Total Pages : 40 October 2021 Vol 14* Issue 7 100
Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report An Alternative Approach to Understanding Acne Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
Mutifocal Alopecia Areata In A Child Green Nail Syndrome: Treated Successfully With Gentamicin Eye Drops Dermoscopic Assessment of Post Covid Hairfall
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Skin Sciences to Grow In India
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Due to environmental changes and an increasing number of life stressors, skin health has become a growing concern. Skin diseases are a major health problem affecting a high proportion of the population in India. Skin diseases can place a heavy emotional and psychological burden on patients that may be far worse than the physical impact. Many factors determine the pattern and prevalence of cutaneous diseases among the youth such as gender, race, personal hygiene, quality of skin care, environmental milieu and diet. Recently, both UV damage and environmental pollution have been shown to accelerate skin-related injury. Increased consciousness especially among the youth of their body and beauty further aggravates their anxiety. Most research in the field of skin science has focused on the avoidance of skin diseases and the protection of skin health.Moreover, considering the recent progress in scientific and technological basic research on the skin, the fields of dermatology and cosmetology have substantially advanced. This issue has a wide range of clinical Dermatology articles from Allergic Contact Dermatitis, Alternative Approach to Understanding Acne, Multifocal Alopecia Areata in a Child to Dermoscopic Assessment of Post Covid Hair fall.
- Dom Daniel Executive Editor & Publisher
All rights reserved. Reproducing in any manner without prior written permission prohibited.
Published for the period of October-2021
October 2021
3
Dr. Shru takir
MD, DVD
Allerg ic C Leadin ontact Der Dermat g To Eczem matitis at itis: A Case R ous eport Dr. Atul Gir Allergic
itis Leading
oi
tous Dermat
Dr. Atul Girdhardas Singhania,MBBS,DVD
itis: A
Case
MBBS, DVD s Singha Skin Spec nia ialist, Vene Cosmetolo reologist gist , Leprolog Shree Skin ist, and and Hair Akola, Care Clini Maharash c, tra
swaramm
Profess or and HOD Departm ent of DVL Guntur Medica l College Guntur, , Andhra Pradesh
07 Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report
To Eczema
dharda
Dr. S. Nage
MD
Contac
t Dermat
thi D. Shen
Profess or and Head, Departm ent of Dermat Kanach ology, ur Institut e of Mangal uru, Karnata Medical Science ka s,
a
Dr. D. Indir
Introd uction Conta ct derma exoge titis is comm nous allerge on inflam one of n to which matory the have previo characterize skin diseas humans usly d by been pruritic erythe e Common sensit matou skin lesion etiolog s and allergi ical allerge ized. 4 contact s that c conta occur with a ns for ct derma after balsam Conta titis are of Peru, ct derma foreign subst nickel, chrom ance. 1 forma titis is irritant ium, neom ldehyd contact divided e, thiom ycin, derma into mix, cobalt contact ersal, titis and fragrance , and parthe derma allergic conta titis. 2 Each differe ct derma nium. 2 nt mech type has Allergic titis can anism presentatio a products (e.g., be from while the topica n is medic l contact the same. clinical adhesive ines, cosm 3 derma tape) etics, Irritan reactio titis often non–im t ns mune-modu is caused produ with by the borde 1 ces of the well-d lated rs. Clinica emarc skin by irritatio ated lly it is a subst to skin n by local skin characterize ance, chang 1 rash, itchine leading papul es. It d chemicals es, vesicle is produ ss, redne s, follow ced by and ss, toxic effect or metal ions dry skin, ed by that exert being scaling s withou swellin response g, t induci mainly ng a T-cell test. diagnosed and lesions, (conta ct irritant contact However, by the derma s). 2 Allerg patch many titis (ACD) hypersensit ic been report disabilities is ed a delaye ivity reactio such as have psych foreign osocia pain, itch, n in which d substance l conse and quenc 4,5 with the comes a The es. into skin; most skin chang contact after reexp comm allergic on sympt es occur osure Gener oms to the contact pruritu ally it of substance. derma s, along 1 chemicals is caused by titis are stingin that modif small reactiv g. Allerg with burnin induce g and e comm ic conta y protei innate only ns and ct derma and adapt responses presents titis erythe ive immu (conta ct allerge ne and matous, indura acutely with Allergic ns). 2 plaques, ted contact papules vesicu and for 20% derma lation, bullae titis accou edema of the formation nts cases. derma cases titis. It Chron in severe of conta ic allergi inflammator is an adver ct dermatitis c conta se cutan can prese y reactio eous lichenificatio ct direct nt with n cause contact n, and scaling, d by the conta of the skin fissuring. ct derma with a Allerg titis specific with a well-d typically prese ic nts efined , expos ure-
a MBBS, MD, DVL Assista nt Profess or Gandhi Medica l College Secund , erabad, Telanga na
07
Octobe
r 2021
7
An Alternativ
e Approach
to Understa
An Alter nativ Underst e Approach to anding Acne nding Acne
10
An Alternative Approach to Understanding Acne
Dr. Vina
y
MD, DTCD Kumar Sinh a , MACP, Skin Care MCGP and Laser West Borin Centre, g Patna, Bihar Canal Road,
Dr. Vinay Kumar Sinha, MD, DTCD, MACP, MCGP
The presen t dissert on my ation is experie based therefo re has nce with acne pustule tropica its relevan and regardi s. Tomes l ce in have been live in. settings that ng the formati the and It written on of comed researc climatic may not hold we Indians h has conditions. factors true in ones enuncia other and hormondiscovered The ted his es that many own experieauthor has role in the formati may or may on of acne. play a nce which put, acne the prevale not be in may appear Simply effect nt view. consonance believe followin of them, of differen Neverth s g the eless giving rises t combinations views andthat he should expres he lesions: to the followin so the of conflict s his article. of g skin or indirect interest of any He has no 1) Comed sort, directly onal acne group or ly, with any either organiz industr which ation or ial house. can be Acne a) Blackh sebace is a disease contain eads: When ous unit of the ing follicle the comed sebace ous glands and particupilo- and the comed has its mouth one by the and is charac larly or one showin open presen ce g through terized affecte d areas. of comedones , in the b) Whiteh The affecte contain eads: When ing the comed the face, d areas with a thin follicle has its one are typicall should film of epithelimouth closed upper y arms and ers, upper um. chest, In these occasio phases nally the upper back of acne, disease and does not buttock of fade away adolescence s. It is a presence seem to react the body of acne. and tends as the by its presen adultho It is not to the to od, althoug adolescent bothere ce. into late d h it may enters 2) Papule adultho persist od. s and papule papulo These forms are the when therepustules: A respon secretio se of the n is the areas where is minima of the comed skin to child greates oil the presen l reache one. s adolesc t when a skin has androg started In other words ce enic hormon ence. getting play an the The the presence es are annoye importa believe d by increas nt role d to mild inflamm of the comed e in sebace in the secretiothe sudden the formati atory reactio ones. A ous glands n causes on of ns of the sebace ous secretio. In the body the that comedonal a papule around the said orifice. the extrava ns are areas. It sation greates of fluid means t in the comedones Comed minima has started inside ones l. form within are keratin but is causing This extrava sated a reactio the follicula plugs that tissue and are n in the fluid is surroun r openin formati frequently associa adnexa g The adnexa ding the on of l comed ted erythem ones. a, nodule with forming pus may react at the orifice still further s and to the formati and leading on of have the papulo a pustule. Now pustula we r acne
10
10
16
October
"A
Perfect Protein Doesn't Exist: A Rare Case Report of Fixed Food Eruption Triggered by Egg Ingestion"
2021
"A Perfect
Protein
Doesn't
"A Perfe A Rare ct Protein Do Case Re esn't Ex Eruptio port of Fixed ist: n Tr Food Egg Ingeiggered by stion"
Dr. Mahajabeen S. Madarkar, MBBS, MD Dr. S.V. Smitha, MBBS
Exist: A
Rare Case
Report
of Fixed
Food Eruption
Dr. Mah
ajabeen
MBBS,
MD
Triggered
by Egg
Ingestion
"
S. Madarka
r
Associate Professor Department of Derm S. Nijali atology, ngappa Venereology Medical and Lepro College, sy Bagalkot, Karnataka, India
Dr. S. V.
Smi
tha MBBS Junior Resid ent Department of Derm S. Nijali atology, ngappa Venereology Medical and Lepro College, sy Bagalkot, Karnataka, India Abstra ct
20 Green Nail Syndrome: Treated Successfully With Gentamicin Eye Drops
16
Fixed food hyperse eruption nsitivity (FFE) is of hyperse reaction a rare type recurren nsitivity in which t fixed reaction after consum cutaneo occurrin ption of us lesions g appear at in the form some food the same items exposure of recurren site on to the patches t erythem re, bullae, offendin atous Even though g food. [1] vesicle, the same fixed drug or pustule site after eruption at FFE have in commo ingestio s and or related n recurrin food produc n of same at the same g lesions food items location ts. Various and , variable were listed timing nature causing of in FFE include the literature food eruption the lesions in fixed ground s sugges tree nuts, mechan nuts, legume ts differing isms. The like kiwi, s, lentils, exact strawbe of fruits FFEs is mechan rry and yet to be Here we ism tonic water. be present elicited multifac and may a rare torial. [2] triggere case of Here we d by intake FFE rare case present of eggs. of FFE a triggere of eggs. Key wordsd by intake Fixed food allergy, eruption hyperpi , egg Case report gmenta tion. Introdu ction A 35 year old homem female Fixed food aker in patient, eruption occupa (FFE) is to skin tion present a unique outpatie ed nt departm recurren ent with t episode s of multiple sharply
16
October
2021
Dr. Mala Bhalla, MD Dr. Amrit Kaur, MD Dermatology
Green
Nail Syndrom
e: Treated
Green Na Success il Syndrome : Treated fully W ith Eye Dr Gentamicin ops Successf
ully With
Gentamic
in Eye
Dr. Mala
MD
Drops
Bhalla
Professor Department of Derm Governmen atology, Venereolog t Medic al Colleg y e and Hospi and Leprosy, tal, Chand igarh
Dr. Amrit
22
Mutifocal Alopecia Areata In A Child Dr. Shrutakirthi D Shenoi, MD, DVD Dr. Shibani Bhatia, MBBS, MD, DNB, FAGE, MRCP (SCE) UK
26
20 20
October
2021
Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
INTRO DUCTI ON Green and progres Nail Syndro sed to known me (GNS), nail. There involve as ‘CHLOR half of also was no the commo history or any n bacteria NYCHIA’ is of diabete other a caused l nail comorb She worked id conditio s infectio by n, ns. aerugin Pseudo cook. She as a domestic osa. It monas help and had taken is charact greenis oral antifung h chromo treatme erized nt with by als from nychia discolo improve i.e greenis outside ration ment. of the with no h On examin is due nails. The and lateral to ation distal color onycho a metabo a pigment lysis was Nail folds pyocya lite was normal present nin, produc pseudo . intact. All ed by and cuticle monas other nails the bacteria 1 were asympt clipping were normal. . Althoug omatic, s were it causes h Nail cosmet sent for hydroxi ic disfigur significa de examin potassi nt ement um emotion ation bacteria leading al and along l and psycho to with which fungal social results culture distress sensitivity. Provisio in the treatme patient nal diagnos and nt. seeking chlornychia due is of to pseudo made and CASE monas gentam REPOR was icin eye given for T drops were topical A applica the nail 50-year tion around and on -old present female the nail drops’. ed bed as patient Bacteri with ‘nail greenis al culture asympt the diagnos h discolo omatic confirm is as ration finger nail ed of Pseudo the growth of left since 2 ring monas was months It had organis aerugin started (FIG-1& m was osa. from the 2). At 3 weeks sensitive to gentam The lateral edge icin. follow showed 80% improve up the patient ment.
Mutifocal
Alopecia
Areata
In A Child
Mutifo
cal Alop ec In A Ch ia Areata ild
Dr. Shru
MD, DVD
ani
ai
22
October
2021
Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
INTRO DUCTI ON Hair loss in children bothers ome compla is one of in dermat ints present the region followin ology clinics. ing g a haircut. conditio gradua Some ns causing lly increas The patch of the tinea capitis, ed in size hair loss lesions appear include and new alopeci ed over trichotil months a areata lomania the next . He compla (AA), and rarely six disorde rs. AA hair shaft but denied habit ined of mild itching is a chronic mediate of had no d disorde immune other compla hair pulling. - he r that scarring ints except He causes had been hair loss. nondiagnos that The commo ed as nephro nly present condition most syndrome 5 years ago tic patches s with treatme and of discrete nt with oral steroids was on It is known alopecia on the scalp. Clinical . to occur autoimm with other smooth examination reveale une disease pernicio d multiple alopeci s like us anaemi c patches vitiligo, varying a, mellitus in size on scalp and thyroid type 1 diabete from 2cm x s 10cm x 6cm this associa disease 2cm to in size althoug tion is coalesc h form larger clinical not commo ing to bald areas practice n in growth of . Here [Fig. 1] case of white hair we report with multifoc in betwee al AA in a was patchy patient n. There a paediat hair loss with nephro ric eyebrows over bilatera tic syndrom as well. CASE l e. reveale REPOR d multiple Nail examination T regular pull test A ten-yea pits. Hair was positive r-old boy of the at the periphe patchy patches present hair loss ry ed with clinical . Looking over the eyebrow picture, at the scalp and with s of six AA was a differen months conside His mother ’ duration red tial of had noticed trichotil . His laborato 6 months the first ry parame lomania. ago over patch unrema ters rkable. the right were parietal
Telangiec
tasia Maculari
s Eruptiva
October 2021
Form of
Cutaneou
s Mastocyt
MD
T. Vani
Professor Departmen t of DVL Guntur Medical College,
Dr. S. Nag
MD
26
26
October
2021
Guntur,
Andhra
eswaram
Professor and HOD Departmen t of DVL Guntur Medical College, ct
4
- A Rare
osis
Abstra
Dr. Rahul Nagar, DNB Dr. Farah Khan, MD
Perstans
Telan Eruptiv giectasia M acula a Pe of Cutan rstans - A Ra ris re eous M astocyto Form sis Dr.
