November 2019 Clinical Advisor by The Clinical Advisor

A PEER-REVIEWED FORUM FOR NURSE PRACTITIONERS

NEWSLINE

■■ Lipoid Pneumonia and Marijuana Oils in E-Cigs ■■ USPSTF Breast Cancer Risk-Reduction Guidance ■■ Botulinum Toxin for Endometriosis Pain ■■ Soft Drink Consumption and Mortality LEGAL ADVISOR

Is Accessing PHI a Violation? CONFERENCE ROUNDUP

Psych Congress 2019

DERMATOLOGY CLINIC

Erythematous, Eczematous, and Pruritic Lesions

CASE STUDY

Extensive Deep Venous Thrombosis

NOVEMBER 2019

| www.ClinicalAdvisor.com

GASTROENTEROLOGY

Therapeutic Potential of Fecal Microbiota Transplant in Obesity The ideal gut microbiome has yet to be determined.

Statement of Ownership, Management, and Circulation

Vice president, content, medical communications, editor Kathleen Walsh Tulley Associate editor Madeline Morr Assistant editor Rita Aghjayan Production editor Kim Daigneau Group creative director, medical communications Jennifer Dvoretz Senior production manager Krassi Varbanov Director of audience insights Paul Silver National sales manager Alison McCauley, 973.224.6414 alison.mccauley @ haymarketmedical.com Associate account manager Michael Deverin, 732.343.4921 michael.deverin@haymarketmedia.com Publisher Kathleen Hiltz, 201.774.1078 kathleen.hiltz@haymarketmedia.com General manager, medical communications Jim Burke, RPh President, medical communications Michael Graziani CEO, Haymarket Media, Inc. Lee Maniscalco All correspondence to: The Clinical Advisor 275 7th Avenue, 10th Floor, New York, NY 10001 For advertising sales, call 646.638.6085. For reprints/licensing, email haymarketmedia@theygsgroup.com or call 800.290.5460. Persons appearing in photographs in “Newsline,” “The Legal Advisor,” and “Features” are not the actual individuals mentioned in the articles. They appear for illustrative purposes only. The Clinical Advisor® (USPS 017-546, ISSN 1524-7317),Volume 22, Number 10. Published 11 times a year, by Haymarket Media, Inc., 275 7th Avenue, 10th Floor, New York, NY 10001. For Advertising Sales & Editorial, call (646) 638-6000 (M–F, 9am–5pm, ET). The Clinical Advisor is available on a paid subscription basis at the following annual rates: $75 USA, $85 Canada, $110 for all other foreign, in U.S. dollars, Single copy price: USA $20, Foreign $30. To order or update a paid subscription visit our website at www. ClinicalAdvisor.com or call (800) 436-9269. Periodicals postage rate paid at NewYork, NY, and additional mailing offices. Postmaster: Send changes of address to The Clinical Advisor, c/o Direct Medical Data, 10255 W. Higgins Rd., Suite 280, Rosemont, IL 60018. All rights reserved. Reproduction in whole or in part without permission is prohibited. Copyright © 2019

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www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 1

CONTENTS NOVEMBER 2019

NEWS 6

Newsline ■■Acute Lipoid Pneumonia Linked to Marijuana Oils in E-Cigs ■■Botulinum Toxin for Chronic Pelvic Pain in Endometriosis ■■Soft Drink Consumption Associated With Mortality ■■Forced Sexual Initiation Linked to Adverse Health Outcomes ■■And more

6 Lipoid Pneumonia and E-Cigs

Conference Roundup Psych Congress 2019

FEATURE 12 Therapeutic Potential of Fecal Microbiota Transplant in Obesity Fecal microbiota transplant may have potential as an effective therapeutic option for the treatment of obesity. 27 Burning, Itchy Rash

DEPARTMENTS 4

Web Roundup A summary of our most recent opinion, news, and multimedia content from ClinicalAdvisor.com.

18 Case Study: Deep Venous Thrombosis A young woman presents with abrupt onset of swelling and pain in the lower extremity. 23 34 PAs and Mental Health Management

Dermatology Clinic ■■Erythematous Plaques With Scaling ■■Erythematous, Eczematous, and Pruritic Lesions

27 Dermatologic Look-Alikes Rash With Burning and Pruritus 39 Legal Advisor Is Accessing PHI a Violation?

39 Privacy Violation Without a HIPAA Breach

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NEWS

FEATURES

ClinicalAdvisor.com/News

ClinicalAdvisor.com/Features

Link Between Altered Microbiota and Cognitive Performance Identified

Inhaler Misuse in Asthma and COPD: Undoing 40 Years of Incorrect Technique Challenges pertaining to the correct use of inhalers for asthma and COPD can limit the effectiveness of treatment.

Cognitive impairment in veterans with cirrhosis was more severe in those with posttraumatic stress disorder (PTSD) vs those without PTSD, and these results were seen in tandem with reduced microbial diversity.

Screening for Cognitive Decline in Primary Care Although an estimated 82 million people worldwide will be affected by dementia by 2030, research demonstrates that cognitive decline often goes unrecognized in primary care settings.

Transversus Abdominis Plane Block May Improve Opioid Pain After Cesarean Section Patients in the TAP vs no TAP group had lower visual analog pain scores 3 hours, 6 hours,12 hours, and 36 hours after surgery.

Secondhand Smoke Exposure, Smoking, and Risk of AFib Researchers found a significant association between parental smoking and offspring smoking, and offspring smoking was associated with increased incident atrial fibrillation.

THE WAITING ROOM

Official Blog of The Clinical Advisor ClinicalAdvisor.com/WaitingRoom Jim Anderson, MPAS, PA-C, DFAAPA Providing Medical Services to Immigrants Seeking Asylum The crisis at the border is an ongoing medical emergency that has not been treated as such by medical organizations, including the AAPA and AANP.

Effect of Health Status on Insulin Use in Type 2 Diabetes Insulin discontinuation in older adults is not aligned with guidelines that advise considering health status in treatment decisions.

PRACTICE MANAGEMENT ClinicalAdvisor.com/MyPractice Majority of Physicians Believe ACA Has Had Positive Impact on Health Care Results of a survey reveal that an increasing number of physicians agree with the overall direction of the ACA and report favorable impressions regarding improved access to insurance and coverage for preexisting conditions.

4 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

Advisor Dx Interact with your peers by viewing the images and offering your diagnosis and comments. To post your answer, obtain more clues, or view similar cases, visit ClinicalAdvisor.com/AdvisorDx. Learn more about diagnosing and treating these conditions, and see how you compare with your fellow colleagues. Check out some of our latest cases below!

DERM DX

Itchy Eruption on the Upper Back and Arm A 50-year-old woman presents with acute onset of an itchy eruption on her upper back and arm following a weekend spent hiking and relaxing at a day spa. As a child she experienced numerous bouts of poison ivy but has had no similar cases for most of her adult life. The patient has been taking lovastatin for the past 18 months. CAN YOU DIAGNOSE THIS CONDITION?

• Herpes zoster • Fire ant bites

• Hot tub folliculitis • Poison ivy

● See the full case at ClinicalAdvisor.com/DermDx_Nov19

In partnership with

ORTHO DX

TheJopa.org

Journal of Orthopedics for Physician Assistants

Bilateral Knee Pain Due to Osteoarthritis A 63-year-old woman presents to the office with bilateral knee pain and a known history of osteoarthritis. Anteroposterior radiograph of the bilateral knees is obtained. The patient was previously told that unloader bracing would be a good option for her knee arthritis. WHICH STATEMENT REGARDING UNLOADER BRACING IS TRUE?

• Shorter patients are better candidates for bracing. • Unloader braces are used for tricompartmental arthritis. • An unloader brace places a valgus stress on the knee in a patient with medial compartment arthritis. • An unloader brace places a varus stress on the knee in a patient with medial compartment arthritis ● See the full case at ClinicalAdvisor.com/OrthoDx_Nov19

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 5

Newsline THE POTENTIAL association between use of marijuana oils or concentrates in electronic cigarettes (e-cigarettes) and lipoid pneumonia was highlighted in a recent Morbidity and MortalityWeekly Report. The authors examined 5 adult cases (ages 18-35) reported from 2 hospitals in North Carolina. Patients had experienced several days of worsening dyspnea, nausea, vomiting, abdominal discomfort, and fever. On examination, patients demonstrated tachypnea with increased work of breathing and hypoxemia. Bilateral lung infiltrates were found on chest radiography. All of the patients had reported recently using marijuana oils or concentrates in e-cigarettes.The devices had refillable chambers or interchangeable cartridges with tetrahydrocannabinol vaping concentrates or oils, which were purchased on the street. Three of the patients studied required intensive care for acute respiratory distress

syndrome, 1 of whom required intubation and mechanical ventilation. Initially, all of the patients were treated for presumed community-acquired or aspiration pneumonia using either a 2-drug combination of ceftriaxone and azithromycin or a fluoroquinolone. However, within 48 hours of admission, they all developed worsening respiratory failure. In addition, blood and sputum cultures were negative for bacterial pathogens, and tests for influenza, Mycoplasma, and Legionella were also negative. Diffuse basilar-predominant infiltrates with a range of ground glass opacities and nodular (or “tree-in-bud”) infiltrates were observed on chest computed tomography. Three patients underwent bronchoscopy with bronchoalveolar lavage, which yielded a combination of neutrophils, lymphocytes, and vacuole-laden macrophages but without evidence of alveolar

Acute Lipoid Pneumonia Linked to Marijuana Oils in E-Cigs

Lipoid pneumonia involves inflammation caused by fat particles in the lungs.

hemorrhage or eosinophilia. Lavage cytology confirmed extensive lipid presence within alveolar macrophages. Based on clinical history, radiography, and laboratory and bronchoscopic diagnostics, all 5 patients were diagnosed with acute exogenous lipoid pneumonia. The patients were treated with intravenous methylprednisone and improved within 24 to 72 hours of administration; all of the patients survived and were discharged home with a taper of oral prednisone.

USPSTF Guidance on Breast Cancer Risk-Reducing Medications THE US PREVENTIVE Services Task Force (USPSTF) has issued final recommendations on the use of medications for reducing the risk of primary breast cancer. As stated in 2013, the USPSTF recommends that clinicians should offer risk-reducing medications (ie, tamoxifen, raloxifene, or aromatase inhibitors) to women aged 35 years and older (without signs or symptoms of breast cancer) who are at increased risk for breast cancer and at low risk for adverse effects associated with these medications (B recommendation).The Task Force also recommends against the use of these agents in women who are not at increased risk for breast cancer (D recommendation).

Based on a review of 10 trials, the USPSTF found that in women at increased risk, over 5 years the incidence of invasive breast cancer was reduced by 7, 9, and 16 events per 1000 women with tamoxifen, raloxifene, and aromatase inhibitors, respectively. “For women with a predicted 5-year breast cancer risk of 3% or greater, the absolute benefits are likely even higher,” the Task Force noted. However, for women at low risk for breast cancer, the USPSTF found that these agents only provided a small benefit that did not outweigh the potential harms associated with therapy (ie, venous thromboembolic events, vasomotor symptoms, endometrial cancer, and cataracts).

6 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

Newsline Botulinum Toxin for Chronic Pelvic Pain in Endometriosis BOTULINUM TOXIN injections were found to relieve chronic pelvic pain in women with endometriosis, suggesting that pelvic floor spasms may contribute to endometriosis-linked pelvic pain, according to study results published in Regional Anesthesia & Pain Medicine. In an open-label, proof-of-concept case series, investigators aimed to determine whether botulinum toxin injections reduce pain and muscle spasm in women with surgically recorded endometriosis who experience chronic pelvic pain despite hormonal and surgical interventions. Following administration of up to 10 mg oral diazepam and 4% lidocaine cream to the vaginal mucosa above the spasms, participants underwent transvaginal injection of onabotulinumtoxinA into pelvic floor muscle spasms; 100-unit vials were suspended in saline and administered to 3 or 4 preidentified areas of spasm. Measures of pain, muscle spasm, disability,

Pelvic floor spasms may contribute to endometriosis-linked pelvic pain.

and pain medication use were recorded at patient visits up to 1 year postinjection. Of the 13 women included in the study, 11 experienced moderate pain and muscle spasms in more than 4 of 6 monitored pelvic muscles. All participants reported complete or significantly reduced spasms by 4 to 8 weeks following

injection; 11 women reported absent or mild pain, 7 women reduced pain medication use, and 6 women experienced a decrease in disability. After treatment, 7 of the 11 women who experienced muscle spasms were followed for up to 1 year and reported 5 to 11 months of lasting relief. “This study provides preliminary evidence that in women with evidence of pain arising from pelvic floor muscles, this approach might best be considered after the visceral aspects driving their pain have been managed, possibly with suppression of menses, and optimization of bowel and bladder function,” the investigators noted. “Importantly, this procedure may offer an opportunity to reduce opioid use.This intervention may then be incorporated into the chronic pain model of care, enabling a precision medicine approach with individualized, multifaceted treatment.”

