The Aestheticians Journal | February 2022 issue | E-Journal by The Aestheticians Journal

Total Pages : 36 February 2022 Vol 14* Issue 12 100

Acrokeratosis Verruciformis of Hopf – At An Unusual Site Aesthetic Secrets of Your Own Blood Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I

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Clinical Dermatology: Aspects of Clinical Practice Dermatology is the science that is concerned with the diagnosis and treatment of diseases of the skin, hair and nails. A dermatologist is the medical expert we should consult if we have any significant problem with our skin. Research in Clinical Dermatology addresses all aspects of clinical practice and fundamental understanding of dermatology and skin care practice through the rapid publication of highquality original research, systematic reviews, meta-analyses and technology reports covering all aspects of the management of dermatological conditions. Some common skin diseases mainly superficial mycoses, viral disorders, acne, androgenetic alopecia etc. There is a great need for standardized recommendations on the treatment of the commonest skin disorders and, eventually, on preventive measures that would take into account the epidemiological characteristics and constraints in developing areas. This issue has articles on Acrokeratosis verruciformis of hopf – at an unusual site,Aesthetic Secrets of Your Own Blood, Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient, Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre, Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation. - Dom Daniel Executive Editor & Publisher

Published for the period of February-2022

February 2022

07 Acrokeratosis Verruciformis of Hopf – At An Unusual Site Dr. Patel Trisha B, 3rd Year Resident Dr. Shah Aishni J, Senior Resident Dr. Patel Jalpa K, 2nd Year Resident Dr. Vora Rita V, Senior Professor and HOD Department of Dermatology, Shree Krishna Hospital, Karamsad

Aesthetic Secrets of Your Own Blood Dr. Sowmya N. Dogiparthi, MD DVL, FAM Associate Professor, Department of Dermatology Shri Sathya Sai Medical College and Research Institute (SSSMC & RI), Chennai

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient Dr. Dheemant M, Consultant Dermatologist Aastha Ortho-Derma Centre, Bengaluru Dr. Hari Kishan Kumar Y, Professor Department of Dermatology, Venereology & Leprosy Rajarajeswari Medical College & Hospital, Bengaluru

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I Dr. Rajesh Rajagopalan, MD., DNB., MNAMS Professor and HOD, Department of Skin, STDs & Leprosy Government Erode Medical College, Erode, Tamilnadu

Dr. V. Sudha, MD., DV, Professor and HOD, Department of Skin, STDs & Leprosy ACS Medical College, Chennai

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation Dr. Sharad Chaurasia, PG Resident Dr. Ipshita Bhattacharya, PG Resident Dr. Paschal Dsouza, Professor Department of Dermatology, Venereology and Leprosy ESI-PGIMSR, New Delhi

February 2022

MITHCHELL AD

Editorial Board Dr. Vora Rita V

Dr. Dheemant M

Dr. Rajesh Rajagopalan

Dr. Patel Trisha B

Senior Professor and HOD Department of Dermatology Shree Krishna Hospital, Karamsad

MD., DNB., MNAMS Professor and HOD Department of Skin, STDs & Leprosy Government Erode Medical College Erode, Tamilnadu

Dr. V. Sudha

MD., DV Professor and HOD, Department of Skin, STDs & Leprosy ACS Medical College, Chennai Retired Director, Professor and HOD Institute of Venereology, Madras Medical College, Chennai

3rd Year Resident Department of Dermatology Shree Krishna Hospital Karamsad

Dr. Shah Aishni J

Senior Resident Department of Dermatology Shree Krishna Hospital Karamsad

Dr. Paschal Dsouza

Dr. Patel Jalpa K

Dr. Hari Kishan Kumar Y

Dr. Sharad Chaurasia

Professor Department of Dermatology, Venereology and Leprosy ESI-PGIMSR, New Delhi

Professor Department of Dermatology, Venereology & Leprosy Rajarajeswari Medical College & Hospital, Bengaluru Director, Dr.Kishan’s Skin Care & Aesthetic Research Centre, Raja Rajeshwari Nagar, Bengaluru

Dr. Sowmya N. Dogiparthi

MD DVL, FAM Associate Professor, Department of Dermatology ShriSathyaSai Medical College and Research Institute (SSSMC & RI), Chennai Consultant - Apollo Hospitals, Chennai DermipureDermaclinic, Chennai

Consultant Dermatologist Aastha Ortho-Derma Centre Bengaluru

February 2022

2nd Year Resident Department of Dermatology Shree Krishna Hospital Karamsad

PG Resident Department of Dermatology, Venereology and Leprosy ESI-PGIMSR, New Delhi

Dr. Ipshita Bhattacharya PG Resident Department of Dermatology, Venereology and Leprosy ESI-PGIMSR, New Delhi

Acrokeratosis Verruciformis of Hopf – At An Unusual Site

Acrokeratosis Verruciformis of Hopf – At An Unusual Site Dr. Patel Trisha B

3rd Year Resident Department of Dermatology Shree Krishna Hospital Karamsad

Dr. Shah Aishni J

Senior Resident Department of Dermatology Shree Krishna Hospital Karamsad

Dr. Patel Jalpa K

2nd Year Resident Department of Dermatology Shree Krishna Hospital Karamsad

Dr. Vora Rita V

Senior Professor and HOD Department of Dermatology Shree Krishna Hospital Karamsad

Keywords: Acrokeratosis Verruciformis of Hopf, Forehead, Middle age Abstract Acrokeratosis verruciformis of Hopf (AKV) is a rare disorder of keratinization

inherited in an autosomal dominant fashion. It usually occurs at birth or in early childhood and manifests in two forms, namely classical and sporadic AKV. It is characterised by multiple flesh-colored or lightly pigmented flat or convex warty papules over February 2022

Acrokeratosis Verruciformis of Hopf – At An Unusual Site

dorsa of hands, feet, knees, elbows, and forearms. We report an atypical sporadic case of AKV on forehead with no acral involvement in a middle aged male. Introduction Acrokeratosis verruciformis of Hopf (AKV) is a rare autosomal dominant cutaneous disorder first described by Hopf in 1931. It is present at birth or appears in early childhood, but the onset may be delayed upto the fifth decade. It affects both sexes but is more common in males as compared to females with a ratio of 3.8:1. It is characterised by multiple, flat topped skin coloured, dull red to brown colored, keratotic papules resembling plane warts. The lesions are basically seen on the dorsal aspect of hands and feet but may extend on to knees, elbows, forearms and other parts of the body. We report a case of 56 years old male with lesion of AKV on forehead without acral involvement.

with mild perivascular lymphocytic infiltration. There was elevation of the epidermis resembling church spires. (Fig 3) The findings confirmed the diagnosis of Acrokeratosis Verruciformis of Hopf. The patient was treated with weekly cryotherapy using liquid nitrogen, after which the lesions subsided.

Case Report A 56-year-old male presented to the skin OPD with multiple raised skin lesions over forehead since 3 months. The lesions then progressed to involve the central part of anterior scalp. There was complaint of itching associated with the lesion. He had similar lesion 5 years ago which subsided with some topical medication. There was no family history of similar lesions. On cutaneous examination numerous skin-coloured to hyperpigmented flat-topped papules, measuring 0.2–0.3 cm over centre of forehead, upto the vertex. (Fig 1 & 2) A single, well defined nodule with few scales present over the forehead. Hands and feet were not affected and no nail involvement was seen. No orogenital lesions. Routine investigations were within normal range. Skin biopsy showed hyperkeratosis with mild acanthosis with mild papillomatosis. The rete ridges were slightly elongated 8

February 2022

Fig-1&2: skin-coloured to hyperpigmented flat-topped papules, measuring 0.2–0.3 cm over centre of forehead, up to the vertex.

infiltration. There was elevation of the epidermis resembling “church spires”(H&E Stain,40 X) Discussion Acrokeratosis verruciformis (AKV) of Hopf is a rare genodermatosis having keratinization disorder which was first described by Hopf in 1931. It is inherited in an autosomal dominant manner with ATP2A gene mutation (Ca+ ATPase family). The same inheritance is observed in Darier’s disease also. [1,2] Familial nature of the disease was described by Niedleman and Mckusick.[3] Classical AKV is seen at Birth or in childhood (Classical AKV) and Sporadic AKV may present till fifth decade of life.[4] Similar cases in the family are usually not found as it has an autosomal dominant pattern of inheritance with incomplete penetrance. Sporadic cases with later onset like in our case have also been reported.[5] It affects both sexes but is more common in males with male:female ratio of 3.8:1. [1] Characteristic findings of AKV include asymptomatic, numerous, flat - topped, polygonal, hyperkeratotic, occasionally verrucous papules are present on the distal part of the extremities, predominantly on the dorsal aspects of the hands and feet. The brownish to skin-colored lesions have hard consistency, and its friction can produce vesicles.[5] Small or isolated papules may develop on the knees, elbows, forearms and also on other parts of the body. The sebaceous areas like forehead, scalp, flexures and the oral mucosa are usually never involved [1, 6, 7] but in our case scalp involvement was seen. In one of the case report by Rege V L et al. they reported the spread of AKV from extremities to trunk and face. [8]

Fig-3: Hyperkeratosis with mild acanthosis with mild papillomatosis. The rete ridges were slightly elongated with mild perivascular lymphocytic

