Gastroenterology Today - Spring 2017

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Volume 27 No. 1

Spring 2017

Gastroenterology Today In this issue

CITY CENTRE

LOCATION

Sheffield Gastroenterology Symposium

BIGGER

Book Review - Gluten Attack

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Park Row

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Millenium Square

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TRAINING FACILITIES

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At-Bristol Science Centre

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2017 INVESTMENT

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CONTENTS

CONTENTS 5

EDITORS COMMENT

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CLINICAL STUDY I s mild-to-moderate iodine deficiency in pregnancy associated with impaired cognition in offspring?

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MEETING REPORT S heffield gastroenterology symposium

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MEETING REPORT Discover the hidden world of the gut

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BOOK REVIEW G luten Attack

18

NEWS

22

BSG POSTERS

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COMPANY NEWS

COVER STORY Prime Endoscopy Bristol, part of the InHealth Group, is looking forward to welcoming patients to the newly opened, state-of-the-art endoscopy suite on Millenium Parade, Harbourside, Bristol. The new location offers direct to test endoscopy services to patients registered with GP practices in Bristol, North Somerset and South Gloucestershire. The need for a new site was driven by increasing demand on the Westbury on Trym location, where services were previously offered. There is plenty of parking close by plus easy public transport links making this location accessible to all. The new unit will offer not only diagnostic and therapeutic endoscopy but also community gastroenterology clinics. Referrals are triaged on a daily basis so patients may go straight to test or, when more appropriate, (or requested by their GP) may attend a community gastroenterology clinic.

This issue edited by: Dr M Goldman BSc, MBBS, MRCP, FFPM c/o Media Publishing Company Media House 48 High Street SWANLEY, Kent BR8 8BQ ADVERTISING & CIRCULATION: Media Publishing Company Media House, 48 High Street SWANLEY, Kent, BR8 8BQ Tel: 01322 660434 Fax: 01322 666539 E: info@mediapublishingcompany.com www.MediaPublishingCompany.com PUBLISHING DATES: February, June and October. COPYRIGHT: Media Publishing Company Media House 48 High Street SWANLEY, Kent, BR8 8BQ PUBLISHERS STATEMENT: The views and opinions expressed in this issue are not necessarily those of the Publisher, the Editors or Media Publishing Company. Next Issue Summer 2017 Subscription Information – Spring 2017 Gastroenterology Today is a tri-annual publication currently sent free of charge to all senior qualified Gastroenterologists in the United Kingdom. It is also available by subscription to other interested individuals and institutions. UK: Other medical staff - £18.00 inc. postage Non-medical Individuals - £24.00 inc. postage Institutions Libraries Commercial Organisations - £48.00 inc. postage

Prime Endoscopy Bristol is also at the forefront of GP education locally, co-ordinating and organising GP update courses in the field of gastroenterology.

Rest of the World: Individuals - £48.00 inc. postage Institutions Libraries Commercial Organisations - £72.00 inc. postage

Our new location also offers training and conferencing facilities thereby supporting the need to develop a competent workforce into the future and promoting a high quality, effective community endoscopy service within Bristol and the surrounding areas.

We are also able to process your subscriptions via most major credit cards. Please ask for details.

Prime Endoscopy Bristol Harbourside 8 Millenium Parade Bristol BS1 5TY www.primeendoscopybristol.co.uk www.inhealthgroup.com

Cheques should be made payable to MEDIA PUBLISHING. Designed in the UK by Hansell Design

GASTROENTEROLOGY TODAY - SPRING 2017

Since its inception in 2010, Prime Endoscopy Bristol has worked closely with the local health care community to provide a meaningful gastroenterology service which seeks to support clinicians to manage their patients more effectively in primary care. We continue to work closely with local GPs, CCGs and with our DGHs and we are developing innovative and more collaborative ways of working; offering the best patient experience as well as delivering better outcomes and faster treatment; providing clinical input into new pathways of care and supporting the development of clinical guidelines and protocols.

Gastroenterology Today

3


A simple solution to the complex symptoms of IBS-C1,5

Constella® is a first-in-class, once-daily, continuous treatment.1,2 Constella® normalises bowel function, providing sustained relief from the pain, bloating and constipation associated with IBS-C.1,3,4 Constella® is generally well tolerated and has an established safety profile.1 One convenient treatment, multiple symptoms relieved.1,3,4

PRESCRIBING INFORMATION (Please consult the Summary of Product Characteristics (SmPC) before prescribing.) Constella® 290 micrograms hard capsules Linaclotide Active Ingredient: contains 290 micrograms of linaclotide. Indication: Constella is indicated for the symptomatic treatment of moderate to severe irritable bowel syndrome with constipation (IBS-C) in adults. Dosage and Administration: The recommended dose is one capsule (290 micrograms) once daily. The capsule should be taken 30 minutes before a meal. Physicians should periodically assess the need for continued treatment. Consult SmPC for further information. Contraindications, Warnings, etc: Contraindications: Hypersensitivity to linaclotide or to any of the excipients or known or suspected mechanical gastrointestinal obstruction. Warnings & Precautions: Use once a diagnosis of moderate to severe IBS-C is established. Patients should be aware of the possible occurrence of diarrhoea and lower gastrointestinal bleeding during treatment. Should prolonged (more than 1 week) or severe diarrhoea occur and/or lower gastrointestinal bleeding occur during treatment, a medical physician should be contacted and temporary discontinuation of linaclotide until diarrhoea episode is resolved may be considered. Exercise caution in patients prone to a disturbance of water or electrolyte balance such as elderly, patients with CV diseases, diabetes, hypertension; and electrolyte control should be considered. Not recommended in patients with chronic

inflammatory conditions of the intestinal tract, such as Crohn’s disease and ulcerative colitis. Elderly: Special attention should be given to these patients and the treatment benefit-risk ratio should be carefully and periodically assessed. Children: Not recommended. Interactions: The efficacy of medicinal products absorbed in the intestinal tract with a narrow therapeutic index such as levothyroxine and oral contraceptives may be reduced. The use of an additional contraceptive method is recommended. Concomitant treatment with proton pump inhibitors, laxatives or NSAIDs may increase the risk of diarrhoea. Pregnancy and lactation: It is preferable to avoid the use during pregnancy. Use during breast-feeding is not recommended. Animal studies indicate that there is no effect on male or female fertility. Ability to drive and use machines: None known. Adverse Effects: These are ranked under heading of frequency using the following convention: very common (≥ 1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100); rare (≥1/10,000 to <1/1,000); very rare (<1/10,000). Very common: diarrhoea. Common: gastroenteritis viral, abdominal pain, flatulence, abdominal distension, dizziness. Uncommon: faecal incontinence, defecation urgency, lower gastrointestinal haemorrhage including haemorrhoidal haemorrhage and rectal haemorrhage, nausea, vomiting, hypokalaemia, dehydration, decreased appetite, orthostatic hypotension, blood bicarbonate decreased. Consult SmPC in relation to other side-effects. Legal Category: POM Marketing Authorisation Number(s): 28 – EU/1/12/801/002 NHS Cost: (excluding VAT) £37.56 – Carton containing HDPE bottle containing 28 capsules.

UK/0839/2016d – January 2017

Constella® is recommended in the NICE CG61 guidelines5

Marketing Authorisation Holder: Allergan Pharmaceuticals International Limited, Clonshaugh Industrial Estate, Coolock, Dublin 17, Ireland. Further information is available from: Allergan Ltd, Marlow International, The Parkway, Marlow, Buckinghamshire, SL7 1YL, UK. Email: uk_medinfo@allergan.com Tele: 01628 494 026. Date of Revision: 08/06/2016 Item code: UK/0461/2016

Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard Adverse events should also be reported to Allergan Ltd. UK_MedInfo@Allergan.com or 01628 494 026 References: 1. Constella® Summary of Product Characteristics. 2. Sood R, Ford AC. Ther Adv Chronic Dis 2013; 4(6): 268–276. 3. Quigley EM, et al. Aliment Pharmacol Ther 2013; 37(1): 49–61. 4. Chey WD, et al. Am J Gastroenterol 2012; 107: 1702–1712. 5. National Institute of Health and Clinical Excellence. Clinical Guideline 61. Published February 2008. Updated February 2015. Available at: https://www.nice.org.uk/guidance/cg61 [Accessed October 2016].


EDITORS COMMENT

EDITORS COMMENT Antisocial Media

There is absolutely no doubt about the fact that social media has penetrated mankind, and is unlikely to go away until the next best thing comes along. The nature of the next best thing remains a little uncertain, and anyone who heard Professor Sir Mark Walport talk at a recent BSG meeting about the Internet of things will not be surprised when it appears and the changes ensuing. Until then we might contemplate how to make the best of the rest. Some of you may have unintentionally or otherwise found yourselves on the end of the web sites where patient rate and recommend their doctors, and it is well known that human resource specialists are likely to look at Facebook profiles before an interview. My interest comes from the idea that the Internet may be the first place to turn to for medical information, but sorting out real stuff from disinformation has proved a challenge. Because of the impact, we are finding that authors are starting to prefer publishing in an open source on-line journal rather than a traditional paper vehicle. Twitter is now a bigger potential source of news, but recent events following the US presidential ‘election’ have shown that fake news is big news, and we should wait for the denials before accepting news announcements. Another of my interests is the disease-specific conversations that occur between patients. Some of this is scary or enlightening material. A new breed of research is using this type of information to investigate patient outcomes and may be used as a platform for alternatives or adjuncts to classic controlled clinical studies. What makes this kind of work really interesting is the way that functional diseases may be investigated, assembling huge numbers of patients who might not be presenting to secondary care and who might be the heartsinks of primary care. Nevertheless, the comments contained or obtained are real enough and can form a basis for real world evidence. So next time you nearly knock down someone on a road who is engaged primarily with their phone and who magically looks up at the last moment, or a patient fails to respond the instant their name is called, consider the possibility of the sphere of influence they might have, and the evidence that they might be providing to help the world progress to the next best thing. Dr M Goldman BSc, MBBS, MRCP, FFPM, Editor

GASTROENTEROLOGY TODAY - SPRING 2017

“We are finding that authors are starting to prefer publishing in an open source online journal rather than a traditional paper vehicle.”

Being nearer to my demise than my birth has permitted me to become somewhat wedged in a time rut. The world has sped up faster than I can keep pace with it, and one of the races I am losing is social media. Don’t get me wrong: I love technology and gadgets. I was messing with computers, the Internet and flat-screen televisions before many of today’s adults were born. I was programming in Algol68 and punching cards with the best of them. Social media has turned out to be another thing, and my cherry picker is having a harder time finding the right crop. I simply do not want to expose my life so openly.

5


CASE REPORT

Happy with her selfie When the symptoms of Crohn’s disease are already harming her self-esteem, steroid-related side-effects can make things even worse.1 Budenofalk is different - it offers the efficacy of a systemic steroid, but the side-effect level is more like mesalazine.2,3

Now that’s something to smile about.

Eudragit L/S coating modified release formulation meaning the drug is released in the terminal ileum and caecum4

50x

greater receptor affinity than prednisolone meaning a lower effective steroid dose is required5,6

90%

pre-systemic clearance meaning the potential risk of side-effects is limited2

Corticosteroids, the Dr Falk way

GASTROENTEROLOGY TODAY - SPRING 2017

Prescribing Information (Please refer to full SPC before prescribing) Presentation: Budenofalk® gastro-resistant granules, each sachet contains 9mg budesonide, Budenofalk® gastro-resistant capsules, each containing 3mg budesonide. Indications: Induction of remission of mild to moderate active Crohn’s disease affecting the ileum and/ or the ascending colon. Induction of remission of active collagenous colitis. Autoimmune hepatitis (capsules only). Dosage: Adults: For Crohn’s disease and collagenous colitis: one sachet or three capsules daily with liquid half an hour before food, without chewing or crushing, or one capsule three times daily. Limit treatment to 8 weeks, then withdraw gradually. For autoimmune hepatitis: one capsule three times daily. Possibly combine with azathioprine. Maintenance of remission: one capsule twice daily. Revert to 3 capsules daily if transaminases ALAT and/or ASAT elevate again. Treat until remission is achieved or 24 months. Children: Not recommended; safety and efficacy not established. Contra-indications: hypersensitivity to any constituent. Hepatic cirrhosis. Warnings/Precautions: Change from other steroids may result in symptoms due to reduced systemic steroids. Use with caution in patients with tuberculosis, hypertension, diabetes mellitus, osteoporosis, peptic ulcer, glaucoma, cataracts or family history of glaucoma or diabetes or any condition in which glucocorticosteroids may have undesirable effects. Not appropriate for upper GI Crohn’s or extraintestinal symptoms. Long term, high dose use may result in glucocorticosteroid systemic effects. Infection: suppression of the inflammatory response and immune function increases susceptibility to infections and their severity. Clinical presentation of infections may be atypical and presentation of serious infections may be masked. Chickenpox and herpes zoster are of particular concern. Passive immunisation needed within 10 days in exposed non-immune patients taking systemic glucocorticosteroids. Urgent specialist care required on confirmed chickenpox. Give normal immunoglobulin immediately after measles exposure. Do not give live vaccines to those with chronic glucocorticosteroid use. Antibody response to other vaccines may be diminished. With severe liver function disorders: increased systemic bioavailability. Suppression of the HPA axis and reduced stress response: supplementary systemic glucocorticoid treatment may be needed. Avoid concomitant treatment with CYP3A4 inhibitors. Do not use in patients with galactose or fructose intolerance, glucose – galactose malabsorption, sucrase – isomaltase insufficiency or Lapp lactase deficiency or congenital lactase deficiency. In autoimmune hepatitis evaluate transaminase levels every 2 weeks for the first month and then every 3 months. Interactions: Beware concomitant administration of cardiac glycosides and saluretics. CYP3A4 inhibitors: avoid concomitant administration. CYP3A4 inducers: may reduce systemic and local exposure, necessitating dose adjustment of budesonide. CYP3A4 substrates: may compete with budesonide increasing plasma concentrations depending on relative affinities. Small, non-

6

significant effect of cimetidine on budesonide kinetic effects. Oestrogens/oral contraceptives may elevate plasma concentrations and enhance corticosteroid effects. Steroid-binding compounds and antacids may reduce budesonide efficacy; administer at least 2 hours apart. Because adrenal function may be supressed, an ACTH stimulation test for diagnosing pituitary insufficiency might show false results (low values). Use in pregnancy and lactation: Avoid use in pregnancy unless essential. Do not breastfeed during Budenofalk treatment. Undesirable effects: Cushing’s syndrome, growth retardation in children, glaucoma, cataracts, dyspepsia, constipation, gastric or duodenal ulcers, pancreatitis, increase in risk of infections, muscle and joint pain and weakness and twitching, osteoporosis, osteonecrosis, headache, pseudotumor cerebri (including papilloedema) in adolescents, depression, irritability and euphoria, psychomotor hyperactivity, anxiety, aggression, allergic exanthema, petechiae, ecchymosis, contact dermatitis, delayed wound healing, increased risk of thrombosis, vasculitis (after withdrawal from long-term treatment), fatigue, malaise. Side effects characteristic of systemic glucocorticosteroid therapy may occur. Exacerbation or reappearance of extraintestinal manifestations when switching from systemically acting glucocorticosteroids may occur. Frequency is likely to be lower than with equivalent dosage of prednisolone. Legal category: POM. Costs: UK NHS: 60 sachets £135; 100 capsules £75.05. Ireland (PtW): 60 sachets: €152.15; 100 capsules: €78.96. Licence holder: Dr Falk Pharma GmbH, Leinenweberstr.5, D-79108 Freiburg, Germany. Licence numbers: (granules) PL08637/0020 (UK) PA573/2/3 (IE) (capsules) PL08637/0002 (UK) PA573/2/1 (IE). Prepared: October 2016. Further information available on request. Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard (UK residents) or at https://www.hpra.ie/homepage/aboutus/report-an-issue/human-adverse-reaction-form (residents of the Republic of Ireland). Adverse events should also be reported to Dr Falk Pharma UK Ltd. References: 1. McDermott E et al. Inflamm Bowel Dis 2015; 21(2): 353-60. 2. De Cassan C et al. Dig Des 2012; 30(4): 368-75. 3. Bar-Meir S et al. Gastroenterol 1998; 115(4): 835-40. 4. Data on file, Dr Falk Pharma. 5. Möllman HW et al. In: Möllman HW, May B. Glucocortcoid Therapy in Chronic Inflammatory Bowel Disease. Dordrecht: Kluwer 1996. 6. He Y et al. Cell Res 2014; 24(6): 713-26. Date of preparation: January 2017

DrF17/023


CLINICAL STUDY

IS MILD-TO-MODERATE IODINE DEFICIENCY IN PREGNANCY ASSOCIATED WITH IMPAIRED COGNITION IN OFFSPRING? WHAT IS THE IODINE SITUATION IN THE UK? WHAT COULD BE DONE TO IMPROVE UK IODINE STATUS? Michael Quinlan M.A., MSc. Nutritional Medicine (Merit) Statistician & Nutritionist

Introduction; Evidence shows that mild-to-moderate iodine deficiency during pregnancy is correlated with poor childhood cognitive and educational outcomes in offspring (1). The evidence comes mainly from intervention and observational studies (2 - 8). There is a need for suitably powered randomised-controlled trials (RCTs) to strengthen the existing evidence base (9, 10).