Soft Drink Consumption Associated With Mortality TOTAL, SUGAR-SWEETENED, and artificially sweetened beverage consumption is associated with all-cause mortality, according to study results published in JAMA Internal Medicine. Investigators conducted a populationbased cohort study across 10 European countries to determine the association between soft drink intake and mortality. Individuals who reported a history of cancer, heart disease, stroke, or diabetes at baseline were excluded from participation. The primary outcomes were total and cause-specific mortality. Of the 521,300 people enrolled, 451,743 were included in the study (mean age, 50.8; 71.1% women).There were 41,693 reported deaths in the 16.4-year mean follow-up; 43.2% of these deaths were

from cancer, 21.8% were from circulatory diseases, and 2.9% were from digestive diseases. Compared with individuals who consumed <1 glass of soft drink per month (low consumption), all-cause mortality was higher among individuals who drank ≥2 glasses per day of total soft drinks

day was positively associated with death from circulatory disease (HR, 1.52). In addition, the consumption of ≥2 glasses per day of artificially sweetened soft drinks was positively associated with death from digestive diseases compared with low consumption (HR, 1.59).

Drinking 2 or more glasses of artificially sweetened soft drinks each day was associated with death from circulatory disease and digestive diseases. (hazard ratio [HR], 1.17), sugar-sweetened soft drinks (HR, 1.08), and artificially sweetened soft drinks (HR, 1.26). Compared with low consumption (<1 glass per month) of artificially sweetened soft drinks, consumption of ≥2 glasses per

8 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

“The role of BMI in the soft drink consumption and mortality outcomes association is complex, with adiposity likely a mediating and confounding factor that varies by cause of death,” the investigators noted.

Newsline

Forced Sexual Initiation Linked to Adverse Health Outcomes

Forced sexual initiation includes coercion, verbal pressure, and physical force.

WOMEN WHO were pressured or physically forced into an unwanted first sexual intercourse were found to have increased rates of adverse reproductive, gynecologic, general health, and functional outcomes, according to study results published in JAMA Internal Medicine. Investigators conducted a cross-sectional analysis to determine the frequency of involuntary sexual initiation among US women and if these encounters would subsequently affect reproductive, gynecologic, and general health outcomes. The primary outcomes measured were the prevalence of forced sexual initiation, the age of the woman and her partner at primary sexual intercourse, and the odds ratios for unwanted pregnancy or abortion, development of pelvic pain, and other reproductive and general health events. Results suggested that women who experienced unwanted primary intercourse were on average 2 years younger than women with voluntary sexual initiation (15.6 years vs 17.4 years, respectively). The average age gap between women included in the study and their sexual partners was 6 years. Of women who reported forced sexual initiation, 74.7% were younger than

18 years at the time compared with 60.5% of women who experienced voluntary sexual initiation; 6.8% of women subjected to forced sexual initiation and 0.1% of women with voluntary sexual initiation were younger than 10 years at the time. Of the women who reported forced sexual initiation, 50% claimed they were coerced by a partner who was larger or older; 54% reported experiencing verbal pressure and 46.3% were physically forced. Women who were forced into their first sexual intercourse also reported being given a drug (22.0%) or experiencing a physical threat (26.5%) or physical harm (25.1%). Compared with women who had voluntary experiences, women who were forced into sexual initiation were more likely to have had an unwanted first pregnancy (adjusted odds ratio [aOR], 1.9), an abortion (aOR, 1.5), or to not have used birth control in their lifetime (aOR, 2.6).Women who were subjected to forced sexual initiation were more likely to experience pelvic inflammatory disease, endometriosis, and ovulation or menstruation-related problems.They were also more likely to have not undergone cervical cancer screening or HIV testing. Illicit drug use (aOR, 3.6), fair or poor health (aOR, 2.0), and difficulty completing tasks owing to a physical or mental health condition (aOR, 2.8) were more frequently reported among survivors of forced sexual initiation. “A substantial proportion of American women may experience forced sexual initiation, and the individual and public health implications of this exposure are far reaching,” the investigators noted. “Although additional research is needed, physicians should incorporate trauma informed measures into their practices while advocating for the reduction of structural causes of sexual violence.”

10 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

USPSTF Screening Recommendations for Asymptomatic Bacteriuria THE US PREVENTIVE Services Task Force (USPSTF) has updated its screening recommendations for asymptomatic bacteriuria by urine culture in pregnant persons (B recommendation), according to a statement published in JAMA. During pregnancy, asymptomatic bacteriuria may develop in a small percentage of women, which may increase the risk for pyelonephritis.To update the 2008 recommendation statement, the USPSTF commissioned a systematic evidence review to evaluate the potential benefits and harms of screening for and treating asymptomatic bacteriuria. The USPSTF concluded with moderate certainty that screening for and treating asymptomatic bacteriuria in pregnant persons has a moderate net benefit in reducing perinatal complications. The USPSTF found inadequate evidence on the harms of screening for asymptomatic bacteriuria in pregnant persons, although these harms are thought to be small. With moderate certainty, the USPSTF concludes that screening for and treating asymptomatic bacteriuria in nonpregnant adults has no net benefit. The harms associated with treatment of nonpregnant individuals include adverse effects associated with antibiotic use and changes to the microbiome. Therefore, USPSTF determined the overall degree of harm to be at least small in this group. The major update to the 2008 recommendation is that the USPSTF changed the grade for pregnant persons from “A” to “B.”

Efficacy, Cost-Effectiveness of Herpes Zoster Vaccination RESULTS FROM A study published in CMAJ found that vaccines against herpes zoster are effective for people aged ≥50 years; in addition, the recombinant subunit zoster vaccine was found to be more cost-effective than the live attenuated zoster vaccine. Researchers compared the incidence of herpes zoster and postherpetic neuralgia, mortality rate, use of health care resources, costs, and quality-adjusted life-years (QALY) lost between vaccinated and unvaccinated adults. The researchers predicted that 90,623 cases of herpes zoster, 13,575 cases of ophthalmic herpes zoster, and 17,502 cases of postherpetic neuralgia would occur among adults aged ≥50 years in Canada, with the highest burden of disease occurring in those aged ≥70 years.The number needed to vaccinate was higher for the live attenuated zoster vaccine than for the

recombinant subunit zoster vaccine for all herpes zoster-related events at all ages. The difference in the number needed to vaccinate between the vaccines increased with increasing age for the live vaccine but not for the recombinant vaccine. Administration of the vaccine in adults aged 65 to 75 years was predicted to result in cost-effective ratios below $45,000 per QALY gained for both vaccines and

The recombinant vaccine was estimated to be more cost-effective.

under all scenarios. For the recombinant vaccine, the median cost-effectiveness ratio predictions varied between costsaving and $25,881 per QALY gained. For those aged ≥60 years, the cost-effectiveness ratios remained stable. For the live vaccine, the median cost-effectiveness ratio predictions varied between cost saving and $130,587 per QALY gained. The cost-effectiveness ratios for the live vaccine were highly sensitive to age at vaccination but remained below $45,000 per QALY gained for those between 65 and 75 years of age. The recombinant vaccine was estimated to be more cost-effective than the live vaccine for all ages at vaccination. Depending on the age at vaccination, the cost for the complete series of the recombinant vaccine could be $150 to $200 more than for the live vaccine and still be considered cost-effective.

Blood Biomarkers Detect Brain Injury Following Trauma THE SERUM BIOMARKERS glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase (UCHL1) were found to be effective in detecting concussion in pediatric and adult patients with normal mental status following trauma, according to study results published in BMJ Paediatrics Open. GFAP was more successful than UCH-L1 at detecting concussion; however, UCH-L1 levels were higher in patients with nonconcussive trauma, especially in children. In a large prospective cohort study, investigators aimed to determine whether GFAP and UCH-L1 concentrations could detect concussion in patients following trauma, and how changes in these concentrations may correlate with concussive and nonconcussive head and body trauma. Primary outcomes were

the presence of concussion and gradients of injury in pediatric vs adult patients. A total of 751 pediatric and adult patients who had normal mental status within 4 hours of injury were enrolled in the study; 712 had complete biomarker data. Of the enrolled partici-

Within 4 hours of injury, both GFAP and UCH-L1 levels gradually increased for all 3 groups, with the lowest increase seen in patients sustaining nonconcussive trauma and the greatest increase seen in patients with concussion. Compared with both control groups, pediatric and

Within 4 hours of injury, both biomarker levels gradually increased for all 3 groups, with the greatest increase seen in patients with concussion. pants, 52% had a concussion, 21% had nonconcussive head trauma, and 27% had nonconcussive body trauma; 25% of participants were children and 75% were adults. Blood samples were repeatedly obtained from adult patients from 4 to 180 hours postinjury.

adult patients with concussive injuries were found to have significantly higher GFAP concentrations. No significant differences in UCH-L1 concentrations were reported between the concussion cohort and head trauma control or between body trauma and head trauma groups. ■

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 11

FEATURE: MICHELLE PETROPOULOS, DMSC, PA-C, DFAAPA

Therapeutic Potential of Fecal Microbiota Transplant in Obesity The human gut microbiota has been identified as a metabolic organ having a significant effect on host metabolism.

Scientific evidence of the human microbiome has existed since the 1880s.

12 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

he World Health Organization defines obesity in adults as a body mass index (BMI) ≥30 kg/m2 and overweight as a BMI ≥25 kg/m2.1 Worldwide, approximately 1.9 billion adults are overweight, with 650 million of those classified as obese.1 This global epidemic is responsible for economic drain and is associated with numerous chronic disorders and comorbidities, including cardiovascular disease, cancer, sleep apnea, liver disease, and infertility. As per the Centers for Disease Control and Prevention, the healthcare cost of obesity in 2008 was $147 billion.2 Effective treatments therefore have the potential to decrease the incidence and ultimately the economic impact of obesity. While it is known that the human microbiome has an impact on disease, this relationship has not been robustly studied until recently. The human gut microbiota has been identified as a metabolic organ having a significant effect on host metabolism. Lean individuals harbor a diverse microbiota that requires extraction of less energy from food sources. In contrast, an obese individual’s microbiota is less diverse and extracts more energy from food. The obese gut microbiome becomes more diverse with weight loss and exercise. Although it is not yet clear how long this change lasts, increased intestinal microbiome diversity has been found to be associated with increased host metabolism. Establishing the ideal gut microbiome has yet to be determined. Probiotics and prebiotics may alter this microbiome, although no clear evidence

exists suggesting that this alteration can diversify in a way to increase metabolism for the long term. However, it is known that antibiotic use can decrease diversity permanently.3 Most widely known as a successful treatment for Clostridioides difficile colitis, fecal microbiota transplant (FMT) may have potential as an effective therapeutic option for the treatment of obesity. FMT is the administration of a solution of fecal matter from a donor into the intestinal tract of a recipient, directly altering the recipients’ gut microbiome. The procedure is performed via enema, encapsulation, colonoscopy, or nasogastric tube. The layman’s view that lean individuals have a faster metabolism than their heavier counterparts is far from the truth. Historically, metabolism has been studied using the basal metabolic rate, which was first defined in 1924.4 The basal metabolic rate is derived from a standard calculation using height, weight, age, and gender as the sole factors affecting metabolism. This tool determines total daily energy expenditure or the number of calories burned at rest.Throughout history, researchers have looked at factors in addition to the basal metabolic rate that have the potential to affect metabolism such as genetics, race, biochemical parameters, environmental factors, health status, and diet composition.5 Identifying the gut microbiota as a metabolic organ combines both old and new information. Scientific evidence of the human microbiome and its impact on disease has existed since the 1880s. This knowledge has only recently expanded with the National Institutes of Health Common Fund Human Microbiome Project of 2007.6 This project was established with the mission of generating research resources that have been the basis for several studies analyzing the human microbiota and its role in overall health and disease.6 Manipulation of the gut microbiome represents a promising therapeutic approach not only for obesity but also for autoimmune diseases, mood disorders, type 2 diabetes, and dermatologic conditions. Clinical Significance of the Gut Microbiota