Interruptions of the dermal ridges in the finger pads and palms, identical to those seen in Grover, Galli–Galli, and Darier’s diseases, are another rather

Acrokeratosis Verruciformis of Hopf – At An Unusual Site

common findings in AKV, but not seen in our case.[9] Nails may be whitish and thickened and have longitudinal ridges breaking at the distal edge. Palmar and plantar keratoses have been reported in classical AKV, [7,10] but not in sporadic AKV. ATP2A2 gene mutations, P602L mutation within the ATP-binding domain of ATP2A2 in classical AKV, A698V codon change in ATP2P2 have also been reported to cause AKV. AKV shows characteristic histopathological features that include papillomatosis (circumscribed epidermal elevations known as “church spires”), acanthosis, hyperkeratosis, and hypergranulosis without parakeratosis. Darier’s disease, AKV, epidermodysplasia verruciformis, plane warts, and seborrheic keratoses can be considered as differential diagnosis of AKV. All these conditions can be differentiated by histopathological findings from biopsy. DD and AKV are believed to be allelic to each other due to the occurrence of similar gene defect in both the diseases.[11] and their co-existence of AKV and DD has been reported in past. [12] The difference between the two is that AKV shows excessive but normal keratinization, whereas in Dariers’s disease keratinization is defective. [13] The most effective treatment modality is superficial ablation. Retinoic acid is useful in some cases. Cryotherapy and destructive lasers such as CO2 or neodymium-doped yttrium aluminium garnet have also been tried. The lesions persist throughout life and tend to increase on sun exposure. Cases with malignant transformation of AKV have also been seen. One of the case report suggests a possible linkage of AKV and nevoid basal cell carcinoma syndrome.[14] Conclusion AVK is commonly found on hand, foot, knees, elbows and forearms.

Occurance of AKV in middle age, with no family history, at an atypical site is a rarity as in our case. Hence we present this case, to show that there are chances of occurrence of AKV at such atypical sites and also how histopathological correlation becomes of utmost importance in diagnosis. So that the probability of AKV over forehead should not be neglected and to show the importance of histopathology in making such a rare diagnosis.

Dermatol 1966;93:305-10.

References

in AcrokeratosisVerruciformis of Hopf. J Turk

1. Ramesh M, Ramya N, MGGopal, Sharath

11. Dhitavat J, Macfarlane S, Dode L, Leslie N, Sakuntabhai A, MacSween R, et al. Acrokeratosisverruciformis of HOPF is caused by mutation in ATP2A2: Evidence that it is allelic to Darier’s disease. J Invest Dermatol 2003;120:229-32. 12. Piskin S, Saygin A, Doganay L, Kircuval D, Gurkan E. Coexistence of Darier’s disease and

acrokeratosisverruciformis

Hopf.

Yonsei Med J 2004;45:956-9. 13. Kalic B, Ozgun E. Isotretinoin treatment AcadDermatol 2013;7(3):1373c3.

BC, Nandini AS. Acrokeratosisverruciformis

14. Humbert P, Laurent R, Faivre B,

of Hopf: An association with polymorphic

Agache P. Nevoid basal cell carcinoma

light eruption. JEMDS 2013;2(48):9310-4

syndrome and acrokeratosisverruciformis.

2. Potekar RM, Bhaswanth P, Ambica C, Arora S, Palur K. JKIMSU 2015;4(4):124-5. 3.

Niedleman

ML,

McKusick

Occurrence of two rare inherited autosomal dominant conditions in the same patient. Dermatologica 1990;180:169-70.

VA.

Acrokeratosisverruciformis (Hopf).A followup study. Arch Dermatol 1962;86:779-82. 4. Mohsin A. Acrokeratosis Verruciformis of Hopf. Available from: http://www.emedicine. com/derm/topic7.htm. [Last accessed on 2004 Mar 02]. 5. Bang CH, Kim HS, Park YM, Kim HO, Lee JY. Non-familial acrokeratosisverruciformisof Hopf. Ann Dermatol. 2011;23:S61–S63 6.

Salman

and

Osman

AcrokeratosisVerrucifomis of Hopf (Hopf Disease). J Infect Dis Ther 2014;2(1):128. 7. Panja RK. Acrokeratosisverruciformis (Hopf)--A clinical entity? Br J Dermatol. Jun 1977;96(6):643-52. 8. Rege V L, Hede R V, Nadkarni N S. Acrokeratosisverruciformis of HOPF. Indian J DermatolVenereolLeprol 1992;58:95-8. 9. Raff M, Szilvassy J. Specific dermatoglyphic patterns: A characteristic manifestation of acantholyticdyskeratoticdermatoses. J Am AcadDermatol 1989;21 (5 Pt 1):958-60. 10. Herndon JH, Wilson JD. Acrokeratosis verruciformis (Hopf) and Darier’s disease. Genetic evidence for a unitary origin. Arch February 2022

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February 2022

Aesthetic Secrets of Your Own Blood

Aesthetic Secrets of Your Own Blood Dr. Sowmya N. Dogiparthi

MD DVL, FAM Associate Professor Department of Dermatology Shri Sathya Sai Medical College and Research Institute (SSSMC & RI), Chennai Consultant - Apollo Hospitals, Chennai Dermipure Dermaclinic, Chennai.

“The Hair brings one’s self-image into focus;

Hamilton Classification of Male Pattern Hair loss includes:

It’s a crown that can never be taken off and

Type I: There is an absence of bilateral recessions along the anterior border of the hairline in the frontoparietal regions.

An expression of self-confidence” - Dermipure Dermaclinic In order to know when to start procedures for hair growth, one needs to understand the patterns of hair loss in both male and female. From early fronto -temporal recession to the stage of residual occipital band, patterned hair loss is the most common cause of hair loss seen in both the sexes after puberty. Typically presenting with progressive thinning, miniaturization, and loss of hair at the affected sites. Researchers have proposed multiple different classification systems for patterned hair loss in both males and females based on the evolutionary stage of hair loss. The commonest classification being Norwood Hamilton’s for male and Ludwig’s classification for females.

Type II: The frontotemporal recession of hairline does not extend further than 2 cm anterior to the midcoronal line. Type III: The frontotemporal recession of hairline extends further than type II and may reach the midcoronal line. Type IV: The frontotemporal recession of hairline has receded beyond the midcoronal line. Type V: The area of denudation includes the vertex. Hair loss more severe than type VA cannot be distinguished from types VI or VII.

February 2022

Aesthetic Secrets of Your Own Blood

platelets/ml. Platelets play a central role in tissue regeneration. The PRP is obtained from the blood of patients before centrifugation. After centrifugation and according to their different density gradients, the separation of blood components (red blood cells, PRP, and platelet-poor plasma [PPP]) follows.

Figure 1: Hamilton Classification of Androgenetic Alopecia (Male pattern baldness).

Similarly, Ludwig classification consisted of three grades of hair loss for females, which include: a. Grade I: Perceptible thinning of the hair on the crown, limited in the front by a line situated 1-3 cm behind the frontal hairline.

For years PRP is successfully being used in dermatology, plastic surgery, aesthetic medicine, orthopaedic medicine and dentistry.

Platelet Poor Plasma

b. Grade II: Pronounced rarefaction of the hair on the crown within the area seen in Grade I. c. Grade III: Full baldness within the area seen in Grades I and II. In females there is preservation of the frontal fringe despite progressive centrifugal loss over the top of the scalp.

Platelet Rich Plasma

Red Blood Cells Figure 3: Platelet Rich Plasma: The sedimentation Ratio of PRP

Figure 2: Ludwig Classification of female pattern hair loss (Female pattern baldness).

At what stage of hair loss are procedures required for Hair growth? For Grade II to early grade III patterned hair loss in both sexes a non surgical procedure known as Platelet Rich plasma therapy can be done as an adjuvant therapy along with topical and systemic management to stimulate hair growth. Platelet Rich Plasma Therapy platelet-rich plasma (PRP) is defined as an autologous blood product containing a platelet concentration higher than the baseline level of 150,000--350,000 12

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4a : RBC pellet at bottom.

Aesthetic Secrets of Your Own Blood

Table 1: Indications of PRP in Dermatology Androgenetic Alopecia Alopecia Areata Skin Rejuvenation Acne scars and contour defects Wound ulcers, Connective tissue disease associated ulcers Striae distensae Lipodermatosclerosus Lichen Sclerosus Preparation of PRP 1. Obtain whole blood by venipuncture in acid citrate dextrose (ACD) tubes. 4b: Clearer image of RBC sedimentation Figure 4a and b: Platelet Rich Plasma obtained after Centrifuge: Notice the RBC pellet sedimentation at the bottom of the tube. Types of PRP 1. Pure Platelet-Rich Plasma (P-PRP) or leucocyte-poor PRP products are preparations without leucocytes and with a low-density fibrin network after activation. 2. Leucocyte- and PRP (L-PRP) products are preparations with leucocytes and with a low-density fibrin network after activation.