Dr. D. Indira, MD (DVL)
Dermoscopic Assessment of Post Covid Hairfall
D. Shenoi
Dr. Shib
Bhatia MBBS, MD, Consultant DNB, FAGE, MRCP Dermatolog (SCE) UK Kaya Skin ist Clinic and Criticare Hospital, Mumb
22
35
takirthi
Professor and Department Head, of Derm Kanachur atology, Institute of Medic Mangaluru, al Scien Karnataka ces,
Dr. T Vani, MD Dr. S. Nageswaramma, MD
30
Kau
r MD Derm atology Consultant Dermatolog AK Clinic ist and s, Ludhi Hair Trans ana, Punja plant Surge b on
Pradesh
ma
Guntur,
Andhra
Pradesh
Mastoc ytosis year old is a group male heterog of patient eneous based , diagno on the by abnorm diseases charac sis terized skin lesions characteristics al infiltrati cells in of the on of and histopa various mast features. organs 1 thologic mastoc Dermo . Cutane ytosis scopy has al ous as a diagno is the been used mast cells prolifer stic aid. ation of in the evidenc skin without Keywo e of any Dermo rds: Cutaneous involve organs 2 ment Mastoc . scopy, of other Telangi ytosis, Telangi ectasia eruptiv ectasia e perstan macula ris Introduction s (TMEP) form of cutane is a rare ous mastoc usually ytosis and Mastocytosis it has a prolong is one TMEP hemato ed course of the is usually poietic rare disorde . 3 by compo increas r sed prolifer charac ed numbe of subtly ation and terized rs of spindle mast cells accum shaped ovoid ulation in several to skin, mast cells of the papillar bone marrow organs such infiltrati y dermis as dilated and surroun ng gastroi , skeleta ntestina superfic l system ding l tract, ial capillar , venules 4 nodes spleen, . and liver. 1,6,7 ies and lymph Clinical of TMEP presen tation Mastocytosis or yellowis shows erythem h-brow atous viz. cutane consist of two n macule telangie ous mastoc types ctasias s with system , mostly ytosis ic mastoc trunk and and ytosis. 1 upper limbs. located on the mastoc 5 Cutane ytosis ous is clinicall We report into five y classifie subtyp a case es it d of TMEP pigmen tosa (UP), includes Urticari in a 18 a Diffuse mastoc ytosis (erythro cutane ous derma) , Bullous
Report
MITHCHELL AD
Editorial Board Dr. Atul Girdhardas Singhania
Dr. Shrutakirthi D. Shenoi
Dr. Vinay Kumar Sinha
Dr. T. Vani
Dr. Mahajabeen S. Madarkar
Dr. S. Nageswaramma
Dr. Dr. S. V. Smitha
Dr. D. Indira
MBBS, DVD Skin Specialist, Venereologist , Leprologist and Cosmetologist, Shree Skin and Hair Care Clinic, Akola, Maharashtra
MD, DTCD, MACP, MCGP Skin Care and Laser Centre, Patna, Bihar
MBBS, MD Associate Professor Department of Dermatology, Venereology and Leprosy S. Nijalingappa Medical College, Bagalkot, Karnataka, India
MBBS Junior Resident Department of Dermatology, Venereology and Leprosy S. Nijalingappa Medical College, Bagalkot, Karnataka, India
Dr. Mala Bhalla
MD Professor Department of Dermatology, Venereology and Leprosy, Government Medical College and Hospital, Chandigarh
Dr. Amrit Kaur
MD Dermatology Consultant Dermatologist and Hair Transplant Surgeon AK Clinics, Ludhiana, Punjab
Dr. Shibani Bhatia
MBBS, MD, DNB, FAGE, MRCP (SCE) UK Consultant Dermatologist Kaya Skin Clinic and Criticare Hospital, Mumbai
6
October 2021
MD, DVD Professor and Head, Department of Dermatology, Kanachur Institute of Medical Sciences, Mangaluru, Karnataka
MD Professor Department of DVL Guntur Medical College, Guntur, Andhra Pradesh
MD Professor and HOD Department of DVL Guntur Medical College, Guntur, Andhra Pradesh
MD (DVL) Associate Professor Department of DVL Osmania Medical College/ Osmania General Hospital Hyderabad
Dr. Rahul Nagar
DNB Associate Professor Department of Dermatology, Venereology and Leprosy Mahatma Gandhi Memorial Medical College and MaharajaYashwant Rao Hospital, Indore, Madhya Pradesh
Dr. Farah Khan
MD 3rd Year PG Resident Department of Dermatology, Venereology and Leprosy Mahatma Gandhi Memorial Medical College and MaharajaYashwant Rao Hospital, Indore, Madhya Pradesh
Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report
Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report Dr. Atul Girdhardas Singhania
MBBS, DVD Skin Specialist, Venereologist , Leprologist and Cosmetologist Shree Skin and Hair Care Clinic, Akola, Maharashtra Introduction Contact dermatitis is one of the common inflammatory skin disease characterized by erythematous and pruritic skin lesions that occur after contact with a foreign substance.1 Contact dermatitis is divided into irritant contact dermatitis and allergic contact dermatitis.2 Each type has a different mechanism while the clinical presentation is the same.3 Irritant contact dermatitis is caused by the non–immune-modulated irritation of the skin by a substance, leading to skin changes.1 It is produced by chemicals or metal ions that exert toxic effects without inducing a T-cell response (contact irritants).2 Allergic contact dermatitis (ACD) is a delayed hypersensitivity reaction in which a foreign substance comes into contact with the skin; skin changes occur after reexposure to the substance.1 Generally it is caused by small reactive chemicals that modify proteins and induce innate and adaptive immune responses (contact allergens).2 Allergic contact dermatitis accounts for 20% of the cases of contact dermatitis. It is an adverse cutaneous inflammatory reaction caused by the direct contact of the skin with a specific
exogenous allergen to which humans have previously been sensitized.4 Common etiological allergens for allergic contact dermatitis are nickel, balsam of Peru, chromium, neomycin, formaldehyde, thiomersal, fragrance mix, cobalt, and parthenium.2 Allergic contact dermatitis can be from topical products (e.g., medicines, cosmetics, adhesive tape) often produces reactions with well-demarcated 1 borders. Clinically it is characterized by local skin rash, itchiness, redness, papules, vesicles, followed by scaling and dry skin, swelling, and lesions, being mainly diagnosed by the patch test. However, many disabilities have been reported such as pain, itch, and psychosocial consequences.4,5 The most common symptoms of allergic contact dermatitis are pruritus, along with burning and stinging. Allergic contact dermatitis commonly presents acutely with erythematous, indurated papules and plaques, vesiculation, edema and bullae formation in severe cases. Chronic allergic contact dermatitis can present with scaling, lichenification, and fissuring. Allergic contact dermatitis typically presents with a well-defined, exposureOctober 2021
7
Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report
dependent distribution, commonly involving the hands, face, or eyelids.6 In some patients allergic contact dermatitis can be chronic and significantly affect the quality of life.2 Here we report a case of allergic contact dermatitis leading to eczematous dermatitis due to Tilak of Kumkum, chronic use. Case Report A 42-year old male presented to our out patient department with complaints ofitching, burning, started with pruritus and redness, followed by papules, vesicles and later on leading to eczematous plaqueson his forehead (Fig. 1) with constant use of Kumkum which he applied on forehead and chin sometimes. There was history of same symptoms when he using of Tilak. The symptoms disappear when he stopped using Tilak for long time.He was a case ofallergic contact dermatitis.The patient does not give family history of atopy like frequent running of nose, red eyes, cough, bronchial asthma and eczema in family members. Baseline investigations like haemoglobin (Hb), Total leucocyte count (TLC), differential leucocyte count (DLC), Erythrocyte sedimentation rate (ESR), Serum Glutamic Pyruvic Transaminase (SGPT), Random blood sugar (RBS), Serum creatinine etc were done. Allergic patch test not possible in his area due to remote rural areas. Chest X-Ray nothing abnormal detected (CXR NAD) in this case.
cap daily for 3 months. Intermittently we have used moisturiser like Venusia cream, Moiste creams etc. The patient responded very well with above treatment. He followed up only twice with complete clearance of patches (Fig. 2). Doctor had warned him of long term side effects of topical corticosteroid like Atrophy of skin, Telangiatesias, cushingoid features etc. Also warned him to avoid the suspected allergens. Kumkum in market is made of Turmeric and Limestone and added impurities, which is toxic to human skin.
Figure 1: Before Treatment
8
October 2021
Allergic contact dermatitis is a multifactorial disease, resulting both from genetic and environmental factors.7 Allergic contact dermatitis is one of the most prevalent occupational disease and the most common form of immunotoxicity in humans.4 It is characterized as type IV delayed hypersensitivity reaction.7 Risk factors for allergic contact dermatitis include age, occupation, and history of atopic dermatitis.2 ACD is a T-cell-mediated skin inflammation resulting from the priming and expansion of allergenspecific CD4+ and CD8+ T cells.4 Allergic contact dermatitis has two phases. The first one is sensitization phase in which antigen-specific effector T cells are induced in the draining lymph nodes by antigen captured cutaneous dendritic cells that migrate from the skin. The elicitation phase includes effector T cells that are activated in the skin by antigen captured cutaneous dendritic cells and produce various chemical mediators, which create antigenspecific inflammation.2 Once one or more potential allergens come in contact with the skin, a series of phases sensitization, elicitation, and inflammatory regulation occur that lead to an inflammatory response to the allergens.7 Conclusion
Base line investigations were within normal limits except Hb of 10 gm% (Normal range 12 to 16 gm%). Doctor had treated him for 6 to 7 months with Antihistamins, antibiotic like Ampoxin 500 bd for 7 days, topical corticosteroids like Topical Momate cream, cap Becozinc etc. We have given Ferrous Ascorbate
Discussion
Figure 2: After treatment
ACD is one of the leading causes of occupational skin diseases and significantly impacts quality of life. The best prognostic indicator for treatment of ACD is early recognition and intervention. Accurate identification of an offending allergen requires a detailed history of potential exposures and a physical examination to confirm the signs of ACD.7
Allergic Contact Dermatitis Leading To Eczematous Dermatitis: A Case Report
If the treatment fails and the diagnosis or specific allergen remains unknown, patch testing should be performed.1 Management of ACD is multifactorial, relying on both prevention (eliminating allergen exposure, using protective equipment, and educating the patient) and medical therapy (typically topical corticosteroids). Topical steroids are the mainstay of ACD symptomatic therapy. The combination of barrier creams with moderate to high potency steroids have repeatedly been shown to successfully control ACD symptoms.7 If allergic contact dermatitis involves an extensive area of skin (greater than 20 percent), systemic steroid therapy is often required and offers relief within 12 to 24 hours.1
practice,
2019,
3797536.
https://doi.
org/10.1155/2019/3797536 6. Owen, J. L., Vakharia, P. P., & Silverberg, J. I. (2018). The Role and Diagnosis of Allergic Contact Dermatitis in Patients with Atopic Dermatitis. American journal of clinical dermatology, 19(3), 293–302. https://doi. org/10.1007/s40257-017-0340-7 7. Weintraub GS, Lai IN, Kim CN. Review of allergic contact dermatitis: Scratching the surface. World J Dermatol 2015; 4(2): 95102. Available from: URL: http://www.wjgnet. com/2218-6190/
full/v4/i2/95.htm
DOI:
http://dx.doi.org/10.5314/wjd.v4.i2.95
References 1. Usatine, R. P., & Riojas, M. (2010). Diagnosis and management of contact dermatitis. American family physician, 82(3), 249–255. 2. Litchman G, Nair PA, Atwater AR, et al. Contact Dermatitis. [Updated 2021 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/ NBK459230/ 3.
Al-Otaibi,
S.T.,
Alqahtani,
H.A.M.,
Management of contact dermatitis, Journal of Dermatology & Dermatologic Surgery (2015),
http://dx.doi.org/10.1016/j.
jdds.2015.01.001 4. Brites, G. S., Ferreira, I., Sebastião, A. I., Silva, A., Carrascal, M., Neves, B. M., & Cruz, M. T. (2020). Allergic Contact Dermatitis: from pathophysiology to development of new preventive strategies. Pharmacological Research,
105282.doi:10.1016/j.
phrs.2020.105282 5. Kalboussi, H., Kacem, I., Aroui, H., El Maalel, O., Maoua, M., Brahem, A., El Guedri, S., Chatti, S., Ghariani, N., & Mrizak, N. (2019). Impact of Allergic Contact Dermatitis on the Quality of Life and Work Productivity.Dermatology
research
and October 2021
9
An Alternative Approach to Understanding Acne
An Alternative Approach to Understanding Acne Dr. Vinay Kumar Sinha MD, DTCD, MACP, MCGP Skin Care and Laser Centre, Patna, Bihar
The present dissertation is based on my experience with acne and therefore has its relevance in the tropical settings that we Indians live in. It may not hold true in other climatic conditions. The author has enunciated his own experience which may or may not be in consonance of the prevalent view. Nevertheless he believes that he should express his views and so the article. He has no conflict of interest of any sort, directly or indirectly, with any organization or group or industrial house. Acne is a disease of the pilosebaceous unit and particularly sebaceous glands and is characterized by the presence of comedones in the affected areas. The affected areas are typically the face, shoulders, upper chest, upper arms and upper back and occasionally the buttocks. It is a disease of adolescence and tends to fade away as the adolescent enters adulthood, although it may persist into late adulthood. These are the areas where oil secretion is the greatest when a child reaches adolescence. The androgenic hormones are believed to play an important role in the sudden increase in the secretions of the sebaceous glands. In the body the sebaceous secretions are greatest in the said areas. Comedones are keratin plugs that form within the follicular opening and are frequently associated with formation of erythema, nodules and 10
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pustules. Tomes have been written regarding the formation of comedones and research has discovered many factors and hormones that play a role in the formation of acne. Simply put, acne may appear following the effect of different combinations of them, giving rises to the following skin lesions: 1) Comedonal acne which can be either a) Blackheads: When the comedone containing follicle has its mouth open and the comedone showing through, or b) Whiteheads: When the comedone containing follicle has its mouth closed with a thin film of epithelium. In these phases of acne, the body does not seem to react to the presence of acne. It is not bothered by its presence. 2) Papules and papulopustules: A papule forms when there is minimal response of the skin to the presence of the comedone. In other words the skin has started getting annoyed by the presence of the comedones. A mild inflammatory reaction causes the formation of a papule around the comedonal orifice. It means that extravasation of fluid inside the comedones has started but is minimal. This extravasated fluid is causing a reaction in the adnexal tissue surrounding the comedones. The adnexa may react still further forming pus at the orifice and leading to the formation of a pustule. Now we have the papulopustular acne
An Alternative Approach to Understanding Acne
and it denotes that the condition is worsening or the comedones are getting infected. Now the skin develops a mild itch which worsens as the condition worsens. When the reaction becomes stronger the skin develops nodulocystic acne. What happens is that the oil glands are blocked at their orifices by the comedones. The oil secretions by the glands continue. If the oil secretions push off the comedones from the orifice, acne subsides and acne heals. If the blockage is such that the comedone is not pushed out, then the back pressure builds up, and the wall of the gland ruptures. The contents of the gland then extravasate into the adnexal tissue surrounding the gland causing the formation of a pustule, a nodule or a cyst – the nodulocystic acne. Abcess forms. These abscesses can coalesce and can form large cysts and sinuses which may or may not discharge their contents. They heal with the formation of scars, which may be atrophic or hypertrophic. Usually the condition is associated with severe seborrhea. The lesions are painful. Still worse is the development of Acne conglobata and acne fulminans. In acne conglobata we have coalescing nodules, cysts, abscesses, ulcerations and deep seated sinuses that involve the face, trunks, back, and sometimes also the gluteal region. Spontaneous remission is rare. Still worse is acne fulminans. This condition generally occurs in teenagers, is of acute onset, has all the features of acne conglobata and additionally is accompanied with fever, malaise, fatigue, arthralgias and elevated CBC. There are many variants of acne and there are many diseases which simulate acne. A few of the variants are: - neonatal acne, acne excoriee, acne mechanica, tropical acne, occupational acne, acne cosmetic, chloracne, steroid acne, drug induced acne and gram negative folliculitis. Sapho and Papa syndromes are nonpyogenic acne with multiple tissue involvement and pyogenic acne with multi tissue involvement respectively. They may have multi-organ involvement also. These conditions are rare. In short acne affects the face chest,
upper arms and back. It occurs mostly in the teenagers when the sebaceous secretions of the oil glands are at their peak. Propionibacterium acnes is believed to be a key factor in the formation of pustules along with male hormones and excessive keratinisation of the follicular orifice. The same areas are affected by seborrhic dermatitis and a favorite of malassezia furfur, the fungus that causes pityriasis versicolor. M. furfur causes oval hypopigmented or hyperpigmented patches which are mildly scaly. The fungi are lipophilic. They grow more profusely when the body secretes increased amounts of sebum. They may proliferate and grow down into the follicular orifice of the gland if the sebum secretion is profuse or if topical steroids are applied to control their itch. After the topical steroids they tend to form erythematuos nodules which can be mistaken for gram negative folliculitis or acne, not responding to conventional treatment. The fungi are living organisms and therefore they will have a metabolism; they will intake food and excrete their waste products. This fungus thrives on sebaceous secretions and fats and excretes fatty acids, lactic acid, pyruvic acid and the like. These acids denature the proteins and fats present in the sebum, causing an inspissation of the latter. This inspissated protein and denatured fat solidifies forming a keratin plug which eventually appears as a comedone. The keratin plug blocks the mouth of the follicle, but the oil secretion continues behind the block continuously. A backpressure develops enlarging the follicle, which is now visible as a comedone. It may appear as a blackhead if the follicular orifice is open, or as a whitehead if the follicular opening is covered by a thin film of epidermis. The backpressure also causes enlargement of the follicle. Because of enlargement, the walls of the follicle thin out and the contents of the follicle get released into the surrounding adventitial tissue. The contents are antigenic to the adventitia so a reaction follows. The acne now is inflamed and the comedone can now be called a redhead. On healing it may or may not leave a scar.
