The Aestheticians Journal I October'2022 issue

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Dom Daniel

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Published for the period of October-2022

Beauty Is More Than Skin Deep

Our skin is the largest organ in our body. The skin protects us from all kinds of harsh effluents and work as a barrier to prevent pathogens and other harmful agents from penetrating into our body. Everybody wants their skin is as smooth and youthful as possible. Healthy skin depicts a healthy life. Keeping our skin healthy means we are protecting our body against germs as well as damage to our bones, muscles and internal organs. Besides keeping harmful microbes out and our body infection free, our skin also keeps fluids inside our body to prevent dehydration. Moisturizing our skin is one of the most important things to safeguard our skin’s barrier function and prevent the onset of premature skin aging. Use a good moisturizer that has a simple list of ingredients. A skin product should normalise the skin pH balance.

With growing responsibilities and struggling to balance work and personal life, we all tend to stress out because we hardly stay indoors. The first signs of stress are shown on our skin. Also, frequent exposure to dust, harmful pollutants, and other poisonous gases and rays deplete the natural texture of our skin. Skin experts always help to suggest various steps that we can take to maintain our skin and look charming. Because skin health is very essential to achieve the glow that we long for.

In this issue we have the articles on Exogenous. Ochronosis, Extragenital Bowens Disease, Radiofrequency for Nevus, Dietary Supplements for Hair Loss Treatment, Scar Site Bullous Pemphigoid.

- Dom Daniel Executive Editor & Publisher

Exogenous Ochronosis

Dr. Rashmi Modak, MBBS, DDVL

Scar Site Bullous Pemphigoid- A Rare Presentation and a Clinician Dilemma

Dr. Shadab R. Doi, MD (Dermatology), Fellow in Aesthetic Medicine (AUS) Dr. Zeba Harsolia, M.D.S.Prosthodontics & Crown & Bridge

Case Report of Extragenital Bowens Disease

Dr. Priyanka B S, 3rd Year Resident

Dr. Mangala H C, MBBS, MD (Dermatology)

Radiofrequency (RF) For Nevus

Dr. Srushti Jain Gupta, MBBS, DDV, FAM [Fellowship in Aesthetic Medicine]

Scar Site Bullous Pemphigoid-A Rare Presentation and

Dietary Supplements for Hair Loss Treatment Part-II

Dr. Sonali Kohli, MBBS, MD (Skin and Venereal Disease), M.Sc. (Facial Aesthetics)

Editorial Board

Dr. Mangala H C

MBBS, MD (Dermatology)

Professor

Department of Dermatology

Jagadguru Jayadeva Murugarajendra Medical College (JJMMC), Davangere, Karnataka, India

Dr. Sonali Kohli

MBBS, MD (Skin and Venereal Disease), M.Sc. (Facial Aesthetics)

Department of Aesthetic Dermatology

Sir H. N. Reliance Foundation Hospital and Research Centre, Mumbai

Dr. Srushti Jain Gupta

MBBS, DDV, FAM [Fellowship in Aesthetic Medicine] Consultant Dermatologist

Host Clinic Gwalior and Arogyadham Hospital, Madhya Pradesh

Dr. Shadab R. Doi

MD (Dermatology), Fellow in Aesthetic Medicine (AUS)

Visiting Consultant Dermatologist, Sanket Super speciality Hospital, Ahmedabad,

Visiting Consultant Dermatologist, Fatema Multi speciality Hospital, Himatnagar, Gujarat, India

Dr. Priyanka B S

3rd Year Resident Department of Dermatology

Jagadguru Jayadeva Murugarajendra Medical College (JJMMC), Davangere, Karnataka, India

Dr. Zeba Harsolia

M.D.S.Prosthodontics & Crown & Bridge Senior Lecturer Karnavati school of Dentistry Ahmedabad, Gujarat, India

Dr. Rashmi Modak

MBBS, DDVL Consultant Dermatologist and Owner Ra’Derm Clinic, Mulund, Mumbai

Exogenous Ochronosis

Dr. Rashmi Modak

MBBS, DDVL Consultant Dermatologist and Owner Ra’Derm Clinic, Mulund, Mumbai

Introduction

Ochronosis is a rare disorder characterized by blue-black or grayblue pigmentation clinically, while microscopically it shows ochercolored pigment deposition in the tissues.[1,2] It commonly affects the skin and sometimes the cartilages of ears and sclera of eyes. Exogenous ochronosis is a cutaneous disorder caused commonly due to abuse of hydroquinone containing creams. Hence, early diagnosis is important to necessitate immediate discontinuation of hydroquinone, rather than increasing the concentration in attempt to clear it. It is a cosmetically displeasing and psychologically debilitating disease which is difficult to treat. One needs to keep it in mind as a differential in patient with facial pigmentation, as the diagnosis is commonly missed in clinical practice and hence under reported.

Types of Ochronosis

Two types of ochronosis have been described, namely endogenous ochronosis and exogenous ochronosis.[1]

Endogenous Ochronosis (Alkaptonuria or Black urine disease):

It is an inherited autosomal recessive disorder of metabolism caused by

deficiency of enzyme homogentisate 1, 2 dioxygenase, leading to accumulation of homogentisic acid (1,2-dihydroxyphenolacetic acid, HGA) in the liver. This accumulated phenolic acid, soluble in water, polymerizes to ochre (yellowish) pigments that bind irreversibly to collagenous structures giving rise to the classical triad of (1) homogentisic aciduria, (2) pigmentation of skin, sclera, cartilages, etc and (3) degenerative ochronic arthropathies.[1,3]

Exogenous Ochronosis:

It is an acquired condition resulting from topical application of hydroquinone,[4] phenol, resorcinol, picric acid, mercury, as also with use of quinine injections[5] and oral anti-malarials. Although clinically and histopathologically similar to alkaptonuria, it has no systemic manifestations. We will be discussing about exogenous ochronosis in detail in this article.

History

The name ochronosis is derived from the Greek word “ochre”, which refers to yellow discoloration.[6] The chronological proceedings have been described in Table 1.

Table 1: Sequence of events describing evolution of exogenous ochronosis

Year Author Event

1866 Virchow[7]

Described the term ochronosis (for classical pigmentation).

1906 Pick[8] Described exogenous ochronosis (exogenous cause of ochronosis).

1912 Beddard and Plumtre [9]

Described exogenous ochronosis when a patient used phenol for the treatment of leg ulcer.

1975 De Beer[10]

Epidemiology

Described exogenous ochronosis in patients that used hydroquinone containing topical lightening agents.

The first case of exogenous ochronosis from India was reported in 2004 by Zawar and Mhaskar,[11] in a female using hydroquinone containing cream for more than 3 months. Later many more such cases were reported by Gandhi et al [12] and Jain et al.[13]

Globally, the exact incidence is not known. Due to under-diagnosis and under-reporting of cases, the actual incidence may be much higher than actually reflected in the global literature. The largest series of cases were reported from black population in South Africa.[14, 15, 16, 17, 18] However lately published reports show that exogenous ochronosis is also seen in many fair-skinned individuals.[19,20] USA has reported an incidence of 22 cases in about 50 years.[21, 22] Increasing incidence has been seen in China, Thailand, and Singapore. [23]

Etiology

Exogenous ochronosis has been known to occur following long-term application of skin-lightening creams containing hydroquinone, phenol or resorcinol.[2] Out of these, hydroquinone is known to have the strongest association.[4] The pigmentation may develop gradually over a period of 6 months to 3 years or longer.[4] Various other factors may predispose to its development and are listed in Box1.

Exogenous

Box1: List of predisposing factors

Prolonged unprotected sun-exposure. Outdoor occupation.

Presence of a number of viable melanocytes.[24]

Prolonged use of skin-lightening agents containing hydroquinone [4], phenol, resorcinol.

Application of hydroquinone [11, 12, 23] -over a larger area, in large quantity, alcoholic preparations. [25]

Pathogenesis

The exact pathogenesis of exogenous ochronosis is not known, although it is postulated that hydroquinone inhibits the enzyme homogentisic oxidase, thus interfering with skin pigmentation. It is also known to inhibit synthesis of DNA and RNA.[26] Various speculated theories have been listed in Table 2.

Table 2: Various theories explaining the pathogenesis of exogenous ochronosis

Year Author Theory

1975 Findlay et al [4] Hydroquinone, with prolonged use, passes down in the papillary dermis to be engulfed by the fibroblasts leading to attachment of phenolic degradation products and subsequent polymerization.

1983 Cullison et al [27]

Hydroquinone, oxidized to quinine, to form hydroxylated indoles that are similar to melanin precursors.