2. Do not chill the blood at any time before or during platelet separation. 3. Centrifuge the blood using a ‘soft’ spin at 1500rpm for 15mins. 4. Transfer the supernatant plasma containing platelets into another sterile tube (without anticoagulant). 5. Centrifuge tube at a higher speed (a hard spin) at 3500rpm for 15mins to obtain a platelet concentrate. 6. The lower 1/3rd is PRP and upper 2/3rd is platelet-poor plasma (PPP). At the bottom of the tube, platelet pellets are formed. 7. Remove PPP and suspend the platelet pellets in a minimum quantity of plasma (2-4 mL) by gently shaking the tube. This technique is called a double spin method. There are also other techniques such as single centrifugation or automatic methods, however that last one is much more expensive than the others, and is rarely used in practice.

3. Pure platelet-rich fibrin (P-PRF) or leucocyte-poorplatelet-rich fibrin preparations are without leucocytes and with a high-density fibrin network. These products only exist in a strongly activated gel form, and cannot be injected or used like fibrin glues. 4. Leucocyte- and platelet-rich fibrin (L-PRF) are preparations with leucocytes and with a high-density fibrin network. Figure 5: Preparation of PRP for Scalp (Steps of PRP).

February 2022

Aesthetic Secrets of Your Own Blood

The PRP Priming Diet and Fluid Intake: Advice the patient to increase intake of fluid the day before the procedure by simply drinking 2 glasses of water in the morning, 2 glasses at lunch, and 2 glasses at dinner, in addition to the normal intake of water. Day of Procedure: • Should shower in the morning of the treatment and wash the hair very thoroughly using your regular shampoo.

patient head end of the bed should be raised at 45 degree angle; the injection process is meticulous with injections beginning across the scalp, approximately at every half inch over the area of thinning hair. A dermaroller of size 0.5mm to 1.00mm needles can be gently rolled over the scalp, to allow better penetration of the injection. The entire procedure takes less than a half hour. There is better penetration entire procedure takes is less than a half minimal downtime,ofifthe anyinjection. needed aThe warm shower in the evening hour. There is minimal downtime, if any needed a warm shower the evening recommended post procedure; as the hot temperature will enhance inblood flow isand recommended post procedure; circulation throughout the scalp.as the hot temperature will enhance blood flow and circulation throughout the scalp.

Table 2: Mechanism of Growth factors in PRP for Hair growth

PDGF

TGF-β VEGF

Inhibits hair growth in vitro – Hair-cell proliferation and regeneration – Expressed in DP cells in the anagen phase – Probably regulates perifollicular angiogenesis – Increases perifollicular vessel size during the anagen growth phase.

• Should not apply sprays, gels, or any other styling products to your hair.

EGF

Angiogenesis stimulator – Hair-cell proliferation and regeneration

• Should eat a normal breakfast or lunch the day of PRP session.

HGF FGF

Angiogenesis stimulator – Increases hair growth by inducing the anagen phase of HF – Promotes DP cell proliferation – Increases the HF size in mice – Angiogenesis stimulators

IGF-1

– Increases hair growth – Maintains HF growth in vitro – Angiogenesis stimulator

• Should drink a bottle of water (500 mL) at least 2 hours before the session. Mechanism of Action in Hair Growth The growth factors and the bioactive molecules present in PRP promote 4 main actions in the local environment of the administration, such as proliferation, migration, cell differentiation, and angiogenesis; refer to table 2. Once the scalp is cleaned; either topical anaesthesia 30 minutes prior to the procedure can be applied or frontal block at the time of procedure can be given to reduce the pain. Most patients get injections without any numbing, as there is minimal discomfort. However, cool air or vibrators maybe used to minimize pain. The patients head end of the bed should be raised at 45 degree angle; the injection process is meticulous with injections beginning across the scalp, approximately at every half inch over the area of thinning hair. A dermaroller of size 0.5mm to 1.00mm needles can be gently rolled over the scalp, to allow 14

– Increases hair growth – Vascularization – Angiogenesis stimulator

February 2022

Legend: PDGF, platelet-derived growth factor; TGF, growth Legend: PDGF, platelet-derived growth factor; TGF, transforming growthtransforming factor; VEGF, vascular endothelial growthvascular factor; DP, dermal papilla; EGF, epidermal growth factor; HGF, hepatocyte factor; VEGF, endothelial growth factor; DP, dermal papilla; EGF, epidermal growth factor; HGF, hepatocyte growth factor; FGF, fibroblast growth factor; IGF-1, insulin-like growth factor 1; HF, human follicle(s).

6a: before starting PRP. Photo courtesy: Dr Yogesh B

6b: After 4 sessions of PRP 3 weeks interval. Photo Courtesy: Dr.Yogesh B

Figure 6a and b: PRP for Androgenetic Alopecia

Aesthetic Secrets of Your Own Blood

proliferation, angiogenesis and cell migration. Matrix metalloproteinase proteins (MMP) are involved in aging process by degradation of collagen and other extracellular matrix (ECM) proteins, this mechanism can be used to benefit rejuvenation. They can help regeneration of dermis through omission of collagen fragments that are harmful to the dermal connective tissue, and so, provide an appropriate foundation for new collagen deposition.

7a: Before: Alopecia Areata of Chin.

As we all know; Hyaluronic acid absorbs water and makes hyaluronic acid matrix swell, which increases skin volume and turgor. It also promotes cell proliferation, extracellular matrix synthesis and helps to the adjustment of the collagen fibres diameter.

7b: After 4 sessions of PRP – 30 days Interval

Figure 7a and b: PRP injections for Alopecia Areata Platelet-rich rejuvenation

plasma

skin

The main facial treatments in aesthetic medicine are dermal stimulation and augmentation via non-surgical methods. When it comes to skin rejuvenation, the theory is that PRP, through various secreted growth factors and cytokines, may promote collagen production and fibroblast multiplying in damaged skin. Once injected into the target tissue, platelets are activated endogenously by coagulation factors following their attachment to special receptors on the cell surfaces, some intracellular processes are activated, that facilitate extracellular matrix (ECM) accumulation leading to improved cell proliferation and differentiation. Tissue regeneration results from cell

Another mechanism of PRP for skin rejuvenation, is through acceleration of hyaluronic acid production. Overall, it could enhance skin elasticity contributing to tissue rejuvenation through PRP. The platelets collected in PRP are activated by the addition of thrombin and/or calcium gluconate, which induces the release of these factors from alpha granules. Improvement in skin texture and tone is noticeable within 3 weeks. Full collagen regeneration requires 3 months. STEPS OF PRP IN SKIN REJUVENATION AND SCARS TREATMENT 1. Collection of blood : Withdraw approximately between 5 and 15ml of blood, from a vein in the arm. The vial is then sealed. 2. Centrifuge ( PRP Concentration) : Blood sample is then placed in a centrifuge machine. Platelets are activated to release the growth factors during this process,

stimulating their normal function properties for the healing of tissues. The centrifuge process takes place within 15 minutes. Second centrifuge process can be done in order to achieve a super concentrated PRP extract. This is done is to attain more growth factors in the concentration for the patient’s benefit which helps to achieve the best results in the shortest time possible. 3. Micro-needling: The patient’s skin should be cleansed, ready for the treatment application process. A numbing agent (cream or ointment) is applied to a patient’s face or other treatment area before the micro needling device is used for approximately 20 – 30 minutes. Use the device (DermaPen, DermaRoller or similar treatment device) gently to create tiny needle wounds (holes) in the skin. Depending on the treatment area Dermaroller/ pen needles size can vary from 0.5mm to 2.5mm. Gently glide the device over the area to be treated, in order to penetrate the outer layers of the skin (epidermis), approximately 2mm deep. It is this needling and the depth of it that results in the mild redness and swelling of the skin, which will normalize few days. The process of needling before applying the serum activates the build-up of collagen beneath the skin being treated. The stimulation of collagen quickly improves fine lines, skin texture and scars, priming the treatment area for the next step. 4. The PRP bit: The areas being treated (face, neck, décolletage etc. which can all be safely done in one session if desired): coat the treated (micro – needled) area with the now developed PRP concentration, through a re-needling back into the skin with the micro February 2022

Aesthetic Secrets of Your Own Blood

needling device gently in strokes to allow penetration of the concentration.

7. Can provide outstanding results either with or without the use of underlying fillers.

The growth factors work quickly, stimulating multi-potent stem cells which already exist in the skin. This ‘tricks’ the cells into ‘thinking’ the skin surface is injured (triggering an acceleration of the healing cascade) and the generation of new tissue. The skin responds to this acceleration action by plumping up and thickening, getting to work on those wrinkles, lines or scars.

Table 3: Contraindications for PRP procedure Contraindications for plateletrich plasma treatment: 1. Pregnancy and breast-feeding. 2. Under 18 years of age or over 65 years. 9a: Before: Note the Post Infammatory

3. Smoking of tobacco products.

pigmentation.

4. Immunosuppression.

Skin will begin to feel tighter shortly after the session as its texture, colour and tone start to adjust. Skin will feel softer too and will progressively improve in the weeks to come.