The comedone may also develop pus which may be sterile or may get secondarily infected by commensals in the follicle. The most common organism found infecting is propionobacterium acnes (P. acnes). P. acnes is always present in the follicle because it is a commensal. It becomes a pathogen only when it gets the right opportunity and the follicle is adversely affected by the process of acne formation. A pustule now forms. All healing from now on will lead to scar formation. The papules and the pustules may coalesce forming nodules, nodulocystic acne and sinuses connecting the cysts. However, at any given time all the forms of acne may be present on the face and thus acne is known as a pleomorphic disease. Once the nodules and cysts appear the acne is then called papulopustular acne. Acne therefore progresses from whiteheads and blackheads and redheads, called papule, to pustules, to nodules, then to cysts and to sinuses which may remain isolated or may drain into each other or to the open and finally healing; leading to varying levels of scarring of the face as a sequel of the disease. Acne may thus be produced by 1) Too much oil on the face, which may be produced intrinsically or added onto the face extrinsically. 2) Too much rubbing of the face i.e. friction of the skin of the face leading to minor abrasions and consequently closure of the orifice of the sebaceous glands. 3) Occlusion of the orifice of the sebaceous glands leading to a backpressure in the gland e.g. heavy make-up or powdering of the face. 4) The influence of drugs and chemicals. There are certain drugs that influence the facial skin in a way that it produces acne, e.g. isonex, corticosteroids, oral contraceptives and androgens. Acne may be produced under the influence of one or more of the above factors and in varied combinations of the same. This leads to the varied manifestations of acne. Acne may manifest as: comedones blackheads, whiteheads; papules and papulopustules – papulopustular October 2021
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An Alternative Approach to Understanding Acne
acne; nodules and cysts – nodulocystic acne. They may appear as having sinuses and burnt out acne may show as scars. These have been described earlier.
compounds, usually hydrocarbons, which are present in pesticides, insecticides and herbicides and in electrical goods manufacturing industries.
What can be done about it? A doctor can do nothing unless the patient comes to him. But, if it is possible the treatment should be started early, the earlier the better.
For ease of understanding, acne has been graded into four grades, from the mildest being grade I and the severest being grade IV. Beyond that one has grade V – nodulocystic acne and grade VI - acne conglobata.
Acne cosmetica – Occurs due to the use of oily and comedogenic cosmetics. Hair oil also comes under this heading. Hair oil, when applied onto the hair spreads onto the upper face and the forehead causing an oil overload on the forehead and the face. This overload leads to the formation of acne which is more concentrated on the forehead.
A doctor has to deal with bacteria, fungus, comedones, inflammation, pus and scars. For Malassezia furfur (P. ovale) one can give an appropriate anti fungal. What will happen if one gives an antifungal orally? Nothing. Antifungals do not cure the condition. The fungi are situated deep in the follicle and antifungals cannot reach there in sufficient concentration. Moreover antifungals are bacteriostatic; It means that the total quantity of fungi remains the same at the end of the treatment as compared to before the start of the treatment.
The other forms of acne that one encounters are: Neonatal acne – On the nose and cheeks of newborns; said to be formed under the influence of maternal hormones. It occurs because of transiently excessive production of sebum. It thus is self healing. Acne excoree – Acne associated with excoriations and scarring. The acne is minimal but the excoriation is predominant. Acne causes a minor itch of the face. The affected person, instead of accepting the minor itch as normal, goes after the problem and picks on all the lesions that he or she can see and derives a certain pleasure in doing so. The person may be getting obsessed with the problem of acne. This picking of the lesions leads to excoriations, scaling and patchy pigmentation of the face. Acne mechanica – Acne at those places where there is pressure and friction applied of the face, be it through rubbing, scrubbing or toweling of the face or always holding the face in the palms. Tropical acne – This is a severe form of acne which affects the face, back, chest buttocks and the lesions get infected by many other organisms other than P. acnes. The most common organism is staph. albus and staph aureus. They thus should be classified as folliculitis instead of acne and treated as such, but they continue to be called tropical acne. Occupational acne – In many of the professions there is use of oil. In these professions the oil affects the face either through the vapours that are produced by the hot oil or by direct contact of oils which may also be irritant to the skin. This causes acne called occupational acne. Chloracne – This occurs following exposure to chlorinated aromatic 12
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The conditions that we are not going to discuss are Sapho and Papa syndromes. The other conditions that we are not interested in, in this dissertation, are – steroid acne, drug induced acne, acne aestivalis and gram negative folliculitis. These conditions, even though they have the appearance of acne they are not acne so are not being discussed at the present dissertation. These diseases can be discussed in the differential diagnosis of acne. The other conditions that come under the differential diagnosis are staph folliculitis, pseudofolliculitis barbae, rasacea, perioral dermatitis, superficial mycotic folliculitis and other acne like conditions. In summary acne therefore is basically an effect of the following conditions – a) Excessive, abnormal or irritant oils on face, either by exposure, by direct application or by indirect spread from hair onto the face. b) Overgrowth of fungi, followed by bacteria, into the sebaceous follicles c) There is a possibility that there can be more than one microorganism involved which we have not investigated. d) Formation of a keratin plug. e) Backpressure behind the plug with distension of the plug and an inflammatory reaction to the situation created. f) Rupture of the follicle with discharge of the contents into the adnexa followed by acute inflammatory response, formation of pus and scar and finally loss of confidence from the damage done.
More than that, the infection in the follicle is of mixed type. So we need to add an antibiotic that is effective against the next in command – propionobacterium acnes. We now need to give an antibiotic to take care of the bacteria. What happens when we add an oral antibiotic? Virtually nothing. Over the ages we have seen that giving antibiotics is not a remedy for acne. Even though the organism is sensitive to all antibiotics, the drugs do not reach the site of infection and the bacteria keep on growing merrily. What would happen if we applied the antifungal topically, again the results are just about the same. Acne may reduce by a few grades but that is all. The same holds true for topical antibiotics. To have some result we have to tease out the comedones from the path so that the follicle opens up to treatment, both by oral and topical drugs. For this we need to give acne specific topical irritants. By their very nature they are mild or have to be used in a manner that they cause a mild irritation. Irritation causes exfoliation of the superficial layers of the skin opening up the pores. Irritation also causes erythema and swelling of the face. This increases the pressure inside the tissues of the face. The atmospheric pressure is normal pressure but the pressure inside the tissues is higher and so there is a pressure exerted on the follicle from behind the comedone block. Thus the comedone is slowly pushed out of the orifice with minimal damage to the skin. Once the
An Alternative Approach to Understanding Acne
comedone is out then the antibiotics start working and the secretions, that were abnormal till now start settling down and acne starts healing.
to return if isotretinoin is stopped, which it must after a certain period of time. The search for the stressors that cause acne becomes important.
The specific topical drug that has been found to be most effective are tretinoin, which is acne specific acid and also a mild irritant, and benzoyl peroxide which is a topical antibiotic and also a mild exfoliating agent. They both work better when given together about 12 hours apart, because they react with each other destroying one another. Thus both the drugs neutralize each other when given together of the antibiotics that are suitable for acne tetracycline is the most suitable because it can be given for a prolonged period and has a broad range. But then, it is a bacteriostatic; it cannot kill the bacteria and relies on the bacteria being shed by the body. Even then it is the most suitable of the antibiotics, because it is seen that virtually all antibiotics behave like a bacteriostatic whatever their potency against P. acnes and all need to be given for a prolonged period for them to show any effect. In such a scenario tetracyclines are the least toxic of them.
The stressors that are commonly present and need to be addressed could be the androgens, the testosterones, growth hormones, chronic elevation of the stress hormones adrenaline and noradrenaline, thyroid hormone, drugs that stress the body, medicines, lack of proper sleep, chronic stress at the workplace associated with frustration, and chronic infections like H. pylori, gram negative or candidal infection. They have to be tackled also, otherwise they will cause a rebound of acne during the treatment or after the treatment is stopped.
Any hypopigmenting agent or a modified Kligmans regimen then takes care of the post inflammatory pigmentation. More than 70% acne lesions get cured by following this regimen. This may lead to a permanent cure of acne provided the treatment is continued for a sufficiently prolonged period of time – the author continues the treatment for at least 3 months and then starts withdrawing the drugs one by one over a period of another three months leaving the topical for another six to ten months and tapering them off also. The stressors and other causes of abnormal sebum and the causes for abnormal amount of sebum have also been taken care of, to ensure a full cure.
Follicular Stimulating Hormones
Still, there will be many cases that do not respond or respond only partially to the above regimen. The tough part starts now. Does one indulge in the standard practice of giving isotretinoin orally or go in for investigating other causes that could cause acne. The author prefers to delay their use in the management of acne and first search for other causes – reason being that if one did not search for the cause of acne and treat it first it is bound
One needs to check out if the stressors are persisting. For that one may take recourse to lab tests, even though, most of the time the lab tests are normal. The following tests may be done but the list is not exhaustive and many more tests may be required depending upon the disease condition of the patient. S. Testosterone
Leutinising Hormones and DHEA-S (to rule out PCOS and hyperandrogenism) One needs to test for hepatic and renal functions, and triglyceride and cholesterol levels if one is planning initiation of isotretinoin. The author presently start all the relevant drugs even in mild cases of acne because he believes that it is important to get rid of the condition as soon as possible, it is important not to allow the disease to progress because the damage that it may cause is not visible most of the time, the damage may show months after the disease has subsided and the damage shakes the confidence of the affected person. Early cure leads to prevention of scarring, prevention of ugly looking mottled pigmentation of the face, restoration of confidence with its attendant glow of the face, increase in value of person in the marriage market, and a greater confidence in the person when searching for a job or facing an interview. A special mention needs to be made regarding acne associated with
obesity, because of the increasing prevalence of obesity in teenagers and younger adults; upto 30% of acne patients come under this category who visit my clinic. Obesity is defined as a person having a BMI greater than 30. BMI is defined as Height of the patient in cms, divided by the square of his weight in kg., even though it applies to persons above the age of 18 years, there is a tendency to use it in persons of younger age groups because of its convenience of delivering information. A BMI above 30 in a teenager or young adult denotes insulin resistance and consequent acne. There are two conditions that come under this heading – Polycystic Ovarian Syndrome and Metabolic Syndrome. In the PCOS cysts form in the ovary or around it and they start producing androgens (male hormones). The cysts also cause an imbalance of hormones in the body and cause insulin resistance. The two together cause obesity, irregular cycles, acne and hirsutism. To diagnose the condition lab tests along with ultrasound of the lower abdomen needs to be done and treated with anti-androgens along with the standard acne treatment. The other condition is Metabolic Syndrome. It is defined as a cluster of conditions that increase the risk of heart disease, stroke and diabetes. This condition should be diligently searched for because of its connotation regarding the future. This condition includes hypertension, high blood sugar levels, excessive body fat around the waist, abnormal cholesterol, increased risk of heart attacks and strokes. This condition seems to be very common in Indians and now among the teenagers of the affluent in the society. Acne is an associated symptom and appears as the warning sign of this condition, but most of the other conditions associated with this condition do not have any symptom. Insulin resistance is the underlying cause for both the conditions. Insulin is an anabolic hormone and promotes the absorption of glucose and carbohydrates from the blood into the liver, fat and skeletal muscles. It then converts the absorbed glucose into glycogen via glycogenesis and into fats via lipogenesis, or in the case October 2021
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An Alternative Approach to Understanding Acne
of liver into both. Glucose production and secretion by the liver is inhibited by high concentration of insulin in the blood. High levels of insulin causes storage of low molecular weight glucose into the liver, adventitia and muscle in the form of high molecular weight glycogen which is inert in the sense that it does not involve itself in any of the body activity unless compelled to do so under the influence of glucagon, the hormone that is secreted by the alpha cells of the pancreas, which has an effect opposite that of insulin. Glucagon stimulated the liver to release glucose in the blood by glycogenolysis and neoglucogenesis. Glucagon is secreted when insulin levels and blood sugar levels are low. In a normal person they balance well, but in the insulin resistant the insulin levels are high but the cells are full of fats and glycogen and because of that their functions are impaired. Because of the impairment the cells suffer from starvation of sorts and to cover it the glucagon level also rises. Because of raised glucagon level catabolism increases. Thus the raised levels of both insulin and glucagon causes increased wasting of the muscles and the parenchymal tissues like kidneys, liver, blood vessels, brain and the heart which end up ageing faster, and show up as diseases of premature ageing and weak muscles and bones, fatty liver, incipient renal failure, worsening the condition. On the skin the effects of these hormones show as eczema, acanthosis, obesity and acne. When this imbalance upsets the levels of other hormones varied combinations of disease complexes appear. Treatment can help but cannot cure the condition. Lifestyle changes are important. They are the mainstay of treatment. It includes cessation of smoking, weight loss regimen, a lot of exercise, regulation of blood sugar and cholesterol levels and medication for the same. Metformin seems to be a very promising drug especially suited for the management of this condition, but the cure lies in becoming thin and doing a lot of workouts to remain thin. Finally the scars have to be addressed and this may be done by non medical means such as chemical peels, lasers, dermabrasion, UVR etc. In case all these measures fail then one needs to take the help of 14
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isotretinoin orally and intralesional and oral steroids, but the situation for the use of steroids orally is really rare. Dr. V. K. Sinha ends his dissertation on his understanding of Genesis and basic Management of Acne.