Supplementation studies in pregnancy with outcome measures for child cognition; Berbel et. al (2009) (2) divided women into three groups according to stage of pregnancy, in a part of Spain known for mild iodine deficiency. Each group was supplemented with 150 μg iodine. There were limitations to this study (e.g. groups not randomised, small numbers of children tested). Nevertheless the study did find that supplementing with iodine early in pregnancy gave significantly better cognitive outcomes in offspring than when iodine was supplemented later. In another Spanish region with mild iodine deficiency Velasco et al. (2009) (3) compared the cognitive outcomes of children whose mothers were given 230 μg of iodine in the first trimester to those of children whose mums were not given iodine during their pregnancies. IQ scores of children whose mums received iodine supplements were significantly higher than their counterparts. However cognitive testing of offspring was conducted at significantly different stages for both groups (5.47 versus 12.44 months for the no supplement control group). The study’s control group was also not placebo controlled. These factors should be considered when interpreting these results.

Some studies (11 - 13) where iodine has been given in pregnancy as part of a multivitamin/mineral supplement have questioned benefits of supplementation for offspring cognitive outcomes. It is not possible however to relate findings of these studies to effects of iodine only (11 - 13).

Studies have investigated for correlation between thyroid function in pregnancy and cognitive outcomes of offspring (14). However, as thyroid function is dependent on many factors not just iodine, there was a need to investigate specifically for association between poor iodine status during pregnancy and cognition of offspring, particularly in the UK (1). This was done in a 2013 UK (5) study in a group of 1,040 expectant women who had been recruited originally to the Avon Longitudinal Study of Parent and Children (ALSPAC) (5) in the 1990s. The participants were classed as mildly-to-moderate deficient on the basis of a median UIC of 91.1 μg/L. The study found significant association between iodine deficiency in pregnancy and poor cognitive and reading ability of offspring when aged 8 and 9 respectively. The study also showed that cognitive outcomes worsened as iodine status in pregnancy fell. The odds of poor cognitive outcomes increased further when the researchers adjusted their initial findings to account for twenty one possible confounders (e.g. gender of child, age of mum, iron intake). Largely similar findings have been made in various studies in various countries (6, 7, 8). Not surprisingly relative iodine status at baseline in pregnancy is a key factor when comparing these studies. Other factors to consider include the sample sizes used, and whether iodine measurements were adjusted for urinary creatinine concentration. Notwithstanding differences and some limitations in individual studies, correlation between poor iodine status during pregnancy and poor cognitive outcomes in offspring is a common finding now in studies from the UK, Spain, Australia and the Netherlands (5 - 8). Not surprisingly studies of pregnant women with sufficient baseline iodine status do not report similar associations (15).

Iodine situation in the UK Significant iodine deficiency existed in the UK population right up to the 1960s, with goitres common (e.g. “Derbyshire neck”) (16). Deficiency was largely addressed by increasing the iodine levels in milk and also by increasing the consumption of milk (16, 17). There was a lack of statistics on UK iodine population status until as recently as 2011 (18). Results from the National Diet and Nutrition Survey (NDNS) show that in the UK people rely on milk and dairy consumption for iodine intake. However NDNS data indicates a declining trend for iodine intake in recent years (19, 20). The World Health Organisation (WHO) now describe the UK population as being mildly iodine deficient on the basis of a 2011 national study of

GASTROENTEROLOGY TODAY - SPRING 2017

Finally Santiago et al (2013) (4) conducted a study in a region of Spain with significantly higher baseline urinary iodine measures (median iodine concentration (UIC) of 145 μg /L) than areas chosen in the previous Spanish studies above. Women were randomly divided into three groups (n=38 with iodised salt, n=55 with 150 μg iodine and n=38 with 230 μg iodine). The study found no difference in either maternal thyroid function or in offspring cognitive outcomes (measured between 6 and 18 months). Small numbers in each group, higher baseline status of all participants allied to the fact that there was an absence of any control group not getting iodine are limitations in this study.

Observational studies in pregnancy with outcome measures for child cognition;

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CLINICAL STUDY schoolgirls (14-15 years) (21). The median UIC from this survey was 80.1 μg/L confirming mild deficiency (21). Deficiency has also been highlighted in various studies among key population cohorts (especially among expectant women and those of child-bearing age) (1, 5, 22 - 26).

10. Stagnaro-Green, A., Sullivan, S., & Pearce, E. (2012). Iodine Supplementation During Pregnancy and Lactation. JAMA, 308(23), 2463-2464.

The evidence now of UK iodine deficiency (especially during pregnancy) and of the significant correlations between mild-to-moderate iodine deficiency in pregnancy and poor cognitive outcomes highlights a major public health concern (1, 27).

11. Rebagliato, M., et al. (2010). Iodine intake and maternal thyroid function during pregnancy. Epidemiology, 21(1), 62-69.

In conclusion - options to improve iodine status in the UK population

13. Rebagliato, M. et al. (2013). Iodine Supplementation During Pregnancy and Infant Neuropsychological Development: INMA Mother and Child Cohort Study. Am J Epidemiol, 177(9), 944- 953.

12. Murcia, M., et al. (2011). Effect of Iodine Supplementation During Pregnancy on Infant Neurodevelopment at 1 Year of Age. Am J Epidemiol, 173(7), 804812.

Actions that could improve the iodine status in the UK include;

14. Melse-Boonstra, A., & Jaiswal, N. (2010). Iodine deficiency in pregnancy, infancy and childhood and its consequences for brain development. Best Pract Res Clin Endocrinol Metab, 24(1), 29-38.

1. Producing nationally-representative statistics of iodine status among pregnant women. Spot iodine urinary measurements for pregnant women could be included in the NDNS.

15. Ghassabian, A. et al. (2014). Maternal urinary iodine concentration in pregnancy and children’s cognition: results from a population-based birth cohort in an iodine-sufficient area. 477 BMJ Open, doi: 10.1136/ bmjopen-2014-005520.

2. Giving official dietary advice on iodine needs during pregnancy and lactation to pregnant women and women preparing for pregnancy. Education and training should be given to health carers to facilitate this.

16. Phillips, D. I. (1997). Iodine, milk, and the elimination of endemic goitre in Britain: the story of an accidental public health triumph. J Epidemiol Community Health, 51(4), 391-393.

3. Giving UK school girls nutritional advice on iodine and its general importance at various life stages through an innovative national campaign (e.g. use of social media, mobile app.). Others at risk of deficiency could be similarly targeted (e.g. low dairy/ low fish consumers). The concise British Dietetic Association Iodine Food Fact Sheet could be used as input (29). 4. A suitable analysis of the pros and cons of a food iodisation / fortication programme should be conducted by public health makers and timely decisions made based on the outcome of same. Actions here should ensure that the strategy of reducing iodine deficiency is complementary with other major public health goals (e.g. population salt reduction goals) (30, 31).

GASTROENTEROLOGY TODAY - SPRING 2017

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doi:10.1210/jc.2012-4249. 9. Bath, S. C., Jolly, K. B., & Rayman, M. P. (2013a). Iodine supplements during and after pregnancy. 439 JAMA, 309(13), 1345, doi:10.1001/jama.2013.2237.

17. Wenlock, R. W. et al. (1982). Trace nutrients. 4. Iodine in British food. Br J Nutr, 47(3), 381-390. 18. de Benoist, B., McLean, E., Andersson, M., & Rogers, L. (2008). Iodine deficiency in 2007: global progress since 2003. Food Nutr Bull, 29(3), 195202. 19. Henderson, L. et al. (2003). The National Diet & Nutrition Survey: adults aged 19 to 64 years. Volume 3: Vitamin and mineral intake and urinary analytes. London: HMSO. 20. Bates, B. et al. (2014). National Diet and Nutrition Survey, Results from Years 1-4 of the Rolling Programme. www.gov.uk/government/uploads/system/ uploads/attachment_data/file/310995/NDNS_Y1_to_4_UK_report.pdf. 21. Vanderpump, M. P. et al. (2011). Iodine status of UK schoolgirls: a crosssectional survey. Lancet, 377(9782), 2007-2012. 22. Bath, S. C., et al. (2014b). Iodine deficiency in pregnant women living in the South East of the UK: the influence of diet and nutritional supplements on iodine status. Br J Nutr, 111(9), 1622-1631.

References:

23. Rayman, M. P., et al. (2014). Effect of selenium on markers of risk of preeclampsia in UK pregnant women: randomised, controlled pilot trial. Br J Nutr, 112(1), 99-111.

1. Bath SC, Rayman MP. (2015) ‘A review of the iodine status of UK pregnant women and its implications for the offspring’. Environ Geochem Health, Netherlands: 37 (4), pp. 619-629.

24. Furmidge-Owen, V., Bath, S. C., Redman, C. W. G., & Rayman, M. P. (2014). A longitudinal study of iodine status throughout gestation in UK women. Proc Nutr Soc, 73, OCE1 E38.

2. Berbel, P., et al. (2009). Delayed neurobehavioral development in children born to pregnant women with mild hypothyroxinemia during the first month of gestation: the importance of early iodine supplementation. Thyroid, 19(5), 511-519.

25. Barnett, C. et al. (2002). Inadequate iodine intake of 40% of pregnant women from a region in Scotland. J Endocrinol. Invest., 25, (Supp. No. 7) 90, P110.

3. Velasco, I., et al. (2009). Effect of iodine prophylaxis during pregnancy on neurocognitive development of children during the first two years of life. J Clin Endocrinol Metab, 94(9), 3234-3241.

26. Bath, S. C., et al. (2014a). Iodine intake and status of UK women of childbearing age recruited at the University of Surrey in the winter. Br J Nutr, 112(10), 1715-1723. 27. Bath SC, Rayman MP. (2013) ‘Is iodine deficiency during pregnancy a public health concern in the UK?’. Nutrition Bulletin, 38 (4), pp. 400-404.

4. Santiago, P., Velasco, I., et al. (2013). Infant neurocognitive development is independent of the use of iodised salt or iodine supplements given during pregnancy. Br J Nutr, 110(5), 831-839, doi:10.1017/s0007114512005880.

28. Volzke at al. Ensuring Effective Prevention of Iodine Deficiency Disorders. Thyroid. 2016 Feb;26(2):189-96. doi: 10.1089/thy.2015.0543. Epub 2016 Jan 25.

5. Bath SC, Steer CD, Golding J, Emmett P, Rayman MP. (2013) Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC). Lancet., 382(9889):331-7.

29. https://www.bda.uk.com/foodfacts/Iodine.pdf - Written by Dr Sarah Bath, Dietitian and Professor Margaret Rayman, RNut.

6. Costeira, M. J., et al. (2011). Psychomotor Development of Children from an Iodine-Deficient Region. J Pediatr, 159(3), 447-453. 7. van Mil, N. H., Tiemeier, H., et al.(2012). Low Urinary Iodine Excretion during Early Pregnancy Is Associated with Alterations in Executive Functioning in Children. J Nutr. vol. 142 no. 12 2167-2174. 8. Hynes, K. L., et al. (2013a). Mild Iodine Deficiency During Pregnancy Is Associated With Reduced Educational Outcomes in the Offspring: 9-Year Follow-up of the Gestational Iodine Cohort. J Clin Endocrinol Metab,

30. Trieu K. et al. (2015) Salt Reduction Initiatives around the World – A Systematic Review of Progress towards the Global Target. PLoS ONE 10(7): e0130247. doi:10.1371/ journal.pone.0130247. 31. World Health Organization. Salt reduction and iodine fortification strategies in public health: report of a joint technical meeting convened by the World Health Organization and The George Institute for Global Health in collaboration with the International Council for the Control of Iodine Deficiency Disorders Global Network. Sydney, Australia: World Health Organization; 2013 [cited 2014 29 October]. Available: http://apps.who.int/iris/ bitstream/10665/101509/1/9789241506694_eng.pdf?ua=1.


FEATURE

Can ENDOCUFF VISION® improve visualisation, control and the effectiveness of colonoscopy?

Presenting the innovative ENDOCUFF VISION®, a simple to use, disposable device that securely fits* around the colonoscope tip.

*Please refer to the Compatibility Schedule available from Norgine. Norgine and the sail logo are registered trademarks of the Norgine group of companies. ENDOCUFF VISION is a registered trademark of Arc Medical Design Limited. Date of preparation: August 2016. UK/ECV/0416/0004(1).

GASTROENTEROLOGY TODAY - SPRING 2017

To find out more about how ENDOCUFF VISION® can increase the success of your colonoscopies, visit http://hosted.bmj.com/endocuff. Alternatively speak to your local Norgine representative or call 0800 269865 for further information.

9


PROMOTIONAL FEATURE This feature has been created by AbbVie Ltd. AbbVie has had full editorial control of the content.

INFLAMMATORY BOWEL DISEASE BIOLOGICS SERVICES: MEETING DEMAND TODAY AND IN THE FUTURE There are an estimated 620,000 people in the UK that may be

“Patient experience feedback has been positive. Through

living with inflammatory bowel disease (IBD).1 With no known

responsibly increasing and managing care at home, these patients

cause or cure,2 this number will only increase over time.3 IBD

don’t have to come to the clinic for bloods and tests, which frees up

can be managed long-term using biologic medication. With the

clinic time for new patients,” said Andrew.

NHS Shared Planning Guidance 2017-2019 focus on sustainability in local services,4 IBD biologics service providers may now be

Staff and internal resources were also reviewed. As well as securing

considering longer-term, sustainable optimisation over shorter-

additional clinical resource, the practicalities of managing a growing

term capacity gains to meet growing service demands.

service demanded attention. Funding for a biologics coordinator was secured, which transformed clinic administration and enabled consistent

Everyone in an IBD biologics service – consultants, nurses,

high quality service data entry and updates. The increased headcount

commissioners, managers – has an important role to play in

allowed Andrew to become more actively involved in commissioning

safeguarding the sustainability of their service.

and CCG work regarding how pathway changes could deliver long-term value and enhance clinical outcomes.

Considering the advent of new biologics, including biosimilars in IBD, increasing infusion capacity may be considered a solution to capacity

Understanding the pathway, recruiting a biologics coordinator and

constraints. However, only focusing on one area may mean other

making the most of all treatment options and delivery settings has

opportunities to optimise, which deliver long-term sustainability, are missed.

positively impacted how Aintree deliver care.