5. Emotional illnesses

instability,

mental

6. Disorders in the coagulation system. 7. Number of platelets below 100 000 /ul. 8. Purpura 9. Some infectious diseases. 10. Use of anticoagulants. 9b: After 3 sessions, 4 weeks interval

Figure 9a and b: Postacne pigmentation with dyschromia: treatment with dermaroller and PRP. 8a: Before Procedure: photo courtesy-

Advantages of PRP Rejuvenation 1. Uses body’s own natural platelets so there is no risk of allergic reaction

Dr Yogesh B

2. Natural collagen is formed in response to the presence of the activated platelets 3. PRP is ideal for the patient who does not want any synthetic fillers 4. There is little to no swelling, bruising or lumping as the fluid assimilates in the natural skin environment

8b: After 6 sessions 4 weeks interval between sessions

5. PRP can be used to enhance Laser procedures for faster and improved healing 6. PRP Therapy is equally as effective in men as in women

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11. Use of NSAIDs within 10 days before the planned treatment. 12. Use of corticosteroids. 13. Susceptibility to keloids. 14. Hemoglobin levels below 12 g / dl in women and 14 g / dl in men. 15. Active inflammation at the site of the planned surgery. 16. Some chronic diseases: chronic renal failure, diabetes, hepatic insufficiency / hepatitis, cardiovascular failure.

Aesthetic Secrets of Your Own Blood

Table 4: After Care of PRP for skin (Rejuvenation /Scar treatment) • Continue to avoid anti-inflammatory medications for 3 days after procedure (if possible for 7 days). • A gentle cleanser and tepid water to cleanse the face for the following 72 hours. • A gentle moisturizer is used as needed. • Excessive sun exposure, including tanning booths to be avoided, a broadspectrum sunscreen daily of SPF 30 or higher should be applied. • Avoid warm environments (i.e., hot tubs, jacuzzis, steam rooms, hot yoga, saunas, etc.) for 3 days post treatment.

References 1. Mehta S, Watson JT. Platelet rich concentrate: basic science and current clinical applications. J Orthop Trauma. 2008;22:432-438. 2. Redaelli A, Romano D, Marciano A. Face and neck revitalization with platelet-rich plasma (PRP): clinical outcome in a series of 23 con¬secutively treated patients. J Drugs Dermatol. 2010;9:466-472. 3. Shin MK, Lee JH, Lee SJ, et al. Plateletrich plasma combined with fractional laser

• By day two or three, the skin may feel a bit dry. This is normal and will resolve on its own.

therapy for skin rejuvenation. Dermatol Surg.

• Return to skin care products and makeup when skin is not irritated, typically 4 -5 days after treatment. • One will begin to see improvements in the overall texture and tone shortly after the treatment, but the overall effects take up to 3 months, for optimal improvement.

4. EBISAWA K., KATO R., OKADA M.,

• New collagen formation takes 4-6 weeks to develop; counselling to the patient. • It is recommended to have a minimum of 3 treatments, 4 weeks apart for maximum benefit. PRP as an add-on therapy to laser acne scar treatments, to deliver the best results possible to our acne scar patients.

2012; 38: 623-630.

KAMEI Y., MAZLYZAM A.L.,NARITA Y., KAGAMI H., UEDA M. Cell therapy for facial anti-aging.Med. J. Malaysia. 2008 Jul ; 63 Supp A : 41. 5. Beitzel K, Allen D, Apostolakos J, et al. US definitions, current use, and FDA stance on use of platelet-rich. 6. Plasma in sports medicine. J Knee Surg. 2015 Feb;28(1):29-34. 7. Alves R, Grimalt R. A Review of Platelet-

Table 5: After care – Post PRP Scalp procedure

Rich Plasma: History, Biology, Mechanism of Action, and Classification. Skin Appendage

1. For pain and discomfort – Anti-inflammatory agents to be prescribed

Disord. 2018 Jan;4(1):18-24.

2. Avoid vigorous exercise, sun and heat exposure for at least 2 days after treatment.

8. Dohan Ehrenfest DM, Rasmusson L,

3. Do not wet your hair for at least 3 hours after treatment.

Albrektsson T. Classification of platelet concentrates: From pure platelet-rich plasma (P-PRP) to leucocyte- and platelet-rich fibrin

4. Should take a hot shower and wash your hair that evening, after the treatment, to promote the effects of PRP.

(L-PRF) Trends Biotechnol. 2009;27:158–

5. Avoid saunas, steam rooms, swimming for 2 days after treatment.

9. Dhurat R, Sukesh M. Principles and

6. Avoid alcohol, caffeine, and smoking for 3 days after treatment. Smokers do not heal well and problems recur earlier and results may take longer.

Rich Plasma: A Review and Author’s

7. Avoid resuming Minoxidil, hair coloring, and straightening for 3 days. 8. Continue increased water intake the first week after your treatment. 9. Should not use blood thinning agents such as vitamin E, vitamin A, Ginko, Garlic, Flax, Cod Liver Oil, Essential Fatty Acids at least one week after treatment Acknowledgement Art courtesy by Dr. Mohan Ram Kumar

67.

Methods

Preparation

Platelet-

Perspective. J CutanAesthet Surg. 2014 Oct-Dec;7(4):189-97. 10.

Laver L, Marom N, Dnyanesh

L, et al. PRP for Degenerative Cartilage Disease: A Systematic Review of Clinical Studies. Cartilage. 2017 Oct;8(4):341-364. 11. Hussain N, Johal H, Bhandari M. An evidence-based evaluation on the use of platelet rich plasma in orthopedics—a review of the literature. SICOT J. 2017;3:57.

February 2022

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient Dr. Dheemant M

Consultant Dermatologist Aastha Ortho-Derma Centre, Bengaluru

Dr. Hari Kishan Kumar Y

Professor Department of Dermatology, Venereology & Leprosy Rajarajeswari Medical College & Hospital, Bengaluru Director Dr. Kishan’s Skin Care & Aesthetic Research Centre Raja Rajeshwari Nagar, Bengaluru Introduction Leprosy, a chronic infectious disease caused by the Mycobacterium leprae, continues to be one of the public health challenges for countries like India, which accounts for more than half of the world’s new leprosy cases. [1] Dysfunction of peripheral nerves resulting in skin anaesthesia is one of the salient clinical manifestations of leprosy, which further leads to disabilities, including ulcers. [2] Plantar ulcers are one of the commonest complications of leprosy leading to Grade 2 disability (G2D) and occur in about 10% to 20% of patients. [3] Recently launched global leprosy strategy of WHO aims to reduce the 18

February 2022

number of G2D among new cases. The current G2D rate stands at 1.7 per million populations, with India accounting for 39.8% of cases. [4] Plantar ulcers are typically painless and increase in size without healing for weeks to months. [5] Knowledge accrued from the study is expected to provide new leads for better care for plantar ulcers in leprosy. Managing chronic trophic ulcers is challenging. When all the conservative and medical methods fail, surgical management of ulcers may be the only ray of hope. Many Hansen’s patients are unable to cope with

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

the expenses in the treatment of non-healing trophic ulcers. There is a need for an economical as well as an effective mode to treat such ulcers. Cutaneous wound repair is a multifaceted process involving clot formation, cell migration, and finally dermal and epidermal reconstitution. [6]

Autologous non-cultured Epidermal Cell Suspension (ECS) has already gained popularity in stable vitiligo because of superior results, requirement of only smaller donor area, and is suitable to treat difficult areas. Like cultured keratinocyte allograft, autologous epidermal cell suspension stimulate the growth factors and extracellular matrix proteins. [7] Thus, if used in ulcers, it may promote migration or multiplication of acceptor keratinocytes and formation of extracellular matrix proteins. To prepare cultured keratinocytes for grafting, a minimum of 3-4 weeks is required, [8] whereas epidermal cell suspension is easily trypsinized and economically prepared in few hours.[7]

Methodology: After obtaining approval from the Institutional Ethics Committee, the method, expected outcome, variable results, and relapse were explained to the patient; informed consent was also taken. The procedure was performed on a chronic non-healing trophic ulcer of a Hansen’s disease patient under local anaesthesia in an outpatient setting. The ulcer size in terms of length, breadth and depth were measured. Basic investigations to find out the primary cause of the ulcer were done, including random blood sugar, pus culture and sensitivity, skin biopsy. Primary infection, was treated using antibiotics and surgical debridement was done. Procedure: Step 1 - Harvesting Epidermal Cell Suspension (ECS) (Figs. 1 and 2) The antero-lateral aspect of thigh was chosen as donor site. The parts were prepared and anaesthetized using topical anaesthesia; a mixture of Lidocaine 25mg and Prilocaine 25mg under occlusion, was applied for one hour. Ultrasplit thickness graft measuring 5x5 cm2 was then harvested from the donor site using a razor blade holding dermatome. The graft harvested was placed in 10ml Trypsin-EDTA (Trypsin-Ethylenediaminetetraacetic acid) solution with the epidermis facing upwards in a petri dish and incubated at 37°C for 50 minutes. After incubation, the graft was transferred to DMEM (Dulbecco’s Modified Eagle’s Medium) in another petri dish. Using blunt forceps and agitation, the epidermis was separated from the dermis. The cell suspension obtained was then transferred to a 15ml centrifuge tube.

Hair follicles (HFs) act as ulcer promoters.[9] The restoration of epithelium after injury takes place by migration of epithelial cells from the old epithelium adjoining an ulcer or by centrifugal migration from any HFs remaining within the ulcer.[10] Thus, follicular unit grafting into ulcer beds is feasible and represents a promising therapeutic alternative for managing non-healing chronic leg ulcers. [11] Hence, we took up this novel procedure combining autologous smashed follicular dermal grafts with epidermal cell suspension, which contributes to wound healing by being a source of follicular stem cells, epidermal keratinocytes, and dermal collagen.