1984 Engasser [28] Hydroquinone in higher concentrations stimulates melanocytes and hence produce more melanin.

1985 Penneys [29] Hydroquinone causes local competitive inhibition of the enzyme homogentisic oxidase, leading to local accumulation of homogentisic acid and its metabolic products which polymerizes to form the ochronotic pigment in the papillary dermis. (most accepted theory)

Exogenous

Clinical Features

Exogenous ochronosis presents with hyper pigmentation of photo-exposed areas, especially bony prominence (zygoma) in a symmetrical pattern.[30,31,32]

The pigmentation is usually seen as blue-black or grayish-brown macules with dark, pinpoint, and caviar-like papules.[4]

Clinical classification has been suggested by and described in boxes 2,3,4,5 –

Box 2: Exogenous ochronosis in three clinical stages by Dogliotti and Leibowitz in 1979 [18]

Stage I – Erythema and mild hyper-pigmentation (clinically indistinguishable from melasma).

Stage II – Progressive hyper-pigmentation, pigmented colloid milium (caviar-like lesions) and scanty atrophy.

Stage III – Papulonodular (sarcoid-like) lesions.

Box 3: Grading of exogenous ochronosis by Phillips et al in 1986 [17]

Mild – Coarsening and darkening of the skin.

Moderate – Large black papules; skin in between papules is of normal pigmentation.

Severe – Larger, coalescing, caviar-like papules, which are relatively dark in color.

Box 4: Grading of exogenous ochronosis based on epidemiological studies by Hardwick et al in 1989 [33]

Grade I – Faint macular sooty pigmentation.

Grade II – Distinct macular stippling/small papules.

Grade III – Dark deposits and papules.

Grade IV – Colloid milia (1 mm and greater).

Grade V – Keloid-like nodules and cysts.

Box 5: Two extremes of exogenous ochronosis by Jordaan and Van Niekerk in 1991 [31]

Milder variant- coarsening and darkening of skin.

Severe variant - caviar-like black papules and skin atrophy.

Diagnosis

Clinically, diagnosis of exogenous ochronosis may pose a dilemma as it may be easily confused with melasma. As also the two conditions may co-exist. Furthermore exogenous ochronosis may be treated with hydroquinone containing creams in lieu of melasma, thus aggravating the condition. Various invasive and non-invasive techniques are available in aiding diagnosis of exogenous ochronosis [2] and are described in table no 3.

Table 3: Various techniques for diagnosis of exogenous ochronosis

Technique

Features

Non-invasive. Difficult to differentiate between exogenous ochronosis and melasma. Dermoscopy[35,36] Non-invasive.

Wood's lamp examination and ultraviolet light photography [34]

Presence of dark brown globules and globular-like structures on a diffuse brown background.

D/d – melasma, nevus of ota.

Reflectance confocal microscopy[20]

Superior, non-invasive.

Presence of hyporefractile oval-to-banana-shaped spaces in the dermis corresponding to the banana-shaped bodies on histopathology.

Histopathology[37] Gold standard but invasive.

Presence of the ochrecolored, banana-shaped fibers in the dermis.

Homogenization and swelling of collagen bundles in the papillary and reticular dermis.

Treatment

Exogenous ochronosis is a difficult to treat condition with often inconsistent and unpredictable results. Various non-pharmacological, pharmacological modalities and procedures are available[2] for its treatment and are described as below.

Box 6: Non-pharmacological measures

Stop further use of the offending agent. Avoid sun-exposure.

Use of wide-brimmed hat, sun-goggles, sun-protective clothing.

Table 4: Pharmacological measures

Agents Actions

Physical and chemical sunscreens[25]

Topical retinoid acid, glycolic acid, low potency corticosteroids[25]

Antioxidants, high doses of Vitamin E and C[38]

Tetracycline[39]

Table 5: Procedures

Provide photo protection. Prevent further worsening of skin pigmentation.

Exfoliating, De-pigmenting agents.

Clinical improvement in appearance of lesions.

Assist dilution of the pigment. Provide photo protection.

Improvement in papular- sarcoid lesions.

Despite multitude of treatments being available, none of them have shown a satisfactory result. Consequently, it is important to diagnose the condition early and thus prevent further progression by timely interruption of hydroquinone application.

Referrences:

1. Longo N. Inherited disorders of amino acid metabolism presenting in adults. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, editors. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw Hill; 2001. p. 2307.

Procedure Result

Chemical peeling (glycolic acid or tricarboxylic acid) [25]

Improvement in pigmentation.

Dermabrasion [25,40] Improved pigmentation.

Q-switched 755-nm alexandrite laser [41]

Enhance the clearance of ochronotic pigment fibers from dermis.

Decreased dermal pigmentation.

Lightening of pigmentation of the lesional skin.

2. Prachi A Bhattar, Vijay P Zawar,1 Kiran V Godse, Sharmila P Patil, Nitin J Nadkarni, and Manjyot M Gautam. Exogenous Ochronosis. Indian J Dermatol. 2015 NovDec; 60(6): 537–543.

3. Tharini G, Ravindran V, Hema N, Prabhavathy D, Parveen B. Alkaptonuria. Indian J Dermatol. 2011;56:194–6. [PMC free article] [PubMed]

Q-switched 1064-nm neodymium-doped yttrium aluminium garnet (Nd: YAG) laser [42]

Satisfactory improvement in dyschromia.

Q-switched ruby laser [18] Improvement in pigmentation. Carbon-dioxide laser [32] Improved pigmentation in combination with dermabrasion.

Conclusion

Exogenous ochronosis is an under-diagnosed and difficult to treat entity and pose a challenge to the dermatologist. Hydroquinone containing creams being the leading cause, needs to be used cautiously and at a concentration of < 1%.[43] Reflectance confocal microscopy is a superior emerging noninvasive tool aiding in the diagnosis of exogenous ochronosis. Q switch Nd YAG laser appears to be an upcoming and promising modality of treatment, useful in patients not responding to medical line of therapy.

4. Findlay GH, Morrison JG, Simson IW. Exogenous ochronosis and pigmented colloid milium from hydroquinone bleaching creams. Br J Dermatol. 1975;93:613–22. [PubMed]

5. Bruce S, Tschen JA, Chow D. Exogenous ochronosis resulting from quinine injections. J Am Acad Dermatol. 1986;15(2 Pt 2):357–61. [PubMed]

6. Online Etymology Dictionary. [Last accessed on 2013 oct 06]. Available from: http://www.etymonline.com.

7. Virchow R. Ein fall von allegemeiner ochronose der knorpel aud knorpelahnlichen theile. Virchows Arch Pathol Anat. 1866;37:212–9.

Exogenous Ochronosis

Exogenous Ochronosis

8. Pick L. Uber die Ochronose. Klin Wochenschr. 1906;43:478–80.

9. Beddard AP, Plumtre CM. A further note on ochronosis associated with carboluria. Q J Med. 1912;5:505–7.

10. Findlay GH, de Beer HA. Chronic hydroquinone poisoning of the skin from skin-lightening cosmetics. A South African epidemic of ochronosis of the face in dark-skinned individuals. S Afr Med J. 1980;57:187–90.

11. Zawar VP, Mhaskar ST. Exogenous ochronosis following hydroquinone for melasma. J Cosmet Dermatol. 2004;3:234–6. [PubMed]

12. Gandhi V, Verma P, Naik G. Exogenous ochronosis after prolonged use of topical hydroquinone (2%) in a 50-year-old Indian female. Indian J Dermatol. 2012;57:394–5. [PMC free article] [PubMed]

13. Jain A, Pai SB, Shenoi SD. Exogenous ochronosis. Indian J Dermatol Venereol Leprol. 2013;79:522–3. [PubMed]

14. Weiss RM, del Fabbro E, Kolisang P. Cosmetic ochronosis caused by bleaching creams containing 2% hydroquinone. S Afr Med J. 1990;77:373. [PubMed]

15. Bentley-Phillips B, Bayles MA. Cutaneous reactions to topical application of hydroquinone. Results of a 6-year investigation. S Afr Med J. 1975;49:1391–5. [PubMed]

16. DeCaprio AP. The toxicology of hydroquinone – Relevance to occupational and environmental exposure. Crit Rev Toxicol. 1999;29:283–330. [PubMed]

17. Phillips JI, Isaacson C, Carman H. Ochronosis in black South Africans who used skin lighteners. Am J Dermatopathol. 1986;8:14–21. [PubMed]

18. Dogliotti M, Leibowitz M. Granulomatous ochronosis – A cosmeticinduced skin disorder in blacks. S Afr Med J. 1979;56:757–60. [PubMed]

19. Kramer KE, Lopez A, Stefanato CM, Phillips TJ. Exogenous ochronosis. J Am Acad Dermatol. 2000;42(5 Pt 2):869–71. [PubMed]

20. Gil I, Segura S, Martínez-Escala E, Lloreta J, Puig S, Vélez M, et al. Dermoscopic and reflectance confocal microscopic features of exogenous ochronosis. Arch Dermatol. 2010;146:1021–5. [PubMed]

21. Snider RL, Thiers BH. Exogenous ochronosis. J Am Acad Dermatol. 1993;28:662–4. [PubMed]

22. Levitt J. The safety of hydroquinone: A dermatologist's response to the 2006 Federal Register. J Am Acad Dermatol. 2007;57:854–72. [PubMed]