Andrew Kneebone, Lead IBD Clinical Nurse Specialist at Aintree

“We are tracking the impact of these changes and have seen faster

Hospital’s IBD service describes how a broader approach to optimising

access for patients into the service. Optimising all aspects of the

service capacity helped positively transform the service.

service means we are confident we can sustainably manage our patient numbers for years to come,” said Andrew.

“Aintree is a busy service with daily IBD clinics managing upwards of 300 patients per week. This is three times the number of patients we were managing five years ago. We knew we had to make service changes to meet patient demand in the future. We identified key areas to improve and optimise the patient experience and ensure long-term capacity within our service,” said Andrew. The first step was to review and map the IBD pathway. Interrogating the pathway allowed the team to:

Service Sustainability: Key Areas to Consider • Current service capacity and future demand • Consulting patients and offering choice in care strategies • Opportunities to optimise e.g. medicines and care pathways • Service evaluation via data collection e.g. patient outcomes and spend • Partnerships with colleagues and decision makers at Trust and Clinical Commissioning Group level

• Review what medications were offered and where they were delivered i.e. in hospital (infusion), at home (self-administered subcutaneous) or via shared care with local GPs • Target educational resources and training to deliver maximum impact GASTROENTEROLOGY TODAY - SPRING 2017

10

• Truly understand the patient experience via the active Aintree patient panel “This work enabled us to make key clinical, staffing and patient-centric adaptations to the service,” said Andrew, “Once we understood the variety of reasons for patients missing appointments, clinic times could be changed and treatment offered in the centre and also at home to increase patient choice.” Aintree has also implemented a dedicated at-home treatment service, AbbVie Care, which has been beneficial to both patients and the IBD service. The at-home service provides dedicated nurses who arrange faecal calprotectin tests and check clinical disease activity scores at home, which are then analysed at Aintree. The AbbVie Care nurse works closely with the Aintree team to ensure consistent, high quality care and information sharing. References 1 The IBD Standards Group. Standards for the Healthcare of People who have Inflammatory Bowel Disease. Available at http://www.bsg.org.uk/images/stories/docs/clinical/ibd_standards_13.pdf Accessed December 2016 2 NHS Choices: IBD. Available at: http://www.nhs.uk/conditions/Inflammatory-bowel-disease/Pages/Introduction.aspx Accessed December 2016

“Everyone has a role to play in optimising the service. There are simple areas to review and identify changes that can bring great benefits. We have a responsibility to our patients to make our services as patient-centric as possible and make sure that our services are fit for years to come,” said Andrew.

Useful information sources: • NHS RightCare Initiative • IBD Standards • Five Year Forward View • NHS Shared Planning Guidance

For further information about Humira (adalimumab), AbbVie Care and additional examples of successful optimisation in IBD biologics services, please visit http://hosted.bmj.com/humiraIBD 3 Molodecky, NA. et al. Gastroenterology. 2012;142(1):46-54 4 NHS England Sustainability and Transformation Plans. Available at https://www.england.nhs.uk/ourwork/futurenhs/deliverforward-view/stp/ Accessed December 2016


PROMOTIONAL FEATURE This feature has been created by AbbVie Ltd. AbbVie has had full editorial control of the content. Some patients may not be suitable for Humira. You are strongly advised to read the prescribing information (PI) below. Prescribing Information (PI) Humira (adalimumab) 40 mg solution for injection in pre-filled pen or pre-filled syringe or paediatric vial containing 40 mg solution for injection. Refer to Summary of Product Characteristics (SmPC) for full information. Presentation: Each single dose pre-filled pen (0.4 ml), pre-filled syringe (0.4 ml) or vial (0.8 ml) contains 40 mg of adalimumab. Indications: Rheumatoid arthritis (RA), adults: In combination with methotrexate (MTX) for moderate to severe, active RA with inadequate response to disease-modifying anti-rheumatic drugs (DMARDs) including MTX. In combination with MTX for severe, active and progressive RA when not previously treated with MTX. Can be given as monotherapy if intolerance to or when continued treatment with MTX is inappropriate. Reduces rate of progression of joint damage on X-ray and improves physical function, in combination with MTX. Polyarticular juvenile idiopathic arthritis (pJIA), paediatrics 2 years and above: In combination with MTX, for active pJIA with inadequate response to one or more DMARDs; or monotherapy if intolerance to or when continued treatment with MTX is inappropriate. Enthesitis-related arthritis (ERA), paediatrics 6 years and above: For active ERA with inadequate response or intolerance to conventional therapy. Ankylosing spondylitis (AS), adults: For severe active AS with inadequate response to conventional therapy. Axial spondyloarthritis without radiographic evidence of AS (nraxSpA), adults: For severe nr-axSpA with objective signs of inflammation (elevated CRP and/or MRI), and an inadequate response to or intolerance to nonsteroidal anti-inflammatory drugs (NSAIDs). Psoriatic arthritis (PsA), adults: For active and progressive PsA with inadequate response to DMARDs. Reduces rate of progression of peripheral joint damage on X-ray in polyarticular symmetrical subtypes of the disease and improves physical function. Psoriasis, adults: For moderate to severe chronic plaque psoriasis who are candidates for systemic therapy. Psoriasis, paediatrics 4 years and above: For severe chronic plaque psoriasis with inadequate response, or if topical therapy and phototherapies are inappropriate. Hidradenitis suppurativa (HS), adults and adolescents from 12 years of age: For active moderate to severe hidradenitis suppurativa (acne inversa) in patients with an inadequate response to conventional systemic HS therapy. Crohn’s disease (CD), adults: For moderately to severely active CD with inadequate response, contraindication or intolerance to corticosteroid and/or an immunosuppressant therapy. Crohn’s disease (CD), paediatrics 6 years and above: For moderately to severely active CD with inadequate response, contraindication or intolerance to conventional therapy including primary nutrition therapy and a corticosteroid, and/or an immunomodulator. Ulcerative colitis (UC), adults: For moderately to severely active UC with inadequate response, contraindication or intolerance to conventional therapy including corticosteroids and 6-mercaptopurine (6-MP) or azathioprine (AZA). Uveitis, adults: For the treatment of non-infectious intermediate, posterior and panuveitis in adult patients who have had an inadequate response to corticosteroids, in patients in need of corticosteroid-sparing, or in whom corticosteroid treatment is inappropriate.

Contraindications: Active tuberculosis (TB), severe infections (e.g. sepsis), and opportunistic infections; moderate to severe heart failure (NYHA class III/ IV); hypersensitivity to adalimumab or any excipients. Warnings and precautions: Clearly record trade name and batch number of administered product to improve traceability of biological products. Infections: Patients are more susceptible to serious infections especially if impaired lung function. Monitor for infections, including TB, before, during and for 4 months after treatment. Do not initiate treatment with an active infection, until it is controlled. Consider risk/benefit prior to treatment in patients exposed to high risk of TB or endemic mycoses. Evaluate new infections during treatment and monitor closely. Stop treatment if new serious infection or sepsis, and treat appropriately. Exercise caution in patients with a history of recurring infections or who are predisposed to infections. Serious infections: Serious infections, including those with hospitalisation or death, reported in patients receiving treatment. TB: Consult SmPC for details. Reactivation and new onset TB, both pulmonary and extrapulmonary (disseminated) reported. Screen all patients before therapy initiation for active or latent TB. If latent TB suspected, consult physician with appropriate expertise and follow local treatment recommendations for prophylaxis prior to initiation of Humira. Despite prophylaxis, TB reactivation has occurred on Humira. If active TB is diagnosed, do not initiate treatment. Other opportunistic infections: Opportunistic infections observed in patients receiving Humira. Stop treatment in patients with signs and symptoms of such infections. Consult with physician with appropriate expertise for diagnosis and administration of empiric antifungal therapy in these patients. Hepatitis B reactivation: Reactivation has occurred in chronic carriers (surface antigen positive) tested for HBV infection before initiating treatment. HBV carriers should consult a specialist physician and be closely monitored for reactivation of HBV infection throughout therapy and for several months following termination of treatment. If reactivation occurs stop treatment and initiate appropriate anti-viral and supportive treatment. Neurological events: Caution in patients with pre-existing or recent-onset central or peripheral nervous system demyelinating disorders.

Rare association with new onset or exacerbation of symptoms and/or radiographic evidence of central and peripheral demyelinating disease. Discontinuation of treatment should be considered if any of these disorders develop. Neurologic evaluation should be performed in patients with noninfectious intermediate uveitis prior to initiation of treatment and regularly during treatment, to assess for existing or developing central demyelinating disorders. Allergic reactions: Reports of serious allergic reactions including anaphylaxis received. For serious allergic or anaphylactic reaction stop Humira immediately and initiate appropriate therapy. Malignancies and lymphoproliferative disorders: A possible risk of malignancy, including lymphomas and leukaemia, in all patients, including paediatric patients, treated with TNF antagonists. Examine all patients, especially those with a medical history of extensive immunosuppressant or PUVA treatment, for non-melanoma skin cancer prior to and during treatment; caution in COPD patients, and in patients with increased risk for malignancy due to heavy smoking. Consider the potential risk with the combination of AZA or 6-MP and Humira (hepatosplenic T-cell lymphoma has occurred). Risk of hepatosplenic T-cell lymphoma cannot be excluded. Caution in patients with a history of malignancy. Risk of developing dysplasia or colon cancer is unknown. Patients with UC, history of dysplasia or colon carcinoma to be screened for dysplasia before and during treatment. Haematologic reactions: Adverse events of the haematologic system reported with Humira. Patients should seek immediate medical attention if signs and symptoms of blood dyscrasias. Vaccinations: Patients may receive concurrent vaccinations, except for live vaccines. Bring paediatric patients up to date with all immunisations prior to Humira treatment. Congestive heart failure: See contraindications. Caution is advised with mild heart failure (NYHA class I/II). Discontinue treatment for new or worsening symptoms of congestive heart failure. Autoimmune processes: Autoimmune antibodies may form. Stop treatment if development of a lupus-like syndrome with positive antibodies against double-stranded DNA. Surgery: Consider the long half-life of Humira for planned surgical procedures. Monitor for infections. Small bowel obstruction: Failure to respond to treatment for CD may indicate the presence of fixed fibrotic stricture requiring surgical treatment. Elderly patients: Serious infections were higher in patients over 65 years of age, some of whom had a fatal outcome. Consider risk of infections. Interactions: Combination of adalimumab with other biologic DMARDs (e.g. anakinra and abatacept) or other TNF-antagonists is not recommended. Fertility, pregnancy and lactation: Not recommended during pregnancy. Women of childbearing age to use adequate contraception, and continue its use for at least 5 months after the last treatment. Women must not breast feed for at least 5 months after the last treatment. Side effects: Very common ≥ 1/10: Infections, leucopaenia, anaemia, lipids increased, headache, abdominal pain, nausea and vomiting, elevated liver enzymes, rash (including exfoliative rash), musculoskeletal pain, injection site reaction. Common ≥ 1/100 to < 1/10: skin cancer excluding melanoma (including basal cell carcinoma and squamous cell carcinoma), benign neoplasm, leucocytosis, thrombocytopaenia, hypersensitivity, allergies (including seasonal allergy), hypokalaemia, uric acid increased, blood sodium abnormal, hypocalcaemia, hyperglycaemia, hypophosphatemia, dehydration, mood alterations (including depression), anxiety, insomnia, paraesthesias, migraine, nerve root compression, visual impairment, conjunctivitis, blepharitis, eye swelling, vertigo, tachycardia, hypertension, flushing, haematoma, asthma, dyspnoea, cough, GI haemorrhage, dyspepsia, gastroesophageal reflux disease, sicca syndrome, worsening or new onset of psoriasis (including palmoplantar pustular psoriasis), urticaria, bruising (including purpura), dermatitis (including eczema), onychoclasis, hyperhidrosis, alopecia, pruritus, muscle spasms (including blood creatine phosphokinase increased), renal impairment, haematuria, chest pain, oedema, pyrexia, coagulation and bleeding disorders, autoantibody test positive, blood lactate dehydrogenase increased, impaired healing. Serious, including fatal, side effects have been reported including infections/sepsis, intestinal perforation, opportunistic infections, TB, endemic mycoses, demyelinating disease, malignancies including lymphoma, (including hepatosplenic T-cell lymphoma), leukaemia and skin cancer (including melanoma and Merkel cell carcinoma), cytopenias, worsening heart failure, myocardial infarction, pulmonary embolism, pleural effusion, pulmonary fibrosis, cerebrovascular accident, interstitial lung disease, Stevens-Johnson syndrome, angioedema, anaphylaxis, sarcoidosis, hepatitis, liver failure and worsening of symptoms of dermatomyositis. Other less common and rarely reported side effects are listed in the SmPC. Basic NHS price: £704.28 (for 2 pens or 2 syringes or 2 vials). Legal category: POM. Marketing Authorisation numbers: EU/1/03/256/001, EU/1/03/256/013, EU/1/03/256/017. Further information: available from AbbVie Ltd., Maidenhead, SL6 4UB, United Kingdom. Date of revision of PI: December 2016, PI/Humira(combined)/37.

GASTROENTEROLOGY TODAY - SPRING 2017

Dosage and administration: A specialist physician experienced in diagnosis and treatment of the indicated condition, to initiate and supervise treatment. Provide patients with special alert card. Patients may self-inject after proper injection training, with physician approval and appropriate medical follow-up. Optimise other concomitant therapies. RA, adults: 40 mg dose every other week. Concomitant MTX should be continued. During monotherapy, patients may require 40 mg each week if they have experienced a decrease in clinical response. Treatment beyond 12 weeks should be reconsidered if no clinical response in that time. Consider need for dose interruption, e.g. before surgery or if serious infection occurs. Reintroduction after 70 day dose interruption gave same magnitudes of clinical response and similar safety profile as before dose interruption. pJIA, paediatrics 2 years and above: Treatment beyond 12 weeks reconsidered if no clinical response in that time. pJIA, paediatrics 2-<4 years: 24 mg/m² body surface area up to 20 mg maximum single dose every other week (see vial SmPC for height/weight dosing chart). pJIA, paediatrics 4-12 years: 24 mg/m² body surface area up to 40 mg maximum single dose every other week (see vial SmPC for height/weight dosing chart). pJIA, paediatrics 13 years and above: 40 mg every other week regardless of body surface area. ERA, paediatrics 6 years and above: 24 mg/m² body surface area up to 40 mg maximum single dose every other week (see SmPC for height/weight dosing chart). AS, nraxSpA and PsA, adults: 40 mg every other week. Treatment beyond 12 weeks should be reconsidered if no clinical response in that time. Psoriasis, adults: 80 mg induction dose at week 0, 40 mg every other week from week 1. Treatment beyond 16 weeks should be reconsidered if no clinical response in that time. Beyond 16 weeks, patients with inadequate response can increase dosing frequency to 40 mg every week. If adequate response is achieved with an increased dosing frequency, the dose may subsequently be reduced to 40 mg every other week. If there is inadequate response to the increased frequency, carefully reconsider treatment. Psoriasis, paediatrics 4 years and above: 0.8 mg/kg body weight (maximum 40 mg/dose) weekly for the first 2 doses then every other week (see vial SmPC for weight dosing chart). Treatment beyond 16 weeks should be reconsidered if no response in that time. HS, adults: 160 mg initially at Day 1 (given as four 40 mg injections in one day or as two 40 mg injections per day for two consecutive days),