NEWS
Candida fungus seen among recovering Covid patients; herpes, hair fall, nail issues other problems
Fungal infections of the skin, hair, and nails are a common public health problem worldwide. The prevalence of skin fungal infection is increases. The prevalence of skin fungal infection differs by social, geographic, economical status, and life environment. According to the skin care experts coronavirus patients even after being discharged from hospitals or having finished their home quarantine period should watch out skin inflammation. From reactivation of herpes infection to loss of hair, several Covid patients in recovery phase are facing one dermatological complication or another due to lowered immunity. Many postCovid patients with skin complications are rushing to OPDs, fearing they have contracted mucormycosis or black fungus but people should be cautious not paranoid. Several Covid patients in recovery phase are facing skin complications and the most common one being reported to the cases of herpes. In many patients with a history of herpes it is get retriggered and in others they are just contracting it afresh, both due to lowered immunity. Infection with herpes simplex virus, commonly known as herpes, can be due to either herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2). Herpes labialis which occurs around the lip area with lesions in cluster preceded by burning pain is caused by HSV. Herpes zoster is viral infection that occurs with reactivation of the varicella-zoster virus. It is usually a painful but self-limited dermatomal rash. Skin experts, who are seeing post-Covid patients, say cases of herpes zoster are being reported more than herpes from HSV. Cases of infection from Candida fungus have also been seen among the Covid patients who are in recovery phase. It is a mould like infection and can result from excessive medication or use of steroids. This infection can cause white patches on genitalia. Candidiasis is a fungal infection caused by a yeast (a type of fungus) called Candida.COVID-19 compromises the immunity of a patient leading to multifarious complications, including in skin, hair and nails. Though there is no clinical study to correlate the two but herpes infection is being reported in large number of Covid patients during recovery phase even a month later. Besides hair loss and nail complications are too happening with many patients.
Treating the ‘root’ cause of baldness with a dissolvable microneedle patch
The most common hair loss condition is called androgenic alopecia, also known as male- or female- pattern baldness. Androgenetic alopecia (AGA) is one of the commonest reasons for dermatological consultation. Hair loss is permanent for people with the condition because there aren't enough blood vessels surrounding the follicles to deliver nutrients, cytokines and other essential molecules. In addition, an accumulation of reactive oxygen species in the scalp can trigger the untimely death of the cells that form and grow new hair. Androgenetic alopecia has always been recognized as having significant psychological effects on affected patients. Previously, researchers determined that cerium-containing nanoparticles can mimic enzymes that remove excess reactive oxygen species, which reduced oxidative stress in liver injuries, wounds and Alzheimer's disease. However, these nanoparticles cannot cross the outermost layer of skin. So, the researchers wanted to design a minimally invasive way to deliver ceriumcontaining nanoparticles near hair roots deep under the skin to promote hair regrowth. Now, researchers have designed a preliminary microneedle patch containing cerium nanoparticles to combat both problems, regrowing hair in a mouse model faster than a leading treatment. As a first step, the researchers coated cerium nanoparticles with a biodegradable polyethylene glycol-lipid compound. Then they made the dissolvable microneedle patch by pouring a mixture of hyaluronic acid -- a substance that is naturally abundant in human skin -- and cerium-containing nanoparticles into a mold. The team tested control patches and the cerium-containing ones on male mice with bald spots formed by a hair removal cream. Both applications stimulated the formation of new blood vessels around the mice's hair follicles. However, those treated with the nanoparticle patch showed faster signs of hair undergoing a transition in the root, such as earlier skin pigmentation and higher levels of a compound found only at the onset of new hair development. These mice also had fewer oxidative stress compounds in their skin. Finally, the researchers found that the cerium-containing microneedle patches resulted in faster mouse hair regrowth with similar coverage, density and diameter compared with a leading topical treatment and could be applied less frequently. Microneedle patches that introduce cerium nanoparticles into the skin are a promising strategy to reverse balding for androgenetic alopecia patients. October 2021
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"A Perfect Protein Doesn't Exist: A Rare Case Report of Fixed Food Eruption Triggered by Egg Ingestion"
"A Perfect Protein Doesn't Exist: A Rare Case Report of Fixed Food Eruption Triggered by Egg Ingestion" Dr. Mahajabeen S. Madarkar
MBBS, MD Associate Professor Department of Dermatology, Venereology and Leprosy S. Nijalingappa Medical College, Bagalkot, Karnataka, India
Dr. S. V. Smitha
MBBS Junior Resident Department of Dermatology, Venereology and Leprosy S. Nijalingappa Medical College, Bagalkot, Karnataka, India
Abstract
hypersensitivity reaction in which
Fixed food eruption (FFE) is a rare type of hypersensitivity reaction occurring after consumption of some food items in the form of recurrent erythematous patches, bullae, vesicle, or pustule at the same site after ingestion of same or related food products. Various food items were listed in the literature causing
FFE
include
tree
nuts,
groundnuts, legumes, lentils, fruits like kiwi, strawberry and tonic water. Here we present a rare case of FFE triggered by intake of eggs. Key words- Fixed food eruption, egg allergy, hyperpigmentation. Introduction Fixed food eruption (FFE) is a unique 16
October 2021
recurrent fixed cutaneous lesions appear at the same site on reexposure to the offending food.[1] Even though fixed drug eruptions and FFE have in common recurring lesions at the same location, variable nature and timing of the lesions in fixed food eruptions
suggests differing
mechanisms. The exact mechanism of FFEs is yet to be elicited and may be multifactorial.[2] Here we present a rare case of FFE triggered by intake of eggs. Case report A
35
year
old
female
patient,
homemaker in occupation presented to skin outpatient department with recurrent episodes of multiple sharply
"A Perfect Protein Doesn't Exist: A Rare Case Report of Fixed Food Eruption Triggered by Egg Ingestion"
demarcated
violaceous
eruptions
Yanguas et al reported two cases
on lips and back which heals with
of FFE triggered by Lentils. There
hyperpigmentation (figure 1). The
were erythematous lesions on wrist
lesions were associated with mild
and dorsa of hands with burning
itching. It was the second episode
sensation.
since the onset 6 months back which
was positive after 15 minutes and
occurred on the same spot. Patient
histopathology
was otherwise a healthy female
showed hydropic degeneration of
and did not take any drugs before
the basal cell layer and scattered
the appearance of the lesions. On
dyskeratotic
elaborated history taking, she gave
epidermis and mixed inflammatory
history of raw egg intake on the
Figure
previous night before the eruption of
of FFE on back lesion depicting
lesion. Dermoscopy was done using
multiple grouped black to brown
Illuco dermoscope (×10) in polarized
dots of variable size (yellow arrows)
mode
interspersed with eccrine openings
on
back
lesion
depicted
multiple grouped black to brown
2:
Dermoscopic
image
(red arrows).
lesional
keratinocytes
skin
in
the
infiltrate in the dermis.[4] Muso et al reported two cases of FFE caused
by consumption of
tonic water containing quinine on previous night. The lesions were
hyperpigmentation.
Oral rechallenge test was done after
Here
patients
showed positive patch testing results
1 month which showed positive
for quinine sulphate after 48-78 hours.
response after 2 hours after intake of
[5]
raw egg. There was slight erythema
Parker et al reported a case of FFE
with almost immediate onset after
and itching sensation noticed over
ingestion of cashews and peanuts,
the previous lesional sites. Skin
implying
biopsy was done on the back lesions
that
FFE
might
occur
alongside IgE-mediated symptoms.[2]
and we noticed prominent vacuolar
Sohn et al reported a case of well
degeneration of basal keratinocytes,
seen in the upper dermis (figure 3).
of
test
patches which healed by leaving
with eccrine openings (figure 2).
and few pigment laden macrophages
rechallenge
sharply demarcated erythematous
dots of variable size interspersed
perivascular lymphocytic infiltration
Oral
Figure 3: Histopathological picture of FFE depicts prominent vacuolar degeneration of basal keratinocytes (black
arrows),
perivascular
lymphocytic infiltration (green arrow) and few pigment laden macrophages in the upper dermis (red arrow). [H and E, ×40]
demarcated eruptions on wrist after ingestion of hardy kiwi leaves. Skin prick test and oral rechallenge tests were positive. The skin biopsy results showed and
perivascular
eosinophilic
elevated
lymphocytic
infiltration
melanophage
with levels.
Immunohistological analysis of the effector T cell response induced by FFE was positive for CD8+T-cells.
Discussion
He proposed a combination of type
The term “Fixed Food Eruptions”
I and IV hypersensitivity reactions as
was first coined by Keslo in 1996.
the underlying mechanisms for FFE.[6]
He reported the 1 case of FFE as st
hyperpigmented macule over the Figure 1: Clinical image depicting ill-defined hyperpigmented patches over vermilion border of lips (red circles).
buttock appeared after 2 days of fresh strawberry intake. Immediate skin prick test and patch test to strawberry were negative and oral rechallenge test was positive.[3]
Volz et al reported a case of sharply marginated erythema on forearm and chest few hours after ingestion of tinned asparagus. Skin prick test and patch tests were negative on non-lesional sites and positive on lesional sites. Punch biopsy was done October 2021
17
"A Perfect Protein Doesn't Exist: A Rare Case Report of Fixed Food Eruption Triggered by Egg Ingestion"
and immunohistochemical analysis showed large quantities of CD3+ CD8+T lymphocytes in both dermis and infiltrating epidermis.[7] Sharma
et
al
noticed
1.
Devaraj
NK.
BMJ
2019;12:e228355.
Case
Rep
doi:10.1136/bcr-
2018228355
eruption
of FFE due to egg consumption in 3.7% of their study patients.[8] Egg is an encapsulated
source
major micro and macronutrients. It contains major part as proteins
2. Parker AL, Pinson ML, Wohltmann WE, Gomez R. Fixed food eruption caused by peanut and cashew: A case report and review of the literature. J Allergy Clin Immunol Pract 2015;3:119-22.
such as apolipoproteins, albumin,
3. Kelso JM. Fixed food eruption. J Am Acad
immunoglobulins
Dermatol 1996;35:638-9.
etc.
Five
major
allergenic proteins from the egg of the domestic chicken (Gallus domesticus) have been identified. They include ovomucoid, ovalbumin, ovotransferrin and lysozyme. Although ovalbumin
4. Yanguas I, Oleaga JM, González-Güemes M, Goday JJ, Soloeta R. Fixed food eruption caused by lentils. J Am Acad Dermatol 1998;38: 640-1.
(OVA) is the most abundant protein
5. Muso Y, Kentarou O, Itami S, Yoshikawa
comprising
K. Fixed eruption due to quinine: report of
hen’s
egg
white,
ovomucoid (OVM) has been shown to be the dominant allergen in egg. The importance of OVM may be due to its unique characteristics such as relative stability against heat and digestion with proteinases, and its strong allergenicity, compared with
two cases. J Dermatol 2007;34:385-6. 6. Sohn KH, Kim BK, Kim JY, et al. Fixed Food Eruption Caused by Actinidia arguta (Hardy Kiwi): A Case Report and Literature Review. Allergy Asthma Immunol Res. 2017;9(2):182184. doi:10.4168/aair.2017.9.2.182
other egg white components. People
7. Volz T, Berner D, Weigert C, Röcken M,
with egg allergy shows specific IgE
Biedermann T. Fixed food eruption caused
antibodies against ovomucoid.[9]
by asparagus. J Allergy Clin Immunol
Parker et al implicated the role of
2005;116: 1390-2.
IgE as one among the multifactorial
8. Sharma L, Agarwal R, Chopra A, Mitra
mechanisms underneath the FFE.
B. A cross‑sectional observational study of
Although the exact underlying
clinical spectrum and prevalence of fixed
pathophysiology driving FFE is not
food eruption in a tertiary care hospital.
definitively known, the mechanism
Indian Dermatol Online J 2020;11:361‑6.
[2]
may be similar to that involved in fixed drug eruption, whereby drug-specific CD8 + T cells that persist in the skin are reactivated on drug re-exposure, leading to induction of apoptosis of keratinocytes and resulting in the phenotypic cutaneous lesion. Definitive diagnosis of FFE relies on replication of rash onset following oral food challenge to the suspected culprit food.[1]
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References
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9. Caubet JC, Wang J. Current understanding of egg allergy. Pediatr Clin North Am. 2011 Apr;58(2):427-43.