23. Zawar V, Chuh A. Exogenous ochronosis in Asians. Int J Dermatol. 2010;49:101. [PubMed]

24. Hull PR, Procter PR. The melanocyte: An essential link in hydroquinone-induced ochronosis. J Am Acad Dermatol. 1990;22:529–31. [PubMed]

25. Levin CY, Maibach H. Exogenous ochronosis. An update on clinical features, causative agents and treatment options. Am J Clin Dermatol. 2001;2:213–7. [PubMed]

26. Martins VM, Sousa AR, Portela Nde C, Tigre CA, Gonçalves LM, Castro Filho RJ. Exogenous ochronosis: Case report and literature review. An Bras Dermatol. 2012;87:633–6. [PubMed]

27. Cullison D, Abele DC, O’Quinn JL. Localized exogenous ochronosis. J Am Acad Dermatol. 1983;8:882–9. [PubMed]

28. Engasser PG. Ochronosis caused by bleaching creams. J Am Acad Dermatol. 1984;10:1072–3. [PubMed]

29. Penneys NS. Ochronosislike pigmentation from hydroquinone bleaching creams. Arch Dermatol. 1985;121:1239–40. [PubMed]

30. O’Donoghue MN, Lynfield YL, Derbes V. Ochronosis due to hydroquinone. J Am Acad Dermatol. 1983;8:123. [PubMed]

31. Jordaan HF, Van Niekerk DJ. Transepidermal elimination in exogenous ochronosis. A report of two cases. Am J Dermatopathol. 1991;13:418–24. [PubMed]

32. Diven DG, Smith EB, Pupo RA, Lee M. Hydroquinone-induced localized exogenous ochronosis treated with dermabrasion and CO2 laser. J Dermatol Surg Oncol. 1990;16:1018–22. [PubMed]

33. Hardwick N, Van Gelder LW, Van der Merwe CA, Van der Merwe MP. Exogenous ochronosis: An epidemiological study. Br J Dermatol. 1989;120:229–38. [PubMed]

34. Zawar V, Tan SK. Exogenous ochronosis: A review for clinicians. Expert Rev Dermatol. 2012;7:171–80.

35. Charlín R, Barcaui CB, Kac BK, Soares DB, Rabello-Fonseca R, Azulay-Abulafia L. Hydroquinone-induced exogenous ochronosis: A report of four cases and usefulness of dermoscopy. Int J Dermatol. 2008;47:19–23. [PubMed]

36. Romero SA, Pereira PM, Mariano AV, Francesconi F, Francesconi VA. Use of dermoscopy for diagnosis of exogenous ochronosis. An Bras Dermatol. 2011;86(Suppl 1):S31–4. [PubMed]

37. Tan SK. Exogenous ochronosis in ethnic Chinese Asians: A

clinicopathological study, diagnosis and treatment. J Eur Acad Dermatol Venereol. 2011;25:842–50. [PubMed]

38. Burke KE. Interaction of Vitamins C and E as better cosmeceuticals. Dermatol Ther. 2007;20:314–21. [PubMed]

39. Fisher AA. Tetracycline treatment for sarcoid-like ochronosis due to hydroquinone. Cutis. 1988;42:19–20. [PubMed]

40. Lang PG., Jr Probable coexisting exogenous ochronosis and mercurial pigmentation managed by dermabrasion.

J Am Acad Dermatol. 1988;19(5 Pt 2):942–6. [PubMed]

41. Bellew SG, Alster TS. Treatment of exogenous ochronosis with a Q-switched alexandrite (755 nm) laser. Dermatol Surg. 2004;30(4 Pt 1):555–8. [PubMed]

42. Tan SK. Exogenous ochronosis –Successful outcome after treatment with Q-switched Nd: YAG laser. J Cosmet Laser Ther. 2013;15:274–8. [PubMed]

43. Andersen FA, Bergfeld WF, Belsito DV, Hill RA, Klaassen CD, Liebler DC, et al. Final amended safety assessment of hydroquinone as used in cosmetics. Int J Toxicol. 2010;29(6 Suppl):274S–87. [PubMed]

Scar Site Bullous PemphigoidA Rare Presentation and a Clinician Dilemma

Dr. Shadab R. Doi

MD (Dermatology), Fellow in Aesthetic Medicine (AUS)

Visiting Consultant Dermatologist, Sanket Super speciality Hospital, Ahmedabad, Gujarat, India

Visiting Consultant Dermatologist, Fatema Multispeciality Hospital, Himatnagar, Gujarat, India

Dr. Zeba Harsolia

M.D.S., Prosthodontics & Crown & Bridge

Senior Lecturer

Karnavati school of Dentistry

Ahmedabad, Gujarat, India

Abstract

Bullous pemphigoid (BP) is the most common autoimmune subepidermal blistering disease. Its onset is usually after 60 years of age. Characteristically, BP is an intensely pruritic eruption with widespread blister formation. However, in our case, patient characteristically developed lesions on 15th day post total knee replacement surgery and localised around surgical site. This indicates, physical trauma in form of surgical site incision as trigger. Localised BP is rare in itself and can be confused with irritant contact dermatitis, allergic contact dermatitis, bullous cellulitis. Early recognition of this entity is important so as to determine prognosis and course of disease.

Background

India is a country with population of almost 1.2 billion people. Number of

people going for knee arthroplasty in year 2020 was around 2,00,000. It’s one of the safest orthopedic operation with high success rate. Trend is on rise due to bell shaped population curve of INDIA. 74% of total TKRs (total knee replacement) being done in India are posterior stabilised as compared to cruciate retaining implants 11% and remaining 15% were rotating platform, constrained knees (e.g. LCCK (Legacy Constrained Condylar Knee), RHK (Rotating Hinge Knee) from Zimmer and TC 3, Noiles Hinge from DePuy J and J).[1]

Common skin complication post TKR includes post operation wound infections, blistering as a result of soft tissue swelling, allergic reactions to dressing material or topical agents.

Post-surgical occurrence of bullous pemphigoid is a rare but, known entity. However, post TKR only 5 case reports are reported in literature [2,3,4,5,6] and this being 6th.

Case Presentation

A 64 year old female, known case of diabetes mellitus and on TENELIGLIPTIN 20mg and METFORMIN 500mg 1 BD. Patient underwent total knee arthroplasty with tibial insert fixed bearing curved plus, tibial tray fixed bearing modular titanium cemented, femoral cruciate retaining cemented (all from Depuy, Johnson & Johnson). TKR itself was uneventful and patient was discharged after 24 hours. TKR relieved off patients knee pain and range of motion gradually increased upto 95 degree by day 14.

During, stapler removal on day 15th, patient noticed a small single papular eruption in scar line, which was slight pruritic. Treating doctor (orthopaedic) was consulted and cleaning with betadiene 10% was adviced. 3 days post suture removal (18th day post operation), patient noticed large number of bullous eruption in and around scar line (more marked centrally) [figure 1]. Bulla were tense, intensely itchy and ruptured to form erosions. For this dermatologist was consulted later, who treated on line of bullous cellulitis and started tab LINID 600mg 1 BD and supirocin ointment TDS for 7 days. However, no clinical improvement on lesion was seen. Antibiotic was changed to tab Rifampicin 600mg 1 OD on follow up for next 7 days, but new lesions kept on appearing. Meanwhile, patient was completely afebrile and good range of motion was present in operated knee. Patient was adviced to stop dressing the lesion with betadiene 10% and was just asked to apply supirocinoint.

Nikolsky was negative and intense itching probed us to point towards localized bullous pemphigoid. Afebrile patient, no pain and swelling at site ruled out cellulitis. Recurrent appearance of bulla, excluded irritant dermatitis.

re-occurred. PIH (Postinflammatory hyperpigmentation) and crusting at few site was seen on day 30th of treatment and no new lesion occurred [figure 2]. Patient was continued on tab Niacinamide 250mg BD, Levocet 5mg BD, FUCIBET HS application and moisturizer was added. Patient is under observation and is supposed to undergo TKR in right joint anytime soon. Word of caution is adviced to patient regarding same.

Investigation

HEMOGRAM was performed to rule out developing cellulitis and it revealed total count of 8,000/ cmm, DLC (Differential Leukocyte Count) (Neutrophils-65%, Lymphocytes-40, Eosinophils-3%, Basophils-0%), CRP (C-reactive protein)-08mg/L. Biopsy was not performed as consent was denied by patient in fear of secondary infection spreading to joints and risk implant infection.

Treatment

Patient was then, started on low dose deflazacort (12mg) once daily in morning, cap Doxycycline 100mg 1 BD, tab Niacinamide 250mg 1 BD, tab Levocet 5mg 1 BD, topical FUCIBET cream BD (betamethasone + fusidic acid) for 20 days to which patient responded drastically. No new lesions appeared post 20 days and itching subsided. Steroid was tapered and stopped in next 10 days followed by. No new lesions

Figure 2: Day 40th post operation

Discussion

BP is most frequent auto-immune blistering disorder which is caused by auto antibodies against BP 180 and BP 230. Trigger factors include- thermal or electrical burns, surgical procedures, trauma, ultraviolet irradiation, radiotherapy, chemical preparations, transplants, and infections. Drugs like thiazides, cephalosporins, ciprofloxacin, NSAID’s (Non-steroidal antiinflammatory drugs) are common association.