followed by 80 mg two weeks later at Day 15 (given as two 40 mg injections in one day). Two weeks later (Day 29) continue with a dose of 40 mg every week. Antibiotics may be continued if necessary. Concomitant topical antiseptic wash on HS lesions should be used on a daily basis. Treatment beyond 12 weeks should be reconsidered in a patient with no improvement in that time. Reintroduction after interruption: 40 mg every week. Evaluate periodically the benefit and risk of continued long-term treatment. HS, adolescents from 12 years of age weighing at least 30 kg: 80 mg initially at week 0 (given as two 40 mg injections on day one). 40 mg injection in week 1 followed by 40 mg every other week. In adolescent patients with inadequate response to Humira 40 mg every other week an increase in dosing frequency to 40 mg every week may be considered. Antibiotics may be continued if necessary. Concomitant topical antiseptic wash on HS lesions should be used on a daily basis. If no improvement after 12 weeks refer to SmPC for guidance. CD, adults: Induction: 80 mg Week 0 and 40 mg at Week 2. For a more rapid response: 160 mg at Week 0 (either as 4 injections in 1 day or 2 injections/day for 2 consecutive days) and 80 mg at Week 2; risk of adverse events higher during induction. Maintenance: 40 mg every other week. If decrease in clinical response, can increase dose to 40 mg weekly. Corticosteroids may be tapered in maintenance phase in accordance with clinical guidelines. Patients with no response by Week 4 may benefit from continued therapy to Week 12. Treatment beyond 12 weeks should be reconsidered if no clinical response in that time. CD, paediatrics 6 years and above < 40 kg: Induction: 40 mg Week 0, 20 mg at Week 2. For a more rapid response: 80 mg Week 0 (2 injections in 1 day), 40 mg at Week 2; risk of adverse events higher during induction. Maintenance: 20 mg every other week. If insufficient response, consider 20 mg every week. Treatment beyond 12 weeks should be reconsidered if no clinical response in that time. CD, paediatrics 6 years and above ≥ 40 kg: Induction: 80 mg Week 0, 40 mg at Week 2. For a more rapid response: 160 mg at Week 0 (4 injections in 1 day or 2 injections/day for 2 consecutive days), 80 mg at Week 2; risk of adverse events higher during induction. Maintenance: 40 mg every other week. If insufficient response, consider 40 mg every week. Treatment beyond 12 weeks should be reconsidered if no clinical response in that time. UC, adults: Induction: 160 mg at Week 0 (as 4 injections in 1 day or 2 injections/ day for 2 consecutive days) and 80 mg at Week 2. Maintenance: 40 mg every other week. During maintenance, corticosteroids may be tapered in accordance with clinical guidelines. If insufficient response, consider 40 mg every week. Treatment beyond 8 weeks should be reconsidered if no clinical response in that time. Uveitis, adults: 80mg induction dose at week 0, maintenance dose; 40 mg every other week starting at week 1. Treatment can be initiated in combination with corticosteroids and/or with other nonbiologic immunomodulatory agents. Concomitant corticosteroids may be tapered in accordance with clinical practice starting two weeks after initiating treatment with Humira.

Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard. Adverse events should also be reported to AbbVie on ukadverseevents@abbvie.com Date of preparation: January 2017 Job code: AXHUM162017

11


MEETING REPORT

SHEFFIELD GASTROENTEROLOGY SYMPOSIUM Dr Sabina Beg (BSc MBBS MRCP) Endoscopy Research fellow, Nottingham University Hospitals, Meeting held on 23rd September 2016 The Sheffield Gastroenterology Symposium is an annual

technique of Per Oral Endoscopic Myotomy (POEM) were critically

meeting designed to provide an update on a range of

analysed. The topic then changed to bleeding lesions with a review

topics, as well as give a glimpse at future developments in

of the endoscopic techniques for managing variceal hemorrhage and

gastroenterology. Now in its 8th year, this event attracts over

vascular lesions of the gastrointestinal tract. An inflammatory bowel

300 delegates including allied health professionals, nurses,

disease perspective was given with a guide to tailoring and optimising

trainees and consultants. This event is hosted within the grand ballroom of the historic grade II listed Royal Victoria hotel. The central location, with free parking, lends it self to easy access for the delegates and faculty who travel from throughout the UK. Due to generous support from industry sponsors, the symposium remains free to attend. The morning kicked off with a selection of talks on endoscopic therapy.

therapy with anti-TNF and biosimilars. A personal highlight of this meeting was the Bardhan State of the Art lecture. This award is reserved for individuals who have made a significant contribution to the understanding and management of gastrointestinal disease, with previous awardees including Professor Paul Swain and Professor Matthias Lohr. This year’s address was given by Professor Robin Spiller from the NIHR Biomedical Research Unit of the University of Nottingham. The 30-minute lecture was a

This included a review of the evidence upon which the diagnosis

whistle stop tour of a career devoted to the understanding of the

and management of achalasia is based. The results ScheBo_GastroToday_Jan_2017 12/01/2017 17:18of the emerging

pathophysiology of functional gut disorders. This included novel work on magnetic resonance imaging of small bowel motility and water in both health and disease. This wealth of work convincingly demonstrated the altered response of the small bowel to a variety of foodstuffs and the relationship with symptoms in irritable bowel syndrome. Lunch was followed by a session focusing on colorectal disease. With first a review of the various methods that can be used to increase a colonoscopists’ adenoma detection rate to achieve improved patient outcomes. These ranged from optimising technique with patient positioning, to a range of gadgets that can be used as adjuncts to the endoscope to improve mucosal views. A radiography perspective was then provided, with a discussion on the pros and cons of the increasing use of CT colonography. The audience was then asked to take a leap into the future when the novel potential future modality of

GASTROENTEROLOGY TODAY - SPRING 2017

virtual reality colonoscopy was demonstrated. This innovation provided a radically different view of the colon with the operator travelling within the colonic lumen in search of polyps. The viewer was able to appreciate the topography of the reconstructed bowel, although for some this process resulted in a dose of motion sickness! The day was completed with a session devoted to hepatology, which included a thorough examination of the hepatobiliary manifestations of gastrointestinal disease to the case studies of the management of acute liver diseases. This day was a comprehensive update of both general and esoteric topics. In addition to the high quality talks there was a welcoming atmosphere, with the opportunity to rub shoulders with experts. The Sheffield Gastroenterology Symposium is highly recommended for anyone with an interest in innovation within gastroenterology.

12


OCTASA 400mg Modified Release Tablets (mesalazine) and OCTASA 800mg Modified Release Tablets (mesalazine) - Prescribing Information

Adverse events should be reported. Reporting forms and information can be found at https://yellowcard.mhra.gov.uk. Adverse events should also be reported to Tillotts Pharma UK Ltd. (address as above) Tel: 01522 813500. References 1. Data on file, Tillotts Pharma UK Limited. [Price change – withdrawal from PPRS]. 2. MIMS. Accessed online, December 2016. UK/OC/0017/1116a. Date of preparation: December 2016.

You can maintain MORE patients with Octasa® for the same cost as Asacol®* 1 , 2 ●

For £50,000, you can maintain 54 more patients at 2.4g/day for a year with Octasa® 400mg than with Asacol® 400mg*†1,2

123

Asacol® 400mg2

Octasa® 400mg1

69

Small changes add up to modified modified release release mesalazine mesalazine and 800mg For mild to moderate ulcerative colitis BIG savings 400mg

GASTROENTEROLOGY TODAY - SPRING 2017

Presentation: Modified Release tablets containing 400mg mesalazine or 800mg mesalazine. Indications: Ulcerative Colitis - Treatment of mild to moderate acute exacerbations. Maintenance of remission. Crohn’s ileocolitis - Maintenance of remission. Dosage and administration: 400mg tablets – Adults: Mild acute disease: 6 tablets (2.4g) once daily or in divided doses, with concomitant steroid therapy where indicated. Moderate acute disease: 6 to 12 tablets (2.4g – 4.8g) daily. 2.4g may be taken once daily or in divided doses, higher doses should be taken in divided doses. Maintenance therapy: 3 to 6 tablets (1.2g – 2.4g) once daily or in divided doses. 800mg tablets - Adults: Mild acute disease: 3 tablets (2.4g) once daily or in divided doses with concomitant steroid therapy where indicated. Moderate acute disease: 3 to 6 tablets (2.4g – 4.8g) daily. 2.4g may be taken once daily, higher doses should be taken in divided doses. Maintenance therapy: 2 to 3 tablets (1.6g - 2.4g) once daily or in divided doses. 400mg and 800mg tablets – No more than 2.4g should be taken at one time. Tablets must be swallowed whole. Elderly: Normal adult dose may be used unless liver or renal function is severely impaired. Children: Limited documentation of efficacy in children >6 years old. Dose to be determined individually. Generally recommended that half the adult dose may be given to children up to a body weight of 40 kg; and the normal adult dose to those above 40 kg. Contra-indications: Hypersensitivity to salicylates, mesalazine or any of the excipients, severe impairment of hepatic or renal function (GFR less than 30 ml/min). Warnings and Precautions: Urinary status (dip sticks) should be determined prior to and during treatment, at discretion of treating physician. Caution in patients with raised serum creatinine or proteinuria. Stop treatment immediately if renal impairment is evident. Haematological investigations are recommended prior to and during treatment, at discretion of treating physician. Stop treatment immediately if blood dyscrasias are suspected or evident. Caution in patients with impaired hepatic function. Liver function should be determined prior to and during treatment, at the discretion of the treating physician. Do not use in patients with previous mesalazineinduced cardiac hypersensitivity and use caution in patients with previous myo- or pericarditis of allergic background. Monitor patients with pulmonary disease, in particular asthma, very carefully. In patients with a history of adverse drug reactions to sulphasalazine, discontinue immediately if acute intolerance reactions occur (e.g. abdominal cramps, acute abdominal pain, fever, severe headache and rash). Use with caution in patients with gastric or duodenal ulcers. Intact tablets in the stool may be largely empty shells. If this occurs repeatedly patients should consult their physician. Use with caution in the elderly subject to patients having normal or non-severely impaired renal and liver function. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption, should not take this medicine. Interactions: No interaction studies have been performed. May decrease the anticoagulant activity of warfarin. May increase the myelosuppressive effects of azathioprine, 6-mercaptopurine or thioguanine. Monitoring of blood cell counts is recommended if these are used concomitantly. Fertility, pregnancy and lactation: Only to be used during pregnancy and lactation when the potential benefit outweighs the possible risk. No effects on fertility have been observed. Adverse reactions: Common: dyspepsia, rash. Uncommon: eosinophilia (as part of an allergic reaction), urticaria, chest pain. Rare: myocarditis, pericarditis. Very rare: altered blood counts (aplastic anemia, granulocytosis, pancytopenia, neutropenia, leucopenia, thrombocytopenia), hypersensitivity reactions (such as allergic exanthema, drug fever, lupus erythematosus syndrome, pancolitis), peripheral neuropathy, allergic and fibrotic lung reactions (including dyspnoea, cough, bronchospasm, alveolitis, pulmonary eosinophilia, lung infiltration, pneumonitis), interstitial pneumonia, eosinophilic pneumonia, lung disorder, acute pancreatitis, changes in liver function parameters (increase in transaminases and cholestasis parameters), hepatitis, cholestatic hepatitis, impairment of renal function including acute and chronic interstitial nephritis and renal insufficiency, renal failure which may be reversible on withdrawal, nephrotic syndrome, oligospermia (reversible). Not known: lupuslike syndrome with pericarditis and pleuropericarditis as prominent symptoms as well as rash and arthralgia. Consult the Summary of Product Characteristics in relation to other adverse reactions. Marketing Authorisation Numbers, Package Quantities and basic NHS price: 400mg PL36633/0002; packs of 90 tablets (£16.58) and 120 tablets (£22.10). 800mg - PL36633/0001; packs of 90 tablets (£40.38) and 180 tablets (£80.75). Legal category: POM. Marketing Authorisation Holder: Tillotts Pharma UK Ltd, The Larbourne Suite, The Stables, Wellingore Hall, Wellingore, Lincolnshire, LN5 0HX, UK. Octasa is a trademark. ©2010 Tillotts Pharma UK Ltd. Further Information is available from the Marketing Authorisation Holder. Date of preparation of API: January 2017

For mild to moderate ulcerative colitis

* Using the same daily maintenance dose of 2.4g/day for a year. † Rounded down to the nearest whole patient. There are no clinical comparisons of Octasa® 400mg and 800mg vs Asacol® 400mg and 800mg. SmPCs may differ; consult individual SmPCs before prescribing.

13


MEETING REPORT

DISCOVER THE HIDDEN WORLD OF THE GUT How nutritional management of infant gut health can help intestinal disorders, feeding problems and parental anxiety

between natural birth – where the baby’s head passes through the

Infant feeding problems are one of the most common reasons why parents turn to primary care for help.

explaining that a course of antibiotics wipes out huge numbers of

About 50% of infants will suffer a feeding problem in the first few months of life. The vast majority of visits by desperate parents of newborn babies to health care professionals (HCPs) are to seek advice on a problem that relates to a functional gastro-intestinal disorder (FGID). Some 30% of infants will experience reflux or regurgitation - when a baby visibly brings up milk during or after feeding - 20% colic and 15% constipation. What many HCPs often fail to identify is which of these problems is causing the discomfort and how they can best support parents. Moreover, it’s only recently that studies have shown that early-life gut development - during the first 1,000 days of pregnancy and life - plays an important role in a person’s genetic and biological make up. This has a huge impact on the health and wellbeing of the baby and is linked inextricably with the health and wellbeing of the family, child development, parental welfare and children safeguarding problems. This complex world of the developing infant gut was the subject of a series of presentations by leading experts in paediatric gastroenterology, epigenetics and gut microbiology at Nutricia Early Life Nutrition’s recent ‘Discover the hidden world of the gut…’ event at the At-Bristol Science Centre. Professor Tim Spector - Professor of Genetic Epidemiology, Kings College London; Director of Twins UK Registry & Project Lead, British Gut Project; author, Identically Different & The Diet Myth – ‘The hidden ecosystem inside of you’ GASTROENTEROLOGY TODAY - SPRING 2017

14

birth canal, exposing the baby to a mix of fertilisers for microbes - and caesarean section, whereby these microbes are different.” Professor Spector warned against the use of antibiotics in child health, microbes: “By three years old an average baby in the UK has had more than two courses of antibiotics, most of them unnecessary. Some children have 10 courses in a row. They’re like a nuclear bomb to the gut, studies have shown this is potentially linked to obesity and allergies later in life.” Dr Nikhil Thapar – Academic Lead for Gastroenterology, University College London’s Institute of Child Health; Honorary Consultant, Great Ormond Street Hospital – ‘Gut health, development and well-being in the first 1000 days’ Dr Nikhil Thapar stressed the focus should be on the first 1,000 days of pregnancy and life, from conception through to toddler, during which time babies need to have balanced nutrition from the womb. The consequences of this are far reaching for the infant. As an example, he highlighted research showing that infants are 10 times more likely to overcome most life threatening childhood diseases with a balanced microbiome. “Focus on nutrition in the first 1,000 days and you’ll end up with children who are generally healthier, suffer less infections, do better in school and grow up with healthier families,” Dr Thapar said. He added that researchers are now exploring whether they can programme the gut earlier in life: “We understand now that there’s a cross talk between immune cells, between the microbiome, between the nerves in the gut and between the brain itself.” Dr Thapar said children who have functional GI disorders are generally unhappy and the condition is linked with learning disabilities in infants: “There are new studies that suggest it might influence the central nervous system, resulting in conditions such as autism. So all this is

Professor Tim Spector discussed the diverse genetic components that

influenced by the microbiome, nerves and muscles in the gut.”

make up each individual’s gut microbiome. His study of gut microbes has shown that calorie controlled diets are largely based on popular

Dr Thomas Ludwig – Principle Scientist of Paediatric

myths, often around lifestyle and cultural issues.

Gastroenterology, Danone Nutricia Research – ‘Functional gastrointestinal disorders in infancy – what’s the impact?’