Obesity is a comorbid disease that also carries social stigma. The media often correlate beauty with low body weight, as is reflected by the vast majority of advertisements depicting the typically thin model selling everything from tools to fashion. Television and movies follow suit. Coupled with the increased health risks that obesity imposes, these social constructs can have a detrimental effect on an obese individual’s self-esteem, body image, and overall well-being. Identifying factors that affect metabolism has the potential to provide a pathway to success for those who struggle to attain an appropriate body weight. Diet and exercise are not the only contributors to a successful weight loss program. Recognition of the gut microbiota as a metabolic organ may change the way we view and think about obesity. Unidentified variables influencing body habitus exist and until recently, the intestinal microbiota was one of them. Several

intestinal microbiome studies currently in progress are focusing on this relatively newer thought process; however, enough information currently exists to enhance the understanding of the role the human microbiota has on body composition. Although clinical applications and benefits are still in the early stages of research, the correlation between the lack of diverse gut microbiota and obesity may identify opportunities for novel treatment options. Therapeutic Potential of FMT

The idea of incorporating FMT as a treatment for obesity emerged in 2004 with a study that looked at gut microbiota as a factor in metabolism. Conducted at the Washington University School of Medicine, this study involved feeding stool from traditionally raised mice to germ-free mice. The outcomes of the study demonstrated a 60% increase in body fat content and insulin resistance in germ-free mice 14 days after intestinal colonization, despite no change in caloric intake.7 Launched in 2007, the Human Microbiome Project identified our metabolic landscape, revealing a connection between the variable human microbiome and disease.6 This project was an international summary reflection of multiple works connecting medical and environmental microbiology to identify new pathways of disease intervention. This framework created the opportunity to intentionally manipulate gut microbiota, subsequently optimizing an individual’s host metabolism. We now know that the digestive capacity of the gut microbiota influences the nutrient and caloric value of food. Turnbaugh and colleagues initially identified the gut microbiome as a

POLL POSITION Which of the following is the least abundant bacterial-dominant phyla in the human gut? 7.68% ■ Chloroflexi ■ Firmicutes

13.68%

29.06%

■ Proteobacteria ■ Actinobacteria ■ Bacteroidetes

21.37% 28.21%

For more polls, visit ClinicalAdvisor.com/Polls.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 13

GASTROENTEROLOGY

contributing factor in the pathophysiology of human obesity.8 Further research has uncovered that the obese microbiome has an increased capacity to harvest energy from food and that the intestinal microbiota not only differs between the lean and obese but is also transferable between human subjects. What Is in the Gut?

The human gut microbiota is primarily made up of bacterial organisms residing in the colon, with a smaller percentage of Archaea, eukaryotes, and viruses.The 2 major bacterial-dominant phyla in the human gut include Firmicutes and Bacteroidetes, followed by Proteobacteria and Actinobacteria, which altogether account for 97% of the gut microbe population.3 A greater percentage of body fat correlates with a greater ratio of Firmicutes to Bacteroidetes; hence, obesity is associated with changes in the amount of at least 2 of these major phyla.9 Generally, Bacteriodetes are decreased and Firmicutes are increased in obesity, resulting in an increased Firmicutes-to-Bacteroidetes ratio (Table). A number of small studies have reported controversial and conflicting results regarding the optimal microbiota profile and the different phenotypes associated with BMI. This is most likely the result of the various less-abundant species of each phylum, different methodologies employed in each study, and an increase in more recent data and knowledge.10 Although current evidence is preliminary, multiple factors including genetic, environmental, diet, exercise, and psychological stress are considered to contribute to the incidence of TABLE. Generalization of Lean and Obese Intestinal Microbiome* Obese

Lean

Microbial Diversity

↓

↑

Firmicutes

↑

↓

Bacteroidetes

↓

↑

Proteobacteria

↑↓

Actinobacteria

Equivocal or ↑

Equivocal or ↓

↑

↓

Firmicutes/Bacteroidetes ratio

*Conflicting data exist regarding the optimal microbiota for weight loss. Possible explanations include (a) Firmicutes are more effective as an energy source than Bacteroidetes, resulting in increased calorie absorption; (b) the association between the relative proportion of gut anaerobic and blood glucose levels; (c) the abundance of various species within each phylum; (d) different study methodologies; and (e) the dietary habits of participants in specific geographic locations.3,11,12,14,20

obesity. Jayasinghe and colleagues identified the connection between obesity and metabolic disorders in relation to the potential of FMT as a treatment for obesity. Gut microbiota were found to affect host metabolism by promoting uptake of monosaccharides, storage of triglycerides, digestion of dietary fiber, and the synthesis of hormonal precursors.11 Short-chain fatty acids (SCFA) are microbial metabolites responsible for several physiologic effects. Complex carbohydrates are metabolized by intestinal microbiota to oligosaccharides and monosaccharides, and then fermented to SCFA such as butyrate, propionate, and acetate.12 Once absorbed in the colon, propionate and acetate act as substrates in the liver and peripheral organs for gluconeogenesis and lipogenesis. SCFA reduce intestinal permeability and regulate such processes within the gastrointestinal tract as absorption of water and electrolytes. The types and amount of SCFA produced are determined by how much carbohydrate is consumed and the composition of the gut microbiota. A higher number of SCFA is associated with obesity due to the increased dietary energy harvest, which translates to more calories absorbed from the diet compared with a lower amount of SCFA. Two important points to recognize are that obesity is associated with microbial dysbiosis, characterized by decreased microbial gut diversity and lack of bacterial richness, and that lean individuals have a more diverse gut microbiome and more optimal metabolic homeostasis.13 Multiple factors contribute to the composition of the gut microbiome, dysbiosis, and fecal microbiota diversity. These variables result in a lack of consistency in an obese individuals’ microbiota composition and complicating the relationship between gut microbiota and energy homeostasis. Allen et al established a relationship between exercise and changes in the gut microbiota.14 This small study of 32 lean and obese individuals reported the presence of a more diverse gut microbiota with regular exercise, which was sustained only if exercise continued. A study by Graessler et al evaluated patients following bariatric surgery and found increased microbial diversity during weight loss that was not sustained in those gaining weight 2 years following the procedure.15 De Clercq and colleagues introduced the role of the gut-brain axis and microbial diversity in metabolism.16 The investigators highlighted the link between host metabolism and behavior via bidirectional signaling between the gastrointestinal tract and the brain. The effect of SCFA on energy homeostasis through the regulation of gastrointestinal hormones such as cholecystokinin, glucagon-like peptide-1, peptide tyrosine-tyrosine, and leptin has also been the focus of research. Preclinical studies show that modifying the microbiota of rodents through FMT results in alterations of these hormones, which affect not only metabolism but also behavior. Whether these findings translate to human Continues on page 17

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GASTROENTEROLOGY

The Human Microbiome Project was established to analyze the role of the human microbiota in overall health and disease. metabolism is as yet unclear. However, the ideal microbiome may have the potential to command the gut-brain axis and positively influence the pathophysiology of metabolic disease.

4. McNab BK. On the utility of uniformity in the definition of basal rate of metabolism. Physiol Biochem Zool. 1997;70(6):718-720. 5. Taousani E, Savvaki D, Tsirou E. Regulation of basal metabolic rate in uncomplicated pregnancy and in gestational diabetes mellitus. Hormones (Athens).

FMT in Obesity

2017;16(3):235-250.

Given that gut dysbiosis has been implicated in obesity, and FMT improves gut flora, further research is warranted to clarify this connection and assess treatment potential. A case report published in 2015 identified an individual experiencing a disproportionate weight gain after undergoing FMT.17 A 32-year-old woman with recurrent C difficile infection underwent FMT from an obese donor. This patient experienced a rapid weight gain of >30 lb despite a supervised high-protein liquid diet and exercise program. In addition, a review by Marotz and Zarrinpar describes the exciting potential of FMT as a treatment for metabolic syndrome but cites the lack of randomized controlled trials that currently exist, which supports the need for and usefulness of further investigation into this topic.18 In a randomized, double-blind, controlled trial using gut microbiota transfer via gastroduodenal tube from a lean donor vs the subjects’ own gut microbial infusion, a statistically significant improvement in peripheral insulin sensitivity was seen 6 weeks following treatment.19 As of this writing, researchers at Helsinki University Hospital in Finland have initiated a randomized control trial to assess FMT as a treatment for morbid obesity. A total of 40 patients meeting the criteria for obesity surgery have been enrolled and will undergo FMT via gastroscopy 6 months prior to obesity surgery; 20 of the patients will receive a fecal transplant from a thin donor and 20 will receive a transplant of their own feces. Changes in weight, laboratory values, general wellbeing, and stool microbiota will be measured up to one year after the surgery. Outcomes from this study are anticipated in early 2021. ■

6. Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R, Gordon JI. The human microbiome project. Nature. 2007;449(7164):804-810. 7. Bäckhed F, Ding H, Wang T, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A. 2004;101(44):15718-15723. 8. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006;444(7122):1027-1031. 9. Million M, Lagier JC, Yahav D, Paul M. Gut bacterial microbiota and obesity. Clin Microbiol Infect. 2013;19(4):305-313. 10. Million M, Maraninchi M, Henry M, et al. Obesity-associated gut microbiota is enriched in Lactobacillus reuteri and depleted in Bifidobacterium animalis and Methanobrevibacter smithii. Int J Obes (Lond). 2012;36(6):817-825. 11. Jayasinghe TN, Chiavaroli V, Holland DJ, Cutfield WS, O’Sullivan JM. The new era of treatment for obesity and metabolic disorders: evidence and expectations for gut microbiome transplantation. Front Cell Infect Microbiol. 2016;6:15. 12. Tremaroli V, Bäckhed F. Functional interactions between the gut microbiota and host metabolism. Nature. 2012;489(7415):242-249. 13. Martinez KB, Pierre JF, Chang EB. The gut microbiota: the gateway to improved metabolism. Gastroenterol Clin North Am. 2016;45(4):601-614. 14. Allen JM, Mailing LJ, Niemiro GM, et al. Exercise alters gut microbiota composition and function in lean and obese humans. Med Sci Sports Exerc. 2018;50(4):747-757. 15. Graessler J, Qin Y, Zhong H, et al. Metagenomic sequencing of the human gut microbiome before and after bariatric surgery in obese patients with type 2 diabetes: correlation with inflammatory and metabolic parameters. Pharmacogenomics J. 2013;13(6):514-522. 16. de Clercq NC, Frissen MN, Groen AK, Nieuwdorp M. Gut microbiota and the gut-brain axis: new insights in the pathophysiology of metabolic syn-

Michelle Petropoulos, DMSc, PA-C, DFAAPA, works in a private practice family medicine office in Madison Heights, Michigan.

drome. Psychosom Med. 2017;79(8):874-879. 17. Alang N, Kelly CR. Weight gain after fecal microbiota transplantation. Open Forum Infect Dis. 2015;2(1):ofv004.

References

18. Marotz CA, Zarrinpar A. Treating obesity and metabolic syndrome with

1. World Health Organization. Obesity. World Health Organization website.

fecal microbiota transplantation. Yale J Biol Med. 2016;89(3):383-388.

https://www.who.int/topics/obesity/en/. Accessed August 20, 2019.

19. Vrieze A, Van Nood E, Holleman F, et al. Transfer of intestinal microbiota

2. Centers for Disease Control and Prevention. Adult obesity causes and conse-

from lean donors increases insulin sensitivity in individuals with metabolic

quences. Centers for Disease Control and Prevention website. https://www.cdc.

syndrome. Gastroenterology. 2012;143(4):913-916.e7.

gov/obesity/adult/causes.html. Updated August 29, 2017. Accessed August 20, 2019.

20. Jumpertz R, Le DS, Turnbaugh PJ, et al. Energy-balance studies reveal

3. Ursell LK, Haiser HJ,Van Treuren W, et al.The intestinal metabolome: an inter-

associations between gut microbes, caloric load, and nutrient absorption in

section between microbiota and host. Gastroenterology. 2014;146(6):1470-1476.

humans. Am J Clin Nutr. 2011;94(1):58-65.

www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 17

Case Study | INTERVENTIONAL RADIOLOGY PHYSICAL EXAMINATION Vital signs are within normal limits with the exception of an increased heart rate of 114 beats per minute. Lungs are clear to auscultation. Significant swelling that is dark red in color is noted in the left lower extremity. Sensation of the extremity is intact. Skin is warm and dry to touch. Posterior tibial and pedal pulses are 2+. Positive Homan sign is noted, and no palpable cords are present.