Figure 1: Harvesting ultra-split thickness graft.

February 2022

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

Step 3- Dressing of Donor area Firm compression with dressing paraffin gauze dressing was applied over the donor area. Step 4- Application of Dermal Grafts and ECS to ulcer bed (Fig. 4) The mixture of smashed dermal grafts and ECS harvested above in the 15ml centrifuge tube was centrifuged at 3000 rpm for ten minutes. The pellet thus obtained was spread evenly over the ulcer bed. The ulcer bed was then covered with paraffin gauze and Johnson and Johnson 3M Dynaplast.

Figure 2: Graft is transferred to a petri dish containing Trypsin-EDTA and then incubated. The incubated specimen is then subjected vigorous agitation to separate epidermis and dermis. Step 2- Harvesting Dermal Grafts (Fig. 3) After taking graft for ECS, follicular dermal grafts were harvested using punches of size 2.5mm from the same donor site, as for the ECS procedure, spaced at least 5mm from each other, ensuring that each graft consists of a hair follicle. Number of grafts required were to be approximately two grafts per cm2 of ulcer area. The grafts were then transferred to a petri dish containing normal saline. Dermal grafts were minced with surgical blade number 15 to form smashed dermal grafts. The smashed dermal graft was transferred into the same 15ml centrifuge tube which contained ECS from step one.

Figure 3: (a) Harvesting follicular dermal grafts with biopsy punch. (b) Follicular grafts obtained after smashing.

February 2022

Figure 4: (a) Pellet thus obtained after centrifugation. (b) Application of smashed follicular dermal graft and ECS mixture to the ulcer bed.

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

Post-procedure instructions:

Statistical Analysis:

The patient was instructed to take complete rest and to avoid all vigorous physical activities for seven days. The patient was also prescribed oral antibacterial agents for five days.

Analysis was done using SPSS 26 software. Independent t-test was used and a P value of <0.05 was considered statistically significant.

Follow up: Dressing on both donor and recipient site was removed after seven days postsurgery and regular follow up was done with regular paraffin gauze and saline dressing at every week till 12 weeks and then once a month till 6th month or complete healing, whichever was earlier. Photographic assessment was done at every follow-up visit. Baseline and at every follow-up visit, wound area was measured by the formula Length x Width x 0.7854 (an ellipse is closer to a wound shape than a square or rectangle); and volume measured by Length x Width x Depth x 0.7854. [12] A percentage reduction of 100% in size of ulcer was defined as complete healing and anything less than that was considered as incomplete healing. Percentage of change in volume and area of the ulcer[11] = (Baseline measurement – Assessment day measurement) x 100% Baseline measurement

Results Area in the of ulcer The baseline area of the ulcer was 8.06 cm2. The area of ulcer with respect to baseline was 3.48 cm2 after 1 week of treatment, which reduced to 0.09 cm2 in 3 weeks, that later healed completely in 5 weeks (Table 1). Table 1: Area of ulcer at different study points. Time of follow up

Area of ulcer (cm2)

P value

Baseline

8.06

0.302

1st week

3.48

0.024**

2nd week

1.04

< 0.001**

3rd week

0.09

< 0.001**

4th week

0.04

< 0.001**

5th week

0.00

** P value < 0.05 = Significant

Figure 5: (a) Before procedure. (b) 1 week post procedure. (c) 3 weeks post procedure. (d) 5 weeks post procedure.

February 2022

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

Volume of the ulcer The baseline volume of the ulcer was 6.65 cm 3. The volume of ulcer with respect to baseline was 4.16 cm3 after 1 week of treatment, which reduced to 0.03 cm3 in 3 weeks, that later healed completely in 5 weeks (Table 2). Table 2: Volume of ulcer at different study points. Time of follow up

Volume of ulcer (cm3)

P value

Baseline

6.65

0.107

1st week

4.16

0.048**

2nd week

0.30

< 0.001**

3rd week

0.03

< 0.001**

4th week

0.01

< 0.001**

5th week

0.00

** P value < 0.05 = Significant Discussion: The technique involving ECS was invented to enable the possibility of treating larger wounds with a small piece of donor skin.[12] In a pilot study on the effect of autologous ECS in chronic nonhealing wounds by Shukla et al.,[7] 6 (40%) out of 15 patients had completely healed at 12 weeks, 1 patient (7%) at 16 weeks, and 2 patients (13%) at 20 weeks post procedure. In a study by De Angelis et al.,[13] on the use of a noncultured autologous ECS in chronic ulcers, complete ulcer healing, defined as 100% reepithelialization, was observed between 40 and 60 days in 14 patients (70%). At day 60 post procedure, 80% reepithelialization was present in 5 patients (25%),whereas 1 patient with concomitant psoriasis had 50% reepithelialization. In a study on follicular unit grafting in chronic nonhealing leg ulcers by Budamakuntla et al.,[11] a total of 15 patients with 17 ulcers were treated 22

February 2022

with follicular unit graft. The baseline mean area of the ulcer was 6.72 cm2 and baseline volume was 2.87 cm3. The final area of the ulcer at the end of 18 weeks after the procedure was 3.84 cm2 and the final volume was 1.21 cm3, which was statistically significant. In a randomized controlled study on HF containing punch grafts in chronic ulcers by Martínez et al.,[14] ulcer healing measured as the average percentage reduction, 18 weeks post intervention was significantly increased (P = 0.002) in the HF group with a 75.15% ulcer area reduction compared with 33.07% in the control group (nonhairy grafts). Nagaraju et al.,[15] in his study noted that in the technique of autologous smashed follicular dermal graft with ECS in 12 cases of chronic nonhealing ulcers, 41.6% of the ulcers healed within 4 weeks post procedure, and 100% ulcers had completely healed by the 8th week. Ulcers healed both from the periphery as well as in a centrifugal manner, Hypertrophic granulation tissue was seen in two of the regular normal saline dressing. The donor site in all cases showed complete healing by 7 days post procedure with mild pigmentation. No other adverse effect was noted in any case. The results from all the above studies infer that noncultured ECS is one of the better surgical modalities in treating chronic nonhealing ulcers as it seems to be an effective, simple, economical, and time saving method and larger area can be treated with smaller donor area. Similarly, hair follicular dermal grafting is a minimally invasive surgical procedure that appears to be effective as a therapeutic tool for chronic leg ulcers. Hence, epithelial cells from ECS, HFs, and collagen from dermis may enhance the ulcer healing process and reduce the duration of ulcer healing.

Conclusion Trophic skin ulceration in Hansen’s disease is a complex phenomenon, the management of which has always been challenging. The rapid healing of ulcers improves the patient’s quality of life by reducing the morbidity. The success of any alternative measure depends on insights into the intricacies of trophic skin ulceration. Hence, a search for viable alternative treatment methods are always on the lookout. With improvising the surgical graft technique, there is certainly a great improvement in the treatment of chronic non-healing ulcers. The use of autologous smashed follicular dermal graft with epidermal cell suspension is simple technique, manageable even on an out-patient basis that quickly reduces and hastens the re-epithelialization of ulcer. Thus we conclude that by using autologous smashed follicular dermal graft and epidermal cell suspension, it is possible to achieve faster rate of granulation tissue and a faster recovery of the ulcer. References 1. Sengupta U. Elimination of leprosy in India: An analysis. Indian J Dermatol Venereol Leprol 2018;84:131-6. 2. Riyaz N, Sehgal VN. Leprosy: Trophic Skin Ulcers. Skinmed 2017;15:45-51. 3. Nagaraju U, Sundar PK, Agarwal P, Raju BP, Kumar M. Autologous Platelet-rich Fibrin Matrix in Nonhealing Trophic Ulcers in Patients with Hansen's Disease. J Cutan Aesthet Surg 2017;10:3-7. 4. World Health Organization. Global leprosy update, 2016; accelerating reduction of disease burden [Internet]. Switzerland: Weekly epidemiological record; 2017 [Updated 2017 September 1; cited 2021 Feb 16]. Available from: https://www.who.int/ lep/resources/who_wer9235/en/

Autologous Smashed Follicular Dermal Graft and Epidermal Cell Suspension in the Treatment of Chronic Non-healing Trophic Ulcer in a Hansen’s Patient

5. Srinivasan H. Management of Ulcers in Neurologically Impaired Feet in Leprosy Affected Persons. In: Schwarz R, Brandsma W, editors. Surgical Reconstruction and Rehabilitation in Leprosy and other Neuropathies, 1st ed. Kathmandu: Ekta Books; 2004. pp. 193-226. 6. Svensjö T, Yao F, Pomahac B, Eriksson E. Autologous keratinocyte suspension accelerate wound healing in pigs. J Surg Res 2001;99:211-21. 7. Shukla VK, Tiwary SK, Barnwal S, Gulati AK, Pandey SS. Effect of autologous epidermal cell suspension transplantation in chronic nonhealing wounds: a pilot study. Can J Surg 2010;53:6-10.