There are only three cases reported in literature with such acute onset.

Kim et al. described a case of generalized BP that started 3 days after surgery and spread to the

Scar

Figure 1: Day 18th post operation

operative knee 1 week later.[3] S. Sudahet al.[7] described a case of localised BP that started on day 14 and spread to medial side of operated knee on day 17th. Truss et al [2] described in which localised BP appeared and spread in 4 days.

In working up for diagnosis in a patient with bullae or vesicles appearing after a TKA (Total knee arthroplasty ), it is of prime importance to consider a complete differential diagnosis, including, postoperative skin blistering secondary to soft tissue oedema post operation, allergic or irritant contact dermatitis, bullous cellulitis and localised bullous pemphigoid. Post operation wound infection can be devastating as it can put risk of implant failure. It can be ruled out as it will have pus discharge, redness, swelling occasional bullae and patient will be febrile. Other cause of acute bullous eruption is ACD/ICD (Allergic contact dermatitis/Irritant contact dermatitis) due to bandage, dressing material or topical agents used for dressing. This presents as pruritic, bullous eruption. However, removal of culprit agent and changing dressing material should result in complete remission. This was not so in our case, as despite ceasing dressing, bullous eruptions continued.

Occurrence of bullous pemphigoid post trauma and surgery is being linked with “theory of immune compromised district” which states that, tissue damage interfering with local immune and cutaneous processes, leaving the potential for secondary disorders such as BP to occur.[4] [6]

This case, educates clinicians (dermatologist and orthopaedic) to be aware of this rare entitiy which can hinder proper patient care. Timely diagnosis can improve patients prognosis and reduce

psychological trauma to patients.

Conflicts of interest

There are no conflicts of interest.

References

1. Pachore, J., Vaidya, S., Thakkar, C., Bhalodia, H. K., & Wakankar, H. (2013). ISHKS joint registry: A preliminary report. Indian Journal of Orthopaedics, 47(5), 505. doi:10.4103/0019-5413.118208

2. Truss A, Papalexandris S, Gardner S, et al. BMJ Case Rep 2019;12:e227440. doi:10.1136/bcr-2018- 227440

3. Kim YB, Choi HS, Cho HK. Diagnosis and treatment of bullous pemphigoid that developed twice after total knee replacement arthroplasty: a case report. BMC MusculoskeletDisord 22, 118.

4. Kosi L., Peric J., Pantovic M. Localized bullous pemphigoid on the site of knee arthroplasty: a case report. Serbian J DermatolVenereol. 2016;8:39.

5. Kavak A., Parlak A.H., Cetinkaya R. Bullous pemphigoid on an incision scar of total knee prosthesis. Indian J Dermatol. 2006;51(1):70

6. S. Sudah et al. / Arthroplasty Today 9 (2021) 53e57

7. Vassileva S. Drug-induced pemphigoid: Bullous and cicatricial. Clin.Dermatol. 1998;16:379–387. doi: 10.1016/s0738081x(98)00008-x

FDA warns of dangers from skin lightening creams

Skin lightening products can be dangerous for consumers when they contain harmful ingredients that are illegal for over-the-counter sales, the U.S. Food and Drug Administration warned recently.The potentially harmful ingredients are hydroquinone or mercury. People who have used products with hydroquinone have suffered side effects that included rashes, facial swelling, and permanent skin discoloration, the FDA warned. Meanwhile, mercury is highly toxic and can damage the nervous, digestive and immune systems, as well as the lungs, kidneys, skin and eyes.

Skin lightening products are marketed as treatments for uneven skin tone, acne, age spots, freckles and wrinkles. Companies may describe skin lightening products as skin bleaching, brightening or whitening products. These products limit the skin's production of melanin, responsible for skin, hair and eye color. But hydroquinone and mercury can build up in the body over time.

Skin lightening products containing hydroquinone are not approved for over-the-counter sale, the FDA said. However, patient can get a prescription skin product containing hydroquinone from their health care provider. The use of mercury in skin lightening products is banned.

Consumers should check product labels and avoid those containing hydroquinone or mercury. Mercury may be listed as mercurous chloride, calomel, mercuric,mercurio or Hg. Illegal products may be inaccurately labeled. Avoid products with handmade labels, labels in languages other than English, or no label at all, the FDA said. Report any bad reaction from a skin product to health care provider and to the FDA.

Psoriasis diagnoses in primary care may be delayed by up to five years

Psoriasis is a skin disorder that causes skin cells to multiply up to 10 times faster than normal.Psoriasis can appear anywhere on the body, even on the eyelids, ears, lips, skin folds, hands, feet, and nails. Psoriasis is long-term disease which substantially affects patient’s quality of life and is linked with other serious medical conditions such as arthritis, heart disease and depression.

According to research, psoriasis may be underdiagnosed in primary care settings.The findings show that missed opportunities for early diagnosis of the potentially debilitating condition are relatively common in general practice. Doctors already know that delays in the diagnosis and initiation of treatment are associated with deterioration in patients' quality of life. GPs are most often the first point of contact for people with the condition, rather than dermatologists.

Patients who are later diagnosed with psoriasis, find the researchers, are twice as likely to be prescribed steroid or antifungal creams than people without psoriasis, which may mask the signs and symptoms of psoriasis and contribute to a further delay in diagnosis. The research team includes members of Dermatological Societies. We already know that early diagnosis of psoriasis can improve the effectiveness of treatment for psoriasis, so these findings are pertinent, said lead researcher. The World Health Organization has highlighted how many people suffer needlessly from psoriasis due to missed or delayed diagnosis. That is why researchers think it is essential to design additional dermatology training for primary care professionals to improve their diagnostic skills for psoriasis.

The researchers carried out extensive analysis of electronic health records of general practices comparing clinical diagnoses and treatments between people with and without psoriasis. Patients with psoriasis were up to eight-times more likely than those without psoriasis to be diagnosed with pityriasisrosea a minor skin condition at six months before the diagnosis of psoriasis, they found. They were twice as likely to be diagnosed with eczema or tineacorporis a fungal skin infection one year before diagnosis. They were also more likely to report symptoms of psoriasis such as dry skin, rash, skin texture changes and itching than controls up to five years before diagnosis. And they were prescribed topical corticosteroids or topical antifungals in the year before diagnosis twice as often as those without psoriasis.

The findings from this study suggest the diagnosis of psoriasis may be missed or delayed by up to five years for some individuals hence leading to a potentially detrimental delay in establishing an appropriate treatment regimen. It is crucial that diagnosis and treatment start as soon as possible, if patients are to reduce the risk of life-long impairment.

Advisory Board

Dr.

Dr. Satish Bhatia

Dr. Farida Modi MD

and

Center,

Case Report of Extragenital Bowens Disease

Dr. Priyanka B S

3rd Year Resident Department of Dermatology

Jagadguru Jayadeva Murugarajendra Medical College (JJMMC), Davangere, Karnataka, India

Dr. Mangala H C

MBBS, MD (Dermatology) Professor Department of Dermatology

Jagadguru Jayadeva Murugarajendra Medical College (JJMMC), Davangere, Karnataka, India

Introduction

Bowen’s disease is considered an intraepidermal/in situ squamous cell carcinoma (SCC) as long as it has not spread beyond the basal membrane. Spreading into the dermis is a time-consuming process, and when it happens, it grows as an invasive SCC.[1] This precancerous nature of Bowen’s disease was first recognised by John Templeton Bowen in 1912.[2]

The risk of progression to invasive SCC is estimated to be 3-5% for extragenital lesions and 10% for genital lesions.[3] Referring to these assertions, its potential lateral spreading through the epidermis is expected. By this gradual progress, with time, Bowen’s disease gets an unusual giant dimension.

Clinical presentation as a large erythemosqamous patch or plaque can be mistaken with various other dermatological differential diagnoses.[4],[5]

Chronic UV irradiation exposure (solar, iatrogenic and sunbeds) is considered the most obvious trigger of Bowen’s disease. Etiological causes also inspected are age, genetic factors, arsenic exposure and other carcinogens, human papilloma viruses (HPV), immunosuppression, trauma, x-ray irradiation etc.[4]

Case Report

A 65-year-old male was referred to our department with a history of slowly enlarging scaly erythematous lesion on the right arm, developed over the last 4 years (Figure 1). Completely asymptomatic, it has caused only cosmetic disturbance. Patient has reported unprotected exposure to the sun in the last 20 years. He declined previous cutaneous carcinomas of any kind. The attempts to treat it with topical corticosteroids creams did not reveal any improvement.

On local examination it was scaly, slightly elevated erythematous plaque with dimension 2x3cm and well demarcated borders from the surrounding skin.