DIAGNOSTIC ASSESSMENT

Extensive Deep Venous Thrombosis A 22-year-old woman presents with abrupt atraumatic swelling and pain in the left lower extremity. JENNIFER VINCENT, PA-S; E. RACHEL FINK, MPA, PA-C

Basic metabolic panel and complete blood count are within normal limits except for a mild elevation in calcium of 10.6 mg/dL and a white blood cell count of 13,110 cells/µL. Prothrombin time is 13.4 seconds, international normalized ratio is 1.0, and partial thromboplastin time is 23.6 seconds. Electrocardiogram shows sinus tachycardia with intermittent premature ventricular contractions. Ultrasound of the left lower extremity reveals an occlusive thrombus throughout the deep venous system of the left leg from the external iliac vein to the common femoral vein, the femoral vein (Figure 1), the popliteal vein, and the posterior tibial vein. No thrombus was noted in the external iliac vein (Figure 2) and common iliac vein of the right leg.

MANAGEMENT

THE CASE A 22-year-old woman presents to the emergency department with abrupt onset of atraumatic swelling and pain in the left lower extremity. She explains that her leg began to swell spontaneously after showering 2 hours before arriving to the emergency department. She characterizes the pain as heaviness. The patient denies numbness, weakness, saddle paresthesia, loss of bowel or bladder control, chest pain, or shortness of breath. She denies a family history of blood clotting disorders and a personal or family history of deep vein thrombosis (DVT). She has no smoking history and denies alcohol, illicit drug, or tobacco use. Medical and surgical history are noncontributory. The patient takes drospirenone/ethinyl estradiol 3 mg/0.02 mg 1 tablet daily.

The patient was admitted and placed on a heparin drip due to the extensiveness of the thrombus. Interventional radiology was consulted for management of catheter-directed therapy with tissue plasminogen activator (tPA). Hematology was consulted, and a hypercoagulable work-up was initiated given the patient’s young age. Results of the work-up revealed that the patient was a heterozygous carrier of the factor V Leiden mutation, adding to her risk factors for thrombosis. The interventional radiology physician determined that the patient was a candidate for catheter-directed thrombolysis. Since the patient Continues on page 20

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Case Study

FIGURE 1. Ultrasound of the left femoral vein showing noncompressible echogenicity.

iliac vein. A bolus of 8 mg of tPA was infused over 8 minutes. Thrombolysis was successfully initiated at 0.5 mg/h, and the patient was admitted to the intensive care unit overnight for close monitoring. Left lower extremity venogram performed through the existing catheter the following day demonstrated resolution of the DVT. Improvement of blood flow through the left external vein was noted, but complete occlusion of the left common iliac vein was present. The stenosed areas of both the left external iliac vein and left common iliac vein were serially treated with angioplasty up to 12 mm. A stent with 2 overlapping stents was placed in the left common iliac vein. Follow-up venogram was performed and showed the venous system to be widely patent. Computed tomography (CT) with contrast of the abdomen and pelvis (Figure 5) performed the following day determined that the IVC filter was in good position below the level of the renal veins. The stent in the left common iliac and left external iliac vein was patent. The patient tolerated all procedures well, and discharge planning was initiated.

OUTCOME FIGURE 2. Ultrasound of the right external iliac vein showing normal venous blood flow.

had 2 known risk factors for DVT (oral contraceptive use and factor V Leiden mutation), suspicion for venous stenosis or occlusion of the left pelvis was high. A retrievable inferior vena cava (IVC) filter was prepared for placement to prevent emboli from migrating to the lungs. The right internal jugular vein was accessed with ultrasound guidance and documented as patent. Vena cavagram (Figure 3) demonstrated a normal caval diameter and poor inflow from the left iliac vein consistent with thrombosis of the left pelvic deep vein. A small floating thrombus was found to extend from the left iliac vein into the IVC. The IVC filter was successfully placed in its normal configuration and positioned below the lowest renal vein. The left popliteal vein was accessed with ultrasound following placement of the IVC filter. A venogram (Figure 4) was obtained, which showed extensive defects in filling in the external iliac vein and common femoral vein. The left common iliac vein was poorly visualized, supporting chronic occlusion. Collateral venous structures were noted to cross the midline and drain via the contralateral iliac vein. An EKOS™ microcephalic infusion catheter was positioned in the left

The patient made a full recovery, and the extensive DVT resolved after 5 days of inpatient treatment. The patient was started on aspirin 81 mg/d, clopidogrel 75 mg/d for 3 months, and rivaroxaban 15 mg twice daily for 21 days and then 20 mg/d thereafter. She was discharged with instructions to resume normal activities. Follow-up with hematology and vascular surgery was scheduled. The patient was educated on her nonmodifiable risk factor of having 1 allele of the factor V Leiden mutation. She was advised to seek appropriate care to avoid recurrent venous thromboembolism, recurrent miscarriages, complications with pregnancy, or possible arterial thrombosis. The patient’s family members were also encouraged to consider genetic testing to understand their risk for thromboembolism. Results of serial follow-up ultrasounds of the left lower extremity were negative for DVT and confirmed resolution of the left-sided DVT. The IVC filter was successfully retrieved via the right jugular vein by interventional radiology 6 months after the DVT was diagnosed. CT of the pelvis with contrast performed 15 months after diagnosis revealed patent pelvic venous structures, as well as the stent in the left iliac vein. The patient was able to safely discontinue anticoagulant therapy and was discharged from the care of hematology and vascular surgery. No complications occurred.

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Continues on page 22

Case Study

FIGURE 3. Vena cavagram demonstrating poor inflow from the left common iliac vein.

FIGURE 4. Venogram of the left lower extremity showing formation of collateral veins.

lower extremities, also represent a risk factor for DVT but may be less commonly thought of by providers.1 May-Thurner syndrome, also known as iliac vein compression syndrome, is one example of many causes of venous narrowing that could potentially lead to the formation of DVT. In individuals with normal anatomy, the right common iliac artery crosses over the left common iliac vein without complications. In some patients, however, the pulsations from the right common iliac artery can place pressure on the underlying left common iliac vein, pushing it against the lumbar vertebrae. This pressure can become even more elevated, especially while walking, which subsequently alters blood flow, leads to venous stasis, and ultimately causes DVT.2-4 This anatomic variant is present in approximately 20% of the population and is one of the leading causes of treatment failure and recurrent DVT.2,3 This risk factor was first noted when catheter-directed thrombolysis was beginning to be performed in the 1990s for the treatment of larger DVTs. Nearly 50% of these patients were found to have narrowing of the iliac vein.4 From this case, clinicians should be reminded that the risk factors for formation of DVT are additive. The patient in this case recovered without any complications from treatment. The floating thrombus found in the inferior vena cava could have advanced into the lungs or brain to cause pulmonary embolism or stroke if care had been delayed. It is imperative that providers assess a patient’s baseline risk for thrombosis before initiating oral contraceptive therapy. Education must be provided to female patients regarding the risks associated with taking estrogen-containing birth control. Empowering patients with the knowledge of the signs and symptoms of DVT, pulmonary embolism, and stroke, as well as stressing the importance of seeking immediate care are crucial to reducing the burden of thrombotic events. ■

FIGURE 5. CT scan of the abdomen and pelvis demonstrating a widely patent stent in the left common iliac and left external vein.

Jennifer Vincent, PA-S, is a student and E. Rachel Fink, MPA, PA-C, is an assistant professor in the physician assistant program of Augusta University, in Augusta, Georgia.

DISCUSSION

References 1. Patel K, Fasanya A, Yadam S, Joshi AA, Singh AC, Dumont T. Pathogenesis

The young woman in this case was found to have 3 significant risk factors for the development of extensive DVT. It was unclear which of the risk factors — the use of oral contraceptives, the chronically occluded left common iliac vein, or the factor V Leiden mutation — most likely provoked the sudden thrombosis. FactorV Leiden mutation and the use of oral contraceptives are known, common risk factors for the development of DVT. Anatomic anomalies, particularly in the venous system of the

and epidemiology of venous thromboembolic disease. Crit Care Nurs Q. 2017;40(3):191-200. 2. Adams SK, Sinyangwe I. Acute iliofemoral DVT in the presence of MayThurner syndrome. Nursing. 2017;47(3):38-39. 3. Carroll S, Moll S. Inferior vena cava filters, May-Thurner syndrome, and vein stents. Circulation. 2016;133(6):e383-e387. 4. Birn J, Vedantham S. May-Thurner syndrome and other obstructive iliac vein lesions: meaning, myth, and mystery. Vasc Med. 2014;20(1):74-83.

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Dermatology Clinic CASE #1

Erythematous Plaques With Scaling ANNA D. POLINER, BSA; MCKENNA E. BOYD, BS; CHRISTOPHER RIZK, MD

A 42-year-old African American man with a 15-year smoking history presents with well-demarcated erythematous plaques with scale on his ears, arms, and cheeks. He reports that the condition has persisted for the past 2 years. He has no personal or family history of psoriasis and has not started any new medications or used any new products. On examination, the patient has multiple erythematous and hyperpigmented plaques with white sclerotic centers. What is your diagnosis? Turn to page 24

CASE #2

Erythematous, Eczematous, and Pruritic Lesions JONATHAN LO, BA; MICHELLE E. LEE, BA; CHRISTOPHER RIZK, MD

A 41-year-old man presents with a 3-year history of progressively worsening generalized erythematous, eczematous, and pruritic skin lesions along with lichenifications of the flexural surfaces.The patient describes experiencing xerosis and erythematous and edematous plaques that progressed to the trunk and legs. His body is now covered with erythematous plaques, with scaling on the scalp. Painful erosions as a result of severe scratching are also present. He denies history of asthma or allergic rhinitis. What is your diagnosis? Turn to page 25 www.ClinicalAdvisor.com • THE CLINICAL ADVISOR • NOVEMBER 2019 23

Dermatology Clinic CASE #1

Discoid Lupus

Cutaneous lupus erythematosus (CLE) is associated with a diverse array of dermatologic pathology. Under this umbrella is discoid lupus erythematosus (DLE), the most common subtype of chronic cutaneous lupus erythematosus (CCLE).1,2 Like all forms of CLE, discoid lupus can be, but is not always, associated with systemic disease. In fact, cutaneous lupus is 2to 3-times more common than systemic lupus erythematosus (SLE) and thus often occurs independently.3 DLE most commonly presents in African American women as well-demarcated, coin-shaped lesions with central clearing that are susceptible to scarring alopecia.1,3 These lesions are diagnosed clinically, although histology and lupus band testing can be useful diagnostic tools.3 Treatment involves sun protection, smoking cessation, and medical therapy such as topical corticosteroids, topical calcineurin inhibitors, and systemic antimalarial therapy.1,3,4 DLE falls within the broad category of lupus erythematosus and more specifically cutaneous lupus. For context, the 4 major subtypes of CLE include CCLE, acute CLE (ACLE), subacute CLE (SCLE), and intermittent CLE (ICLE).2,3 Within the CCLE subtype is DLE, lupus erythematosus profundus, chilblain cutaneous lupus, and lupus erythematosus tumidus.3 DLE may occur in the setting of SLE; however, only one-quarter of patients diagnosed with SLE develop discoid cutaneous lesions.1 Conversely, only approximately 5% to 10% of those diagnosed with DLE will have progression to SLE.3 As many as 25% of patients with ACLE will have progression to SLE; consequently, the discoid variant is considered a relatively benign disease compared with the other cutaneous subtypes.3 The development of DLE involves an interplay between genetic, environmental, and immunologic factors.1,5 Some implicated genes include TYK2, IRF5, and CTLA4; these genes are also associated with development of SLE.1 Environmental risk factors for DLE include smoking, sun exposure, and certain medications; viruses have also been implicated as a potential inciting factor.1,4 Sun exposure and smoking are also particularly important for the development of CLE. Although the exact mechanism is unknown, some evidence suggests ultraviolet (UV) radiation triggers keratinocyte morphologic change and apoptosis.4 Analogously, smoking may increase apoptosis and increase photosensitivity.1 In addition, both risk factors stimulate the immune response. UV light induces the release of several factors, namely interferon (IFN), tumor necrosis factor (TNF)-α,

interleukin (IL)-1, IL-10, and IL-17, from keratinocytes.4 These cytokines recruit inflammatory cells, initially CD4+ and eventually CD8+ T cells. Similarly, smoking has been shown to induce T-cell proliferation.1 In accordance with these immunologic factors, IFN types I (α and β) and II (γ) have been associated with the development of DLE.5 Increased production of type I IFNs by plasmacytoid dendritic cells has been found to contribute to the accumulation of autoimmune debris that causes DLE via increased production of apoptotic factors, such as TNF-related apoptosis-inducing ligand (TRAIL).5,6 INF-γ induces differentiation of naive T-cells to Th1 cells; in DLE specifically, cutaneous inflammatory infiltrates are predominately Th1 mediated.1,4-6