2015;12:32-9. 14. Martínez ML, Escario E, Poblet E, Sánchez D, Buchón FF, Izeta A, et al. Hair follicle-containing punch grafts accelerate chronic ulcer healing: A randomized controlled trial. J Am Acad Dermatol 2016;75:100714. 15. Nagaraju U, Kashyap P, Raveendra L. Autologous smashed follicular dermal graft with epidermal cell suspension in chronic nonhealing leg ulcers. J CutanAesthetSurg 2020;13:38-42.

8. Rouabhia M. Permanent skin replacement using chronic epithelial cultured sheets comprising xenogenesic and syngenetic keratinocyte. Transplant 1996;61:1290-300. 9. Navsaria HA, Ojeh NO, Moiemen N, Griffiths MA, Frame JD. Reepithelialization of a full-thickness burn from stem cells of hair follicles micrografted into a tissue-engineered dermal template (Integra). Plast Reconstr Surg 2004;113:978-81. 10. Brown JB, McDowell F. Epithelial healing and the transplantation of skin. Ann Surg 1942;115:1166-81. 11. Budamakuntla L, Loganathan E, Sarvajnamurthy SA, Nataraj HV. Follicular unit grafting in chronic nonhealing leg ulcers: A clinical study. J Cutan Aesthet Surg 2017;10:200-6. 12. Zhao H, Chen Y, Zhang C, Fu X. Autologous epidermal cell suspension: A promising treatment for chronic wounds. J Tissue Viability 2016;25:50-6. 13. De Angelis B, Migner A, Lucarini L, Agovino A, Cervelli V. The use of noncultured autologous cell suspension to repair chronic ulcers. Int Wound J February 2022

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I Dr. Rajesh Rajagopalan

MD., DNB., MNAMS Professor and HOD Department of Skin, STDs & Leprosy, Government Erode Medical College, Erode, Tamilnadu

Dr. V. Sudha

MD., DV Professor and HOD Department of Skin, STDs & Leprosy, ACS Medical College, Chennai Retired Director, Professor and HOD Institute of Venereology Madras Medical College, Chennai ABSTRACT Background: Vulvovaginal candidiasis (VVC) is the leading cause of vaginitis with more than ¾th of women has at least on episode in their life time, with parturition being a predisposing factor. If untreated in pregnancy, it can lead to chorioamnionitis with abortion, premature labour and congenital neonatal candidiasis. In this study, we aimed at determining the prevalence, species profile and symptomatology variations among HIV and Non HIV pregnant women.

February 2022

Methods: A prospective cross sectional study in which 260 study participants attending STD OPD at Institute of STDs, Madras Medical College, Chennai for whom high vaginal swab samples were taken after informed written consent during the study period for culture and species differentiation. Their vaginal smears were subjected to KOH mount, Gram stain. Candida isolates were identified using germ tube test, sugar assimilation tests. Relevant statistical methods were used. Results : The prevalence of genital candidiasis in our study group subjects was 50%. Albicans and Non –albicans

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I

(NAC) had a prevalence of 85.5% and 14.5 % respectively. Candida albicans was the most common species, followed by C.glabrata, C.keyfr, C.parapsilosis and C.tropicalis. There was no significant association between participant’s socio demographic details and clinical presentations. However, severe symptoms was observed more in HIV positive antenatal women. Conclusion: The prevalence of VVC was high in the study area. C.albicans was the most common isolated organism in culture among antenatal women attending STD clinic with or without symptoms. NAC were seen emerging ones with diseased related symptomatology is severe among HIV antenatal women. Keywords: Pregnancy, Candida, Species, HIV INTRODUCTION Candidal vaginal infections are classically considered with other STDs. Physiological changes, anatomical changes in genital tract, immunological alterations (alterations in host defense mechanisms) in a pregnant female have been postulated to influence the course of STDs which pose a special risk of infection for both mother and fetus.1,2 Candida albicans is present in the vagina of approximately 25% of sexually active women.3 Symptomatic vulvovaginal candidiasis (VVC) affects 15% of pregnant women. Clinical signs of infection could be detected in all pregnant women from whom the fungus was isolated, even those with those without symptoms. Severe vulvar pruritus is the most common symptom. Carriage rates and the risk of clinical vaginitis are highest in the third trimester. There is an increased prevalence of VVC in HIV infection and pregnancy. There are rare case reports of

intrauterine acquired candidiasis (ascending maternal vaginal infection) resulting in spontaneous abortion. Also, there are occasional reports of candidal chorioamnionitis and prematurity in pregnant women, congenital infection of the neonate and pelvic inflammatory disease (PID) resulting in infertility in non-pregnant women.4 Most common route of perinatal infection is by direct contact during delivery through an infected vagina and oral thrush of the neonate is the most common problem. So prepartal vaginal yeast colonization should be treated to protect the newborn. Clinical appearance is confirmed by wet mount for KOH, gram stain and culture. Gram stain examination of vaginal discharge may reveal diagnostic pseudohyphae in 30-50% cases. Culture in Sabouraud’s (most commonly employed) dextrose agar or Nickerson medium is even more sensitive. Ability to identify various Candida species (albicans Vs non –albicans Spp) can be done using (a) Germ tube test (Raynauld’s – Braude Phenomenon) (b) ability to form chlamydospores in cornmeal agar (c) Carbohydrate fermentation test. Candida albicans is responsible for 80–92% of episodes of VVC. Recently, an increased frequency of other candida Spp especially in HIV positive individuals particularly C.glabrata have been reported. Therapeutic failure often occurs when vaginitis is caused by non-C. albicans species such as C.glabrata, C.tropicalis and C.parapsilosis. Antenatal attendees are a section of population routinely used as a reference point for STD prevalence in the general population of women. AIMS AND OBJECTIVES • To determine the prevalence of genital candidiasis among the pregnant women attending the STD

clinic at the Institute of Sexually Transmitted Diseases • To study the species profile of isolated candida Spp among them • To assess the clinical differences among HIV and Non HIV population with regards to vaginal candidiasis MATERIALS AND METHODS It is a cross sectional study to find out the prevalence of candidiasis among pregnant women attending the STD clinic at Institute of Sexually Transmitted Diseases, Madras Medical College & Research Institute, during the study period of May 1998 to July 1999. 260 consecutive pregnant women at various trimesters who attended the STD clinic at the Institute of Sexually Transmitted Diseases, Madras Medical College & Research Institute, were included in the study. Majority of the pregnant women were referred from Institute of Obstetrics and Gynaecology, Egmore, Chennai and Kasturbha Gandhi Hospital for Women and Children, Triplicane, Chennai. Also many attended on their own for various genitourinary symptoms. Majority of the unmarried pregnant women were referred to be screened for sexually transmitted infections including HIV infection, prior to Medical Termination of Pregnancy (MTP). A well structured, pre-tested proforma was prepared and used for the study. It consists of various information including their age, socioeconomic status, marital status, sexual history and obstetric history apart from detailed clinic history. Pregnant women were screened for candidiasis along with other STDs and a provisional diagnosis was made. Investigations including KOH/ gram stain / Culture in Sabouraud’s glucose agar were done accordingly to confirm the diagnosis. Species February 2022

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I

differentiation using germ tube test and carbohydrate assimilation test was done from culture isolates. Sabouraud’s Medium is the commonest fungal culture media used. It consisted of ingredients like glucose, cycloheximide, agar etc. Sterile vaginal swabs were used for taking specimens. Cultures were incubated at room temperature (22OC) for 2 weeks. Identification was based on the colony appearance (creamy, white, mucoid) and the morphology of the fungus by microscopy. The method of identifying Candida albicans was based on its ability to form germ tubes within two hours when incubated in human serum at 37oc. RESULTS In this study 260 pregnant women were examined and the following results were derived. AGE DISTRIBUTION AGE DISTRIBUTION Age group in years

Total No.

Percentage (%)

15-19

18.5

20-24

144

55.4

25-29

19.2

30-34

6.2

35-39

0.8

MARITAL STATUS OF THE PREGNANT WOMEN Marital Status

Total No.

Percentage (%)

Married

200

76.9

Single (Unmarried)

23.1

PRESENTING COMPLAINTS OF PREGNANT WOMEN

Majority of the pregnant women had visited the STD clinic for checkup (n=62, 47.7 %). Genital discharge and genital sore were the most common presenting complaints in 36 (27.7%) and 17 (13.1%) patients respectively, followed by itching in genitalia in 15 (11.5%) and growth in genitalia in 10 (7.7%) patients. Some pregnant women also had other symptoms like burning micturition (n=6,4.6%), lower abdominal pain (n=6, 4.6%), fever (n=3, 2.3%),cough (n=2, 1.5%), low stools (n=2, 1.5%), loss of weight (n=2, 1.5%), frequency of micturition (n=2, 1.5%), swelling of genitalia (n=2, 1.5%), loss of appetite (n=1, 0.8 %) and dysuria (n=1, 0.8 %). PREMARITAL /EXTRA MARITAL CONTACTS AMONG MARRIED PREGNANT WOMEN (n=200) Contacts

Total Percentage% No.

EMC

PMC

EMC+PMC

PAST HISTORY OF STDs

COMPLAINTS

TOTAL NO.

PERCENTAGE (%)

Past History of STDs

Checkup

124

47.7

Present

8.5

Absent

238

91.5

Genital discharge

27.7

Genital sore

13.1

Itching in genitalia

11.5

Growth in genitalia

7.7

Burning micturition

4.6

Lower abdominal pain

4.6.