Dermoscopy showed glomerular or dotted blood vessels and yellow white opaque scales on an erythematous background. (Figure 2, 3)

Histopathological examination (H/E) revealed parakeratosis in stratum corneum with atypia in cells throughout the epidermis. Individual dyskeratotic cells and increased mitotic figures were evident in spinous layer (Figure 4). Hence the diagnosis of bowen’s disease.

Figure 4: H/E revealed parakeratosis in stratum corneum with atypia in cells throughout the epidermis

Treatment

Treatment with 5% imiquimod cream was given thrice weekly for 4 months followed by twice weekly for the next 2 months. Since the patient was lost to follow up we could not assess the treatment outcome.

Discussion

Although the clinical presentation can argue about plentiful of dermatological diseases, dermoscopic findings strongly

suggestive for Bowen’s disease were recently defined.[6] Anyway, histopathology remains the ‘gold standard’ for an accurate diagnosis of Bowen’s disease.[7]

The period for full expression of the Bowen’s lesion is variable, from 2 years to maximum 40 years, a finding which is strongly in favour of the slow, lateral spreading of Bowen’s disease.

Asymptomatic as it is, the early lesions of Bowen’s disease are very subtle and overlap with clinical features seen in many other dermatological conditions (seborrheic keratosis, superficial basal cell carcinoma, actinic keratosis, eczema, tinea, psoriasis vulgaris, seborrhoeic dermatitis etc).[8]

Although early dermatological consultation can be accessed by the patient, these clinically not specific changes of Bowen’s disease often mislead the dermatologist in making the correct diagnosis. Undiagnosed Bowen’s disease ultimately advances to invasive SCC.[9]

Treatment modalities for Bowen’s disease are topical immunosuppressive/ immunostimulating creams, cryotherapy, curettage, photodynamic therapy, radiotherapy, laser and finally surgical excision.[10] The therapeutic choice can be influenced by the age group, number, size and localisation of the lesion, preferable and comfortable solution by the patient and affordability of the therapeutic modalities.[1]

Therefore, we strongly recommend self-skin examination to be carried out, especially in older patients. Also, regular dermoscopy performed on every long-standing

Figure 1: Scaly erythematous lesion on the right arm

Fig. 2

Fig. 3 Figure 2&3: Dermoscopy showed glomerular or dotted blood vessels and yellow white opaque scales on an erythematous background

Case Report of Extragenital Bowens Disease

erythemosquamous skin lesion should be a rule. Early recognition of Bowen’s disease and prevention of its undeniable progression into an invasive SCC is very important.

Conclusion

Early recognition of bowen’s disease and prevention of its progression into an invasive SCC is very important.

Reference

1. Bath-Hextall FJ, Matin RN, Wilkinson D, et al. Interventions for cutaneous Bowen's disease. Cochrane Database of Syst Rev. 2013;6:CD007281. https:// doi.org/10.1002/14651858.CD007281. pub2. [PMC free article] [PubMed] [Google Scholar]

2. Bowen JT. Precancerous dermatosis:a study of two cases of chronic atypical epithelial proliferation. J Cutan Dis Syph. 1912:241–55. In:ArchDermatol. 1983; 119(3):243-60. https://doi.org/10.1001/ archderm.1983.01650270061020

PMid:6297414. [PubMed] [Google Scholar]

3. Kao GF. Carcinoma arising in Bowen's disease. Arch Dermatol. 1986;122:1124–1126. https://doi.org/10.1001/ archderm.1986.01660220042010

PMid:3767398. [PubMed] [Google Scholar]

4. Kallini JR, Hamed N, Khachemoune A. Squamous cell carcinoma of the skin:epidemiology, classification, management, and novel trends. Int J Dermatol. 2015;54(2):130–40. https://doi. org/10.1111/ijd.12553 PMid:25428226. [PubMed] [Google Scholar]

5. Wozniak Rito AM, Rudnicka L. Bowen's disease in dermoscopy. ActaDermatovenerol Croat. 2018;26:157–161. https://doi.org./10.2340/000155551328 PMid:29989873. [PubMed] [Google Scholar]

6. Sotiriou E, Lallas A, Apalla Z, et al. Treatment of giant Bowen's disease with sequential use of photodynamic therapy

and imiquimod cream. Photodermatology, Photoimmunology& Photomedicine. 2011;27:164–166. https://doi. org/10.1111/j.1600-0781.2011.00586.x PMid:21535173. [PubMed] [Google Scholar]

7. Park JY, Kim SK, Cho KH, et al. Huge Bowen's disease:A pitfall of topical photodynamic therapy. Photodiagnosis and Photodyn Ther. 2013;10(4):546–

8. https://doi.org/10.1016/j. pdpdt.2013.05.001 PMid:24284109. [PubMed] [Google Scholar]

8. Bakardzhiev I, Chokoeva AA, Tchernev

G. Giant extragenital Bowen's disease. Wien Med Wochenschr. 2015;165(2324):504–7. https://doi.org/10.1007/ s10354-015-0396-z PMid:26542410. [PubMed] [Google Scholar]

9. Shankar AA, Pinto M, Shenoy MM, et al. Giant pigmented Bowen's disease:A rare variant at a rare site. Indian Dermatol Online J. 2015;6:S63–4. https://doi. org/10.4103/2229-5178.171048 PMid:26904458 PMCid:PMC4738524. [PMC free article] [PubMed] [Google Scholar]

10. Baykal C, Buyukbabani N, Babuna G, et al. Giant Bowen's disease histologically showing Borst- Jadassohn phenomenon and complicated with squamous cell carcinoma development. J EurAcadDermatolVenerol. 2016;30:88–89. https://doi.org/10.1111/jdv.13335 PMid:26373350. [PubMed] [Google Scholar]

Researchers develop painless tattoos that can be self-administered

A tattoo is a form of body modification made by inserting tattoo ink and it can be temporary or permanent images in the skin, delivered by needles injecting ink into the dermis. The ink is injected into the dermis by a machine that delivers thousands of tiny pricks per minute via needle.To make the tattoos typically use large needles to puncture repeatedly into the skin to get a good image, a time-consuming and painful process.

The researcher’s team has developed microneedles that are smaller than a grain of sand and are made of tattoo ink encased in a dissolvable matrix. Because the microneedles are made of tattoo ink, they deposit the ink in the skin very efficiently. In this way, the microneedles can be pressed into the skin just once and then dissolve, leaving the ink in the skin after a few minutes without bleeding.Instead of sitting in a tattoo chair for hours enduring painful punctures, imagine getting tattooed by a skin patch containing microscopic needles. Researchers have developed low-cost, painless, and bloodless tattoos that can be self-administered and have many applications, from medical alerts to tracking neutered animals to cosmetics.

Researchers have miniaturized the needle so that it's painless, but still effectively deposits tattoo ink in the skin. This could be a way not only to make medical tattoos more accessible, but also to create new opportunities for cosmetic tattoos because of the ease of administration.Tattoos are used in medicine to cover up scars, guide repeated cancer radiation treatments, or restore nipples after breast surgery. Various cosmetic products using microneedles are already on the market mostly for anti-aging but developing microneedle technology for tattoos is new.

Researcher has studied microneedle patches for years to painlessly administer drugs and vaccines to the skin without the need for hypodermic needles. They saw this is an opportunity to leverage their work on microneedle technology to make tattoos more accessible. They thought others might prefer a tattoo that is simply pressed onto the skin and does not hurt. Researcher’s goal is to create new opportunities for patients and people who want a painless tattoo that can be easily administered.

A Dermatologist on recognizing the monkeypox rash

Human monkeypox is a zoonosis caused by monkeypox virus, an orthopoxvirus and close relative of variola virus (smallpox). The clinical symptoms is characterised by fever, rash and lymphadenopathy. Complications of monkeypox can include pneumonitis, encephalitis, sight-threatening keratitis, and secondary bacterial infections.

Dermatology society offers some tips for helping distinguish monkeypox from other health issues that cause rashes and for getting care. The dermatologist said monkeypox looks different, while past outbreaks of monkeypox have started with fever and flu-like symptoms and a rash that could include more than 200 bumps, this time it's more common for people with monkeypox to get fewer skin bumps. They may also not have fever or flu-like symptoms. During this particular outbreak, we're seeing that the rash may start in the groin, genital region, or around the anus and sometimes stay in the spot that it started instead of spreading. People may have only one or two blisters, pus-filled bumps or open sores, which can be very painful. A dermatologist can narrow down the causes of a rash by its pattern on the skin and where it appears, confirming suspected monkeypox with a swab sent to a lab. While the monkeypox rash can be mistaken for chickenpox, shingles or herpes, there are differences between these rashes. Monkeypox is contagious and can spread until the bumps are gone, which is about two to four weeks.

The dermatologist said not every new rash is monkeypox. However, if you do think you have monkeypox, it's important to see your doctor quickly. Patients who delay getting medical attention may be diagnosed later when fewer treatment options are available. Waiting also means that you can expose more people to the virus, so family and others may develop monkeypox. Patients should call their doctor's office instead of going in, explaining symptoms first and then getting advice about what to do. People can contract this virus in several ways, including through touching the rash or scabs of an infected person during intimate contact. This is the most common type of transmission. The virus can also less commonly spread through respiratory droplets. It can also be passed by touching unwashed clothing or bedding from an infected person.