The development of DLE involves an interplay between genetic, environmental, and immunologic factors. Clinically, DLE presents as well-demarcated, round, erythematous plaques that slowly become indurated with associated adherent follicular hyperkeratosis.1-3,7 Removal of this scale is painful and reveals keratotic spikes commonly known as the carpet tack sign.1-3 Peripheral expansion leaves an atrophic, hypopigmented central depression with telangiectasias.1,4 Active lesions eventually resolve; however, patients may experience persistent scarring alopecia as lesions tend to extend into the hair follicle.3 On rare occasions squamous cell carcinoma arises from old lesions.1,3,4 Aside from rash, arthralgia is the most common systemic complaint in patients with DLE.8 Of note, patients of any age can be affected by DLE; however, it most commonly affects middle-aged women.1,3 The distribution of lesions can further classify DLE into localized and disseminated variants. DLE occurs predominantly above the neck on the face, scalp, and ears.1,4 Localized DLE is limited to this distribution above the neck, while disseminated DLE presents with lesions below the neck as well.1 Only 20% of patients develop disseminated DLE, but this variant is associated with higher rates of SLE.1,2 Lesions on the trunk or extremities without distribution above the neck are uncommon in DLE.1 Mucosal surfaces such as the lips and the nasal, oral, and genital mucosa may also be involved.1,9 In some patients, these lesions display a classic photodistribution; however, development of lesions in sun-protected areas is also possible, and the role of UV radiation in the development of DLE is unclear.1,4 The diagnosis of DLE is made clinically based on patient history and physical examination; however, histology, direct immunofluorescence (DIF), and serologic studies may be necessary for confirmation when the diagnosis is unclear.3

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Histologic examination of DLE lesions reveals a lichenoid reaction characterized by vacuolar degeneration and apoptotic keratinocytes (Civatte bodies).4 Lymphocytic infiltrate, follicular plugging, mucin deposition, and thickening of the basement membrane are also classic features of DLE.1,3,10 The lupus band test is another useful diagnostic tool with positive results in the majority of patients with DLE.1,3 This test detects the deposition of immunoglobulins and complement at the dermal-epidermal junction and is especially useful for the differentiation of SLE and CLE. Both diseases are associated with positive band testing of active lesions; however, only SLE will be positive for uninvolved skin.1 DLE bands most commonly consist of C3 and IgM deposits with lower incidence of certain antibodies, including antinuclear, dsDNA, anti-Smith (anti-Sm), and SSA/ Ro antibodies, when compared with other CLE subtypes.3 The differential for DLE depends on the stage, location, and variant of disease. Early lesions can mimic psoriasis, sarcoidosis, and cutaneousT-cell lymphoma.3 Especially given limited mucosal involvement, buccal mucosal DLE can be mistaken for lichen planus. Hypertrophic lichen planus and keratoacanthomas can also mimic the rare hypertrophic variant of DLE. Other differentials include other CLE such as ACLE and SCLE, as well as scleroderma, mixed connective tissue disease, and rheumatoid arthritis.1,3 Early treatment is vital in DLE as lesions frequently lead to permanent hypopigmentation, scarring, and alopecia, which can be disfiguring, especially for darker-skinned individuals.1 Although no medications have been approved specifically for the treatment of DLE, topical corticosteroids and calcineurin inhibitors and systemic antimalarial agents are used as first-line treatment.1,3,4 Sun avoidance and protection as well as smoking cessation are recommended for all patients.3,4 Intralesional administration or short courses of oral corticosteroids may be necessary for chronic lesions that are unresponsive to topical corticosteroids or calcineurin inhibitors.1 For refractory cases, immunosuppressive agents such as methotrexate, mycophenolate mofetil, and azathioprine; biologics such as rituximab; immunomodulators such as dapsone and thalidomide; or retinoids may be considered.3,4 Thalidomide and lenalidomide have been shown to be effective for DLE; however, they are not considered first-line treatment as patients frequently relapse once medication is discontinued.1,4 A skin biopsy was performed on the patient in our case, the results of which were consistent with DLE. Oral hydroxychloroquine and topical corticosteroids were prescribed, and the patient was advised to stop smoking and avoid sun exposure.Although his lesions have improved, hypopigmented scars remain. Anna D. Poliner, BSA, and McKenna E. Boyd, BS, are medical students at Baylor College of Medicine in Houston,Texas. Christopher Rizk, MD, is a dermatologist with Elite Dermatology in Houston,Texas.

References 1. McDaniel B, Tanner LS. Discoid lupus erythematosus. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2019. 2. Kuhn A, Landmann A. The classification and diagnosis of cutaneous lupus erythematosus. J Autoimmun. 2014;48-49:14-19. 3. Okon LG, Werth VP. Cutaneous lupus erythematosus: diagnosis and treatment. Best Pract Res Clin Rheumatol. 2013;27(3):391-404. 4. Ribero S, Sciascia S, Borradori L, Lipsker D. The cutaneous spectrum of lupus erythematosus. Clin Rev Allergy Immunol. 2017;53(3):291-305. 5. Kahn JS, Deverapalli SC, Rosmarin DM. JAK-STAT signaling pathway inhibition: a role for treatment of discoid lupus erythematosus and dermatomyositis. Int J Dermatol. 2018;57(8):1007-1014. 6. Zhang Y, Wu J, Han Y, Shi Z, Wang L. Pathogenesis of cutaneous lupus erythema associated with and without systemic lupus erythema. Autoimmun Rev. 2017;16(7):735-742. 7. Walling HW, Sontheimer RD. Cutaneous lupus erythematosus: issues in diagnosis and treatment. Am J Clin Dermatol. 2009;10(6):365-381. 8. Oh EH, Kim EJ, Ro YS, Ko JY. Ten-year retrospective clinicohistological study of cutaneous lupus erythematosus in Korea. J Dermatol. 2018;45(4):436-443. 9. Salah E. Clinical and dermoscopic spectrum of discoid lupus erythematosus: novel observations from lips and oral mucosa. Int J Dermatol. 2018;57(7):830-836. 10. Elman SA, Joyce C, Nyberg F, et al. Development of classification criteria for discoid lupus erythematosus: results of a Delphi exercise. J Am Acad Dermatol. 2017;77(2):261-267.

CASE #2

Erythroderma

First identified in 1868 by Von Hebra, erythroderma — also known as exfoliative dermatitis — involves redness and scaling of more than 90% of skin, leading to uncontrolled skin dysmetabolism.1 The incidence of erythroderma is approximately 1 in 100,000 annually.1 Although erythroderma can occur at any age and in any sex, it is more common in older adults and males.2 Erythroderma presents later in men than in women, with differing age and length of hospital stay due to underlying etiology.3 Erythroderma is a clinical diagnosis with a variety of underlying causes. The most prevalent cause of erythroderma is exacerbation of a preexisting inflammatory skin condition, most commonly atopic dermatitis or psoriasis. Other triggers include drug reactions and cutaneous T-cell lymphoma.3 For patients with psoriasis, risk factors include systemic illnesses, phototherapy damage, medications, sudden discontinuation

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Dermatology Clinic of corticosteroids or immunosuppressants, or HIV.4 Drugs reportedly associated with erythroderma include penicillins, carbamazepine, sulfa drugs, antiepileptic agents, antihypertensive medications, and calcium channel blockers.While carbamazepine and penicillin are the most common inciting agents, it is important to consider an idiopathic etiology for any patient taking medications who presents with urticarial, lichenoid, or morbilliform rashes that develop into erythroderma.1,5 Other patterns of drug-induced exfoliative dermatitis include DRESS (drug rash with eosinophilia and systemic symptoms) syndrome, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis.6 A less common cause of erythroderma is CD4+ cutaneous T-cell lymphoma. This disease is subclassified as mycosis fungoides, the most common form of which can present similarly to a benign erythroderma, and Sezary syndrome, which is a more aggressive form with more extensive hematologic and internal organ involvement.1 Some cases of erythroderma have no identified etiology and are thus classified as idiopathic. The molecular pathogenesis of erythroderma is poorly understood but is generally thought to involve interactions of cytokines, chemokines, and intracellular adhesion molecules that cause inflammation of the skin. Specifically, elevated serum levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin are seen in patients with erythroderma secondary to psoriasis, eczema, and Sezary syndrome.7 The increased inflammatory cell recruitment results in increased turnover of the epidermis, leading to a dysmetabolic state and associated complications such as dehydration, electrolyte imbalance and infection. Common clinical findings include pruritus, peripheral edema, fever, palmoplantar keratoderma with desquamation, nail changes, hepatosplenomegaly, psoriatic arthritis, and lymphadenopathy.3 Laboratory findings are generally nonspecific in erythroderma and not useful for diagnosis. Findings include mild anemia, eosinophilia, elevated erythrocyte sedimentation rate, hypoalbuminemia, hyperuricemia, and elevated immunoglobulin (Ig)-E levels.8 Histology also tends to yield nonspecific features such as hyperkeratosis, acanthosis, and perivascular inflammatory infiltrates with or without eosinophils. In a retrospective study, a blinded histopathology examination was only able to identify the correct diagnosis in 61% of cases.9 This points to the lack of an exclusive pathognomonic finding for erythroderma. The differential diagnosis for erythroderma includes acanthosis nigricans, cutaneous sarcoidosis, allergic/irritant contact dermatitis, bullous pemphigoid, lichen planus, pityriasis rubra pilaris, and reactive arthritis. Erythroderma can also occur secondary to these conditions.4 The major differentiating factor is the extensive skin surface area involved in erythroderma. Erythroderma is a

clinical diagnosis based on erythema and warmth of ≥90% of the body surface, often with pain and pruritus. Treatment for erythroderma involves initial management of the acute presentation followed by individualized treatment based on etiology. Patients who are hemodynamically unstable will require hospitalization. Use of heating blankets may be necessary due to the loss of thermoregulation from skin dysmetabolism. Monitoring of blood pressure and pulse is also required as skin vasodilation could lead to high-output cardiac failure; adequate hydration and maintenance of electrolyte status are also necessary. For pain and pruritus, emollients and wet dressings are beneficial. Treatments such as topical corticosteroids, oral antihistamines, systemic antibiotics for Staphylococcus aureus, or antiviral agents for herpes simplex can also be added as necessary.10 As the underlying cause is identified, targeted treatment can be initiated. After presentation, the patient in this case was diagnosed with erythroderma secondary to an exacerbation of atopic dermatitis. Systemic treatment including topical corticosteroids, phototherapy, and emollients resulted in remission of the atopic dermatitis flare and associated erythroderma. ■ Jonathan Lo, BA, and Michelle E. Lee, BA, are medical students at Baylor College of Medicine, in Houston,Texas. Christopher Rizk, MD, is a dermatologist with Elite Dermatology in Houston,Texas. References 1. Okoduwa C, Lambert WC, Schwartz RA, et al. Erythroderma: review of a potentially life-threatening dermatosis. Indian J Dermatol. 54(1):1-6. 2. Li J, Zheng HY. Erythroderma: a clinical and prognostic study. Dermatology. 2012;225(2):154-162. 3. César A, Cruz M, Mota A, Azevedo F. Erythroderma. A clinical and etiological study of 103 patients. J Dermatol Case Rep. 2016;10(1):1-9. 4. Rothe MJ, Bernstein ML, Grant-Kels JM. Life-threatening erythroderma: diagnosing and treating the “red man.” Clin Dermatol. 2005;23(2):206-217. 5. Khaled A, Sellami A, Fazaa B, Kharfi M, Zeglaoui F, Kamoun MR. Acquired erythroderma in adults: a clinical and prognostic study. J Eur Acad Dermatol Venereol. 2010;24(7):781-788. 6. Yacoub M-R, Berti A, Campochiaro C, et al. Drug induced exfoliative dermatitis: state of the art. Clin Mol Allergy. 2016;14:9. 7. Groves RW, Kapahi P, Barker JN, Haskard DO, MacDonald DM. Detection of circulating adhesion molecules in erythrodermic skin disease. J Am Acad Dermatol. 1995;32(1):32-36. 8. Wilson DC, Jester JD, King LE Jr. Erythroderma and exfoliative dermatitis. Clin Dermatol. 1993;11(1):67-72. 9. Megna M, Sidikov AA, Zaslavsky DV, et al.The role of histological presentation in erythroderma. Int J Dermatol. 2017;56(4):400-404. 10. Mistry N, Gupta A, Alavi A, Sibbald RG. A review of the diagnosis and management of erythroderma (generalized red skin). Adv Skin Wound Care. 2015;28(5):237-238.