Fever

2.3

Frequency of micturition

1.5

Swelling in genitalia

1.5

Loss of weight

1.5

Cough

1.5

Loose stools

1.5

Loss of appetite

0.8

Dysuria

0.8

February 2022

Total Percentage No. (%)

DISTRIBUTION STDs (n=22) Disease

Total No.

Percentage (%)

Genital ulcer

63.6

Genital discharge

27.3

Genital warts

9.1

Prevalence and Species Profile of Genital Candidiasis Among Pregnant Women Attending STI/RTI Clinic At a Tertiary Referral Centre Part-I

BOH AMONG THE PREGNANT WOMEN (n = 68) BOH

Total No.

Percentage (%)

Spontaneous abortion

58.8

Still birth

23.5

8.8

Neonatal death Spontaneous Still births

abortion

CLINICAL SIGNS IN THE STUDY GROUP Clinical Signs

Total No.

Percentage (%)

Cervical erosion

152

29.2

Soddening of vulva

100

19.2

Genital ulcer

13.8

Genital wart

7.7

Bilateral inguinal Iymphadenopathy

5.4

Condylomatalata

3.1

Skin rash

2.3

Excoriations of vulva

1.5

Intertrigo groin

1.5

Molluscum Contagiosum

0.8

Scabies

0.8

Tinea cruris

0.8

Cervical erosion was the most common clinical sign followed by soddening of vulva. NATURE OF THE GENITAL DISCHARGE AMONG THE STUDY GROUP Nature of the discharge

Total No.

Percentage (%)

Mucopurulent

104

Mucoid

36.9

Curdy white

Frothy

2.3

Serosanguinous

0.8

Vaginal discharge for culture of candida species in Sabouraud`s dextrose ager medium revealed growth in 114 cases (47.7%). Candida albicans was the most frequently isolated candida species in 106 cases (85.5%). Rest of them were non albicans Spp. SEROLOGY RESULTS AMONG THE PREGNANT WOMEN VDRL REACTIVITY/TPHA Serological Patients Percentage test with (%) reactive VDRL/ TPHA VDRL

25.4

PREVALENCE OF HBs Ag Serological Patients Percentage test positive for HBs Ag HBs Ag

17.7

PREVALENCE OF HIV INFECTION Serological Total Percentage (%) test No. of patients positive for HIV antibodies HIV

6.2

Majority of the pregnant women had mucopurulent discharge. RESULTS OF INVESTIGATIONS IN THE STUDY GROUP (n = 260) Investigations

Positive results

Percentage (%)

(Total No.) Culture of candida spp.

124

47.7

Gram stain for candida

KOH mount for candida

21.5

Wet film for Trichonomas vaginalis

10.8

Gram stain for clue cells

2.3

Urine culture (routine)

2.3

February 2022

NEWS

Scarless wound healing for technology development in surgical and cosmetic medicine Scars form as a part of the healing process after your skin has been cut or damaged. The skin repairs itself by growing new tissue to pull together the wound and fill in any gaps caused by the injury. Scar tissue is made primarily of a protein called collagen. Scars are a natural part of the body's healing process. Scars can result from accidents, diseases, skin conditions such as acne, or surgeries. Scars form when the dermis (deep, thick layer of skin) is damaged. The body forms new collagen fibers (a naturally occurring protein in the body) to mend the damage, resulting in a scar. The new scar tissue will have a different texture and quality than the surrounding tissue. Researchers examined skin regeneration over two years in various body parts of the adult newt, Cynops pyrrhogaster. Their wounds were very quickly healed over several days without prolonged inflammation. Because of this rapid healing, granulation/ dermal fibrosis, and therefore scarring, did not occur. The skin was able to fully regenerate. These findings provide evidence that this newt species may be an ideal model system to study and prevent scar formation in human skin. Although human skin heals from injuries and wounds, many of us have scars that are left behind. Scar formation happens in adult mammals because skin regeneration does not fully occur. This poses a challenge to physicians who wish to conduct surgeries without scars appearing afterwards. In a newly published study investigated the use of the adult newt, Cynops pyrrhogaster, as a model system for studying scarless wound healing for technology development in surgical and cosmetic medicine.After an injury occurs, the epidermis, which is the outer layer of the skin, can grow and migrate to fill in the wound. This is known as re-epithelialization. Although this takes place, the original skin color and texture is sometimes not retained, leading to the appearance of what we know as a scar. Processes called granulation and dermal fibrosis underpin scar formation, making them a focus for scientists aiming to minimize scarring following clinical procedures. Amphibians have been used as animal models for studying this, because they do not scar prior to metamorphosis. However, it is not clear what happens to fully mature amphibian skin. Researchers chose to examine the adult Japanese fire-bellied newt, which is a type of salamander that is well understood on the genetic level. They know adult newts are capable of complicated tissue, organ, and limb regeneration. Despite that, their ability to regenerate skin has not been scientifically demonstrated. The team excised a small piece of skin from various body parts of adult newts, including the head, trunk, limbs, and abdomen. They periodically observed the skin healing and regeneration progression for up to two years, making note of re-epithelialization and dermal fibrosis, as well as recovery of texture, appendage, and color. Interestingly, they found that the adult newts could successfully and fully regenerate their skin at each part of the body that they examined. Re-epithelialization occurred at all locations, while no dermal fibrosis was observed at all. However, the original color pattern of the dorsal-lateral and ventral skin was not restored. Because humans do not have such color patterns, the researchers believed this to be a newt-specific issue. Thus, they concluded that Cynops pyrrhogaster could be a perfect model system for investigating skin regeneration and scar formation in humans. The team also further studied skin regeneration in these newts at the morphological and molecular level. The wounds tended to heal within only a few days, while skin regeneration took up to two years to complete. Inflammatory gene markers were only briefly expressed during wound healing. Dermal fibrosis is often characterized by prolonged inflammation at the wound site. Scar-free skin occurred in the newts through rapid re-epithelialization and skipping of granulation and dermal fibrosis. Overall, these findings will be crucial for future studies in humans focusing on efforts to prevent scarring in human skin following various medical procedures.

Dermatologists Seeing High Rates of Hair Loss after COVID-19 Hair loss (alopecia) can affect just your scalp or your entire body, and it can be temporary or permanent.Alopecia areata is a disease that develops when the body’s immune system attacks hair follicles, causing hair loss. It can be the result of heredity, hormonal changes, medical conditions or a normal part of aging. Baldness typically refers to excessive hair loss from scalp. Hereditary hair loss with age is the most common cause of baldness. Some people prefer to let their hair loss run its course untreated and unhidden. Recent study found that 22 percent of hospitalized COVID-19 patients were dealing with hair loss months after being discharged. According to dermatologist the hair loss that occurs after COVID-19 infection occurs because of overactive inflammation in the body. The inflammation can cause a shift in the hair cycle.Hair loss after a COVID-19 infection typically begins anywhere from several weeks to 3 months post infection. How long it lasts can vary from patient to patient but usually 6 to 9 months. Hair loss after a stressful situation is not unusual. People can experience hair loss after childbirth or a major surgery, and we’re now seeing the same results after COVID-19 infection in some people. 28

February 2022

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation Dr. Sharad Chaurasia

PG Resident Department of Dermatology, Venereology and Leprosy, ESI-PGIMSR, New Delhi

Dr. Ipshita Bhattacharya

PG Resident Department of Dermatology, Venereology and Leprosy, ESI-PGIMSR, New Delhi

Dr. Paschal Dsouza

Professor Department of Dermatology, Venereology and Leprosy, ESI-PGIMSR, New Delhi

Introduction Erythroderma, or generalized exfoliative dermatitis, is an inflammatory disorder characterized by erythema and scaling of greater than 90% of the body's surface. Erythroderma is a potentially fatal dermatosis even when properly managed, mainly due to its metabolic complications. In majority of cases, erythroderma is the morphological presentation of a variety of cutaneous and systemic diseases. Hence it is 30

February 2022

essential to establish its etiopathology in order to facilitate precise management. The most common cause is an exacerbation of preexisting dermatoses such as psoriasis and atopic dermatitis. Uncommon causes include cutaneous T-cell lymphoma and other internal malignancies, drugs, pemphigus foliaceus. Pemphigus is an autoimmune disease of the skin and mucous membranes that manifests as

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation

vesicles (blisters) or bullae, which ultimately break down to form chronic painful ulcers. It is an autoimmune disorder in which the immune system produces antibodies against the desmosomal proteins - desmoglein 1 and desmoglein 3, in the skin and mucous membrane resulting in loss of keratinocyte adhesion leading to a typical intra-epidermal acantholytic blister that is evident on histology. Patients with pemphigus foliaceus, who have anti-Dsg 1 antibodies alone, exhibit skin blistering without mucosal involvement. In pemphigus vulgaris, where anti-Dsg 3 antibodies predominate there is generally marked mucosal blistering. Erythrodermic presentation in a patient of pemphigus foliaceus is known but not in pemphigus vulgaris which prompted us to report this case.

to haemorrhagic crusting and raw areas over the body. On examination patient had generalized large, moist, thick yellowish adherent crusts almost all over the body including scalp face, trunk and extremities sparing palms and soles (Fig 1 A& 1 C). Patient also had haemorrhagic crusting predominantly over the anterior aspect of bilateral thighs and few large erosions over back. Patient’s hair over the vertex were matted and had thick yellowish adherent crusts.