NEWS
Gene for sex hormone synthesis could play key role in eczema
Eczema (also known as atopic dermatitis) is a chronic, relapsing, and itchy inflammatory skin condition, which usually develops in early childhood. We often think of eczema as a dry-skin condition and treat mild cases with moisturizers. Here, the new study showing that a gene that's important for making sex hormones seems to play a role in the skin making its own moisturizers. If we could alter this gene's activity, we could potentially provide relief to eczema patients by helping the skin make more oils and lipids to moisturize itself. The researcher explained that previous research has linked AD to overactivity in genes responsible for the production of two inflammatory immune molecules, interleukins 4 and 13 (IL-4 and IL-13). A relatively new drug called dupilumab -- a monoclonal antibody that reduces the amount of the inflammatory molecules -- has been extremely effective in many patients with moderate to severe AD. However, the molecular mechanisms behind how IL-4 and IL-13 contribute to this form of eczema was unknown. To investigate this question, researcher’s team focused on sebocytes, the cells that make up sebaceous glands. These glands produce an oily, waxy barrier that coats the skin, helping it retain moisture. The researchers dosed human sebocytes growing in petri dishes with IL-4 and IL-13, then used a technique called RNA sequencing to get a readout on gene activity for the entire genome and compared it with gene activity in sebocytes that weren't treated with these immune molecules. They found that a gene called HSD3B1, which makes an enzyme called 3b-hydroxysteroid dehydrogenase 1, became up to 60 times more active when exposed to the two interleukins. The finding was a surprise, because this enzyme is well known for playing a key role in the production of sex hormones such as testosterone and progesterone, but it had never been linked to atopic dermatitis and skin lipid production. Databases of human gene activity showed that HSD3B1 tends to be overactive in patients with eczema; a single study of patients on dupilumab showed that this drug appears to lower HSD3B1's activity. Both pieces of evidence suggest that IL-4 and IL-13 drive up the activity of this gene. To determine how this gene affects sebum output, the researchers manipulated HSD3B1's activity in sebocytes growing in petri dishes. They found that when they made this gene less active, the levels of sex hormones decreased, and skin sebum production increased. The reverse was also true, with more gene activity leading to higher amounts of sex hormones and less sebum. The researchers made similar findings in a mouse model of AD, with sex hormone production decreasing the production of skin lipids. These findings suggest that HSD3B1 could be a new target for fighting AD and potentially other forms of eczema. "Changing the output of this gene could eventually offer a way to treat AD that's completely different from any treatment that currently exists.
Sunlight exposure guidelines may need to be revised
Vitamin D is sometimes called the “sunshine vitamin” because it’s produced in our skin in response to sunlight.Vitamin D is integrally connected to the skin for its synthesis, metabolism, and activity. It has several important functions; it regulates many physiological processes in the skin ranging from cellular proliferation, differentiation, and apoptosis to barrier maintenance and immune functions. A study by researchers has tested the optimum ultraviolet radiation (UVR) wavelengths for human skin production of vitamin D in sunlight.UVR from sunlight can cause sunburn and skin cancer, however, it is the most important source of vitamin D that is essential for healthy bone development and maintenance.Public health advice on sunlight exposure takes both risk and benefits into account. Calculating the potential risks and benefits from sunlight exposure is not simple because the health outcomes from UVR exposure vary considerably with wavelength within the sun's UVR spectrum. For example, the sun's UVR contains less than 5% short wavelength UVB radiation but this is responsible for over 80% of the sunburn response. Each health outcome from solar exposure has its own unique wavelength dependency. The association between specific UVB wavelengths and vitamin D production was determined more than thirty years ago in skin samples (ex vivo). However, the finding is less well established and there have been doubts about its accuracy. These doubts compromise risk/benefit calculations for optimal solar exposure. Researchers measured blood vitamin D levels in 75 healthy young volunteers, before, during, and after partial or full body exposure to five different artificial UVR sources with different amounts of UVB radiation, to weigh the trade-off between the benefits of solar exposure, which include vitamin D synthesis, versus the risks of sunburn and skin cancer.They then compared their results with those that would be predicted from the old ex vivo vitamin D study and found the previous study is not an accurate predictor of benefit from UVR exposure. The new study means that many risk benefit calculations for solar UVR exposure must be reviewed with a revised version of the wavelength dependency for vitamin D.Their study shows that risk versus benefit calculations from solar exposure may need to be re-evaluated. The results from the study are timely because the global technical committee, Commission internationale de l'éclairage, that sets UVR standards will be able to discuss the findings of this paper to re-evaluate the wavelength dependency of vitamin D. Further research from their group will determine the risk/benefit calculations. October 2021
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Green Nail Syndrome: Treated Successfully With Gentamicin Eye Drops
Green Nail Syndrome: Treated Successfully With Gentamicin Eye Drops Dr. Mala Bhalla
MD Professor Department of Dermatology, Venereology and Leprosy, Government Medical College and Hospital, Chandigarh
Dr. Amrit Kaur
MD Dermatology Consultant Dermatologist and Hair Transplant Surgeon AK Clinics, Ludhiana, Punjab
INTRODUCTION Green Nail Syndrome (GNS), also known as ‘CHLORNYCHIA’ is a common bacterial nail infection, caused by Pseudomonas aeruginosa. It is characterized by greenish chromonychia i.e greenish discoloration of the nails. The color is due to a pigment pyocyanin, a metabolite produced by the pseudomonas bacteria.1 Although asymptomatic, it causes significant cosmetic disfigurement leading to emotional and psychosocial distress which results in the patient seeking treatment. CASE REPORT A 50-year-old female patient presented with asymptomatic greenish discoloration of left ring finger nail since 2 months (FIG-1&2). It had started from the lateral edge 20
October 2021
and progressed to involve half of the nail. There was no history of diabetes or any other comorbid conditions. She worked as a domestic help and cook. She had taken treatment with oral antifungals from outside with no improvement. On examination distal and lateral onycholysis was present. Nail folds was normal and cuticle were intact. All other nails were normal. Nail clippings were sent for potassium hydroxide examination along with bacterial and fungal culture and sensitivity. Provisional diagnosis of chlornychia due to pseudomonas was made and gentamicin eye drops were given for topical application around the nail and on the nail bed as ‘nail drops’. Bacterial culture confirmed the diagnosis as the growth was of Pseudomonas aeruginosa. The organism was sensitive to gentamicin. At 3 weeks follow up the patient showed 80% improvement.
Green Nail Syndrome: Treated Successfully With Gentamicin Eye Drops
Figure 1 Figure.3: After 3 weeks of treatment Bae Y et al. have earlier successfully used tobramycin (aminoglycoside) eye drops for GNS treatment. The better than expected results with these topical applications may be because the affected lesion acted like a dead space with moist environment resulting in easy percolation and increased concentration of the drug.3 Figure 2 Figure 1 & 2: Baseline DISCUSSION Certain predisposing factors have been identified for GNS like moist conditions, micro trauma, onychotillomania, elderly debilitated patients with diabetes, etc and rarely pre-existing nail disorders e.g. psoriasis. Most of the antipseudomonal antibiotics are used intravenously and have systemic adverse effects. Gentamicin, tobramycin (aminoglycoside) are indicated for the treatment of P. aeruginosa, Klebsiella species, Enterobacter species, and others. Treatment of nail is challenging as these drug preparations penetrate the nail plate poorly and are unable to reach the affected site in the required concentration.2 Topical gentamicin eye drops (3mg/ml) for 3 weeks twice daily showed 80% improvement with promising results (FIG-3).
Thus it is important to remember that nail infections may not always be due to fungus and topical preparations are also effective in treating them. References 1. Chiriac A, Brzezinski P etal; Chloronychia: green
nail
syndrome
caused
by
Pseudomonas aeruginosa in elderly persons. ClinInterv Aging. 2015; 10: 265-67. 2. Muller S, Ebnother M etal; Green Nail Syndrome (Pseudomonas aeruginosa nail infection); treated with topical nadifloxacin, an acne medication. Case Rep Dermatol. 2014; 69(2): 180-184. 3. Bae Y, Mo G etal; Green nail syndrome treated with the application of Tobramycin eye drops. Ann Dermatol. 2014; 26(4): 51416.
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21
Mutifocal Alopecia Areata In A Child
Mutifocal Alopecia Areata In A Child Dr. Shrutakirthi D. Shenoi
MD, DVD Professor and Head, Department of Dermatology, Kanachur Institute of Medical Sciences, Mangaluru, Karnataka
Dr. Shibani Bhatia
MBBS, MD, DNB, FAGE, MRCP (SCE) UK Consultant Dermatologist Kaya Skin Clinic and Criticare Hospital, Mumbai
INTRODUCTION Hair loss in children is one of the bothersome complaints presenting in dermatology clinics. Some of the conditions causing hair loss include tinea capitis, alopecia areata (AA), trichotillomania and rarely hair shaft disorders. AA is a chronic immunemediated disorder that causes nonscarring hair loss. The condition most commonly presents with discrete patches of alopecia on the scalp. It is known to occur with other autoimmune diseases like vitiligo, pernicious anaemia, type 1 diabetes mellitus and thyroid disease although this association is not common in clinical practice. Here we report a case of multifocal AA in a paediatric patient with nephrotic syndrome. CASE REPORT A ten-year-old boy presented with patchy hair loss over the scalp and eyebrows of six months’ duration. His mother had noticed the first patch 6 months ago over the right parietal 22
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region following a haircut. The patch gradually increased in size and new lesions appeared over the next six months. He complained of mild itching but denied habit of hair pulling. He had no other complaints except that he had been diagnosed as nephrotic syndrome 5 years ago and was on treatment with oral steroids. Clinical examination revealed multiple smooth alopecic patches on scalp varying in size from 2cm x 2cm to 10cm x 6cm in size coalescing to form larger bald areas [Fig. 1] with growth of white hair in between. There was patchy hair loss over bilateral eyebrows as well. Nail examination revealed multiple regular pits. Hair pull test was positive at the periphery of the patches. Looking at the clinical picture, AA was considered with a differential of trichotillomania. His laboratory parameters were unremarkable.
Mutifocal Alopecia Areata In A Child
of “going white overnight”. This occurs as the immune process acts against melanin in hair bulb, hence sparing the non-pigmented hair.
1 (a)
1 (b)
Figure 1(a) & 1(b): Multiple smooth alopecia patches over scalp Dermoscopic evaluation showed black dots, broken hair, exclamation mark hair, coudability hair and pohlpinkus constrictions. [Fig 2]. On basis of clinical examination and dermoscopic evaluation trichotillomania and tinea capitis were ruled out thus confirming the diagnosis of alopecia areata.
Figure 2 – Trichoscopic image showing: a) Black dots & broken hair b) Exclamation mark hair c) Coudability hair d) Pohl pinkus constrictions DISCUSSION AA is a chronic inflammatory disease that affects the hair follicles causing non-scarring type of hairloss. It is also known as Pelade or Area Celsi. The prevalence of AA is about 1 in 1000 people with a life time risk of around 2 percent. The exact etiopathogenesis is unknown but is thought to be mediated by autoreactive T-cells against hair follicle. Human Leucocyte antigen (HLA) genes play a role in AA particularly HLA haplotypes DQ3, DR4 and DR11. It is also known to
be associated with atopy, Down’s syndrome and other autoimmune diseases such as vitiligo, pernicious anaemia, thyrotoxicosis and diabetes insipidus. AA can affect any of the hair bearing areas of the body, out of which scalp is most commonly affected. There are various patterns of AA such a patchy, ophiasis, sisaphio, reticulate, diffuse, subtotal, alopecia totalis and alopecia universalis of which patchy AA is the most common. It is characterized by smooth, well defined round or oval patches, that often go unnoticed by the patient initially. Hair can regrow back on its own or can expand and form confluence of patches leading to alopecia totalis. There is sparing of white hair and patients may complain
Nail changes are seen in 10-66% of patients with AA. The commonest nail change is superficial, uniform pitting of nails giving it a Scotch plaid appearance. It has to be distinguished from nail pitting in psoriasis which has coarse, deep and irregular pits. Other nail changes like trachyonychia, red lunula, nail thinning and ridging, dystrophy and discoloration of nails have been reported. AA is usually a clinical diagnosis but it can be confused with other conditions like tinea capitis and trichotillomania, especially in children. Tinea capitis presents with patchy areas of hair loss with overlying scales and broken off hairs. Diagnosis is established by Woods lamp examination, fungal culture of hairs and dermoscopy. Trichotillomania presents with patches of alopecia which are asymmetrical, geometrical or in unusual shapes, principally present over accessible areas like parietal and vertex regions. The patches are associated with scratching, bleeding and hair of uneven length. Nail changes like onychophagia and onychotillomania can be found on examination. The histopathological features vary depending upon the stage of the disease. The earliest and the most important feature in the acute stage is peribulbar lymphocytic infiltrate, which may extend into the epithelium and hair matrix likened to a ‘swarm of bees’. In the later stages, inflammation may be diminished or absent. Dermoscopy is a non-invasive tool and helps in quick diagnosis of AA. It also helps distinguish it from tinea capitis or trichotillomania. Dermoscopy features of AA include October 2021
23
Mutifocal Alopecia Areata In A Child
broken hair, exclamation hair, black dots, yellow dots, coudability hair and pohlpinkus constrictions. Whereas, dermoscopy of tinea capitis shows comma hair, corkscrew hair, black dots, broken hair and morse code hair. Trichotillomania shows tulip hair, broken hair of different lengths, haemorrhagic spots, flame hairs and black dots. In 50% of patients spontaneous hair growth occurs by one year although many will relapse months or years later. In children the standard first line treatments are topical steroids applied with or without occlusion or application of irritants such as anthralin. Intralesional steroids are usually not preferred as children may not be co-operative for injections. The concentration of anthralin used varies from 0.5 % applied for 5 minutes to 1.0 % for 30 minutes. Contact sensitizers such as diphencyprone and squaric acid dibutylester may be used for extensive cases. Topical minoxidil 2–5% has been tried in conjunction with topical steroids. Systemic steroids are used in rapidly spreading disease in the dose of 1 mg/kg body weight tapered over 4–6 weeks. Disease modifying agents such as sulfasalazine and immunosupressants such as azathioprine and methotrexate are rarely used in children. Among the newer treatments, JAK inhibitors have been tried. Topical tofacitinib 2% and ruxolitinib 1% ointment may be applied twice daily until hair regrowth. Oral tofacitinib in the dose of 5mg once to twice daily has also been studied. Excimer laser emitting monochromatic UVB light 308 nm may be combined with topical therapies. Our case was unusual in that the child was a known patient of nephrotic syndrome and developed AA despite being on systemic steroids. In less 24
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than 2% of cases AA has been associated with nephrotic syndrome. CONCLUSION AA in children may be associated with systemic disease. Dermoscopic examination plays a key role in differentiating AA from other alopecias in children. FOR FURTHER READING 1. Darwin E, Hirt PA, Fertig R, Doliner B, Delcanto G, Jimenez JJ, et al. Alopecia areata: Review of epidemiology, clinical features, pathogenesis, and new treatment options. Int J Trichology 2018;10:51–60. 2. Gandhi V, Baruah MC, Bhattacharaya SN. Nail changes in alopecia areata: incidence and pattern. Indian J DermatolVenereolLeprol 2003;69:114–5. 3. Spano F, Donovan JC. Alopecia areata: Part
1:
Pathogenesis,
diagnosis,
and
prognosis. Can Fam Physician 2015;61:751– 5. 4. Seetharam KA. Alopecia areata: An update.