26 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

Dermatologic Look-Alikes Rash With Burning and Pruritus JESSICA C. SHEU, BA; MICHELLE E. LEE, BA; CHRISTOPHER RIZK, MD

CASE #1

CASE #2

A 54-year-old man with a history of asthma presents to the dermatology clinic in the springtime with a burning, itchy rash on his lateral neck. He denies any other medical history. On physical examination an erythematous plaque with scale is noted around his entire neck. The remainder of the physical examination is unremarkable. The patient says that he has tried applying moisturizer but without relief. Upon further questioning, the patient admits that he has been wearing a new necklace that was given to him recently as a gift.

A 62-year-old man presents to the clinic complaining of a painful rash on both cheeks for the past 4 months. On examination the rash appears as faint erythematous patches with mild scale over the central cheeks bilaterally. The patent says that the rash worsens during the week, with mild abatement during the weekend.After extensive questioning, the patient offered that he works with toxic gases and is required to wear a protective gas mask daily at his job. The patient has no other medical problems.

www.ClinicalAdvisor.com â&#x20AC;˘ THE CLINICAL ADVISOR â&#x20AC;˘ NOVEMBER 2019 27

Dermatologic Look-Alikes CASE #1

Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) is a T-cell-mediated, delayed-type IV hypersensitivity reaction to exogenous agents.1,2 ACD and irritant contact dermatitis (ICD) frequently exist together, which contributes to the difficulty in measuring the prevalence of ACD on its own. In many European countries, occupational dermatitis has been found to occur in 500 to 1900 workers per year.3 The pathogenesis of ACD is a 2-step process. When an allergen or benign substance contacts skin initially, it goes through the skin via the stratum corneum. During the sensitization phase, the surface of Langerhans cells in the epidermis becomes coated with the allergen.The Langerhans cells move to surrounding lymph nodes, where naive Th1 cells come into contact with this complex of allergen and proteins.The newly sensitized Th1 cells undergo clonal proliferation and produce memory Th1 cells.The second phase of the delayed hypersensitivity reaction occurs once the patient comes in contact with the allergen again. Memory T cells produce a rapid inflammatory response, resulting in spongiosis.3,4 In the adult population, a common cause of ACD is urushiol, a highly allergenic chemical found in various plants including oak, poison ivy, and sumac. In a patch-testing study, nickel and fragrances each triggered ACD in 14% of patients, and neomycin caused ACD in 11% of patients.5 In pediatric patients, contact sensitization often begins in early childhood through exposures to vaccinations, cosmetics, topical medications, and piercings.6 In addition, pediatric patients with atopic dermatitis frequently also present with ACD. At work and home, risk factors for ACD include contact with chemicals in cleaning supplies, nail and hair products, and skin care products.3 ACD can vary in presentation depending on the time course and severity. Acute, mild reactions present with erythema, edema, and pruritus only at the contact points. More severe reactions also involve vesicular lesions that burst and crust afterward. In particular, when a patient comes in contact with poison ivy, the rash that often appears looks like a line of vesicles from the pattern of contact.After chronic exposure to the allergen, the skin thickens and fissures, with an appearance similar to eczema. Particularly in chronic cases, the rash is more widespread although particularly severe in the allergen contact location.Although the hands are most commonly affected by ACD, any exposed areas of the skin are susceptible.3,5

The histology of ACD in its initial stages predominantly consists of spongiotic vesicles in the lower epidermis. In the later stages, spongiosis can be seen throughout the epidermis. In addition, groups of Langerhans cells, lymphocytes, and macrophages cluster around the superficial vessels in the upper dermis. Absence of eosinophils does not exclude ACD, although eosinophilic exocytosis is often seen in ACD. In patients with chronic ACD, epidermal proliferation, scale crust, and papillary fibrosis of the dermis mostly characterize the skin histology, with limited spongiosis and vesicles.7 The differential diagnosis for ACD includes ICD, atopic dermatitis, psoriasis, rosacea, erythroderma, lichen planus, xerotic eczema, stasis dermatitis, and seborrheic dermatitis.3,7

Allergic contact dermatitis can vary in presentation depending on the time course and severity. If ACD appears in the groin, it must be distinguished from extramammary Paget disease, Candida, erythrasma, or inverse psoriasis. Due to the preservatives in topical preparations, ACD of the diaper area is often seen and can be distinguished from Candida by its characteristic “satellite lesions.” If ACD appears on the face, particularly in the perioral region, nutritional deficiencies, periorificial dermatitis, or rosacea should be considered.7 To date, patch testing has been the gold standard of ACD diagnosis. Patch testing involves placing numerous small patches onto the patient’s back; the allergens that produce a more severe ACD reaction than the control irritant are identified as triggers. While the possible causes of ACD are numerous, diagnosis can be reached via allergen testing specifically considering the patient history and rash distribution.1,3 When patch testing does not reveal a specific etiology, skin biopsy can establish a diagnosis. When tinea is in the differential, the periodic acid-Schiff (PAS) stain can help rule out that diagnosis.7 Treatment and prevention of ACD rely on allergen avoidance. However, this often proves to be difficult due to work or environmental situations. In these types of environments, patients need to be counseled into engaging in protective measures; examples of these include using barrier creams or donning appropriate protective equipment.3 When patients still experience ACD despite attempts at avoidance, topical treatments can be pursued.Topical corticosteroids are the first-line

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AGA=American Gastroenterological Association. References: 1. Schiller LR, Emmett M, Santa Ana CA, Fordtran JS. Osmotic effects of polyethylene glycol. Gastroenterology. 1988;94(4):933-941. 2. Hammer HF, Santa Ana CA, Schiller LR, Fordtran JS. Studies of osmotic diarrhea induced in normal subjects by ingestion of polyethylene glycol and lactulose. J Clin Invest. 1989;84(4):1056-1062. 3. Survey of 672 consumers, August 2017, Bayer Consumer Health. 4. Bharucha AE, Dorn SD, Lembo A, Pressman A; American Gastroenterological Association. American Gastroenterological Association medical position statement on constipation. Gastroenterology. 2013;144(1):211-217.

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Dermatologic Look-Alikes treatment for localized ACD.8 However, chronic use can result in skin atrophy. As a result, topical calcineurin inhibitors such as tacrolimus or pimecrolimus are prescribed following brief topical steroid use in areas with a thin epidermis.3,9 Although rare, chronic ACD may require immunosuppressive treatment with cyclosporine, azathioprine, or mycophenolate.3 Based on the patient’s history (wearing a new necklace), ACD was suspected. The patient underwent patch testing and was determined to have an ACD reaction to nickel.The patient stopped wearing the necklace and was treated with topical triamcinolone ointment. The patient’s rash resolved within 1 week.

CASE #2

Irritant Contact Dermatitis

Irritant contact dermatitis (ICD) is a localized inflammatory skin reaction to physical or chemical agents. It is the most common form of contact dermatitis and is distributed on the hands more frequently than allergic contact dermatitis.10,11 Infants are the most sensitive to skin irritants and therefore prone to developing ICD.12 In the adult population, individuals involved in “wet work” are at high risk for occupational ICD.13 “Wet work” is defined as washing hands, wearing gloves, or touching water for >2 hours per day.10 This commonly includes workers in health care, mechanics, cleaning, or food industries.13 ICD commonly affects women more than men, likely due to increased domestic and occupational exposures.11 The pathophysiologic mechanism of ICD is dependent upon innate immune system activation. As such, ICD can develop with the first exposure to a skin irritant, unlike ACD, which requires initial sensitization.3 The first step in acute ICD development is damage to the epidermal skin barrier, resulting in cytokine release and leukocyte recruitment.14 Exposure to water causes the stratum corneum to swell and the skin lipids to separate.15 Detergents and alkaline substances also damage hydrophobic lipids in the skin via saponification, and acids act by denaturing proteins. Physical irritants such as fiberglass and wood break the skin through repetitive trauma. Environmental factors also play a role in ICD pathogenesis. In high heat and humidity, the skin barrier is more susceptible to irritant entry. However, cold temperatures also contribute to ICD because increased water loss compromises the skin

barrier.16 The pathogenesis of chronic ICD is more poorly understood, but the long-term exposure to an irritant is believed to down-regulate immune responses and induce skin proliferation.17 The acanthosis and hyperkeratosis that result are known as a “hardening phenomenon.”18 The clinical presentation of ICD is highly variable depending on irritant strength and skin sensitivity. The mildest form involves skin dryness and erythema, and the most severe presentation includes skin necrosis. In acute ICD, patients often complain of a stinging or burning pain. It is characterized by vesicles, edema, erythema, and scaling. Corrosive chemicals can elicit ulcers and necrosis. Chronic ICD presents with dry, fissured skin, hyperkeratosis, and a glazed appearance.19 In both acute and chronic ICD, the rash is sharply circumscribed and defined by the area of contact.8 Histologically, acute ICD shows spongiosis, epidermal bullae or vesicles, edema, and keratinocyte necrosis. Microscopically, chronic ICD has hyperkeratosis, parakeratosis, acanthosis, and hypergranulosis.20 Of note, histopathology cannot be used to distinguish ACD and ICD.21 The differential diagnosis of ICD includes ACD, eczema, psoriasis, tinea, and scabies. Scabies frequently affects the hands but usually presents with intense pruritus, which is less common in ICD. Psoriasis and chronic ICD can appear very similar on physical examination, but the characteristic presence of nail changes or plaques on the elbows and knees points toward psoriasis.

The clinical presentation of irritant contact dermatitis is highly variable depending on irritant strength and skin sensitivity. Diagnosing ICD depends mostly on detecting localized dermatitis on physical examination, which is supported by an in-depth history revealing exposure to an irritant. Given the similar appearance and histology of ACD, ruling out ACD with the use of patch testing is commonly performed.19 Although CD and ACD can coexist, this is rare and happens most frequently in occupations involving wet work.22 When there is concern for other skin pathologies, skin biopsy can be useful, and a potassium hydroxide prep can rule out fungal infection. The most critical component of ICD treatment is irritant avoidance. For those with work exposures, using plastic instead of rubber gloves and adding cotton liners under gloves can aid in sweat absorption. In addition, thoroughly drying hands after washing can reduce the damaging effects of water on the

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Dermatologic Look-Alikes 5. Usatine RP, Riojas M. Diagnosis and management of contact dermatitis.

Allergic Contact Dermatitis1-9

Irritant Contact Dermatitis10-22

T-cell-mediated, delayedtype IV hypersensitivity

Inflammatory, localized skin response caused by a broad range of physical or chemical agents

Leprol. 2010;76(5):514-520.