“What do microbes do? They produce enzymes and chemicals to breakdown food and extract nutrients,” he said. “They produce a quarter

The nutritional management of FGIDs was discussed by Dr Thomas

of our vitamins and brain chemicals, like Serotonin, essential to our

Ludwig, who explained that the vast majority (80%) of 1,000 mothers

wellbeing. Everyone needs a diverse microbiome to keep the immune

who went to see their HCP after birth visited for GI disorders, and

system in check.”

symptoms of colic accounted for 70% of visits.

Professor Spector added that many problems that develop later in life,

To help distressed parents, paediatricians often prescribe popular FGID

such as obesity, can be determined from birth: “The first three years

remedies, but many of these “do more harm than good”, according to

is essential for the development of the gut. There is a big difference

Dr Ludwig.


MEETING REPORT “The conclusion is that during 2014-15, 3.5 million packs of these remedies went in to 800,000 children,” he said. “The defoaming agent (simeticone), lactase droplets and gripe water, have been found to be not only inefficient, but also frequently there is no basic safety or tolerance data or randomised trials for these popular remedies.”

University Hospitals NHS Trust – ‘Managing GOR and GORD – primary. secondary and tertiary care’

This alarming conclusion shows just how desperate parents are to treat their infant’s discomfort and their own stress and anxiety.

He explained how essential it is for HCPs to identify the crucial distinction between gastro-oesophageal reflux (GOR) and gastrooesophageal reflux disease (GORD). He considers this to be the difference between resolving problems with relatively simple primary treatment and urgent surgery.

“But this is just the tip of the iceberg,” he added. “Parents largely try to do things themselves as well. In 2001, the cost to the NHS of infant crying and sleeping problems in the first 12 weeks of life cost £65 million a year. “These remedies often increase feeding difficulties and there is then a sustained impact on the family. The result is behavioural disorders, parental stress, anxiety, depression.” More worrying still, Dr Ludwig said that the quality of life for such a family remains low years later: “So FGIDs have a long lasting effect on the infant and the family.

The importance of understanding the FGIDs was highlighted in Mr Shailinder Singh’s presentation.

Mr Singh admitted it is difficult in clinical practice to differentiate between GOR and GORD, especially as the terms are used interchangeably by most HCPs. To help the audience understand the difference, he presented statistics: GOR is very common, affecting 40% of infants, usually starting at about eight weeks old. Some 90% of affected infants are younger than one year old, and in the majority of cases no further investigation or treatment is necessary. GORD, meanwhile, is much more serious.

“Basically the gut is the gatekeeper to the entire organism. Gut health is such a holistic and integrated concept that it includes wellbeing and parental bonding.” This latter point is hugely important, he said. Research has pointed to a direct correlation between FGIDs and parental depression and even violence towards the baby, most commonly resulting in ‘shaken baby syndrome’.” Mr Shailinder Singh – Consultant Paediatric Surgeon, Nottingham

“GORD, is when the person or child has GOR, but the symptoms are becoming distressed,” he said. “That is what needs treatment. This is very important. If you suddenly see someone at eight months of age start projectile vomiting or vomiting something green, don’t put it down to GOR.” Mr Singh said the warning signals are always associated with projectile vomiting: “Any child who vomits green has got twisted gut. You lose your entire small gut and part of your intestine within seven to eight hours. If any child is vomiting green refer immediately to the surgical unit.”

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15


MEETING REPORT Peter Richards – Implementation Manager for ‘Coping with Crying’, NSPCC – ‘Supporting parents with crying’

Who Needs That Valuable Clinic Space?

All these FGIDs cause a host of social and familial problems for the baby and parents, which Peter Richards addressed in the final session. Mr Richards said there are no evidence-based services in the UK to support parents to help manage a crying infant. Consequently, the NSPCC has developed the “Coping with Crying” programme to raise awareness and to help parents improve their understanding about

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crying and the dangers of shaking babies. “Regardless of the reason, babies do cry,” he said. “Excessive crying can be for up to eight hours a day. So parents will be exhausted and frustrated, they won’t know why the baby is crying. The result can often have a long-term impact on the parent-child attachment or even worse.” He listed some of these worse case scenarios associated with parents dealing with excessive crying:

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substantial number are three months or younger • Seven times the risk of child death from homicide – risk greatest in first three months • Double the risk of having a child protection plan for neglect. The number of babies estimated to be seriously hurt or killed annually based on the birth rate of 800,000 is 200. Some 25% of these infants will die and 40% will have a learning disability as a result of shaking. Mr Richards warned that research had found a number of these cases

(Subject to availability, Terms and Conditions)

third were not deemed to be risk factors. He concluded: “So this means

As a result, he urged that support is vital: “What’s clear from studies is that parents need emotional support, and support for the practical side of crying.”

Email: marketing@alphalabs.co.uk

Mr Richards concluded his presentation with a film that showed parents explaining how they struggled to cope with infant crying and, in some instances, babies were shaken to such a degree they suffered later

GASTROENTEROLOGY TODAY - SPRING 2017

disabilities - or worse. The film is shown to parents by HCPs and midwives in children’s centres and parents are then encouraged to discuss it afterwards. “We tested delivery of this with 58 health services all over the UK and 57,000 parents had seen the film,” Mr Richards said. “All parents remembered watching the film and it had a very positive impact on each of the settings. “We measured changes in the knowledge and behaviour of those who had viewed it, compared with those who hadn’t. As a result, we

Tel: +44 (0)23 8048 3000 | Web: www.calprotectin.co.uk

saw improvement in knowledge and parents were more likely to feel confident with coping strategies and asking for help. These were very encouraging findings.”

16 Gastro-Today_Half-Ad_Feb17.indd 1

17/01/2017 10:15:57


BOOK REVIEW

GLUTEN ATTACK by David Sanders Paperback: 208 pages Publisher: Vermilion (7 April 2016) ISBN10: 1785040162 ISBN-13: 978-1785040160 I would not normally read and find value in self-help health

Not all gluten sensitivity appears to be coeliac disease, and there are

books. There are so many of them that seek to reinforce the

thought provoking discussions on the relationship between gluten

opinions of the fringe thinkers. I read all of the text in this

and irritable bowel, and also the possible role for gluten sensitivity

intriguing monograph (except for the recipes at the end), and

in inflammatory bowel disease, all supported by scientific literature

felt that I had come out of this knowing much more about some

references. Another interesting excursion in the book is into the world

of the current thinking, and, based on the evidence, with a more

of FODMAPS. It seems that in parallel to the industrialisation of gluten,

open mind on the subject.

there are changes in the western diet that have increased the proportion of fermentable saccharides and polyols, especially fructose, which are

David Sanders, as you many know is Professor of Gastroenterology

fermentable in the gut and also have osmotic properties. In some, it is

at Sheffield. He is the current Chair of the Coeliac UK Health Advisory

thought, these may be the aetiology of gut symptoms in irritable bowel

Council and the elected President of the International Society for the

patients.

Study of Coeliac Disease (ISSCD). I was pleased to be able to review this book because there seemed to be no other person in the country

Alongside the science of provable food sensitivity, Sanders introduces

who could present a more credible view of the topic for the public.

to the term orthorexia nervosa, which could be described as a fixation

Unlike many popular lay medical books, the text is fully referenced to

on righteous eating. These are people, whom we have all met both

relevant recent publications, adding to the credibility of the conclusions

professionally and socially, who spend an excessive amount of time

he draws.

worrying about whether they are eating the right thing, and may embark on faddish diets as a matter of lifestyle rather than medical need. In

The book starts with an overview of gluten intolerance and coeliac

deed, one of the conclusions a reader will come to is that some people

disease. Figures are presented on the prevalence of the disease, and

who place themselves on gluten free diets are doing so without any

figures about how many are using a gluten free diet. According to a

real proof that they are sensitive to gluten, but find it suits them to make

study his group published in a peer reviewed journal, 13% of the UK

themselves special. I guess it is a consequence of a thriving society

population report symptoms after consuming gluten and 2.9% are

where the economy permits a move away from utilitarian eating.

on gluten free diets. About 1% of the population currently has coeliac disease and this is a figure that has grown hugely since the middle of

I was concerned that the picture being painted by Professor Sanders

the last century. The question is whether the remaining symptomatic

might be one sided, in that the book only seems to contain evidence

12% truly have something going on.

that supports his interests and concerns with gluten sensitivity/coeliac disease. There is little reference to publications that do not support his

Sanders offers us explanations why the prevalence figures can have

theories, and none that I found that refuted the associations between

grown in recent history and indicates that this may be down to the way

gluten and symptoms. I spoke with author about his viewpoints, and

that society grows and processes grain for bread and related products.

he remarked that the evidence overwhelmingly supported everything

Similarly gluten sensitivity may have increased by changes in the stimuli

he wrote and his contentions are fact driven. Similarly, he pointed out

that are presented to the human immune system, and this is like a newly

that he had also included the ideas of FODMAPS and orthorexia that

emerged auto-immune condition. It may be that in current society’s

acknowledged that gluten sensitivity is not the whole story.

processing, we may have created a rod for our own backs.

I liked the idea that this book focussed on fact rather than speculation. It gives a solid platform for the journey for those that are proven to

Much of the debate in my mind is how people describe themselves

be sensitive to gluten and have the relevant HLA type. It offers some

in relation to food sensitivity and how the medical profession can

alternate thinking, and debunks those who go gluten free as a lifestyle

approach the problem. A key point that Sanders makes is that if

choice. The book is written in an easy engaging style, and quite frankly

individuals think they are sensitive to wheat, they should get themselves

it is an interesting read with some added obscure take away facts.

tested by a reputable scientific method looking for antibodies, and their

The book has been well received elsewhere by the public. Whether or

HLA genotype. This gives them a solid basis for moving forward. It also

not the recommendation, to individuals who think they are sensitive to

helps with those that may associate the less common symptoms e.g.

gluten, that they should get themselves properly tested, will increase the

neuropsychiatric symptoms to their proven underlying condition. We are

clinical burden has to be considered, but because of the documented

introduced to tissue transglutaminase, an enzyme consequent exposure

complications of coeliac, it seems that the balance of benefit to risk

to gluten in the sensitive, and implicated in neurological changes.

favours having a definitive diagnosis and a plan of management.

Substantial evidence is provided for the systemic effects of gluten sensitivity that go beyond the textbook descriptors for coeliac disease.

GASTROENTEROLOGY TODAY - SPRING 2017

search for growing foods on an industrial scale for factory based

The Editor (no conflict of interest)

17


NEWS The silver lining of an inflammatory bowel disease diagnosis Bethesda, MD (Oct. 18, 2016) -- Twentyfive percent of inflammatory bowel disease (IBD) patients are diagnosed as children or adolescents -- at the peak of their social and educational development. Parents of newly diagnosed patients often inquire about the long-term consequences of IBD on their child’s health and lifestyle.

their parents,” said lead study author Wael El-Matary, MD, MSc, FRCPCH, FRCPC, from the section of paediatric gastroenterology, departments of paediatrics, at the University of Manitoba, Winnipeg, Canada. “We hope our findings reassure families dealing with this diagnosis. Knowing that long-term educational levels attained, occupation and marital status are not worse compared to those without IBD will significantly help in alleviating a great part of this anxiety.”

While there is understandably much anxiety associated with a new IBD diagnosis, children and parents should sleep easier knowing that adults with IBD, who were diagnosed during their childhood, are doing exceptionally well in terms of educational levels attained, annual income and marital status, according to a study published as an article in press in Clinical Gastroenterology and Hepatology(16)30857-6/abstract, the clinical practice journal of theAmerican Gastroenterological Association.

The researchers conducted a cross-sectional analytical study looking at adults diagnosed with IBD in childhood and adolescence between January 1978 and December 2007 at the Paediatric Gastroenterology Clinic at Children’s Hospital, Winnipeg, Manitoba, Canada. IBD patients were compared to age and sex-matched healthy adult controls. Participants were asked questions on educational achievements, employment and marital status. They found that not only were patients with IBD more likely to earn more money per year than their healthy counterparts, but more of these patients went on to receive post-high school education.

“The anxiety associated with a new diagnosis of IBD is significant to both children and

“IBD is not an easy diagnosis. We recognize that it may take several years for patients to find

We don’t want people to die of embarrassment. GASTROENTEROLOGY TODAY - SPRING 2017

18

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a treatment regimen that works best for their disease, hence why we decided to revisit patients many years after their initial diagnosis when they, hopefully, are following a stable and effective treatment plan. What we found was hope at the end of the tunnel,” added Dr. El-Matary.

The IBS Network Supporting the Supports Groups Following The IBS Network’s successful pilot training in Autumn for Support Group Leaders, the charity is now seeking to roll out the scheme across the country throughout 2017. The IBS Network – the national charity that helps people with Irritable Bowel Syndrome (IBS), wants to raise awareness of the importance of self-management through support groups for those living with this debilitating and often misunderstood condition. Self-management is the cornerstone of living well with IBS. If people can share their experience in an open and non-judgemental environment, learn to understand their own illness, and support others, IBS symptoms can


NEWS be much better controlled. The IBS Support Group Leaders’ Training Days are planned for 25 February, 15 July and 18 November 2017. Those attending will gain guidance from healthcare professionals and people who have learned to manage their IBS, as well as practical information on setting up and running groups. For an application form, please email: sam@theibsnetwork.org The IBS Network has provided support to patients and healthcare professionals for over 25 years. The charity receives its funding from various sources, including: annual memberships; an online shop, for purchasing the ‘Can’t Wait’ card, Radar keys and other useful aids, in addition to income from fundraising events and legacies. At any one time, IBS affects around 15-20% of people living in the UK, which equates to approximately 12 million people. The illness is used to describe a collection of otherwise unexplained symptoms relating to a disturbance in the bowels, which can include abdominal pain, bloating, constipation and diarrhoea. More information on the condition and The IBS Network can be found at: https://www.theibsnetwork.org/

Adults with EoE have positive long-term outcomes after diagnosis Ten years after initial diagnosis of eosinophilic esophagitis, most adults with the disease have resolution of symptoms and minimal impacts on quality of life, according to a retrospective study presented at ACG 2016. “There is limited data on the long-term followup of adults ... however in children with EoE, 8 years after initial diagnosis ... approximately 80% demonstrated favourable outcomes,” Alexander Podboy, MD, from the Mayo Clinic, said during his presentation. “So our aim was to assess both symptoms and quality of life 10 years after initial diagnosis in adult patients with EoE.” Podboy and colleagues performed a retrospective cohort study of 59 adults who had EoE for at least 10 years (mean age, 56.2 years; 66.1% men). At their initial diagnosis, 57.6% of the patients were treated with topical steroids and 33.9% were treated with proton pump inhibitors. Ten years later, 31% were not on EoE therapy, 63.8% were taking PPIs, and only 6.8% were

taking steroids. Most of the patients had not had an additional esophagogastroduodenoscopy since their original diagnosis, and only two patients required emergent food disimpaction. During the last month of follow-up, 71.2% reported no difficulty swallowing, while 28.8% did report difficulty swallowing. Moreover, 62.5% reported eating an unlimited diet without caution, while 25% reported eating an unlimited diet with some caution, “with caution indicating excessive amounts of chewing, time, or fluids with their meals,” Podboy said. In addition, 7.1% of patients reported avoiding stringy meats and 3.6% reported avoiding bread. Finally, reduced EoE-related quality of life was trivial to minimal in 57% of patients, mild in 18%, moderate in 16% and severe in 9%. “After 10 years, two patients required emergent food disimpaction, 6.8% of patients were on swallowed steroid therapy, 65% reported no current symptoms, 62% had unlimited to unlimited with caution diet, and 75% reported a trivial to mild decrease in quality of life,” Podboy said. “EoE after initial diagnosis may be more benign than the literature suggests, and further evaluation is warranted to assess the need for long-term medical care.” – by Adam Leitenberger