Indian
J
Dermatol
Venereol
Alopecia
areata
Leprol2013;79:563–75. 5.
Messenger
AG.
:
Management. Available at https://www. uptodate.com/contents/alopecia-areatamanagement?source=history_widget Accessed on 18/04/2019.
.
NEWS
Researchers explore promising treatment for MRSA 'superbug' Skin infections are common and may be caused by bacteria, fungi or viruses. Breaks in the skin integrity, particularly those that inoculate pathogens into the dermis, frequently cause or exacerbate skin infections.These infections trigger the body's immune system and cause inflammation and tissue damage within the skin or wound and slow the healing process. A new study has found the antimicrobial properties of certain stem cell proteins could offer a potential treatment to reduce infection in skin wounds. Treating wounds with the secretion of a type of stem cell effectively reduced the viability of methicillinresistant Staphylococcus aureus -- better known as MRSA -- according to a new study from researchers. Moreover, the secretion stimulated the surrounding skin cells to build up a defense against the bacterial invader, the researchers found. The results showed that secreted factors from equine mesenchymal stromal cells (MSCs), a type of stem cell, significantly decreased the viability of MRSA in their novel skin model. Moreover the researchersdemonstrated that equine MSC secretions increase the antimicrobial activity of the skin cells by stimulating immune responses of the surrounding resident skin cells. The study may point to a possible new approach for treating MRSA. While many people carry MRSA without serious consequences, for those whose health is compromised this "superbug" can be fatal. The key is MSCs -- stem cells that can be isolated from bone marrow, fat, blood and other tissues. Initially, the use of MSCs for tissue regeneration was advocated based on their ability to differentiate into various tissue types. For this reason, it was anticipated that injected MSCs colonize the injury site, differentiate into the appropriate tissue type and regenerate the damaged tissue. However, studies are revealing that only a small portion of administered MSCs actually incorporate into injured tissue.For this reason, it is becoming generally accepted that the beneficial effects in tissue repair and regeneration are more likely indirect, depending on the effects of what these cells secrete. Such cell-free therapies might prove safe and potentially more advantageous alternatives by overcoming the risks and obstacles associated with the use of the cells themselves. Although MSCs have been shown to reduce inflammation in multiple studies, this new study went further, investigating the effect of the MSC secretion -- also known as the secretome -- on the antimicrobial defense mechanisms of skin cells and testing its efficacy on biofilms in a physiologically relevant equine skin model.
Study shows protein that reverses aging of skeletal muscle Aging, progressive physiological changes in an organism that lead to senescence, or a decline of biological functions and of the organism’s ability to adapt to metabolic stress. At the biological level, ageing results from the impact of the accumulation of a wide variety of molecular and cellular damage over time. This leads to a gradual decrease in physical and mental capacity, a growing risk of disease, and ultimately, death. But these changes are neither linear nor consistent, and they are only loosely associated with a person’s age in years. In a series of experiments, researchers overexpressed NANOG in myoblasts, which are the embryonic precursors to muscle tissue. The myoblasts were senescent, meaning they were no longer able to divide and grow. The overexpression ameliorated some of the primary characteristics associated with age-related deterioration of cells, including autophagy, energy homeostasis, genomic stability, nuclear integrity and mitochondrial function. Most notably, NANOG increased the number of muscle stem cells in the muscle of prematurely aging mice. This demonstrated the feasibility of reversing cellular aging in the body without the need to reprogram cells to an embryonic pluripotent state, a process that's often used in stem cell therapy but runs the risk of tumorigenesis. The researchers work focuses on understanding the mechanisms of NANOG's actions in hopes of discovering druggable targets in signaling or metabolic networks that mimic the anti-aging effects of NANOG. Ultimately, the work could help lead to new treatments or therapies that help reverse cellular senescence, and aid the many people suffering from age-related disorders.
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Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis Dr. T. Vani
MD Professor Department of DVL Guntur Medical College, Guntur, Andhra Pradesh
Dr. S. Nageswaramma
MD Professor and HOD Department of DVL Guntur Medical College, Guntur, Andhra Pradesh
Abstract Mastocytosis is a heterogeneous group of diseases characterized by abnormal infiltration of mast cells in various organs.1 Cutaneous mastocytosis is the proliferation of mast cells in the skin without any evidence of involvement of other organs.2 Telangiectasia macularis eruptive perstans (TMEP) is a rare form of cutaneous mastocytosis and usually it has a prolonged course.3 TMEP is usually composed of subtly increased numbers of ovoid to spindle shaped mast cells infiltrating the papillary dermis and surrounding dilated superficial capillaries and venules.4 Clinical presentation of TMEP shows erythematous or yellowish-brown macules with telangiectasias, mostly located on the trunk and upper limbs.5 We report a case of TMEP in a 18 26
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year old male patient, diagnosis based on the characteristics of the skin lesions and histopathological features. Dermoscopy has been used as a diagnostic aid. Keywords: Cutaneous Mastocytosis, Dermoscopy, Telangiectasia Introduction Mastocytosis is one of the rare hematopoietic disorder characterized by proliferation and accumulation of mast cells in several organs such as skin, bone marrow, skeletal system, gastrointestinal tract, spleen, lymph nodes and liver.1,6,7 Mastocytosis consist of two types viz. cutaneous mastocytosis and systemic mastocytosis.1 Cutaneous mastocytosis is clinically classified into five subtypes it includes Urticaria pigmentosa (UP), Diffuse cutaneous mastocytosis (erythroderma), Bullous
Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
mastocytosis, Solitary mastocytoma and Telangiectasia macularis eruptive perstans (TMEP).8, 9 Cutaneous mastocytosis is clinically characterized by multiple erythematous and pigmented macules, papules, plaques and localized blistering that varies in size.1 The main characteristic feature of maculopapular cutaneous mastocytosis (MCM) is presence of multiple hyperpigmented macules, papules or nodules associated with abnormal accumulation of mast cells in the skin. The size and number of lesions is variable, typical range of the size is 1 mm to over 1 cm and in number from 10-1000 lesions. MCM may appear on all regions of the body but the trunk and extremities are most commonly involved. The palms and soles are usually spared. Darier's sign, dermographism and pruritus are also considered as additional features of MCM.10 TMEP is a disputed entity described as a rare variant occurring in adults with the presence of red/ brown telangiectatic macules.10 The lesions are ill defined, nonpruritic telengiectatic tan/brown 2–6 mm macules which may urticate on rubbing. They are located symmetrically over the trunk and extremities and rarely on the face.4 Most cases of TMEP are limited to the skin with a characteristic vascular pattern on dermoscopy and histopathological features. Though more frequent in adults there are case reports affecting younger age group.
discrete and confluent distributed predominantly on lower limbs and upper limbs. Patient denied any systemic symptoms and/or aggravating factors. Darier sign was negative. Systemic examination and lab investigations were unremarkable. Dermoscopy of erythematousbrownish lesions revealed both reticular and globular vascular pattern (superficial vessels more involved), delicate pigment pattern and yellow brown background. HPE showed flattening and hyperpigmentation of the epidermis, thick walled capillaries in upper dermis with superficial perivascular infiltrate of lymphocytes, histiocytes and few mast cells visualized with giemsa stain. Clinical picture, characteristic histopathology and dermoscopic features confirmed the diagnosis of TMEP.
Figure 1: Erythematous-brown coloured macules in front of both legs extending onto the thighs
Diagnosis Diagnosis of TMEP is usually based on clinical examination and confirmed by skin biopsy with histopathological examination,11 which is the gold standard diagnostic method.9 Histologically TMEP involves only a slight increase in mast cells with infiltration of the superficial dermis and epidermal hyperpigmentation. Especially mast cells are located around dilated capillaries and venules of the superficial venous plexus found in the upper third of the dermis.11 To identify the mast cells from histiocytes, Giemsa and toluidine blue stains are very useful in the diagnostic evaluation. It helps to highlight better visualization of mast cells and revealing their metachromatic cytoplasmic granules.2 Tissue sections showing more than 5–10 mast cells are confirmatory for the diagnosis.4 In the presented case of TMEP, dermoscopy has been used as a diagnostic aid which showed reticular and globular vascular pattern, delicate pigment pattern and yellow brown background. (Figure 4, 5, 6, 7).
Case Report An 18 year old male patient presented with 7 months duration of asymptomatic erythematous skin lesions on extremities. Cutaneous examination revealed erythematousbrown coloured macules sizes varying from 1 to >5cms, both
Figure 3: Right forearm with erythematous lesions
Figure 2: Erythematous-brown coloured macules in the back of both legs October 2021
27
Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
DISCUSSION
Figure.4:Dermoscopy-reticular globular vascular pattern
Figure.5: Delicate pigment pattern, yellow brown background
Figure.6:.. Histopathology ........ Examination (HPE) with H&E stain
Figure.7:.. Histopathology ........ Examination (HPE) with Giemsa stain 28
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Cutaneous mastocytosis is commonly restricted to the skin in children and adolescents. Most cases of cutaneous mastocytosis start in childhood. The urticaria pigmentosa is the most common type seen in children. It can be associated with local and systemic symptoms. Systemic involvement should always be suspected if symptoms such as cutaneous flushing, blisters, dyspnea, tachycardia, pruritus, rash, exacerbation of asthma, hypotension, gastrointestinal disorders, gastroesophageal reflux, ulcers, diarrhea and syncope or signs of anaphylaxis are present. These symptoms result from mast cell degranulation with the release of several mediators, histamine being the most significant of all mediators, which can cause both local and systemic reactions.1, 2, 11 There is no specific treatment but it should be targeted to block the mediators’ effects and reduce the mast cell load in affected organs. Commonly used drugs include antihistamines, sodium cromoglicate and H2 blockers. Interferon alpha has produced mixed results. Bone marrow transplant and treatment with drugs like imatinib mesylate are in their infancy.3 TMEP was first described in the 1930s by Parks Weber. It is a very rare cutaneous finding more often in adults than children seen in less than one percent of patients with mastocytosis characterized by reddish macules that occur due to underlying, dilated, dermal, thinwalled blood vessels.2, 11, 12 Though in most cases TMEP is limited to the skin, systemic involvement may occur. Darier sign usually is not positive in patients with TMEP because the lesions are paucicellular. Mast cells may not be adequate
to cause significant degranulation thus resulting in negative darier sign. Presenting patient had no clinical symptoms hence no treatment was advised. Clinical Vignette In 2009, Akay et al studied the dermoscopic pattern in 6 patients with different forms of CM and described the pigment network (urticaria pigmentosa) and reticular vascular pattern (TMEP).8 In 2011, Vano-Galvan et al evaluated the dermoscopic pattern in 127 patients with CM and described 4 distinct patterns namely pigmented network, yellow orange amorphous area, brown amorphous area and telangiectasia with reticular pattern. Correlation was observed between the presence of reticular vascular pattern and the severity of the symptoms. In the present case the lesions were asymptomatic despite the presence of characteristic dermoscopic vascular pattern.5 In 2013 Understell et al and in 2018 Subrata Malakar et al reported cases of TMEP with characteristic dermoscopic features and absent symptoms.9 In TMEP reticular vascular pattern corresponds to dilatation and vascular proliferation and pigment network corresponds to accumulation of melanin in basal keratinocytes associated with the mast cell proliferation in the dermis. Conclusion Mastocytosis has a bimodal distribution with the many cases occurring in childhood age and then peaking again at age 30-50 years. There is equal ratio of men and women affected by mastocytosis but the Caucasian population is reported to be affected more commonly than any other race.11
Telangiectasia Macularis Eruptiva Perstans - A Rare Form of Cutaneous Mastocytosis
The treatment of patients with TMEP depends on the presence of symptoms or clinical appearance, but there is no gold standard medication for the treatment to date. Hence there is need to identify and avoid factors that stimulate the mast cell’s degradation, such as exposure to sunlight, extreme temperature, alcohol, and drugs.2 Patients also require periodic monitoring to identify systemic involvement at the earliest. In conclusion, dermatoscopy can be used as an essential complementary tool for the diagnosis of TMEP as it reveals a characteristic reticular vascular pattern that helps differentiate it from other forms of mastocytosis and skin conditions that present with vascular patterns on dermoscopy. References 1.
findings of urticaria pigmentosa. An Bras Dermatol. 2013;88(6):986-8. 7. Chauhan P, Bhardway N, Shirazi N. Dermoscopy of urticariapigmentosa. Indian Dermatol Online J 2020;11:475-6. 8. Akay BN, Kittler H, Sanli H, Harmankaya K,
Anadolu
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Dermatoscopic mastocytosis.
2009;218(3):226-30.
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10.1159/000182260. Epub 2008 Dec 6. PMID: 19060465. 9. Malakar S, Mukherjee SS. Telangiectasia macularis
eruptive
perstans
under
the
dermoscope in the skin of color. Our Dermatol Online.2018;9(4):458-459. 10. Vano-Galvan Sergio et al. Dermoscopic Features With
of
Skin
Lesionsin
Mastocytosis.Arch
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2011;147(8):932-940. 11.
Watkins
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macularis eruptive perstans: more than skin deep. Dermatology Reports 2011; 3:e12.
Mohammad
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pigmentosa: A case report. NJDVL Vol. 13,
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De lasHeras E, Morgado JM, Matito A,
2. Costa DL, Moura HH, Rodrigues R, PineiroMaceira J, Ramos-E-Silva M. Telangiectasia macularis eruptive perstans: a rare form of adult mastocytosis. J ClinAesthetDermatol. 2011;4(10):52-54.
Vano-Galvan
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3. Balasubramaniam P et al. Telangiectasia
Sep;147(9):1076. Heras, Elena De Las
macularis
rapidly
[corrected to De lasHeras, Elena]; Planas,
progressing to systemic mastocytosis. J AM
Maria Nieves [corrected to Plana, Maria N].
ACAD DERMATOL. MARCH 2005. P61.
PMID: 21844452.
eruptive
perstans
4.
Tumer Gizem, JowTiffany, Lambert
W.
Clark.