Urushiol in oak, poison ivy, and sumac; nickel, neomycin, fragrances

“Wet work” exposures, chemicals

8. Beltrani VS, Bernstein IL, Cohen DE, Fonacier L. Contact dermatitis: a

Inflammatory infiltration, erythema, commonly on hands but any exposed body part is susceptible

Erythema, commonly on hands (dry with fissured skin)

Patch testing

Exclusion of allergic contact dermatitis via patch testing, thorough history, and physical examination

Am Fam Physician. 2010;82(3):249-255. 6. Sharma VK, Asati DP. Pediatric contact dermatitis. Indian J Dermatol Venereol

Pathophysiology

Common Causes

Physical Characteristics

7. So JK, Hamstra A, Calame A, Hamann CR, Jacob SE. Another great imitator: allergic contact dermatitis differential diagnosis, clues to diagnosis, histopathology, and treatment. Curr Treat Options Allergy. 2015;2(4):333-348. practice parameter. Ann Allergy Asthma Immunol. 2006;97(3 Suppl 2):S1-38. 9. Belsito D, Wilson DC, Warshaw E, et al. A prospective randomized clinical trial of 0.1% tacrolimus ointment in a model of chronic allergic contact dermatitis. J Am Acad Dermatol. 2006;55(1):40-46. 10. Clark SC, Zirwas MJ. Management of occupational dermatitis. Dermatol Clin. 2009;27(3):365-383. 11. Thyssen JP, Johansen JD, Linneberg A, Menné T. The epidemiology of

Testing

hand eczema in the general population — prevalence and main findings. Contact Dermatitis. 2010;62(2):75-87. 12. Schwindt DA, Wilhelm K-P, Miller DL, Maibach HI. Cumulative irritation in older and younger skin: a comparison. Acta Derm Venereol. 1998;78(4):279-283. 13. Dickel H, Kuss O, Schmidt A, Kretz J, Diepgen TL. Importance of

skin barrier. Additional therapy includes topical corticosteroids to reduce inflammation, as well as emollients, moisturizers, or barrier creams.These creams restore the skin barrier and should be applied multiple times a day for optimal efficacy.5 At our patient’s next visit, he brought the gas mask he was required to wear at work. It was noted that the mask was coming in contact with his face in the areas of ICD. On further questioning, the patient noted that he was cleaning his gas mask daily with harsh chemicals (required to potentially remove toxic gas residue). The patient was advised to wash off the mask a second time in order to remove the harsh chemicals used during cleaning. This led to resolution of his ICD. ■

irritant contact dermatitis in occupational skin disease. Am J Clin Dermatol. 2002;3(4):283-289. 14. Angelova-Fischer I, Stilla T, Kezic S, Fischer TW, Zillikens D. Barrier function and natural moisturizing factor levels after cumulative exposure to shortchain aliphatic alcohols and detergents: results of occlusion-modified tandem repeated irritation test. Acta Derm Venereol. 2016;96(7):880-884. 15. Spears MJ, McKillop K, Marshall JL, et al. Water disrupts stratum corneum lipid lamellae: damage is similar to surfactants. J Invest Dermatol. 1999;113(6):960-966. 16. Zhai H, Maibach HI. Skin occlusion and irritant and allergic contact dermatitis: an overview. Contact Dermatitis. 2001;44(4):201-206. 17. Visscher MO, Said D, Wickett R. Stratum corneum cytokines, structural proteins, and transepidermal water loss: effect of hand hygiene. Skin Res Technol. 2010;16(2):229-236.

Jessica C. Sheu, BA, and Michelle E. Lee, BA, are medical students at Baylor College of Medicine in Houston,Texas. Christopher Rizk, MD, is a dermatologist with Elite Dermatology in Houston,Texas.

18. Watkins SA, Maibach HI. The hardening phenomenon in irritant contact dermatitis: an interpretative update. Contact Dermatitis. 2009;60(3):123-130. 19. Ale IS, Maibach HI. Irritant contact dermatitis. Rev Environ Health. 2014;29(3):195-206.

References

20. Willis CM, Stephens CJM, Wilkinson JD. Epidermal damage induced by

1. Becker D. Allergic contact dermatitis. J Dtsch Dermatol Ges. 2013;

irritants in man: a light and electron microscopic study. J Invest Dermatol.

11(7):607-619.

1989;93(5):695-699.

2. Saint-Mezard P, Rosieres A, Krasteva M, et al. Allergic contact dermatitis.

21. Frings VG, Böer-Auer A, Breuer K. Histomorphology and immunophenotype

Eur J Dermatol. 2004;14(5):284-295.

of eczematous skin lesions revisited — skin biopsies are not reliable in

3. Kostner L, Anzengruber F, Guillod C, Recher M, Schmid-Grendelmeier

differentiating allergic contact dermatitis, irritant contact dermatitis, and

P, Navarini AA. Allergic contact dermatitis. Immunol Allergy Clin North Am.

atopic dermatitis. Am J Dermatopathol. 2018;40(1):7-16.

2017;37(1):141-152.

22. Schwensen JF, Menné T, Johansen JD. The combined diagnosis of allergic and

4. Nelson JL, Mowad CM. Allergic contact dermatitis: patch testing beyond

irritant contact dermatitis in a retrospective cohort of 1000 consecutive patients

the TRUE test. J Clin Aesthet Dermatol. 2010;3(10):36-41.

with occupational contact dermatitis. Contact Dermatitis. 2014;71(6):356-363.

32 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

877.599.5327 / XLEAR.COM

Conference Roundup Psych Congress 2019

TREATMENT COMBO PROMISING FOR ADOLESCENT BORDERLINE PERSONALITY DISORDER Adolescents with borderline personality disorder (BPD) were found to have significantly higher rates of symptom improvement when prescribed oxcarbazepine and amantadine, according to study results presented at Psych Congress 2019, held October 3 to 6 in San Diego, California. Although psychotherapies have been used successfully to treat BPD, as of 2018 the US and Canadian positions on pharmacologic treatment were, “With regard to evidence-based studies, pharmacological treatment is not recommended and, if ultimately required, should be limited to second-generation antipsychotics.” The investigator countered that “extensive advancements in brainmapping have provided clarity about the various brain dysfunctions underlying the symptoms/traits presenting in BPD, providing new opportunities to address these frontolimbic dysfunctions neuropharmacologically.” The study included 147 female individuals ages 13 to 16 years with a diagnosis of BPD.While at a residential facility, they were started on a protocol consisting of an anticonvulsant (oxcarbazepine) and a dopaminergic (amantadine). Patients were discharged when stable and when they achieved >50% improvement from baseline. Caregivers were surveyed at

6 months and 1 year to determine whether the patient was maintaining improved symptomology. Although adherence to the protocol was requested from the outpatient prescribers, some substituted antipsychotic medication. Of those who were adherent to the medication protocol (n=86), 61 maintained an improvement compared with 19 of the 61 patients whose prescribers switched to antipsychotics. The researcher emphasized the offlabel use of oxcarbazepine and amantadine in this study.

GROWING NUMBER OF PAS TREATING MENTAL HEALTH DISORDERS As a result of the growth of the physician assistant (PA) profession, certified PAs may be an innovative and practical

A survey was deployed to assess PA mental health knowledge and competence.

34 THE CLINICAL ADVISOR • NOVEMBER 2019 • www.ClinicalAdvisor.com

resource to expand the mental health workforce capacity and address unmet needs within mental health services, according to research presented at Psych Congress 2019. Researchers from the National Com mission on Certification of Physician Assistants conducted a web-based survey of PAs to describe the contributions to the mental health field from certified PAs across practice areas.The survey included mental health diseases and disorders as well as knowledge and skill statements that PAs rated from 0 (never) to 5 (daily). Data analysis identified the top 10 psychiatric diseases and disorders seen by PAs.The same diseases and disorders were analyzed from PAs who practice across 5 primary care practice areas: emergency medicine, family medicine, general internal medicine, hospital medicine, and pediatrics. PAs practicing in emergency medicine, family medicine, general internal medicine, and hospital medicine saw patients with depressive/bipolar disorders and anxiety/obsessive compulsive/ trauma/stressor disorders weekly. PAs in primary care saw patients with sleep/ wake disorders, schizophrenia disorders, personality disorders, and disruptive impulse control and conduct disorders monthly or less often. PAs practicing in pediatrics saw patients with attentiondeficit/hyperactivity disorder weekly. PAs in emergency medicine saw patients with psychological emergencies such as suicidal behavior weekly.

Psychiatry & Behavioral Health Learning Network San Diego, CA

PAs practicing in all primary care settings evaluated patients with psychiatric symptoms at least weekly. However, not all PAs conducted risk assessment for suicidal ideation, homicidal ideation, and violence or harm to self or others on a weekly basis (45%). The majority of PAs working primarily in cardiology, family medicine, general internal medicine, pediatrics, and hospital medicine did conduct education on modifiable risk factors with an emphasis on primary and secondary prevention (such as smoking cessation, diet, and exercise). While the majority of PAs working in psychiatry saw patients with substancerelated and addictive disorders weekly to daily, the majority of PAs in primary care treated these patients monthly. “This analysis establishes a baseline to track PA contributions longitudinally and informs efforts to advance PA roles and strengthen partnerships with the mental health community,” the researchers concluded.

DASOTRALINE IMPROVES BODY WEIGHT, COMPULSIVE BEHAVIORS IN BINGE EATING DISORDER For adults with binge eating disorder (BED), treatment with the long-acting dopamine/norepinephrine reuptake inhibitor dasotraline was found to be effective for weight reduction and improvement in binge-related compulsions and obsessive thoughts, according to study results presented at Psych Congress 2019. Having previously found that dasotraline is effective in the treatment of BED, researchers examined the medication’s effects on body weight in patients with overweight/obesity, as well as its effects on obsessions and compulsions related to binge eating. Patients aged 18 to 55 years were randomly assigned to receive once-daily doses of dasotraline (4 mg, 6 mg, or 8 mg) or placebo for 12 weeks. Dasotraline dose

A significant reduction in binge eating days per week was seen with dasotraline.

adjustments were made at the discretion of the investigators and increased to 6 mg/d by week 4 for all patients included in the study. The primary end point was mean change in binge eating days per week. TheYale-Brown Obsessive-Compulsive Scale Modified for Binge-Eating was used to assess the severity of obsessive thoughts and compulsive behaviors. Mixed model for repeated measures analyses were used to evaluate these end points as well as change in mean body mass index (BMI) and weight from baseline. In total, 317 patients were included in the safety population and 315 were included in the intention-to-treat population; 155 received dasotraline (mean age, 38.7 years; 87.7% women) and 160 received placebo (mean age, 37.8 years; 19.4% women). According to BMI at baseline, 5.7% of patients were normal weight, 18.3% were overweight, and 76% were obese (class 1: 24.9%; class 2: 29.3%; class 3: 21.8%). Mean daily dosage of dasotraline was 5.5 mg/d. Compared with the placebo group, patients who received dasotraline had a significant reduction in binge eating days per week (-2.75 vs -3.74 days, respectively; P <.0001).This reduction in binge eating was associated

with significant mean changes in weight (-5.7 kg) and BMI (-2.0 kg/m2) in the dasotraline group by week 12. Patients with obesity (classes 1-3 combined) who received dasotraline had a mean change in weight from baseline to week 12 of -6.2 kg compared with a mean change of +0.3 kg in the placebo group. With regard to binge-related compulsions and obsessive thoughts, individuals who had aYale-Brown Obsessive-Compulsive Scale Modified for Binge-Eating score ≤12 after 12 weeks were categorized as having symptomatic remission. All 10 items measured by the score were significantly improved with dasotraline (P <.001 for all comparisons with placebo) and change in total score was significantly greater with dasotraline vs placebo (-17.05 vs -9.88, respectively; P <.0001). In patients who achieved a Binge Eating Clinical Global Impression-Severity score of 1 (normal; 52.3%), mean end point score for obsessive thoughts and compulsions was 0.5, indicating clinical remission in these measures for the majority of patients. The most frequently reported weightrelated adverse event was decreased appetite, which was more common in the dasotraline vs placebo group. Taken together, these secondary analyses of dasotraline found the medication to be associated with meaningful reductions in binge eating days per week, weight, and BED-related compulsions and obsessions after 12 weeks of treatment. Disclosure: This research was supported by Sunovion Pharmaceuticals. Please see the original references for a full list of authors’ disclosures.

RELAPSE MORE LIKELY WITH SWITCH IN ANTIPSYCHOTIC AGENT Patients with schizophrenia, bipolar disorder, or major depressive disorder who switched antipsychotics were more likely to have a relapse and within a shorter amount of time than patients who did

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not switch, according to results presented at Psych Congress 2019. Patients who switched also had an increased likelihood of healthcare utilization and diagnosis of extrapyramidal symptoms. Investigators used Medicaid data gathered between 2008 and 2017 from 6 US states (Iowa, Kansas, Mississippi, Missouri, New Jersey, and Wisconsin). Patients selected were 18 to 65 years old; had a diagnosis of bipolar disorder, major depressive disorder, or schizophrenia; and had at least 2 refills of an oral antipsychotic medication postdiagnosis. Patients who switched had stable-dose monotherapy for ≥90 days before a change in treatment, and patients who did not switch had stable-dose monotherapy for ≥91 days. Patients were followed for 2 years after the index change until treatment change, end of eligibility, age 65 years, or the end of the study period. A final cohort comprised 10,548 patients who switched antipsychotic medications and 31,644 who remained on their original medication. Patients who switched antipsychotic medications were more likely to have a relapse (adjusted hazard ratio, 1.36; 95% CI, 1.281.44; P <.001) and had a shorter time to disease relapse than those who did not switch (P <.001). Similarly, patients who switched were more likely to have a psychiatric admission, inpatient admission, or emergency department visit within a shorter time during the study period (P <.001). When considering extrapyramidal symptoms, first diagnosis was more likely to happen during the study period for patients who switched antipsychotic medications (adjusted hazard ratio, 1.28; 95% CI, 1.06-1.55; P <.05). “Decisions on antipsychotic switching for patients who require maintenance antipsychotic treatment should be individualized and carefully considered, taking into account the potential risk of relapses in some patients with

[schizophrenia, bipolar disorder, or major depressive disorder],” the investigators concluded. Disclosure: This study was funded by Teva Pharmaceutical Industries.All authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

FACTORS CORRELATED WITH SUICIDAL IDEATION IN MAJOR DEPRESSIVE DISORDER There are differences in age, disease characteristics, and symptoms between people with major depressive disorder (MDD) and suicidal ideation (MDSI) and people with MDD without suicidal ideation (SI), according to research presented at Psych Congress 2019. PatientsLikeMe is a web-based com munity and research platform of approximately 600,000 members who voluntarily report their symptoms and experiences with their disease, including treatment outcomes. Investigators included data from members who joined between May 2007 and February 2018, comparing individuals with a reported diagnosis of MDSI (n=266) with individuals with MDD and no SI (n=11,963).