GASTROENTEROLOGY TODAY - SPRING 2017

19


NEWS Crohn’s disease may have two distinct genetic subtypes Crohn’s disease may have at least two distinct genetic subtypes that are associated with their own specific clinical features, according to researchers from the University of North Carolina School of Medicine. These findings could provide a molecular explanation for the heterogeneity of disease course and severity observed in Crohn’s disease, and potentially guide more customized treatment options. “The one-treatment-fits-all approach doesn’t seem to be working for Crohn’s patients,” Shehzad Z. Sheikh, MD, PhD, assistant professor in UNC’s departments of medicine and genetics, said in a press release. “It’s plausible that this is because only a subset of patients has the type of disease that responds to standard therapy, whereas, for the rest of the patients, we’re really not hitting the right targets.” Sheikh and colleagues collected non-inflamed, healthy looking colonic mucosa samples from 21 Crohn’s patients and 11 controls without IBD. Then they analysed gene expression using RNA sequencing, and gene regulation based on chromatin accessibility using formaldehydeassisted isolation of regulatory elements. The gene expression analysis showed a “striking clustering pattern,” revealing two distinct groups of Crohn’s patients, and the differential expression of the genes involved was unexpected, according to the release. Crohn’s disease samples that resembled those of the non-IBD controls showed abundant expression of colon-specific genes, while the other subtype showed ileum-specific gene expression patterns. GASTROENTEROLOGY TODAY - SPRING 2017

20

“It was surprising,” Jeremy Simon, PhD, a research assistant professor in UNC’s department of genetics, said in the press release. “Many of the genes that were different between the two Crohn’s subtypes are markers that distinguish the colon from the ileum, despite these being colon biopsies.” The genetic regulation analysis also showed distinction between the two subtypes, suggesting that regulatory activity contributes to the differential colon-like and ileum-like gene expression. As the gene expression profiles of adult Crohn’s patients may vary based on their

treatment history, the researchers sought to confirm their findings by examining previously published gene expression data from ileal biopsy samples collected from 201 treatmentnaive paediatric Crohn’s patients and 40 nonIBD controls. While not as distinct as with the adult samples, the researchers observed the same two colon-like and ileum-like subtypes. “This suggests that these molecular programs or baseline genomic signatures of Crohn’s subtypes exist independently of patients’ ages or treatment histories,” Sheikh said in the press release. Further analyses showed key expression differences in in cellular metabolism and immune pathways. In addition, retrospective analysis of the paediatric samples showed the subclasses were associated with distinct clinical characteristics and outcomes. Patients in the colon-like subgroup were more likely to have both colon and ileum involvement, deep ulcers, macroscopic inflammation, greater rectal disease involvement and eventual need for colectomy. Patients in the ileumlike subgroup were more likely to show no inflammation, have colon-only involvement, have ileal disease and need for postoperative treatment with biologics. The researchers plan to develop a diagnostic test based on these results to better classify Crohn’s disease patients and optimize therapies. “We hope one day to be able to test Crohn’s patients for the subtype of the disease they have, and thus determine which treatment should work best,” Sheikh said in the press release. “The idea is to find the best therapeutic course for each patient as quickly and efficiently as possible.” – by Adam Leitenberger

A dangerous bond New receptors discovered for stomach germ Helicobacter pylori Helicobacter pylori is a spiral bacterium that can colonize the human stomach – sometimes with fatal consequences. A research group led by Prof. Markus Gerhard of the Technical University of Munich (TUM) and Assistant Professor Dr. Bernhard B. Singer of the Institute for Anatomy at the Faculty of Medicine of the University of Duisburg-Essen at Essen University Medical Centre has discovered a completely new approach to preventing or treating infections

with this bacterium as well as secondary complications. This research was done in collaboration with the group of Prof. Han Remaut (VIB – VUBrussels, Belgium). Scientific journal “Nature Microbiology” reports on this in its current edition. Helicobacter pylori infection usually occurs during childhood. The bacterium is widely spread: every third person in Germany and every other person worldwide is a carrier (editor comment: rates of carriage in UK as reported by Public Health England may be much lower). Secondary complications include gastritis, stomach and duodenal ulcers. In addition, there is an increased risk of developing stomach cancer. The typical treatment for Helicobacter pylori infections is currently antibiotics. The disadvantage of this treatment, however, is that it not only destroys the bacterium itself but also the ‘good germs’ of the gut flora. In addition, the bacterium is developing increasing resistance. In order to ensure permanent survival in the human stomach, Helicobacter pylori must attach to the epithelial cells in the gastric mucosa. Research groups in Munich, Essen, and Brussels have now detected a highly specific and exceptionally strong variant of this adhesion, in which the bacterial surface molecule HopQ binds itself to so-called “Carcinoembryonic Antigen-Related Cell Adhesion Molecules”, or CEACAMs for short, inside the stomach. Independent of sugar “In contrast to previously known binding partners of the bacterium, this bond is independent of sugar structures. This seems to ensure that it is especially stable in the acid environment of the stomach,” explains Bernhard B. Singer. CEACAMs do not occur in healthy stomach tissue, but primarily when there is an inflammation of the gastric mucosa (gastritis) caused by Helicobacter pylori infection. “One could say that these germs create additional and particularly strong binding opportunities by stimulating the formation of CEACAMs,” adds Singer. Once bound to CEACAM, Helicobacter pylori can transfer additional proteins, so-called virulence factors, to the stomach cells. This secretion system contributes significantly to the development of stomach ulcers and bowel cancer. “Against this backdrop, we assume that HopQ could be used diagnostically and therapeutically,” says Markus Gerhard, Professor at the Institute for Medical Microbiology, Immunology and Hygiene at TUM.


NEWS New approaches to treatment The Scientists are currently researching various approaches in order to replace current types of treatment for Helicobacter pylori infection, due to the aforementioned side effects. The adhesion of the bacterium to stomach cells could be prevented with a soluble version of HopQ or parts of the protein, and the damaging effects of the germ could potentially be suppressed, as the data in the publication indicate. As a further therapeutic option, the researchers are pursuing the approach of using specifically developed antibodies against CEACAMs in order to fight diseases associated with the bacterium. An additional treatment option being considered is immunization against the HopQ protein and thus vaccination against infection with the bacterium. The German Research Foundation (DFG) considers the project a promising approach and will be sponsoring further research over the next three years. Results by a group led by Prof. Wolfgang Haas of Ludwig-MaximiliansUniversity’s Max von Pettenkofer-Institute confirm the data collected by Markus Gerhard and his colleagues. Both articles appear in the current issue of “Nature Microbiology”.

Original publication A. Javaheri , T. Kruse, K. Moonens, R. Mejías-Luque , A. Debraekeleer, I. Asche, N. Tegtmeyer, B. Kalali , N.C. Bach, S.A. Sieber, D.J. Hill, V. Königer, C.R. Hauck, R. Moskalenko, R. Haas, D.H. Busch, E. Klaile , H. Slevogt, A. Schmidt, S. Backert, H. Remaut, B.B.Singer, M. Gerhard M. (2016) Helicobacter pylori adhesin HopQ engages in a virulence-enhancing interaction with human CEACAMs. Nature Microbiology. DOI:10.1038/ nmicrobiol.2016.189

The British Society of Gastroenterology statement The British Society of Gastroenterology has issued the below statement in response to the release of the second Atlas of Variation in Diagnostics in England. The President of the British Society of Gastroenterology, Professor Martin Lombard commented, saying: “The British Society of Gastroenterology

welcomes the second Atlas of Variation in NHS Diagnostic Services in England; it is clear that unwarranted variation in endoscopy quality and access needs to be addressed. It is vital also that we keep our focus on outcomes rather than levels per se. “Integral to high quality diagnostic services is the workforce and this cannot be underestimated in the current environment. Not only is this important for endoscopists but also for the wider team, who increasingly play a fundamental role in the delivery of high quality care. “It is important that endoscopy resources are used in an impactful way and the right types of procedures are better deployed for the patient, such as colonoscopy, capsule endoscopy, flexible sigmoidoscopy and CT colonoscopy whilst procedures such as barium enema, that have no place in modern gastroenterology, are phased out by NHS England.” Find the full report at: http://fingertips.phe. org.uk/documents/DiagnosticAtlas_FINAL.pdf

Helicobacter pylori

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POSTERS

PTU-013: Capsule

Endoscopy in Young P

E Rondonotti1, DE Yung2*, A Giannakou3, B Rosa4, E Toth5, A Lucendo6, R Sidhu7, H B On behalf of the Capsule Endoscopy 1Ospedale

Valduce, Italy;

2Royal

Infirmary of Edinburgh, UK; 8VU

3Open

University of Cyprus, Cyprus; 4Hospital da Senhora da Oliveira

University Medical Centre, Amsterdam; 9Mater Dei Hospital, Malta; 10Universi

Background

Results

Although several studies have shown that the diagnostic yield (DY) of small bowel capsule endoscopy (SBCE) is higher in older patients, recent data imply that patients ≤50 years are at higher risk of sinister SB pathology. We aimed to investigate: (a) DY of SBCE in a large cohort of young patients with iron deficiency anaemia (IDA), and (b) factors associated with neoplastic pathology in this patient cohort.

(262 F/127 M; mean age 3

Final analysis: 220

(122 F/ 98 M; mean age 4

Fig 1: SBCE finding

Materials and Methods

GASTROENTEROLOGY TODAY - SPRING 2017

22

160 140 120 Number of patients

Retrospective, multicentre study (Jan 2010 – Jan 2015) involving consecutive patients ≤50 years undergoing SBCE for IDA at 18 high-volume (>100 SBCEs/year) centres from 12 countries. Exclusion criteria: overt-obscure gastrointestinal (GI) bleeding (ongoing or previous); age >50 or <19 years; comorbidities associated with IDA e.g. inflammatory bowel disease (IBD), coeliac disease. Data retrieved via structured questionnaire: age, gender, indication for SBCE, investigations prior to SBCE (Hb, MCV, ferritin, faecal calprotectin, imaging, upper and/or lower GI endoscopies, biopsies and/or coeliac serology), medications (NSAIDs, antiplatelets, warfarin/heparin), SBCE findings, final diagnosis. Clinical findings were analysed using multivariate logistic regression where the strongest predictors were selected using 500 bootstrap samples with backwards elimination. The Akaike Information Criterion (AIC) was used to include or exclude predictors. P-value <0.05 was considered statistically significant.

389 patients coll

100 80 60

Oth

Other cha

40

Croh

20 0

Angi

Neoplasia

Non-ne clinicall

References 1. 2. 3. 4.

Pennazio M, et al. Small-bowel capsule endoscopy a Endoscopy 2015; 47:352-386. Koulaouzidis A, et al. The use of small-bowel capsule en Goddard AF, et al. Guidelines for the management of ir Sidhu PS, et al. The Utility of Capsule Endoscopy in Pati


POSTERS

Patients with Iron Deficiency Anaemia

Beaumont8, P Ellul9, L Negreanu10, VA Jiménez-García11, JN Plevris2, A Koulaouzidis2 in Young IDA Patients research group

a, Portugal; 5Skåne University Hospital, Malmo, Sweden; 6Hospital General de Tomelloso, Spain; 7Royal Hallamshire Hospital, UK;

ity Hospital of Bucharest, Romania; 11Hospital Universitario Virgen Macarena, Spain

lected

39.4±9.3 years)

169 excluded (43.4%)

Missing data: bidirectional GI endoscopy results, information on Hb/MCV at time of diagnosis/referral, gynaecological examination (where appropriate), negative coeliac serology and/or biopsies to rule out coeliac disease

patients

40.5±8.6 years)

gs in our cohort

r inflammatory anges (25%)

Factor

Estimate

Std Error

Z-value

P-value

-0.0395

0.0186

-2.13

0.03

0.01

0.0058

1.73

0.08

Use of antiplatelets

1.7635

0.9002

1.96

0.05

Use of NSAIDS

1.4065

1.1055

1.27

0.20

Use of warfarin/ heparin

-15.445

1061.731

-0.01

0.99

MCV Clinically insignificant findings e.g. lymphangiectasias, red spots (39%)

Ferritin

Conclusion Normal SBCE (61%)

hn’s disease (25%)

iodysplasias (37%)

eoplastic but ly significant

Table 1: predictive factors investigated in multivariate analysis

Normal/ nonclinically significant

In patients ≤50 years old with IDA, the overall DY of SBCE for significant findings is 32.3% and around 5% are diagnosed with SB malignancy. In this cohort, lower MCV or antiplatelet use have been associated with higher DY for SB neoplasia or clinically significant findings on CE. This could be confirmed by prospective studies with a larger sample of patients.

and device-assisted enteroscopy for diagnosis and treatment of small-bowel disorders: European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline.

ndoscopy in iron-deficiency anaemia alone; be aware of the young anaemic patient. Scand J Gastroenterol 2012; 47: 1094-1100. ron deficiency anaemia. Gut 2011: 2010.228874. ients under 50 Years of Age with Recurrent Iron Deficiency Anaemia: Is the Juice Worth the Squeeze? Gastroenterol res prac 2015:948574.

GASTROENTEROLOGY TODAY - SPRING 2017

hers (13.3%)

Patients were grouped according to final diagnosis into the following groups: neoplastic pathology (11/220; 5.0%); non-neoplastic but clinically significant, findings (60/220; 27.3%); normal or non-clinically significant findings (149/220; 67.7%). (Figure 1) On multivariate analysis, MCV was associated with the occurrence of neoplastic pathology (OR: 0.96; 95%CI: 0.930.99; p=0.033), i.e. the odds of SB neoplastic pathology increased by 4% for every unit of decrease in MCV. Weak evidence existed for the association between use of antiplatelet drugs and risk of SB neoplasms (OR: 5.83; 95%CI: 1.0-34.0; p=0.05). (Table 1)

23


POSTERS Associa'on between midazolam dose and caecal intuba'on rate at colonoscopy

Jason Boyd, Lennard YW Lee, Charlo3e Harper, Sandro Lanzon-­‐Miller Department of Gastroenterology, Milton Keynes NHS FoundaEon Trust, United Kingdom

Results

Introduc'on

6200 paEents were included for analysis. The median age was 62 years and 49.4% were male. The mean midazolam dose was 1.9mg. 1004 paEents had a low dose of midazolam (<2mg), 4618 a standard dose (2mg) and 578 a high dose (>2mg). The CIR in the low dose cohort was 83.6%, in the standard dose cohort was 91.3% and in the high dose cohort was 78.7%. Procedural discomfort was significantly greater in the high dose cohort. When paEents with poor bowel preparaEon were excluded (n=5534) CIR was 85.2% in the low dose cohort vs 92.1% in the standard dose cohort. Pa'ents who received doses of midazolam <2mg or >2mg had a significantly lower CIR than pa'ents who received 2mg, with P < 0.001 in both comparisons.

Midazolam is a short acEng benzodiazepine that is commonly used for sedaEon during colonoscopy. There is no standard dose of midazolam; however, BriEsh Society of Gastroenterology guidelines suggest a maximum of 5mg with lower doses for elderly paEents. Caecal intubaEon rate (CIR) is a commonly used performance indicator for colonoscopy. Data exploring the relaEonship between midazolam dose and CIR is limited.

Methods

A retrospecEve cohort study of all paEents who had undergone a colonoscopy at Milton Keynes Hospital between January 2010 and December 2012. PaEents were idenEfied from the Endoscopy Unit database and their records were reviewed. PaEent details, midazolam dose and depth of inserEon were extracted into a standardized form. Caecal intubaEon was defined as inserEon of the colonoscope to a point proximal to the ileocaecal valve so that the the enEre caecum could be visualised. GASTROENTEROLOGY TODAY - SPRING 2017

24

Conclusion

Midazolam dose

<2mg

2mg

>2mg

n (%)

1004 (16.2)

4618 (74.5)

578 (9.3)

CIR

83.6%

91.3%

78.7%

P-­‐value

<0.001

-­‐

<0.001

In this study we demonstrate that a standard (2mg) dose of midazolam is associated with a significantly higher CIR than lower doses. Following straEficaEon of paEents by adequacy of bowel prepraEon, CIR remained lower in the low dose midazolam group. Appropriate paEent selecEon for standard dose midazolam is important to avoid respiratory and cardiovascular compromise. Further prospecEve studies are warranted.