Telangiectasia
Macularis
Eruptiva Perstans: Report of Three Cases. Blood (2011) 118 (21): 5176.https://doi. org/10.1182/blood.V118.21.5176.5176 5.Unterstell N, Lavorato FG, Nery NS, Mann D, Alves MFSG, Barcaui C. Dermatoscopic findings in telangiectasia macularis eruptive perstans. An Bras Dermatol. 2013;88(4):6435. 6. Benez-Miller MD, Nery NS, Gripp AC, Maceira JP, Nascimento GM. Dermatoscopic October 2021
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Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
Primary Localized Cutaneous Amyloidosis – Clinical Features and Management Dr. D. Indira
MD (DVL) Associate Professor Department of DVL Osmania Medical College/ Osmania General Hospital Hyderabad Introduction Amyloidosis is a term used for a group of diseases where one or more body organs accumulate various insoluble proteins (amyloid) extracellularly in amounts to cause dysfunction of the organ system.1 The word amyloid is derived from Latin word amylum which means starch. This extracellular protein turns brown on incubation with iodine, hence was named amyloid. Awareness and proper management of cutneous amyloidosis is important as it affects the quality of life of patients due to its persistence, lasting pruritus and cosmetic disfigurement. Classification Amyloidosis is classified into cutaneous amyloidosis and systemic amyloidosis. Cutaneous amyloidosis is again classified into Primary Localized Cutaneous Amyloidosis (PLCA) and Secondary Localized Cutaneous Amyloidosis (SLCA). Systemic Amyloidosis is classified into generalized, localized and hereditary types. Systemic amyloidosis is a rare disease. The patients often present to physician with systemic symptoms like fatigue, weight loss, oedema, paraesthesias, macroglossia etc., who in turn refer the patient to 30
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a dermatologist for cutaneous findings. Cutaneous manifestations of systemic amyloidosis include petichae, ecchymosis (pinch purpura) especially around eyes (raccoon sign) and non healing ulcers. Rarely they may present with waxy papules, plaques or with diffuse infiltration of skin. PLCA is a relatively common type of cutaneous amyloidosis and is of more interest to dermatologists. It is characterized by extracellular deposition of heterogenic amyloid protein in the skin without systemic involvement.2 PLCA is classified into Macular Amyloidosis (MA), Lichen or Papular Amyloidosis (LA), Nodular amyloidosis (NA) and rarer variants. Table 1: Classification of Amyloidosis 1. Cutaneous amyloidosisa. Primary Localized Cutaneous Amyloidosis i. Macular amyloidosis ii. Lichen/papular amyloidosis iii. Biphasic iv. Nodular v. Rarer variants
Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
b. Secondary....Localized Cutaneous Amyloidosis (found in association of skin tumours like BCC,SCC, actinic keratosis) 2. Sytemic Amyloidosisa. Generalized i. Primary..amyloidosis
in the overlying epidermis likely plays a role. In one theory cytokeratin released from apoptotic basal keratinocytes is covered with autoantibodies, phagocytosed by macrophages and enzymatically degrade to form amyloid K.5
affected than males. History of friction from usage of nylon brushes, towels, artificial sponges or scratching of skin is often obtained several patients. Lichen amyloidosis or Papular amyloidosis
ii..Familial amyloidotic neuropathy
3. Amyloidosis cutis dyschromica8
iii. Systemic senile amyloidosis
4. Anosacralamyloidosis9
Skin lesions in LA usually present later in life in the 5th or 6th decade. They are more common in males. The lesions are in the form of grouped, firm, pigmented, hyperkeratotic, scaly dome shaped papules of 2 to 4 mm size arranged in linear rows in a rippled or ridged pattern, the appearance of which resembles sea bed or tree bark. The common sites are anterior aspect of shins and other extensor surfaces like thighs and forearms. They may start unilateral initially but eventually become bilateral and symmetrical and is often associated with itching.
Epidemiology
5. Bullous amyloidosis10
Biphasic amyloidosis
PLCA is more common in South America, Middle Eastern countries and in South East Asian countries like Taiwan, Singapore, Thailand, and India. LA is more common in people with Chinese decent. MA is common in women (3-2:1) in contrast, LA is common in men.3 The disease is commonly found in 30 to 50 years age group. Family history is present in 10% of cases and majority of cases occur sporadic.4
6. Pharmaceutical....(Injection) amyloidosis11
Patients exhibit features of both macular and popular lesions of MA and LA in biphasic amyloidosis.
Etiopathogenesis
11. Amyloidosis over auricular concha16
( Immunoglobulin dyscrasias) ii. Secondary amyloidosis ( reactive systemic) iii. Hemodialysis...associated amyloidosis b. Loacalized i. Senile cerebral ii. Endocrine related c. Hereditary i. Familial Mediterranean Fever
The exact etiology of amyloidosis is unknown. Genetic factors, sunlight, atopy and friction are implicated in the etiopathogenesis. 10% have autosomal dominant inheritance. An increase in the pro apoptotic factors and a decrease in anti apoptotic factors are considered in the pathogenesis. Friction and chronic scratching in susceptible individuals in MA and LA is thought to contribute to the deposition of amyloid. Degeneration of basal kerationocytes
Clinical features The various clinical types of PLCA include Macular amyloidosis (35%), Lichen amyloidosis (35%), Biphasic (15%) and Nodular amyloidosis (15%).3 Several rare variants are described in the literature and these include patients presenting with 1. Periorbitalmelanosis6 2. Pigmentation over bony prominences7
7. Poikiloderma like cutaneous amyloidosis12 8. Diffuse macular amyloidosis with incontinentiapigmenti like pattern13 9. Primary cutaneous amyloidosis of glans14 10. Diffuse primary cutaneous amyloidosis15
Macular amyloidosis MA presents as hyperpigmented macules arranged in a rippled or confluent pattern. Itching is present in majority of patients. The sites commonly involved are inter scapular region and extensor surfaces of limbs. Less commonly involved are clavicles, face, neck, axillae, breasts and buttocks. Age of onset is 34.6+/_10.5 years.17 Females are more commonly
Nodular amyloidosis It is a rare form of PLCA. It occurs more frequently in women. 7% of cases can progress to systemic form.18 25% cases are associated with Sjogren’s syndrome. Lesions are solitary or multiple and are in the form of brownish to red papules, nodules or plaques and usually occur over limbs, face and genitalia. Haemorrhages may be seen on the surface of the lesions. They may be associated with itching or asymptomatic. Rare variants Periorbitalmelanosis Patients with macular amyloidosis may have associated dark pigmentation around the eyes. Periorbital pigmentation is rarely reported with systemic amyloidosis.
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Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
Amyloidosis cutis dyschromica This variant is characterized by specked reticular hyperpigmentation with hypopigmented macules and is usually seen in prepubertal girls. Anosacral amyloidosis This occurs in the anal and sacral region of elderly as a hyperkeratotic plaque in the gluteal cleft. It is often mistaken for lichen simplex chronicus or tinea. Pigmentation over bony prominences Somani et al reported 23 cases who presented with pigmentation proximal and distal to bony prominences, all of whom gave history of using nylon scrubbers during bath. Bullous amyoidosis A rare variant of bullous amyloidosis is reported in a 55 year old male with familial biphasic lichen amyloidosis. Bullous lesions are usually associated with systemic amyloidosis. Pharmaceutical (Injection site) amyloidosis Firm subcutaneous nodules or plaques with overlying hyperpigmentation and/or ecchymosis may appear at the sites of injection like abdomen and thighs. Insulin and ART medication enfuviritide are known to cause such reactions. Poikiloderma like cutaneous amyloidosis It is characterized by poikiloderma like skin changes, lichenoid papules and blisters. Limbs and trunk are commonly involved. A syndromic form with photosensitivity, short stature and occasional palmoplantar keratosis is described. Unusual forms like diffuse macular amyloidosis with incontinentia pigmenti like pattern, primary 32
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cutaneous amyloidosis of glans and diffuse primary cutaneous amyloidosis exhibiting both macular and lichenoid lesions involving trunk and limbs are reported. Associations Recently, a growing number of reports indicate that primary cutaneous amyloidosis might be associated with various autoimmune disorders, such as systemic lupus erythematosus, rheumatoid arthritis, Hashimotos thyroiditis, sarcoidosis and immunoglobin A nephropathy.19 Investigataions Diagnosis of PLCA is mostly clinical. The diagnosis can be confirmed by routine histopathology, special staining and electronmicroscopy of skin biopsy. In cases of nodular amyloidosis in addition to clinical examination for systemic involvement, investigations should include, CBP, X-Ray examination, metabolic panel, serum and urine electrophoresis, FNAC of abdominal fat, rectal biopsy and bone marrow aspiration. Dermoscopy The primary patterns seen include a central hub, either white or brown, surrounded by various configurations of hyperpigmentation and for cases with prominent hyperkeratois, the central hub is replaced by a scar like white area. Skin biopsy A deep shave biopsy or a puch biopsy is sufficient except for nodular amyloidosis where a deep biopsy including subcutaneous fat is required as amyloid is deposited in dermis, subcutaneous tissue as well as blood vessel walls. Histopathology In both macular MA and LA small globules of pink material (amyloid) are present in superficial dermis,
mostly in dermal papilla between epidermal rete ridges. Overlying epidermis shows increased melanin, basal cell vacuolation, macrophages and pigment incontinence. LA in addition shows hyperkeratosis and acanthosis. Nodular amyloidosis shows diffuse infiltrates of amyloid in the epidermis, dermis, subcutaneous tissue and blood vessel walls. Special stains like methyl violet and crystal violet produce metachromatic staing of amyloid. Congo Red gives apple green birefringence under polarized light. Pagoda red and RIT Scarlet No 5 are more specific as they do not stain hyaline and colloid. Other special stains include PAS, von Gieson and Thioflavin T. Electronmicroscopy shows small areas of extracellular fibrillar material in dermis. The fibrils are rigid, non branching, straight or slightly curved and intertwining. Treatment2 There are vast treatment options for PLCA but none proved satisfactory in achieving complete clinical regression. Treatment should aim at relieving symptoms and improving cosmesis. Friction from itching can be an important cause for cutaneous amyloidosis and treating the underlying itchy condition can improve it. Treatment should be directed at breaking the itch scratch cycle usually present in these patients. Treatment options can be divided into medical, non surgical and surgical procedures (Table 2).
Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
Table 2: Treatment of PLCA Topical therapy
Systemic therapy
Non surgical procedures
Topical , I/L steroids
Acitretin
(with or without occlusion +/keratolytics)
Cyclophosphamide
Transcutaneous nerve stimulation
Retinoids
Colchicines
Capsaicin
Amytryptiline
Calcineurin inhibitors
Phototherapy photochemotherapy
Topical vit D analogues DMSO Menthol Hydrocolloid dressings and wraps (ZnO)
Chemical peels
Cyclosporine
Cryotherapy Lasers
in MA. TCA was found superior to GA.20 -22 Cryotherapy Cryotherapy was found to be unhelpful and was associated with hemorrhage. Surgical therapies
NBUVB
Scraping with scalpel
Electrodessication, scraping with scalpel, dermabrasion and curettage help in the treatment of LA. Nodular lesions can be excised.
PUVA
Dermabrasion
Laser therapy
Re PUVA
Curettage
CO2 laser is most frequently used laser in the treatment of PLCA. Different lasers like Yiterbium/Erbium, Pulse Dye Laser, Q switched NdYag laser were all tried in the management of cutaneous amyloidosis.
Surgical therapy Electrodessication
Excision
Topical and bath PUVA Tretinoin tocoferil
Topical therapies
Systemic therapy
Corticosteroids are the most commonly used treatment for PLCA. They are useful to some extent in relieving itching and improving skin lesions. Potent topical corticosteroids can be used with or without salicylic acid and with or without occlusion. Intralesional steroids can be used for limited disease. Calineurin inhibitors like tacrolimus act as good adjuvant. Topical retinoids with their effects on epidermal differentiation, desquamation and pigment lightening help in clearance of lesions of LA. Apoptosis induced by them can stimulate macrophages and clear amyloid. Tretinoin tocoferil, a combination of tocopherol and retinoic acid is reported to have a mixed outcome. Capsaicin, menthol and topical and bath PUVA helps in relieving itching. Dimethyl sulfoxide (DMSO) is a penetration enhancer and an immunomodulator. It is found useful in the treatment of LA. Side effects of DMSO include irritant and allergic contact dermatitis.
Systemic therapy is indicated for widespread disease. Acitretin helps in relieving itching and flattening of the lesions. Cyclophosphamide in a dose of 50mg daily helped in clearing LA. Amytryptaline, a tricyclic antidepressant is found useful in relieving pruritus but without change in the lesions in a case of familial LA. Colchicine binds to microtubules and inhibits leucocyte function. It is found useful in the management of hyperpigmentation in MA and LA in a clinical trial of 90 days. Cyclosporine helps by decreasing production of pro inflammatory cytokines.
Localized limited disease is treated with topical or intralesional steroids, DMSO, surgical excision and with ablative lasers. Widespread disease is treated with photo/photochemotherapy and systemic agents like acitretin and cyclophosphaide. Nodular lesions are treated with surgical excision or with laser ablation. There is a potential threat of haemorrhage with these treatments. Recurrence is common.
Phototherapy and Photochemotherapy Narrow band UVB, topical, bath and systemic PUVA, Retinoid PUVA all help in relieving itching and clearing the lesions of LA. Chemical Peels Several chemical peels like 15% trichloroacetic acid, Glycolic acid, Retinol and Nomelan Fenol are tried
Figure 1: Macular amyloidosis showing rippled pigmentation
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Primary Localized Cutaneous Amyloidosis – Clinical Features and Management
References 1. Vanessa Ngan. 2003.Amyloidosis, DermNet NZ, accessed on 5th July, 2021, <https://dermnetnz.org/topics/amyloidosis/> 2. Weidner T, Illing T, Elsner P. Primary Localized Cutaneous Amyloidosis: A Systematic Treatment Review.Am J ClinDermatol. 2017 Oct;18(5):629-642.doi: 10.1007/s40257-0170278-9. PMID: 28342017.
Figure 2: Tea bark appearance or sea floor appearance of Lichen amyloidosis
Figure 3: Macular pigmentation over and below clavicular area
3. Schremi S. Cutaneous Amyloidosis. In (Eds) Christopher Griffiths, Jonathan Barker, Tanya Bleiker, Robert Chalmers, Daniel Creamer, (eds). Rook’s Text book of dermatology, Ed 9th Publisher: Wiley-Blackwell, 2016; pp: 58.1 - 58.13. 4. Sakuma TH, Hans-Filho G, Arita K, Odashiro M, Odashiro DN, Hans NR, HansNeto G, McGrath JA. Familial primary localized cutaneous amyloidosis in Brazil. Arch Dermatol.
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15. Bourke JF, Berth-Jones J, Burns DA. Diffuse primary cutaneous amyloidosis. Br J Dermatol.
16. Errol C. Lichen amyloidosis of the auricular concha: report of two cases and review of the literature. Dermatol Online J. 2006 Sep 8;12(5):1. PMID: 16962016.