Monkeypox can also be spread by animals through a bite or scratch, by handling a live or dead infected animal, eating an infected animal or using a cream or powder made from the animal. People vaccinated against smallpox have less risk of developing monkeypox. Though no specific treatment for monkeypox is approved by the U.S. Food and Drug Administration, but people at risk of developing severe disease may receive treatment with an antiviral medication for smallpox known as Tecovirimat.

Radiofrequency (RF) For Nevus

Dr. Srushti Jain Gupta

MBBS, DDV, FAM [Fellowship in Aesthetic Medicine] Consultant Dermatologist Host Clinic Gwalior and Arogyadham Hospital, Madhya Pradesh

Introduction

A Nevus or Mole is an area of growth on skin. Some are present at birth while others develop over the course of lifetime. Many moles develop during adulthood related to sun exposure and effects on melanin production. Most of Nevi are harmless.

Types of Nevus

1. Congenital Nevus:- This is a mole which is by birth. They are generally categorized as being small, medium or giant in size. They vary in color, shape and consistency.

2. Common Nevus:- This is smooth, round mole that’s all one color. This can appear by birth or develop later in childhood.

3. Dysplastic Nevus:- A/C/A atypical mole are benign often resemble as melanoma. They may feature with different colors, asymmetrical or have borders.

4. Blue Nevus:- It is blue colored mole that can be congenital or acquired. Common Blue Nevus may appear flat/ dome shaped.

5. Miescher Nevus:- It is brownish or skin colored, dome shaped mole which appears on face or neck. It’s typically frim, round, smooth with hair coming out.

6. Unna Nevus:- Soft brownish moles located on your trunk, arms

and neck resembling as raspberry.

7. Meyerson Nevus:- These are moles surrounded by small ring of eczema which is itchy, red rash, common in men than women.

8. Halo Nevus:- Halo Nevus is mole with white ring of unpigmented skin around it. Over time mole in center begins to fade from brown to pink.

9. Spitz Nevus:- (<1 cm) It is raised, pink dome shaped mole typically appears before 20. They can have different color. They may bleed or ooze.

10. Reed Nevus:- It is dark brown or black raised dome shaped mole that affects women. This grows quickly.

11. Agminated Nevus:- Cluster of similar moles located on one area of body. These vary in appearance and type.

12. Capillary Malformation:This usually referred to as port wine stain or nevus flammeus. It is most common type of vascular malformation.

13..Riehl Melanosis:- A/C/A Pigmented Contact Dermatitis. It is dark brown to grey brown facial pigmentation that was most pronounced on lateral aspect of face and neck.

Radiofrequency

Management of Nevi

Diagnosis is done clinically and confirmed on biopsy [shave, punch, excisional biopsy]

A – Asymmetrical shape

B – Border

C – Color

D – Diameter

E – Evolving

Treatment

Medical Care –Medical treatment is ineffective and inappropriate for management of nevus like melanocytic nevus.

t/t – Excision

- Shave

- Dermabrasion

- Q-switch LASER

- CO2 LASER

Surgical

Melanocytic nevi can be surgically removed for cosmetic reason and are removed by tangential or shave excision.

Punch excision is done for small lesions.

Larger lesion require complete excision.

Excisional biopsy with suture closure.

Case Report

27 year old female had hyperpigmented patch since childhood over left cheek and under eyes. She was diagnosed as congenital nevus. She has undergone various treatments outside including medi-peel, Q-switch laser, no response was seen. She was given topical agents like retinol, kojic acid, glycolic acid but there was no response. She had visited to us and was advised

trial patch to be treated with RF. Her patch ~1cm area was taken for trial RF and was observed for 1 month. She responded well and as patient wanted only cheeks part to be treated and not under eye pigmentation. RF was successfully done for her left cheek hyperpigmented patch. She had no recurrence and she is under followup since 1 year.

Radiofrequency (RF) For Nevus

Figure 1: Before treatment

Figure 2: Before treatment only trial patch marked Figure 3: After trial patch circle is appreciated

Figure 4: After 2 days of treatment

Figure 5: After 1 month of removal

Figure 6: After procedure healing phase

Figure 7: After 4 months of treatment

Figure 8: After 1 year of treatment

References

1. Damsky WE, Bosenberg M. Melanocytic nevi&melanoma : unraveling a complex relationship. oncogene 2017 october 19.36.

2. Natarajan K, Arunachalam P, Sundar D, Srinivas CR. Congenital Melanocytic nevi : catch then early/ J.CutanAesthet surg.2013 Jan.

3. Patruno C, Scalvenzi M, Megna M, Russo I, Gaudiello F, BalatoN. Meloanocytic Nevi in children of southern Italy. Dermascopic, constitutional Environmental factors. PediatrDermatol 2013 may 31.

4. Harrison SL, Machennan R, buettner PG. sun exposure & the incidence of melanocytic nevi in young Australian children. Cancer epidemiol biomarkers prev. 2008 sep 17.

5. Gallagher RP, Rivers JK, Lee TK, Bajdik CD, Mclean DI, Coldman AJ. Broad spectrum sunscreen use & the development of new nevi in white children. A randomized controlled trial. JAMA 2000 Jun 14.

6. Zalaudek1 ,Schmid k , Marghoob AA , et al . Frequency of dermoscopic nevus subtypes by age & body site . A cross sectional study . Arch dermatol 2011 Jun .

7. HarthY ,friedman - Birnbaum R ,Linn S. Influence of cumulative

sun exposure on the prevalence of common acquired nevi . Jam AcadDermatol. 1992 Jul .

8. Tran KT, Wright NA, Cockerell CJ. Biopsy of the pigmented lesion – when & how. J Am AcadDermatol, 2008 Nov. 59.

9. Smith AD, Waisman M. connective tissue nevi familial occurrence and association with osteopoekilosis. Arch Dermatol. 1960.

10. Solomon LM. The management of congenital melanocytic nevi. Arch Dermatol 1980.

11. Kaplan EM. The risk of malignancy in large congenital nevi. PlastReconstSurg 1974.

12. Curth HO. Unilateral epidermal nevus resembling acanthosis nigricans. Br. J'Deamatol 1976.

13. Hong CE, Lee SH. Multiple excrine nevus with depressed patches . Yonsei Med J.

14. Pippione M, Depaoli MA, Sartirus S, et al. Nevus eccrineDermatologica, 1976.

15. Pack GT, Sunderland DA Nevus uniuslateralis.Arch Surg. 1941.

Radiofrequency

Researchers produce nanodiamonds capable of delivering medicinal and cosmetic remedies through the skin

The skin is one of the largest and most accessible organs in the human body,but penetrating its deep layers for medicinal and cosmetic treatments still eludes science.

A novel approach developed by researchers provides an innovative solution to overcoming two major challenges in delivering medicinal and cosmetic remedies through the skin. Combining techniques in nanotechnology and optics, researchers produced tiny (nanometric) diamond particles so small that they are capable of penetrating skin to deliver these remedies. Next, they created a safe, laser-based optical method that quantifies nanodiamond penetration into the various layers of the skin and determines their location and concentration within body tissue in a non-invasive manner eliminating the need for a biopsy. This innovation was just published by researchers.

The nanodiamonds have also been proven effective antioxidants. This property ensures that particles penetrating the body are both safe and therapeutic, as their chemical properties allow them to be coated with medication prior to their insertion into the body.

The optical method developed by the research team enables them to identify relative nanodiamond concentrations of particles in the different layers of skin (epidermis, dermis and fat) through safe and non-invasive sensing based on a blue wavelength laser, a unique finding in itself given the fact that red wavelength lasers are generally used in human medical exams and treatments. To determine their location in the skin and in what concentration, patients are briefly exposed to the blue laser beam. An optical system creates a photograph-like 3D image through which optical changes in treated tissue can be extracted and compared to adjacent, untreated tissue using a specially-created algorithm. This is a significant development in dermatology and in optical engineering,says a member of the research team. It could open the door to developing drugs applied through the skin alongside modern cosmetic preparations using advanced nanotechnology.

Microneedling improves appearance of surgical scars especially if performed early

Microneedling is a nonsurgical technique that has been used to improve the appearance of the skin in a number of conditions, such as chronic acne scars. In this procedure, after the skin is numbed, a power handpiece with needles of different sizes is used to create tiny channels in the skin.