COMPANY NEWS

IBS: BURDEN ON HEALTHCARE SYSTEMS The IBS Global Impact Report presents key evidence gathered through a literature review of current and recent papers outlining the human, societal and healthcare burden imposed by Irritable Bowel Syndrome (IBS) in order to stimulate discussion on how patients may receive better management and patient outcomes improved. The report represents a consensus view of the members of the Steering Committee* The Global IBS Impact Report has been funded and facilitated by Allergan and coordinated by a secretariat service. The following extract has been taken from the report* • It may take many years for a patient to be formally diagnosed with

*Steering Committee

IBS1. During this time, many people with IBS will have repeated visits to healthcare services in primary and secondary care • IBS puts considerable strain on healthcare resources, incurring a significant financial burden – IBS accounts for up to 50% of

• Professor Maura Corsetti Clinical Professor in Gastroenterology • Professor Jean-Marc Sabaté Professor in Gastroenterology, University Paris Diderot

gastroenterology consultations2 • Professor Nick Freemantle Professor of Clinical Epidemiology and • Greater severity of IBS symptoms results in higher use of more costly healthcare resources: the onset of severe symptoms

Biostatistics, Faculty of Population Health Sciences, University College London, UK

is often associated with referral to a specialist, patients with symptoms of moderate severity consult a general practitioner (GP) and patients with mild symptoms generally do not seek

• Professor Jan Tack Head of Clinic, Gastroenterology; Professor in Internal Medicine, University of Leuven, Belgium

healthcare support. Full editorial control resides with Gastroenterology Today. • Calculations of the level of healthcare resource utilisation and financial burden of IBS are likely to be under-estimated due to

For a copy of the full report please visit Allergan.co.uk

under-diagnosis. References: Adult patients presenting to their GP with lower gastrointestinal tract disorders account for one in 20 of all general practice consultations, with functional disorders, such as IBS, being most prevalent.3 It is estimated that between 33-50% of people who have symptoms suggesting IBS will seek medical advice and those who do consult a physician tend to consult regularly.4 However, IBS patients do not always consult a physician and a substantial proportion meeting IBS criteria may not be diagnosed with IBS5.

1. American Gastroenterological Association. IBS in America: Survey Summary Findings, December 2015. 2. Gunn, MC, Cavin AA, Mansfield JC. Management of irritable bowel syndrome. Postgrad Med J. 2003;79(929):154-8. 3. Spiller R, Aziz Q, Creed F, et al. Guidelines on the irritable bowel syndrome: mechanisms and practical management. Gut 2007;56:1770–98. 4. Canavan C, West J, Card T. Review article: the economic impact of the irritable bowel syndrome. Aliment Pharmacol Ther

healthcare costs for patients with IBS.4 In the UK, people with IBS

2014;40(9):1023-34.

will consult with their primary care physician at rates of 8.1 to 10.7 times per year during the three years prior to and after their first

5. Hungin APS, Whorwell PJ, Tack J, et al. The prevalence, patterns

gastroenterology appointment. 6 This compares with a reported

and impact of irritable bowel syndrome: an international survey of

average of two to three visits per year in the USA.4 IBS is a common

40 000 subjects. Aliment Pharmacol Ther. 2003;17:643–50.

reason for consulting a gastroenterologist, accounting for up to 50% of such consultation. 2 In the UK specifically, 29% of IBS cases are referred to a secondary care specialist and the majority are returned to primary care for long-term management.3 In 2010, the Rome Foundation formulated a diagnostic algorithm for IBS. The algorithm is used for patients who present with recurrent abdominal pain/discomfort with disordered bowel function. A diagnosis of IBS can be made if the patients symptoms fulfil Rome IV criteria for IBS, there are no red flags, and the results of the screening investigations are negative.7,8

6. Canavan C, West J, Card T. Calculating total health service utilisation and costs from routinely collected electronic health records using the example of patients with irritable bowel syndrome before and after their first gastroenterology appointment. Pharmacoeconomics. 2016;34(2):181-94. 7. Spiller RC, Thompson WG. Bowel Disorders. Am J Gastroenterol. 2010;105(4);775-85. 8. Lacy BE, Mearin F, Chang L, et al. Bowel disorders.

GASTROENTEROLOGY TODAY - SPRING 2017

Overall, primary care visits account for up to 30% of the total direct

Gastroenterology. 2016;150:1393-407.

25


COMPANY NEWS

ABBVIE’S INVESTIGATIONAL, PAN-GENOTYPIC REGIMEN OF GLECAPREVIR/PIBRENTASVIR (G/P) SHOWS HIGH SVR RATES IN CHRONIC HEPATITIS C PATIENTS WITH SEVERE CHRONIC KIDNEY DISEASE • 98 percent of patients across all major HCV genotypes (GT1-6)

The EXPEDITION-4 results are the latest to be released from

with severe chronic kidney disease (CKD), including patients on

registrational studies in AbbVie’s G/P clinical development program,

dialysis, achieved SVR12 with 12 weeks of G/P in the primary

designed to investigate a faster path to virologic cure* for all major

intent-to-treat analysis, regardless of previous treatment status

HCV genotypes (GT1-6) and with the goal of addressing areas of

or presence of compensated cirrhosis

continued unmet need.

• 100 percent of patients achieved SVR12 in a modified intent-totreat analysis

“HCV patients with severe chronic kidney disease present a complex challenge for physicians to treat, particularly as kidney

• G/P is an investigational, pan-genotypic, once-daily, ribavirin-

disease progresses, and if the patient has genotype 2 or 3 or has

free, fixed-dose combination for the treatment of chronic HCV

compensated cirrhosis,” said Ed Gane, M.D., professor of medicine

• Development of new regimens to treat HCV patients with CKD

at the University of Auckland in Auckland, New Zealand. “The results

remains a critical unmet medical need across genotypes

1

NORTH CHICAGO, Ill., Nov. 15, 2016 /PRNewswire/ -- AbbVie (NYSE: ABBV), a global biopharmaceutical company, today announced 98 percent (n=102/104) of chronic hepatitis C virus (HCV) infected patients with severe chronic kidney disease (CKD) achieved sustained virologic response following 12 weeks of treatment (SVR12) with its investigational, pan-genotypic regimen of glecaprevir (ABT-493)/ pibrentasvir (ABT-530) (G/P) in the primary intent-to-treat (ITT) analysis. In a modified intent-to-treat (mITT) analysis, SVR12 was achieved in 100 percent (n=102/102) of severe CKD patients; mITT excludes patients who did not achieve SVR for reasons other than virologic failure. These new data from the Phase 3 EXPEDITION-4 study, evaluating patients with chronic HCV infection across all major genotypes (GT1-6) and

seen in EXPEDITION-4 are a positive development in AbbVie’s investigation of the G/P regimen for patients with chronic kidney disease, who currently have limited HCV treatment options.” HCV is common among people with severe CKD, reaching prevalence of up to 80 percent in some regions of the world.2 In the U.S., it is estimated that over 500,000 people have both chronic HCV and CKD.3 Some chronic HCV infected patients with severe CKD, particularly those with GT2 and GT3 HCV infection, currently don’t have access to direct-acting antivirals (DAAs). The development of new, safe and effective regimens to treat HCV in these patients remains a critical unmet medical need.1 “With our investigational, pan-genotypic regimen, our goal is to

severe CKD, will be presented as a late-breaker today at The Liver

provide a safe and effective cure to patients across genotypes,

Meeting , the Annual Meeting of the American Association for the

including patients with severe chronic kidney disease, regardless of

Study of Liver Diseases (AASLD) in Boston.

previous treatment status or presence of compensated cirrhosis,”

®

said Michael Severino, M.D., executive vice president, research and development and chief scientific officer, AbbVie. “Our clinical development program reflects our ongoing commitment to addressing treatment areas of continued unmet need.” GASTROENTEROLOGY TODAY - SPRING 2017

The EXPEDITION-4 study enrolled 104 patients with severe chronic kidney disease, including 85 patients (82 percent) who were receiving dialysis at enrollment and 20 patients (19 percent) who had compensated cirrhosis. The study also included those who were not cured with previous sofosbuvir (SOF) with ribavirin (RBV) or interferon (IFN) with RBV; with or without SOF (44 patients, 42 percent). The majority of treatment related adverse events (AEs) were mild or moderate. The most commonly reported AEs included pruritus, fatigue and nausea. Of the 24 percent of patients who experienced serious AEs, none were considered related to G/P. Four AEs (4 percent) led to the discontinuation of G/P and one patient died after achieving SVR4 due to a serious AE (intracerebral hemorrhage) considered not-related to G/P. *Patients who achieve a sustained virologic response at 12 weeks post

26


COMPANY NEWS About the EXPEDITION-4 Study EXPEDITION-4 is a single-arm, open-label, Phase 3 study evaluating the safety and efficacy of 12 weeks of G/P in patients with GT1-6 chronic HCV infection and chronic kidney disease, including those on dialysis. The primary efficacy endpoint is SVR 12. Patients had severe or end stage kidney disease (stage 4 and 5 CKD), with an eGFR < 30 mL/min/1.73 m2 required at screening. Prior treatment in the study is defined as treatment with IFN/ pegIFN ± RBV, or SOF + RBV ± pegIFN therapy. Additional information on the clinical trials for G/P is available at www.clinicaltrials.gov/.

About AbbVie’s HCV Clinical Development Program AbbVie’s glecaprevir/pibrentasvir (G/P) clinical development program was designed to investigate a faster path to virologic cure* for all major HCV genotypes (GT1-6) and with the goal of addressing treatment areas of continued unmet need. G/P is an investigational, pan-genotypic regimen that is being evaluated as a potential cure in 8 weeks for HCV patients without

Prime Endoscopy Bristol, part of the InHealth Group, is looking forward to welcoming patients to the newly opened, state-of-the-art endoscopy suite on Millenium Parade, Harbourside, Bristol. The new location offers direct to test endoscopy services to patients registered with GP practices in Bristol, North Somerset and South Gloucestershire. The need for a new site was driven by increasing demand on the Westbury on Trym location, where services were previously offered. There is plenty of parking close by plus easy public transport links making this location accessible to all. The new unit will offer not only diagnostic and therapeutic endoscopy but also community gastroenterology clinics. Referrals are triaged on a daily basis so patients may go straight to test or, when more appropriate, (or requested by their GP) may attend a community gastroenterology clinic. Since its inception in 2010, Prime Endoscopy Bristol has worked closely with the local health care community to provide a meaningful gastroenterology service which seeks to support clinicians to manage their patients more effectively in primary care. We continue to work closely with local GPs, CCGs and with our DGHs and we are developing innovative and more collaborative ways of working; offering the best patient experience as well as delivering better outcomes and faster treatment; providing clinical input into new pathways of care and supporting the development of clinical guidelines and protocols.

cirrhosis and who are new to treatment, who make up the majority of HCV patients. AbbVie is also studying G/P in patients with specific treatment challenges, such as genotype 3, patients who were not cured with previous DAA treatment and those with CKD, including patients on dialysis. G/P is an investigational, once-daily regimen that combines two distinct antiviral agents in a fixed-dose combination of glecaprevir (300mg), an NS3/4A protease inhibitor, and pibrentasvir (120mg), an NS5A inhibitor. G/P is dosed once-daily as three oral tablets.

Prime Endoscopy Bristol is also at the forefront of GP education locally, coordinating and organising GP update courses in the field of gastroenterology. Our new location also offers training and conferencing facilities thereby supporting the need to develop a competent workforce into the future and promoting a high quality, effective community endoscopy service within Bristol and the surrounding areas. Prime Endoscopy Bristol Harbourside, 8 Millenium Parade, Bristol BS1 5TY www.primeendoscopybristol.co.uk www.inhealthgroup.com

Glecaprevir (GLE) was discovered during the ongoing collaboration between AbbVie and Enanta Pharmaceuticals (NASDAQ: ENTA) for HCV protease inhibitors and regimens that include protease inhibitors.

Recommendations for Testing, Managing, and Treating Hepatitis C, February 24, 2016, http://www.hcvguidelines.org/full-report/ monitoring-patients-who-are-starting-hepatitis-c-treatment-aretreatment-or-have. Accessed March 15, 2016. 2 Fabrizi F, Poordad FF, Martin P. Hepatitis C infection in the patient with end stage renal disease. Hepatology. 2002;36(1):310. 3 IMS Health, July 2016. Parsippany, NJ; Medivo, July 2016. New York, NY (Estimate based on IMS Health Dx Medical Claims 12/2013-4/2016; IMS Health Life Link Patient Level Data

GASTROENTEROLOGY TODAY - SPRING 2017

1 American Association for the Study of Liver Diseases.

12/2013-4/2016; Medivo Lab Data 12/2013-4/2016).

27


COMPANY NEWS

WHAT GASTROENTEROLOGISTS SHOULD KNOW ABOUT DYSBIOSIS AND ITS MANAGEMENT Researched and written by Dr Ashton Harper, MBBS, BSc, MRCS, Head of Medical Affairs at Protexin The Human Gastrointestinal Microbiota: ‘We are more bacteria than human’ a statement based on the ubiquitous fact that we contain 10 times as many bacterial cells as human. Although this ratio is more accurately 1 to 11 this still means we harbour approximately 40 trillion bacterial cells. Moreover, research in the 1980s showed that mitochondria are of bacterial origin so taken together we shouldn’t be too hasty in dismissing this contemporary aphorism. The array of crucial physiological processes these tiny allies perform is even more impressive from the synthesis of vitamins (K and some B vitamins), to dietary fibre digestion and the development and function of the immune system. Sequencing technologies have identified a staggering level of diversity with each of us harbouring >1000 ‘specieslevel’ phylotypes2 that contribute >3 million bacterial genes; a number that exceeds our human gene complement by ~150 times!

Table 1 Feature

Figure

Bacteria in the gut

~ 40 trillion (~30 trillion eukaryotes) (Sender 2016)

Diversity in the human gut

>1000 species (Lozupone 2012)

Microbiota genes

>3 million (150-fold more than human) (Qin 2010)

“Living in a modern postindustrial age exposes us to numerous insults such as unnatural processed and sterile food, antibiotics and urban dwelling - all of which are prime suspects in the prevalent dysbiosis of Western disease5” disease4. These studies clearly show that diet has an undeniable impact on our microbiota and likely contributes to a range of pathologies. Living in a modern post-industrial age exposes us to numerous insults such as unnatural processed and sterile food, antibiotics and urban dwelling - all of which are prime suspects in the prevalent dysbiosis of Western disease5. There has been immense interest and research into manipulating and augmenting our gut microbiota with live biotherapeutic products (probiotics) to prevent and/or treat a range of pathologies. An update in the

Diversity, dysbiosis and disease:

treatment of dysbiosis relevant to gastroenterologists follows.