6. van den Berg WH, Starink TM. Macular amyloidosis, presenting as periocular hyperpigmentation. ClinExpDermatol. 1983 Mar;8(2):195-7. doi: 10.1111/j.13652230.1983.tb01765.x. PMID: 6851240. 7. Somani V K, Hari S, V L Sita V N, Razvi F. Nylon friction dermatitis: A distinct subset of macular amyloidosis. Indian J DermatolVenereolLeprol 1995;61:145-147
10. Suranagi VV, Siddramappa B, Bannur HB, Patil PV, Davangeri RS. Bullous variant of familial biphasic lichen amyloidosis: a unique combination of three rare presentations. Indian J Dermatol. 2015;60(1):105. doi:10.4103/00195154.147868 11. D'Souza A, Theis JD, Vrana JA, Dogan A. Pharmaceutical amyloidosis associated with subcutaneous insulin and enfuvirtide
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14. Ritter M, Nawab RA, Tannenbaum M, Hakky SI, Morgan MB. Localized amyloidosis of the glans penis: a case report and literature review. J CutanPathol. 2003 Jan;30(1):37-40. doi: 10.1034/j.1600-0560.2003.300107.x. PMID: 12534803.
5. Bohjanen K, Miller D D. 2021. cutaneous manifestations of amyloidosis.Uptodate. Accessed on 5th July, 2021.<https:// www.uptodate.com/contents/cutaneousmanifestations-of-amyloidosis>Feb, 08,2021.
Chinese cases.Br J Dermatol. 2000 Dec;143(6):1266-9. doi: 10.1046/j.13652133.2000.03899.x. PMID: 11122031.
pattern
13. Wan H, Ran Y. Unusual primary cutaneous amyloidosis with an incontinentiapigmenti-like pattern. Int J Dermatol. 2011 Apr;50(4):4857. doi: 10.1111/j.1365-4632.2009.04373.x. PMID: 21413964.
1992 Dec;127(6):641-4. doi: 10.1111/j.13652133.1992.tb14880.x. PMID: 1476924.
9. Wang WJ, Huang CY, Chang YT, Wong CK. Anosacral cutaneous amyloidosis: a study of 10
amyloidosis showing hub and spoke
12. Heng JK, Ho SA, Tan KB. Poikilodermalike cutaneous amyloidosis--a rare presentation of primary localized cutaneous amyloidosis. Dermatol Online J. 2016 Jan 15;22(1):13030/ qt20s8p7qt. PMID: 26990468
2009 Jun;145(6):695-9. doi: 10.1001/ archdermatol.2009.107. PMID: 19528426.
8. Verma S, Joshi R. Amyloidosis cutis dyschromica: A rare reticulate pigmentarydermatosis. Indian J Dermatol 2015;60:385-7
Figure 4: Dermoscopy of macular
administration. Amyloid. 2014;21(2):71-75. doi: 10.3109/13506129.2013.876984
17. Bandhlish A, Aggarwal A, Koranne RV. A clinico-epidemiological study of macular amyloidosis from north India. Indian J Dermatol. 2012;57(4):269-274. doi:10.4103/00195154.97662 18. Groves, R. Cutaneous Amyloidosis ed.Kang S, Amagai M, Bruckner AL et al. 2019. Fitzpatrick's dermatology. 9th ed. New york: McGraw Hill education, pp.754 - 760. 19. Chen JF, Chen YF. Answer: Can you identify this condition?. Can Fam Physician. 2012;58(11):1234-1235. 20. Nandini A. S, Sharath Kumar B. C. TCA peel in the treatment of macular amyloidosis. JMDS.2014 Sept;3(45):11090-11095. 21. Sacchidanand S, Shetty AB, Leelavathy B. Efficacy of 15% trichloroacetic Acid and 50% glycolic Acid peel in the treatment of frictional melanosis: a comparative study. J Cutan Aesthet Surg. 2015;8(1):37-41. doi:10.4103/09742077.155078 22. Wang, Lian& Zhang, Nan & Li, Xiao-Xue& Jiang, Xian. (2018). Biphasic Amyloidosis involved in the face: Effective Treatment with 30% Salicylic Acid. Dermatologic Therapy.32. 10.1111/dth.12743.
Dermoscopic Assessment of Post Covid Hairfall
Dermoscopic Assessment of Post Covid Hairfall Dr. Rahul Nagar
DNB Associate Professor Department of Dermatology, Venereology and Leprosy Mahatma Gandhi Memorial Medical College and MaharajaYashwant Rao Hospital, Indore, Madhya Pradesh
Dr. Farah Khan
MD 3rd Year PG Resident Department of Dermatology, Venereology and Leprosy Mahatma Gandhi Memorial Medical College and MaharajaYashwant Rao Hospital, Indore, Madhya Pradesh ABSTRACT An increased incidence of alpoceia particulary developing in patients recovering from covid infection was noted, we assessed 100 cases of post covid alopecia dermoscopically, which showed the predominant cause of post covid hair fall in females was acute telogen effluvium whereas in males it was androgenetic alopecia. INTRODUCTION There has been a surge in cases of hair loss in post covid times, which has added to the psychological trauma to the already distressed patients recovering from covid infections the two major causes of post covid hair fall noticed are actue telogen effluvium and androgenetic alopecia. Telogen effluvium is due the psychological stress, drugs and the nutritional compromise. An association has been noticed between covid infection and androgenetic alopecia. Patients with Androgenetic alopecia (AGA) were found to have severe Acute
Respiratory Distress Syndrome (ARDS) with poor prognosis.1 Animal experiments with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV) have previously showed that males develop increased viral load in the lungs during infections, and are more susceptible to severe disease at lower viral inoculate, compared to females.2 X-linked inheritance of genetic polymorphisms include Angiotensin-Converting Enzyme 2 (ACE2) gene loci and the androgen receptor (AR), which may make males further vulnerable.3 SARS-CoV-2 infection is likely androgen mediated.4 MATERIAL & METHODS The single center, nonrandomized, open-label, observational study was performed over a period of 6 months in Department of Dermatology, Venereology and Leprosy of Mahatma Gandhi Memorial Medical College, in association with Maharaja Yashwant Rao hospital, Indore, India. Permission was obtained from the ethical committee of our institute prior October 2021
35
Dermoscopic Assessment of Post Covid Hairfall
to initiation of study. Written informed consent was taken from all the patients for participation in study and for publication of clinical photographs. 100 patients with history of post covid hairfall were randomly selected from OPD of MY hospital, Indore. After recruitment all the subjects underwent detailed history taking, clinical and dermatological examination, also subjects were advised basic investigations like complete blood picture and thyroid profile. Patients with deranged basic investigation were excluded from study. Trichoscopic examination of each individual was done by a single observer and other causes of hair loss like alopecia aerata and telogen effluvium were ruled out. All patients were explained about the trichoscopic examination procedure at the start. A midline partition was done by separating the hairs from midline, trichoscope was put in midline 3cm above the anterior hair line in the frontal area and 3 images were capturedin personal computer by putting the trichoscope in 3 different sites in midline, similarly occipital area was examined 3cm above posterior hair line. We counted trichoscopic variables of male pattern hair loss in all 3 images of frontal and occipital area respectively. Major Criteria
2. Ratio of number of single hair pilosebaceous unit of frontal to occipital area >2:1. 3. Ratio of hair follicles with perifollicular discoloration in frontal to occipital area >3:1 Fulfillment of two major criteria or one major and two minor criteria is required diagnosis. CHANGES IN HAIRS 1. Vellus like hairs- thin miniaturized hair. 2. Anisotrichosis- heterogenecity in hair shaft thickness.
Figure 4: Yellow Dot Figure 1: Anisotrichosis CHANGES AROUND FOLLICLES 1. Peripilar sign- the brown perifollicular discoloration corresponds to perifollicular presence of lymphocytic infilterates. 2. Yellow dots- follicular openings with keratotic material and/or sebum. 3. Single hair follicular unitpredominance of follicular unit with only one hair emerging from follicular.
1. More than four yellow dots in four images at a 70 fold magnification in frontal area. 2. Lower average hair shaft thickness in frontal area as compared to occiput. 3. More than 10% thin (<0.03mm) in frontal area.
hairs
Minor Criteria
Figure 2: Peripilar Sign
1. Ratio of number of vellus hairs in frontal to occipital area >1.5:1.
36
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Figure 3: Single Hair Follicle Unit
Diagnosis Diagnosis of acute telogen effluvium is clinical, made on the basis of history of stressor event and diffuse pattern of hair loss.5 Signs like temporal rarefaction, frontal and occipital fringe, is called the acute telogen effluvium triad.6 Dermoscopic findings suggestive of TE are reduced density and single hair follicle unit.
Dermoscopic Assessment of Post Covid Hairfall
STATISTICAL ANALYSIS S.NO BASELINE CHARACTERSTICS 1 AGE 2 GENDER 3 4 5
COVID STATUS SEVERITY OF ARDS/ INFECTION PATTERN OF HAIR LOSS
6
Severity of hair loss
7
DERMOSCOPIC FEATURES S/O
MEAN VALUES 35-50 MALES FEMALES 57 43 POSITIVE MILD MODERATE SEVERE 30 35 35 DIFFUSE PATTERNED MALES FEMALES MALES FEMALES 24 30 33 13 MALES FEMALES MILD 17 MILD 13 MODERATE 19 MODERATE 20 SEVERE 21 SEVERE 10 ANDROGENETIC ACUTE TELOGEN ALOPECIA EFFLUVIUM MALES 33 MALES 24 FEMALES 10 FEMALES 33
RESULT In our study we found the age group that was most frequently affected and presented with post covid alopecia was between 35-50 years of age, amongst the study subjects 57% were males and 43% were females. Out of 57 males 42% males had diffuse hair loss whereas 58% had patterned hair loss, on the other hand 70% females had diffuse hair loss and 30% had patterned hair loss. On the basis of dermoscopic evaluation 53% males and 23.2% females had AGA whereas 42% males and 76% females had acute telogen effluvium. Also an association between AGA and severity of covid infection has been found pointing towards the role of androgen in the pathogenesis of infection.7 DISCUSSION Coronavirus disease 2019 (COVID-19) pandemic fatalities are rare before adrenarche/puberty (<10 years of age), and the vulnerability of males to severe disease8 has been constantly reported.The first biologic step required for potential infectivity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the priming of the spike proteins by transmembrane protease, serine 2 (TMPRSS2). TMPRSS2 activity is regarded as essential for viral spread and pathogenesis in the infected hosts.9 TMPRSS2 may also cleave angiotensin converting enzyme 2 (ACE2) for augmented viral entry.10 Androgen receptor activity has been considered a requirement for the transcription of the TMPRSS2 gene because no other known TMPRSS2
gene promoter has been described in humans to date. Theoretically, the hyperandrogenic phenotype might correlate with COVID-19 increased viral load, increased viral dissemination, and severity of lung involvement. There have been many studies supporting the correlation between AGA and severe covid induced ARDS with poor outcome.11,12,13,14 Also there are studies showing that post covid alopecia is one of the major sequelae faced by recovering patients.15 In our study we assessed the post covid alopecia patients dermoscopically and on the basis of history, clinical examination and dermoscopic findings that found 53% males and 23.2% females had AGA whereas 42% males and 76% females had acute telogen effluvium. The cause of telogen effluvium following covid infection (a stressor event) is quite obvious but the ways it induces or aggravates AGA is still to be eluded. References
4. Wambier CG, Goren A. Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) infection is likely to be androgen mediated. J Am Acad Dermatol. 2020; 83: 308309. 5. Mubki T., Rudnicka L., Olszewska M., Shapiro J. Evaluation and diagnosis of the hair loss patient: part I. History and clinical examination. J Am Acad Dermatol. 2014;71 6. Contin LA, Rocha VB. Acute telogen effluvium triad after resolution. An Bras Dermatol. 2021;96(5):605-608. doi:10.1016/j. abd.2020.10.008 7. Aditya K. Gupta, Literature Review, International Society of Hair Restoration Surgery, 10.33589/31.2.60, 31, 2, (60-61), (2021). 8. Shi Y.Yu X.Zhao H.Wang H.Zhao R.Sheng J.Host susceptibility to severe COVID-19 and establishment of a host risk score: findings of 487 cases outside Wuhan Crit Care. 2020; 24: 108. 9. Hoffmann M.Kleine-Weber H.Schroeder S.et al.SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor.Cell. 2020; : 1-10. 10. Heurich A.Hofmann-Winkler H.Gierer S.Liepold T.Jahn O.Pohlmann S.TMPRSS2 and ADAM17 cleave ACE2 differentially and only proteolysis by TMPRSS2 augments entry driven by the severe acute respiratory syndrome coronavirus spike protein.J Virol. 2014; 88: 12931307. 11. Wambier CG, Vaño-Galván S, McCoy J, et al. Androgenetic alopecia present in the majority of hospitalized COVID-19 patients–the “Gabrin sign”. J Am Acad Dermatol. 2020; 83: 680- 682. 12. Goren A, Vaño-Galván S, Wambier CG, et al. A preliminary observation: male pattern hair loss among hospitalized COVID-19 patients in Spain–a potential clue to the role of androgens in COVID-19 severity. J Cosmet Dermatol. 2020; 19: 1545- 1547. 13. Lee J, Yousaf A, Fang W, Kolodney MS. Male balding is a major risk factor for severe COVID-19. J Am Acad Dermatol. 2020; 83(5): e353- e354.
1. Gustavo Wambier, C, Mehta, N, Goren, A, Cadegiani, F. COVID-19, androgens, and androgenic alopecia. Dermatological Reviews. 2021; 2: 146- 153.
14. Nanes BA. Androgenetic alopecia in COVID-19: compared to what? J Am Acad Dermatol. 2020; 83(6):e451.
2. Channappanavar R, Fett C, Mack M, Ten Eyck PP, Meyerholz DK, Perlman S. Sex-based differences in susceptibility to severe acute respiratory syndrome coronavirus infection. J Immunol. 2017; 198(10): 4046- 4053.
15. Iqbal A, Iqbal K, Arshad Ali S, et al. The COVID-19 Sequelae: A Cross-Sectional Evaluation of Post-recovery Symptoms and the Need for Rehabilitation of COVID-19 Survivors. Cureus. 2021;13(2):e13080. Published 2021 Feb 2. doi:10.7759/cureus.13080.
3. Goren A, McCoy J, Wambier CG, et al. What does androgenetic alopecia have to do with COVID-19? An insight into a potential new therapy. Dermatol Ther. 2020; 33:e13365.
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Introducing
The Next generation Itraconazole
50
SUBA Itraconazole 50 mg Capsules
Equivalent to 100 mg of Conventional Itraconazole
A B C +
A
Absorption
B
=
Bioavailability
C
Clinical Efficacy
Greater...
A B c
Absorption Bioavailability Clinical Efficacy
R.N.I. No.MAHENG/2010/44622 Postal Registration No.MCE/295/2021-23 Posted at Mumbai Patrika Channel Sorting Office Mumbai-1 on 5th & 6th Every Month Published on 1st of Every Month