An online platform may help to identify suicide-related risk in depression.

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The majority of members in both cohorts were women (MDSI: 72.9%; MDD: 83.3%) and white (MDSI: 87.5%; MDD: 86.7%). Members of the MDSI group were younger than members of the MDD group (median age, 36 vs 44 years, respectively), reported earlier onset of disease (before age 30 years; 83% vs 71%, respectively), and reported a longer diagnosis latency (median, 4 vs 2 years). The median number of psychiatric comorbidities was higher in those with MDSI (4 vs 3; P <.01). Compared with the MDD cohort, generalized anxiety disorder was higher in the MDSI cohort (63% vs 44%; P <.001) as was social anxiety disorder (45% vs 18%; P <.001). However, fibromyalgia was considerably lower in the MDSI cohort compared with the MDD cohort (10% vs 31%; P <.01). Members of the MDSI cohort more frequently reported unprompted symptoms such as loneliness (24% vs 1.1%), hopelessness (23% vs 0.7%), and impulsivity (16% vs 0.3%) compared with members in the MDD cohort. Hopelessness, loneliness, anhedonia, social anxiety, and younger age were the major predictors of SI in MDD. People in the MDSI cohort reported lower perceived effectiveness of commonly prescribed antidepressant treatments compared with people in the MDD cohort. The study relied upon self-reported data provided by members of a specific web-based platform, which may not be reflective of the general population. “Overall, results from the study can help guide clinical judgment to identify suicide-related risk among patients with MDD who may not voluntarily report suicidal ideation to health care providers,” the investigators concluded. Disclosure:This study was supported by funding from Janssen Research & Development LLC. All authors are employees of Janssen. Continues on page 38

Conference Roundup

CV events had an onset shortly after dosing and resolved within 1.5 hours.

CV SAFETY OF ESKETAMINE NASAL SPRAY FOR TREATMENT-RESISTANT DEPRESSION Blood pressure should be assessed before treatment with esketamine nasal spray in patients with treatment-resistant depression, according to study findings presented at Psych Congress 2019. Researchers sought to evaluate potential cardiovascular (CV) effects of esketamine nasal spray in patients with treatment-resistant depression.The safety analysis population was derived from 5 double-blind placebo-controlled phase 2/3 studies and 1 open-label phase 3 study of esketamine nasal spray. A total of 1708 patients received esketamine nasal spray plus an oral antidepressant vs 486 patients who received an oral antidepressant plus placebo. The patients were aged 18 to 64 years (5 studies) or ≥65 years (2 studies; mean age, 49.1 years across all studies) and had treatment-resistant depression (defined as a nonresponse to adequate trial of at least 2 antidepressants during the current episode of depression). Patients with CV disease were excluded from the study. Vital signs were measured at baseline and during all dosing visits; blood

pressure and pulse/heart rate measurements were taken after the patient had rested for ≥5 minutes and were measured supine (with either completely automated device or manual techniques); and single, 12-lead electrocardiograms were performed at prespecified time points after patients had rested in a supine position for ≥5 minutes. A total of 1708 patients received ≥1 dose of esketamine in the 6 completed phase 2 and 3 studies, with a combined cumulative exposure to esketamine nasal spray of 611 patient-years in the phase 2/3 treatment-resistant depression studies and 601 patient-years in the phase 3 studies. Of the 1601 patients exposed to esketamine nasal spray in the 5 completed phase 3 studies, 479 were exposed for ≥6 months and 178 for ≥12 months. Increased blood pressure, abnormal heart rate, and CV adverse events of clinical interest in patients treated with esketamine had an onset shortly after dosing and were resolved within 1.5 hours while they were still in the clinic. Approximately 2.0% to 4.9% of patients in the esketamine group experienced an abnormal blood pressure elevation vs 0.0% to 0.9% in the placebo group across all studies. The abnormal blood pressure elevations were generally higher in patients with vs without a history of hypertension and in elderly patients. Fewer than 2% of all patients across the studies discontinued esketamine due to adverse events of increased blood pressure and tachycardia, and there were no hospitalizations reported for any blood pressure elevation. In addition, the researchers did not observe any clinically relevant effect on electrocardiogram parameters. Disclosure: Studies discussed in this poster presentation were supported by funding from Janssen Research & Development LLC. Several authors declared affiliations with the Janssen. Please see the original reference for a full list of authors’ disclosures.

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LOFEXIDINE MAY MITIGATE SYMPTOMS OF OPIOID WITHDRAWAL SYNDROME Treatment with lofexidine may provide better control of the symptoms of opioid withdrawal syndrome compared with placebo, according to research presented at Psych Congress 2019. Lofexidine is a non-opioid, centrally acting agonist of α2-adrenergic receptors that was approved by the US Food and Drug Administration in May 2018 for the management of opioid withdrawal symptoms in adults. Opioid withdrawal syndrome is caused by enhanced activity in the locus coeruleus resulting in excessive noradrenaline release from this structure. In this double-blind, placebo-controlled study, 602 patients aged ≥18 years with opioid use disorder who abruptly discontinued their short-acting opioid regimen were randomly assigned to receive lofexidine 2.16 mg/d (4 daily doses of 0.54 mg; n=229; 70.7% men; 73.8% white; 86.0% using heroin; mean substance use duration, 9.3 years), lofexidine 2.88 mg/d (4 daily doses of 0.72 mg; n=222; 71.2% men; 71.2% white; 82.0% using heroin; mean substance use duration, 7.9 years), or placebo (4 times/d; n=151; 70.9% men; 77.5% white; 80.8% using heroin; mean substance use duration, 8.8 years).The study outcome was the percentage of patients taking supportive medication for opioid withdrawal syndrome as specified in the protocol (eg, acetaminophen, bismuth, antacids, and zolpidem) from day 1 to day 7. A greater percentage of patients taking placebo vs either dose of lofexidine resorted to supportive medication from day 2 to day 5, with greater group differences for the use of acetaminophen and bismuth. Adverse events associated with the use of lofexidine included bradycardia, orthostatic hypotension, hypotension, and dizziness. ■ Disclosure:This study was supported by US WorldMeds, LLC. Both authors are employees of US WorldMeds, LLC.

LEGAL ADVISOR CASE

Is Accessing PHI a Violation?

Remotely accessing patients’ protected health information puts a nurse in a precarious position. ANN W. LATNER, JD

When we hear about privacy issues in the medical field, we almost immediately think about violations of The Health Insurance Portability and Accountability Act (HIPAA).Although many privacy issues do not rise to the level of a HIPAA breach, they still may be significant enough to get a clinician fired or censured by the state nursing board. This month we look at one such case. Ms L was a nurse working in a large suburban hospital. She had many years of experience in general but had been working for the hospital for less than a year. Ms L was assigned to the intensive care unit (ICU). Five nurses were assigned to each shift, and the last one on the list was flexible depending on the number of patients in the ICU. If the patient census was low, the last nurse on the list would be put on call and would not have to work the shift. Nurses could call the charge nurse on the unit earlier in the day to find out if they would be needed for an assigned shift. In order to determine if she would have to come in for a shift, Ms L remotely accessed the patient census list from the hospital from her

Violating an employer’s policies can subject a clinician to a reprimand, a suspension, or worse.

home, using her personal computer.The patient census list from the ICU contained private health information including patient names, ages, diagnoses, medications, and insurers. Over the course of 1 month, Ms L remotely accessed the patient census list 11 times. The hospital discovered the remote access the next month and questioned Ms L about it. “Yes,” she said to her supervisor. “I did access the list. I did it so I could see the capacity in the ICU to know whether I would be needed at work.” “As you know, the hospital’s information security policy prohibits remote access to the computer system without authorization, which you did not have,” said Ms L’s supervisor, Ms S.“Nor did you need to access the list to treat a patient or for any other legitimate job responsibility.” Continues on page 40

Cases presented are based on actual occurrences. Names of participants and details have been changed. Cases are informational only; no specific legal advice is intended. Persons pictured are not the actual individuals mentioned in the article.

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LEGAL ADVISOR The supervisor issued Ms L an employee disciplinary notice, suspended her for 2 shifts, and required her to repeat a HIPAA training class. Additionally, the supervisor filed a complaint with the state Board of Nursing.The Board began its own investigation and found probable cause to file a notice of hearing and statement of charges against Ms L, alleging that she violated state code regarding privacy rights of patients. A hearing took place, after which the Board made the following finding of facts: 1. Ms L had accessed the patient lists for the sole purpose of determining the ICU census so that she could determine whether she would be working her shift the next day or be placed on call. 2. Ms L did not use the information for any other purpose, and she did not share it with anyone. 3. Ms L was not authorized to access the patient lists from remote locations. 4. Ms L did not need the patient list information in order to perform her duties. The Board found that Ms L had committed unethical conduct by violating the confidentiality or privacy rights of patients by accessing protected health information on the census lists without the need to do so. As punishment, the Board imposed a citation and a warning as discipline. Ms L filed an application for a rehearing with the Board, claiming the Board’s finding was unsupported by the evidence and inconsistent with the Board’s findings that she did not use or share the information.

Never access records of patients who are not yours or records that you do not have a legitimate reason to look at. The Board denied her application, repeating that accessing the protected health information without a legitimate reason was sufficient to find that Ms L had violated the confidentiality or privacy rights of patients.The Board also noted that it had fully considered the circumstances of the violation (ie, that Ms L didn’t understand that her actions violated patient privacy, that she did not disclose the information to anyone else, and that the hospital determined her actions were not a reportable HIPAA breach) when it chose to impose the least severe sanction available: a citation and a warning. Unsatisfied, and angry at what she felt was mistreatment, Ms L filed a petition for judicial review, asking the court to overturn the Board’s ruling.

Legal Background

Ms L argued that accessing — without reading or sharing — patients’ protected health information is not sufficient conduct to find a violation of patients’ confidentiality or privacy rights. However, the court disagreed with her assessment.“Ms L admits that she repeatedly accessed the census list, which contained numerous forms of protected health information,” wrote the court in its decision. “Ms L denies reading the parts of the list containing the protected information, but she does not deny that she accessed the information and that the information was not necessary for her to complete her job duties. Accessing the unneeded confidential information is a violation of hospital policies put in place to protect patient confidentiality, which Ms L knew or should have known about.” Based on this determination, the court dismissed her appeal. Protecting Yourself

Ms L did not think she was doing anything wrong when she accessed the patient census list to determine the need for her to work her assigned shift. After all, she didn’t read anything – she just looked at the number of patients. She didn’t share any information. So how was this a violation? It is simple. First, Ms L’s actions represented a violation of her hospital’s policies.Violating your employer’s policies can get you reprimanded, suspended, or worse. Second, Ms L’s actions represented a violation of the state’s administrative code regarding patient privacy as determined by the Board of Nursing. Although Ms L didn’t do anything with the information contained in the census list, the simple act of accessing it in the first place was the violation. The fact that she had no malicious intent when doing it didn’t matter.What mattered was that she was not authorized to access the list via the computerized system, and she had no legitimate patientrelated purpose for doing so. It is essential to know your employer’s policies about information security and patient privacy. Never access records of patients who are not yours or records that you do not have a legitimate reason to look at. Be extremely careful about remotely accessing your employer’s computer system from home; never do so without authorization or without a very specific reason, and never do so if employee policy forbids it. While a privacy violation may not rise to the level of a HIPAA violation, it can still be enough (as in this case) to cause you plenty of misery. ■ Ms Latner, a former criminal defense attorney, is a freelance medical writer in Port Washington, New York.

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