Dysbiosis refers to a shift in bacterial diversity and composition from

GASTROENTEROLOGY TODAY - SPRING 2017

28

healthy to diseased states and is observed in a wide range of conditions

Endoscopy:

from IBS and IBD, to Clostridium difficile diarrhoea, and even autism

Worldwide Helicobacter pylori

and ADHD. Analysis of the microbiota from calcified dental plaque

(H. pylori) is the most infectious

of prehistoric human skeletons3 has shown that the dietary transition

pathogen in humans infecting

from Paleolithic (hunter gatherers >10,000 years before present) to

~1/3 of Western populations

Neolithic (farming - carbohydrate rich diets - ~10,000 years before

and >1/2 of those residing in

present) humans shifted the oral microbiome to a disease-associated

developing countries6. Infection is

composition with a decrease in diversity and a significant increase in

associated with a broad spectrum

oral pathogens (NB: oral bacteria are associated with a range of chronic

of diseases from gastritis and

systemic inflammatory conditions). Faecal microbial comparison between

peptic ulceration to lymphoma

healthy African-Americans and native Africans identified fundamental

and stomach cancer. The effectiveness of triple therapy to treat H. pylori

compositional differences in a recent study4. Major butyrate-producing

is increasingly compromised by the global rise of antibiotic resistance;

groups (butyrate is a SCFA protective against early tumorigenic events)

the major cause of treatment failure7. Probiotic bacteria have been

were significantly more abundant in native Africans, whereas microbial

shown to antagonize H. pylori by a number of mechanisms such as

genes encoding for secondary bile acid production (pro-carcinogenic

inhibiting urease activity8 and disrupting receptor glycolipid binding9.

compounds) were significantly richer in African Americans. These

A 2015 publication reviewing 143 studies on treatment of H. pylori

observations at the microbial level are associated with striking differences

concluded that the addition of probiotics to standard triple therapy

in the incidence of colorectal cancer between the two populations; African

enhanced the efficacy of treatment with the added benefit of improving

Americans are at highest risk globally and native Africans rarely suffer the

tolerance to the medication and reducing gastrointestinal side-effects6.


COMPANY NEWS On the wards: Antibiotic-associated diarrhoea (AAD) is the most common gastrointestinal complication following antibiotic use; incidence 5-62%10 occurring anytime from initiation to 8 weeks following treatment completion. Clostridium difficile associated diarrhoea (CDAD), an archetypal illustration of dysbiosis, accounts for 5-25% of AAD cases in hospital, and those at highest risk are the over 65s on broad-spectrum antibiotics. The economic burden of CDAD for European healthcare systems is staggering with incremental costs of ~£4,500 to nearly £9,000 per case11. Probiotics may prevent AAD and CDAD by numerous mechanisms such as stabilising the barrier force of the resident microflora, augmenting immune functions (e.g.- increasing secretory IgA levels), direct anti-microbial abilities (e.g.- bacteriocins) and maintaining intestinal physiology (e.g. – ectomembrane enzymes)12. Recent meta-analyses have concluded that probiotics may reduce the relative risk of AAD by 42%13, and cases of CDAD by 64%14. This evidence is compelling particularly considering the low cost of probiotic prophylaxis. A number of NHS trusts are currently using probiotics to prevent AAD and CDAD with encouraging results (contact author – Dr. A Harper for further details – ashton.harper@protexin.com). Out-patients: Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are both associated with GI dysbiosis. In IBD a reduction in the diversity of the luminal microbiota is common with a more profound difference observed in Crohn’s than ulcerative colitis (UC)15. Multi-strain probiotics, as adjuncts to conventional therapy in UC, have shown efficacy in both maintaining and inducing remission16. Clinical evidence for a benefit of probiotics in Crohn’s is however currently lacking17.

with approximately 30%19 of patients seeking medical attention (~3.5 million) it is unsurprising that 20-50% of gastroenterology referrals relate to this symptom complex20. A conservative estimate of the economic impact, in the UK alone, considering both direct care costs and costs to industry, is between £1.7 billion - £4.2 billion annually21. The discovery that IBS-D, which accounts for the majority of IBS referrals19, is associated with a significant decrease in GI biodiversity22 has prompted extensive research in this area. In IBS-D host antibodies to bacterial toxins (CdtB) cross react with the host cell adhesion protein vinculin to produce an IBS-like phenotype23; suggesting a post-infectious aetiology. Recent reviews of human clinical trials treating IBS with probiotics have concluded that they are effective therapies24 reducing both pain and symptom severity scores25. This clinical benefit in combination with low treatment costs could equate to substantial savings for the NHS.

GASTROENTEROLOGY TODAY - SPRING 2017

IBS has an estimated 17% UK prevalence18 (>11 million people) and

1 Sender R, Fuchs S, Milo R. Revised Estimates for the Number of Human and Bacteria Cells in the Body. PLoS Biol 2016; 14: 1–14. 2 Lozupone CA, Stombaugh JI, Gordon JI, Jansson JK, Knight R. Diversity , stability and resilience of the human gut microbiota. Nature 2012; 489: 220–30. 3 Adler CJ, Dobney K, Weyrich LS, et al. Sequencing ancient calcified dental plaque shows changes in oral microbiota with dietary shifts of the Neolithic and Industrial revolutions. Nat Genet 2013; 45: 450–5. 4 Ou J, Carbonero F, Zoetendal EG, DeLaney JP, Wang M, Newton K. Diet, microbiota, and microbial metabolitesin colon cancer risk in rural Africans and African-Americans. Am J Clin Nutr 2013; 98. DOI:10.3945/ ajcn.112.056689. 5 Sonnenburg JL, Bäckhed F. Diet–microbiota interactions as moderators of human metabolism. Nature 2016; 535: 56–64. 6 Li B-Z, Threapleton DE, Wang J-Y, et al. Comparative effectiveness and tolerance of treatments for Helicobacter pylori : systematic review and network meta-analysis. Bmj 2015; : h4052. 7 Testerman TL, Morris J. Beyond the stomach : An updated view of Helicobacter pylori pathogenesis diagnosis, and treatment. World J Gastroenterol 2014; 20: 12781–808. 8 Gotteland M, Brunser O, Cruchet S. Systematic review: Are probiotics useful in controlling gastric colonization by Helicobacter pylori? Aliment Pharmacol Ther 2006; 23: 1077–86. 9 Mukai T, Asasaka T, Sato E, Mori K, Matsumoto M, Ohori H. Inhibition of binding of Helicobacter pylori to the glycolipid receptors by probiotic Lactobacillus reuteri. FEMS Immunol Med Microbiol 2002; 32: 105–10. 10 Goldenberg J, Lytvyn L, Steurich J, Parkin P, Mahant S JB. Probiotics for the prevention of pediatric antibiotic-associated diarrhea ( Review ). Cochrane Database Syst Rev 2015; :CD004827.: 1–49. 11 Wiegand PN, Nathwani D, Wilcox MH, Stephens J, Shelbaya A, Haider S. Clinical and economic burden of Clostridium difficile infection in Europe: A systematic review of healthcare-facility-acquired infection. J Hosp Infect 2012; 81: 1–14. 12 McFarland L V. Evidence-based review of probiotics for antibioticassociated diarrhea and Clostridium difficile infections. Anaerobe 2009; 15: 274–80. 13 Hempel S, Maher AR, Wang Z, et al. Probiotics for the Prevention and Treatment of Antibiotic-Associated Diarrhea A Systematic Review and Meta-analysis. JAMA 2012; 307: 1959–69. 14 Goldenberg JZ, Ma SSY, Saxton JD, et al. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. Cochrane database Syst Rev 2013; 5: CD006095. 15 Ananthakrishnan AN. Epidemiology and risk factors for IBD. Nat Publ Gr 2015; 12: 205–17. 16 Cammarota G. The involvement of gut microbiota in inflammatory bowel disease pathogenesis : Potential for therapy. Pharmacol Ther 2015. DOI:10.1016/j.pharmthera.2014.12.006. 17 Lichtenstein L, Avni-Biron I, Ben-Bassat O. Probiotics and prebiotics in Crohn’s disease therapies. Best Pract Res Clin Gastroenterol 2016; 30: 81–8. 18 Khanbhai A, Sura DS. Irritable bowel syndrome for primary care physicians. Br J Med Pract 2013; 6: 1–4. 19 Canavan C, West J, Card T. The epidemiology of irritable bowel syndrome. Clin Epidemiol 2014; 6: 71–80. 20 Wilson S, Roberts L, Roalfe A, Bridge P, Singh S. Prevalence of irritable bowel syndrome: a community survey. Br J Gen Pract 2004; 54: 495–502. 21 Canavan C, West J, Card T. Review article: The economic impact of the irritable bowel syndrome. Aliment Pharmacol Ther 2014; 40: 1023–34. 22 Carroll IM, Ringel-Kulka T, Keku TO, et al. Molecular analysis of the luminal- and mucosal-associated intestinal microbiota in diarrheapredominant irritable bowel syndrome. Am J Physiol Gastrointest Liver Physiol 2011; 301: G799-807. 23 Pimentel M, Morales W, Rezaie A, et al. Development and validation of a biomarker for diarrhea-predominant irritable bowel syndrome in human subjects. PLoS One 2015; 10: 1–12. 24 Zhang Y, Li L, Guo C, et al. Effects of probiotic type, dose and treatment duration on irritable bowel syndrome diagnosed by Rome III criteria: a meta-analysis. BMC Gastroenterol 2016; 16: 62. 25 Didari T. Effectiveness of probiotics in irritable bowel syndrome: Updated systematic review with meta-analysis. World J Gastroenterol 2015; 21: 3072.

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COMPANY NEWS

FIT FOR PURPOSE

Reviewing Faecal Immunochemical Testing for Bowel Cancer Diagnosis by Matthew Davies, Senior Product Manager, Alpha Laboratories Ltd, Eastleigh, UK www.alphalabs.co.uk In June 2015 NICE published the NG12 guidelines and the re-

The introduction of new quantitative FIT methods has also changed

introduction of Faecal Occult Blood tests (FOBT) for patients with

the method of sample collection. This is an important aspect of

suspected colorectal cancers. This sparked controversy regarding

the process as the test NPV is reliant on the ability of the method to

the different types of occult blood tests currently available, as many

distinguish between the detection of occult blood at very low levels

hospital laboratories had discontinued the provision of Guaiac based

versus undetectable levels.

FOBT and did not want to go back to this old subjective technology. In June 2015 NICE published the NG12 guidelines and the re-introduction of Faecal Occult Blood tests (FOBT) for patients with suspected colorectal

Haemoglobin is very unstable and degrades rapidly at temperature. When present in faeces, which contains digestive enzymes, bacteria

cancers. This sparked controversy regarding the different types of

and fungi, it will degrade even quicker. Therefore, to protect the

occult blood tests currently available, as many hospital laboratories had

integrity of the sample it is vital to stabilise the haemoglobin present.

discontinued the provision of Guaiac based FOBT and did not want to go

Some FIT methods like the HM-JACKarc can stabilise the sample for

back to this old subjective technology.

up to 120 days at 4°C or 14 days at ambient temperature (up to 25 °C).

Whilst newer Faecal Immunochemical Test (FIT) methods have been introduced and publications

Consistency of sampling is another key

on such methodology have been increasing since

consideration. Results are expressed as µg

2012, these had not been part of the data review

of Hb / g of faeces, and thus any variation in

for the June 2015 publication. As a consequence

sample size could potentially impact the NPV

NICE have now reviewed FIT data and are due

cut-off. The HM-JACKarc sample collection

to publish new guidelines in April 2017 entitled:

device has been specifically designed to

“Quantitative faecal immunochemical tests to

consistently collect the same amount of

assess symptomatic people who are at low risk

sample. The unique dimpled collection probe

of colorectal cancer in primary care”.

enables uniform sampling, irrespective of the

This assessment is focused on peer reviewed publications of quantitative FIT methods. Some of these publications are based on symptomatic patients where a FIT has been performed on samples from patients already scheduled for colonoscopy1,2,3. The quantitative FIT results have been compared against the clinical findings and these publications identify that the FIT result could be used as a negative predictive value (NPV) for Cancer. In fact, using a cut-off of < 10 µg of Hb/ g of faeces, this NPV was almost 100%. Furthermore, these publications also identify GASTROENTEROLOGY TODAY - SPRING 2017

that faecal haemoglobin (f-Hb) could also be used to provide a high NPV (around 94%) for other serious bowel conditions, such as High Risk Adenomas (HRA) and Inflammatory Bowel Disease (IBD). The NICE Diagnostics Assessment Committee has published a draft document on the internet, detailing the outcome of its review www.nice.org.uk/guidance/indevelopment/gid-dg10005/documents

consistency. The NPV data provided by many publications show cut-offs at the low end of the analytical range of the available technologies. The choice of the laboratory method is therefore important to the clinical evaluation of patients referred to secondary care, not only for its sample preservation, but also for its accuracy and precision at the low end of the detection range. Four FIT systems were evaluated by the Guildford Medical Evaluations Centre (GMEC) in 2013. The resulting report is available online. (http://194.97.148.137/assets/downloads/pdf/activities/ fit_reports/gmec_fit_evaluation_report.pdf) In this study the HM-JACKarc technology was described as one of the more precise methods and its analytical range correlated well

Differentiating patients with serious bowel disease from benign functional

to expected values of spiked faecal samples. The ability to detect

disorders can be challenging and the ability to use a diagnostic test

haemoglobin at both the low and high end of the analytical range

will provide additional assistance in determining the appropriate patient

was confirmed along with the sample stability experiments.

pathway for further investigation. Ahead of this publication, several hospitals and CCG’s have already committed to the provision of FIT as a

For more information on the HM-JACKarc and how this could help with

means of triaging patients scheduled for colonoscopy.

your clinical practice, please visit www.alphalabs.co.uk/fit .

Godber IM, Todd LM, Fraser CG, MacDonald LR, Ben Younes H. Use of a faecal immunochemical test for haemoglobin can aid in the investigation of patients with lower abdominal symptoms. Clin Chem Lab Med 2016;54:595-602 2 Thomas CL, Tomkins C, Widlak M, Smith S, Arasaradnam R. Can immunochemical tests for faecal haemoglobin and faecal calprotectin be used to risk stratify patients for referral to colonoscopy for suspected colorectal cancer? Annals of Clinical Biochemistry 2016;53 Suppl 1:38-9. 3 Auge JM, Fraser CG, Rodriguez C, Roset A, Lopez-Ceron M, Grau J, Castells A, Jimenez W. Clinical utility of one versus two faecal immunochemical test samples in the detection of advanced colorectal neoplasia in symptomatic patients. Chem Lab Med. 2016:54:125-132. 1

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person performing the sampling or the stool


COMPANY NEWS

The BSG Annual Meeting 2017, taking place at the Manchester Central Convention Complex from Monday 19 June – Thursday 22 June 2017, is set to be the best meeting yet. This four day meeting begins on Monday 19 June 2017 with the Gastroenterology Master Class “Dealing with Dilemmas”, which will see world renowned speakers from the UK and abroad provide advice and guidance on how to approach those problematic diagnostic and management challenges which we face in every day practice.

The exhibition opens on Monday evening with a drinks reception to mark the 80th anniversary of the BSG The main scientific programme Tuesday 20 – Thursday 22 June 2017 will include basic and clinical science symposia, state-of-the-art lectures, clinical updates, moderated poster rounds, the new endoscopy village and the industry exhibition. This year we are having themed days at the meeting to facilitate your main areas of interest! Please check out the online programme to make sure you don’t miss the sessions that interest you most!

Register now to benefit from the Early Bird rates These rates are available until 17 March 2017 and offer a significant discount, especially to BSG members. New for 2017 is the addition of a nurse “Unit Registration Fee”, offering a group discount to three nurses of any grade (who are BSG Members) from the same unit when registering together.

Don’t miss the abstract submission deadline of 24 February 2017! Visit www.bsg2017.org.uk to secure your place, view the programme and submit your abstract now.

Sponsorship/exhibition opportunities:

wh sc to prac ere you will b opy tice you e able models , watch r skills on pig demon try out stra ne discuss w technologie tions, s with ex perts h and perfect ow to your te chniqu e.

BSG2017industry@mci-group.com

Conference Secretariat: BSG2017@mci-group.com

#BSG2017

@BritSocGastro

www.BSG2017.org.uk

GASTROENTEROLOGY TODAY - SPRING 2017

Attending Endolive UK 2017? Use your Endolive UK code to receive a 20% discount on Early Bird registration rates.

Endosc opy New fo Village r 2017! In the e xhib be a ha ition area the re will nds-on village endo

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