Sometimes called "minimally invasive percutaneous collagen induction," microneedling works by inducing the body's own healing factors, such as collagen and elastin. Typically, microneedling or other treatments to improve the appearance of surgical scars have been delayed until after the scar has fully matured: between 6 and 12 months. Researcher’s evaluated an alternative approach using microneedling in earlier phases of the healing process, with the goal of reactivating the healing pathway. (Left) Face lift incision scar 13 weeks postoperatively before first microneedling treatment. (Right) Face lift incision scar 8 weeks after third and final microneedling treatment. Performed early after surgery, a procedure called microneedling can improve the final appearance of surgical scars—with best results if done within six to seven weeks, reports a new study.That's in contrast to the "conventional wisdom" that treatments to improve the appearance of surgical scars should be delayed for up to a year, according to the new research. The researchers findings suggest that microneedling 6 weeks after surgery to restart the healing process is an option to improve the final outcomes of postoperative scarring.

The study included 25 women with surgical scars resulting from various plastic/skin surgery procedures, such as benign lesion removal, facelift, or tummy tuck. Each patient underwent microneedling, with the first treatment performed at 6 and 16 weeks after surgery. The second and third treatments were performed 4 and 8 weeks later, respectively.After microneedling, the patients had significant improvement in scar appearance, based on three different standardized assessments. For example, on the Patient and Observer Scar Scale (POSAS, with a range from 6 to 60, with lower scores indicating better appearance), average score decreased from 23.7 before microneedling to 11.7 at follow-up (2 months after the last treatment).

The researchers also compared results for patients who started microneedling earlier, 6 to 7 weeks after surgery; versus later, 13 to 16 weeks. The results showed "markedly better" improvement in POSAS (Patient and Observer Scar Scale) scores for the earlier treatment group: from 16.8 to 8.1, compared with 26.1 to 14.2 in the later treatment group. Outcomes were similar for patients in different age groups and for those with scars located on the body versus face.

Dietary Supplements for Hair Loss Treatment Part-II

Dr. Sonali Kohli

MBBS, MD (Skin and Venereal Disease), M.Sc. (Facial Aesthetics) Department of Aesthetic Dermatology

Sir H. N. Reliance Foundation Hospital and Research Centre, Mumbai

Amino Acids and Proteins

Protein malnutrition, such as in kwashiorkor and marasmus, can result in hair changes that include hair thinning and hair loss. One study examined the role of L-lysine, an essential amino acid that may play a role in iron and zinc uptake. The addition of L-lysine to iron supplementation resulted in a significant increase in mean serum ferritin concentration in some women with chronic TE who failed to respond to iron supplementation alone.5

A variety of amino acids have been studied for the treatment of hair loss. Most notably, cystine and lysine have been evaluated in humans. Other amino acids, including methionine and arginine, are often included in hair nutraceuticals but have not yet been evaluated in clinical studies. Cysteine plays a central role in hair health; it forms dimers that are oxidized to produce cystine, creating disulfide bridges that provide strength and rigidity between keratin strands.6

Oral L-cystine (70 mg) in combination with retinol was evaluated for the treatment of diffuse alopecia, with increases seen in both hair density and anagen rate. In patients with chronic TE, supplementation with

L-lysine (1.5 g), iron (72 mg), vitamin B12, vitamin C, biotin, and selenium resulted in a significant 39% reduction in hair shedding after 6 months, as well as a significant increase in serum ferritin levels in women who had previously failed with iron supplementation alone.6

Methionine is another essential amino acid that is vital for both keratin and procollagen synthesis. Studies have suggested a role for L-methionine in slowing the onset of grey hair in an in vitro model by counteracting hydrogen peroxidemediated oxidative stress and blunting of methionine sulfoxide repair.6

Antioxidants

Antioxidants are compounds that are able to neutralize reactive oxygen species (ROS), preventing oxidative damage. Many substances can be classified as anti oxidants, including zinc, selenium, vitamins A and E, vitamin C, and polyphenols. Oxidative stress has been linked to hair loss. In vitro studies of dermal papilla cells from male AGA patients have shown that oxidative stress may have an important role in the balding phenotype and development of AGA. Additionally, in a study of endogenous antioxidant enzymes

and lipid peroxidation in the scalps of patients with AA, excessive free radical generation was shown to occur in the scalps of patients with AA accompanied by high levels of antioxidant enzymes that were unable to protect against the ROS.5

Discussion

Food supplements are often used to improve hair growth, although the link between the use of specific components and the prevention of hair loss is not always supported by scientific studies.2

Stress and unhealthy lifestyles, combined with genetic conditions, hormonal imbalances, and other types of diseases play an important role in the physiology of the hair and imperfections related to the scalp. When imbalances occur in the delicate biological mechanisms that characterize the trophism of hair, it becomes clear how a targeted and complete food supplementation can give concrete help to the rebalancing and maintenance of the hair physiology. Such deficiencies often have turned into a busy life, food shortages, or physiological deficiencies of the individual. It is good to know which elements are important for hair growth, and therefore able to counteract hair fall.2

Data is available for the use of amino acids, caffeine, capsaicin, curcumin, garlic gel, marine proteins, melatonin, onion juice, procyanidin, pumpkin seed oil, rosemary oil, saw palmetto, vitamin B7 (biotin), vitamin D, vitamin E, and zinc to treat hair loss.6

The nutrients evaluation shown below made it possible to highlight a correlation between the substances analyzed and the treatment of hair loss, based on scientific studies that through different in vitro or in vivo tests allowed to demonstrate

tangible benefits (Table 1).3

Table 1: Summary of nutrients and mechanisms related to hair loss and follicle biology.2

Nutrient

Mechanism

Zinc Zinc is involved in several metabolic pathways and cellular functions, moreover, it contributes to the production of keratin, which represents the 95% of the hair structure. Zinc is a potent inhibitor of hair follicle regression and accelerates hair follicle recovery.

Copper The role of copper in hair biology is not well clarified. It has an important enzymatic role in the production of cross links in elastin and collagen fibers in the dermis, post-translational formation of di-sulfide bonds between cysteine molecules in cytoskeletal proteins of cortical and cuticle proteins.

Selenium Selenium is an essential trace element that plays a role in protection from oxidative damage as well as hair follicle morphogenesis.

Cysteine and Methionine Cysteine, along with methionine, is one of the main constituents of hair, contributing to the formation of keratin for a quarter of the total. The use these amino acids promotes the repair of structural lesions and slows down hair loss. Moreover, they contribute to the normal processes of contrast to the oxidative stress that can lead to hair loss, favoring the production of natural antioxidants such as glutathione.

Vitamin C Vitamin C is an essential cofactor in the enzymatic step forming collagen and in supporting the cross-linking of keratin fibers. Moreover, it is a potent water-soluble antioxidant, helpful in contrasting the oxidative stress responsible of the hair follicles degeneration.

Vitamin B5 The role of vitamin B5 in hair loss is not clear. Probably, like the rest of the B vitamins, an improvement in cellular metabolism can also benefit hair.

Vitamin B6 Vitamin B6 is an important nutrient, acting as a cofactor for several enzymes. It plays a key role in skin development and maintenance, and more important it contributes in cysteine incorporation in hair cells.

Biotin Biotin is an important cofactor that contributes to the normal functioning of enzymes responsible for carboxylation. It has been shown that its deficiency can lead to skin rashes, conjunctivitis and alopecia. Its deficiency is rare, since intestinal bacteria can produce an adequate amount of biotin.

Niacin Niacin is an essential component for the body, contributes to the production of ATP and therefore to the correct energy support for the cells. Its deficiency leads to pellagra, with phenomena such as dermatitis, hyperpigmentation, diarrhea, weakness and hair loss.

Taurine Taurine is a beta-amino acid that, in addition to having an important role in the proper functioning and maintenance of our nervous system and muscle structure, seems to be able to counter androgenetic alopecia, limiting the process of follicular atrophy.

Dietary Supplements for Hair Loss Treatment Part-II

Folic Acid

Folate is a water-soluble B vitamin and includes naturally occurring food folate and folic acid (fully oxidized monoglutamate). Folate is a coenzyme in the synthesis of nucleic acids and in amino acid metabolism.

B Group Vitamins

Other B group vitamins include thiamine (B1), riboflavin (B2) and vitamin B12 which in general, help to keep hair healthy. There are no scientific studies that directly correlate these vitamins with the reduction of hair loss, but it is reasonable to assume that, given their extreme importance in terms of numerous biochemical processes, these may have, albeit to a lesser extent, a role also in growth and hair care.

Table 2 : The role of micronutrients in non-scarring alopecia and premature graying of hair4 Micronutrients

TE/AGA AA Premature hair graying ACP outcome study grading

Vitamin D Study results are conflicting, but most authors agree on supplementing vitamin D in patients with hair loss and vitamin D deficiency

Several studies showed an association between AA and low vitamin D levels Correction of vitamin D deficiency improves AA outcome and enhances response to treatment

Screening for deficiency and supplementation are recommended

Moderate in all studies

Vitamin C Crucial in patients with hair loss associated with iron deficiency

Vitamin E

Data not available

Few studies, thereby precluding recommendations

Conflicting data, thereby precluding recommendations

Data are not available Very low in AA Studies

Iron/Ferritin

Most authors agree on iron supplementation in patients with iron or ferritin deficiency and hair loss

Iron deficiency reported in female patients, likely coincidental

Data are not available Moderate in AA studies

Screening for deficiency and supplementation are recommended

Moderate in all studies

Zinc

Data are not homogenous and findings are too inconsistent to recommend screening

Selenium Toxicity can cause hair loss. There are no data to recommend screening

Most studies revealed low serum levels in AA Evidencebased information on efficacy of zinc supplementation in AA is lacking

No data to provide recommendations

Data are not available Moderate in TE/AGA and AA studies

Screening for deficiency and supplementation are recommended

Low in TE/ AGA and premature graying of hair studies

October 202230 Hair Loss Treatment

Riboflavin

Deficiency can cause hair loss.

Data are too scarce to recommend screening

Biotin Biotin levels can be low in patients complaining of hair shedding

Efficacy of supplementation not supported by evidence-based trials

Exogenous biotin interferes with some laboratory tests, creating false negative or false positive results

Folic acid/Vitamin B12 Data are not sufficient to recommend screening and supplementation

Data are not available Data are not available Very low in TE/ AGA studies

Vitamin A Hypervitaminosis A causes hair loss

Screening is recommended in selected cases

No studies on biotin as monotherapy

Data are not available Low and very low in TE / AGA studies

A few studies suggest that the levels of folate or vitamin B12 might modify progression of AA

Data are scarce for recommending supplementation

Screening for deficiency and supplementation are recommended

-Low in TE/AGA studies Moderate in AA and in premature graying of hair studies

Data are not available Data are not available Low and very low in TE/AGA studies

AA alopecia areata, AGA androgenetic alopecia, TE telogen effluvium, ACP american college of physicians

Conclusion

Traditional nutrients and several commercialized food supplements can help the patient to counteract and reduce hair loss, compensating for possible alterations and nutritional deficiencies that in the long run could accentuate or accelerate the loss of hair. The use of food supplements or the normal intake of vitamins and minerals, together with a healthy lifestyle and a balanced diet, can contribute to the well-being of everyone. These recommendations are essential in the treatment of important pathologies, and at the same time, they are important for dealing with minor pathologies such as hair loss.2

Multiple factors contribute to hair loss, including genetics, hormones, environmental exposure, medications, and nutrition. Treatment of hair loss requires a multimodal approach and the use of CAM (complementary and alternative medicine) may provide added benefits. Vitamins and trace minerals are vital to the hair follicle cycle and maintain homeostasis as enzyme cofactors, hormones, antioxidants, and immuno modulators.6

Indeed, the use of specific vitamins and minerals for the treatment of hair loss is often based on popular traditions or commercial reasons, and several nutrients are

inserted into the dietary supplement composition to adhere to the rule of "one size fits all". The nonpathological treatment of hair loss requires an in-depth analysis of the nutritional deficiencies of each individual in order to restore the biological functions of hair and to reach the normal physiological conditions.2

References

1. Braun N, Heinrich U. What Can Complex Dietary Supplements Do for Hair Loss and How Can It Be Validly Measured—A Review. Applied Sciences. 2020; 10(14):4996. https:// doi.org/10.3390/app10144996

2. Labrozzi A (2020) Nutrients in Hair Supplements: Evaluation of their

Dietary Supplements for Hair Loss Treatment Part-II

Function in Hair Loss Treatment. Hair Ther Transplant 10:150.

3. Ablon G. A 3-month, randomized, double-blind, placebo-controlled study evaluating the ability of an extrastrength marine protein supplement to promote hair growth and decrease shedding in women with selfperceived thinning hair. Dermatol Res Pract. 2015;2015:841570. doi: 10.1155/2015/841570. Epub 2015 Mar 25. PMID: 25883641; PMCID: PMC4389977.

4. Almohanna HM, Ahmed AA, Tsatalis JP, Tosti A. The Role of Vitamins and Minerals in Hair Loss: A Review. DermatolTher (Heidelb). 2019 Mar;9(1):51-70. doi: 10.1007/s13555018-0278-6. Epub 2018 Dec 13. PMID: 30547302; PMCID: PMC6380979.

5. Guo EL, Katta R. Diet and hair loss: effects of nutrient deficiency and supplement use. DermatolPract Concept. 2017;7(1):1-10. Published 2017 Jan 31. doi:10.5826/dpc.0701a01

6. Hosking AM, Juhasz M, AtanaskovaMesinkovska N. Complementary and Alternative Treatments for Alopecia: A Comprehensive Review. Skin Appendage Disord. 2019 Feb;5(2):7289. doi: 10.1159/000492035. Epub 2018 Aug 21. PMID: 30815439; PMCID: PMC6388561.

7. Munkhbayar S, Jang S, Cho AR, Choi SJ, Shin CY, Eun HC, Kim KH, Kwon O. Role of Arachidonic Acid in Promoting Hair Growth. Ann Dermatol. 2016 Feb;28(1):55-64. doi: 10.5021/ad.2016.28.1.55. Epub 2016 Jan 28. PMID: 26848219; PMCID: PMC4737836.

8. Le Floc'h C, Cheniti A, Connétable S, Piccardi N, Vincenzi C, Tosti A. Effect of a nutritional supplement on hair loss in women. J CosmetDermatol. 2015 Mar;14(1):76-82. doi: 10.1111/ jocd.12127. Epub 2015 Jan 8. PMID: 25573272.

9. Hayk S. Arakelyan‘Huys’ International JV Corporation • Interactive Clinical Pharmacology, Treatment Tactics,General Medicine and Clinical Research.

Infants, young children finally get relief from eczema's terrible itch

Eczema, Eczema, also known as atopic dermatitis, is a chronic inflammatory skin disorder characterized by red, dry, often oozing skin and itch that can profoundly affect the lives of affected patients and their families.The first study to treat moderate-to-severe eczema in infants and children 6 months to 5 years old with a biologic drug (monoclonal antibody) rather than immune-suppressing medications shows the drug was highly effective in reducing the signs and symptoms of moderate-to-severe eczema. More than half of children had at least a 75% reduction in signs of eczema and itch. Kids slept through night for first time instead of scratching. Parents saw children's personalities change as they were able to lead a normal life, report researchers involved in a new multisite phase III study.

During the past few years, dupilumab isa new medication which is the first "biologic" drug to treat eczema in a targeted manner, meaning a narrow attack on just what scientists have found is causing the manifestations of the disease in skin. This medication was found to be effective and safe in studies with adults, then adolescents, then other school-aged children. A 16-week course of dupilumab, a medication that targets a key immune pathway in allergies, resulted in more than half the children having at least a 75% reduction in signs of eczema and highly significant reductions in itch with improved sleep. This is the first large-scale, randomized, placebo-controlled trial of a monoclonal antibody in any skin disease, including eczema, in children as young as 6 months. Preschoolers who are constantly scratching, awake multiple times a night with their parents, irritable and markedly curtailed in their ability to do what other children their ages can do improved to the extent that they sleep through the night, change their personalities and have a normal life as babies and children should, researcher said.

The ability to take this dupilumabwill significantly improve the quality of life for infants and young children who suffer tremendously with this disease. As a result of this study, this medication is now available to infants and preschoolers as young as 6 months of age. It has "an outstanding safety profile" and does not even require any laboratory tests before starting the medication, researcher said. As a result of the study, scientists and physicians can start to better understand the relationships between eczema and a variety of allergic disorders and can consider the possibility of using this medication for other disorders that affect these very young children.

Sensory Neurons in Human Skin Play Key Role in Pigmentation

Our skin forms the physical boundary between us and the outside world, yet it still holds a surprising number of secrets. Now, researchers have discovered that sensory nerve cells in our skin do more than just help us feel our way around.A research group has found that sensory neurons play an important role in human skin pigmentation and physiology. Specifically, the neurons secrete a protein known as Repulsive Guidance Molecule B (RGMB), which stimulates melanocytes. This study could lead to the development of new drugs to treat pigmentation disorders.

A researchrevealed that sensory neurons in human skin play an important role in pigmentation. Pigmentation in our skin is caused in part by a group of substances known as melanin, which are produced by skin cells called melanocytes. When melanocytes are damaged or reduced in number, this leads to either increased or limited melanin production, resulting in pigmentation disorders. The researchers explored the relationship between sensory neurons and melanocytes, and found that there was a greater degree of contact between them in skin color patch tissue than control tissue. When cultured with neurons, melanocytes were also found to have higher pigmentation and an increased survival rate. Melanocytes cultured in growth media that had been conditioned with sensory neurons showed increased survival, as well as longer dendrites, these effects were specific to melanocytes. Additionally, researchers identified proteins secreted by sensory neurons, including Repulsive Guidance Molecule B (RGMB). They discovered that melanocyte survival and darkness is promoted by RGMB.

The study revealed that sensory neurons play a role in modulating a number of features of human melanocytes via the secretion of RGMB, which is a key factor that stimulates melanocytes. The study results highlight how important sensory neurons are to skin pigmentation and physiology.The results of this study could lead to the development of new drugs for use with current therapies by enabling the discovery of previously unknown molecules and mechanisms that include RGMB.