Case report A 34-year-old male patient presented with a 3 weeks history of generalized moist dirty yellowish crusting in addition to haemorrhagic crusting and raw areas over the body. Patient was diagnosed with pemphigus vulgaris 2 years back based on clinical, histopathological and direct immunofluorescence findings. Initially patient had been taking Tablet Azathioprine 50mg twice a day and Oral Corticosteroids in varying doses off & on for the past 2 years and he had no major complaints while being on the above said medications. But 4 weeks before he presented to us, the patient had switched to homeopathic medications and had stopped all other medications. Thereafter he initially developed a large clear fluidfilled lesion over the dorsal aspect of feet along with bilateral pedal edema. Subsequently the patient developed similar lesions over hands and later gradually progressed to involve trunk & head over a period of 2 weeks. The bullae ruptured spontaneously to form dirty yellowish crusts in addition

Figure 1 A & C: Pemphigus Vulgaris patient before treatment. B & D : Remarkable clinical improvement 3 weeks after first monthly dose of Dexamethasone Pulse therapy.

February 2022

Pemphigus Vulgaris Presenting as Exfoliative Dermatitis: A Rare Presentation

The lesions involved almost around 90% of the body surface area. Nails were normal. Oral and genital mucosa were normal. A clinical diagnosis of Erythroderma secondary to Pemphigus vulgaris was made. Routine investigations i.e., complete blood count, urinalysis, liver and kidney function tests, chest radiographs were normal. Tzanck smear from a deroofed new bleb revealed multiple acantholytic cells. Skin biopsy from edge of a recent blister showed suprabasal split with acantholytic cells on H & E (Fig 2) & DIF was positive with typical intercellular deposit of IgG in a fish net pattern in epidermis surrounding the suprabasal split (Fig 3).

After admission, patient was managed with prompt fastidious care. Daily dressings were started with Condy’s compresses followed by liberal application of emollients and topical antibiotics and gentle removal of crusts was done over successive days. Initially Intravenous dexamethasone in a dose of 8mg twice a day and IV broad-spectrum antibiotics was started along with other supportive medications and i.v. fluids. High protein diet was also given to compensate for excessive catabolism. With this patient started showing significant improvement and dexamethasone was slowly tapered over 3 weeks. Patient was then planned for monthly Dexamethasone pulse therapy. Tablet dapsone was started at a dose of 100mg HS along with Tablet Azathioprine 50 mg twice daily. After relevant investigations, Dexamethasone pulse therapy using 100 mg of dexamethasone in 500 ml of 5% Dextrose water for 3 consecutive days in a month was started and the lesions almost completely cleared 3 weeks after the 1st pulse (Fig 1 B & D). Patient has received four monthly Dexamethasone pulse so far and has only occasional new lesions. He is under regular follow up. Discussion

Figure 2: H & E of edge of blister showing intraepidermal suprabasal split with multiple acantholytic cells (Magnification x 10X)

Figure 3: DIF showing intercellular IgG deposits in normal looking epidermis in a characteristic fish net appearance along with suprabasal split at one end (Magnification x 10X) 32

February 2022

Erythroderma, or generalized exfoliative dermatitis, is an inflammatory disorder characterized by erythema and scaling of greater than 90% of the body's surface.[1] Causes of erythroderma vary with age group; in general psoriasis, atopic dermatitis & airborne contact dermatitis are among common causes. Pemphigus is a group of chronic autoimmune blistering diseases characterized by the presence of antibodies against desmosomal adhesion proteins. Patients with pemphigus vulgaris possess anti-Dsg 3 predominantly besides anti-Dsg 1 antibodies. Majority of patients have mucosal lesions which may precede cutaneous lesions (i.e., flaccid blister) or may be the only manifestation of the disease. Patients with pemphigus foliaceus have anti-Dsg 1 antibodies alone. Pemphigus foliaceus is usually less severe than pemphigus vulgaris.

Patients present with scaly lesions involving the ‘seborrheic’ areas of the scalp, face, chest and upper back. In severe cases patients may be- come erythrodermic with crusted oozing red skin.[2] There have been very few reported cases of erythroderma secondary to pemphigus foliaceus. [3,4] Our case is unique and unusual as it clinically presented with erythroderma though he was a diagnosed case of pemphigus vulgaris based on histopathology and DIF. He also had no mucosal lesions which are very common in patients of pemphigus vulgaris but uncommon in foliaceus variant. Erythrodermic presentation of pemphigus vulgaris has not been reported till date. Our patient also had abruptly stopped oral steroids and tablet azathioprine by himself, which could have led to relapse of pemphigus and the underlying inflammation may have been aggravated by homeopathic medications leading to his present clinical manifestation. This case also highlights the importance of patient education, counselling and adherence to treatment, all of which might have avoided such serious consequences. References 1. John R. Ingram, Eczematous Disorders, In: Griﬃths C. E. M., Barker J, Bleiker T et al (eds.) Rook’s Textbook of Dermatology. 9thed. UK: Wiley Blackwell; 2016. p. 39.3032 2. Enno Schmidt and Richard Groves, Immunobullous Diseases, In: Griﬃths C. E. M., Barker J, Bleiker T et al (eds.) Rook’s Textbook of Dermatology. 9thed. UK: Wiley Blackwell; 2016. p.50.3-50.5 3. Gopal V, Pinto M, Mala MS. Pemphigus foliaceus: A rare case of exfoliative dermatitis. Clin Dermatol Rev 2017; 1:19-21 4. Patsatsi A, Douma S, Kokolios M, Meltzanidou P, Lambropoulos A, Sotiriadis D. Erythrodermic pemphigus foliaceus: A rare refractory variant. Journal of the American Academy of Dermatology. 2016 May;74(5). AB 145. DOI:https://doi.org/10.1016/j. jaad.2016.02.571

NEWS

FDA Approves Two Oral JAK Inhibitors for Moderate-to-Severe Atopic Dermatitis Atopic Dermatitis is one of the major public health problems worldwide. Atopic Dermatitis is a chronic relapsing eczematous skin disease characterized by pruritus and inflammation and accompanied by cutaneous physiological dysfunction, with a majority of the patients having a personal or family history of atopic diathesis. It can be hard for people to fully appreciate how difficult Atopic Dermatitis can be and the tremendous impact it has on patients. The chronic itch is difficult to cope with and related sleep issues can be exhausting. According to recent data shows the FDA granted a first-ever approval of a topical Janus kinase (JAK) inhibitor for atopic dermatitis (AD). Ruxolitinib cream received approval for short-term, noncontinuous treatment of moderate-to-severe AD that has not been adequately controlled with topical prescription therapies or the therapies are not advisable. The approval specifies use of ruxolitinib cream in non-immunocompromised patients ages 12 and older. Support for the approval came from the randomized, vehicle-controlled, phase III TRuE-AD1 (Topical Ruxolitinib Evaluation in Atopic Dermatitis Study 1) and TRuE-AD2 (Topical Ruxolitinib Evaluation in Atopic Dermatitis Study 2) clinical trials, which involved a combined total of more than 1,200 adults and adolescents with moderate-to-severe AD. Patients in both trials were randomized to twice-daily topical ruxolitinib or a non-medicated cream. The primary endpoint was Investigator's Global Assessment (IGA) of Treatment Success at week 8 (IGA score 0/1). More than half of patients randomized to ruxolitinib cream met the primary endpoint as compared with 15.1% and 7.6% of patients in the control groups (P<0.0001). Additionally, more than half of patients in the ruxolitinib groups had clinically meaningful reductions in itch versus 15-16% of patients randomized to vehicle (P<0.0001).Many patients and their dermatologists are looking for additional options to meet current unmet needs in the management of AD. The approval of Ruxolitinib is exciting news, and we welcome a new treatment option for our community

Novel mechanism linking intercellular adhesion molecule with genetic skin diseases discovered The skin is composed of a variety of cell types expressing specific molecules and possessing different properties that facilitate the complex interactions and intercellular communication essential for maintaining the structural integrity of the skin. The recent study suggests that Desmoglein-1 (Dsg1) deficiency results in an inflammatory gene signature that is seen in patients diagnosed with skin diseases such as psoriasis and may be a promising therapeutic target.Dsg1 is a cadherin, a cellto-cell adhesion molecule and key component of the desmosome, a complex that helps tissues withstand mechanical and environmental stressors. Dsg1 is expressed exclusively within the upper layers of the skin's most outer layer, the epidermis. Previous work suggests that mutations in Dsg1 and ultimately its loss of function are associated with chronic inflammation and the manifestation of skin lesions and allergies. However, the precise intracellular mechanisms that cause this deficiency remained unknown. To uncover these mechanisms, the investigators used gene editing methods to delete Dsg1 from mice genomes. The gene expression profiles of the mice were then compared to the profiles of patients with severe dermatitis, multiple allergies and metabolic wasting (SAM) syndrome, a rare, genetic skin disease caused by Dsg1 deficiency that results in a severe thickening of the skin and increased inflammation. The team found similarities between the genetic profiles of the mice and patients, specifically a shared IL-17/IL-23 inflammatory signature and impaired intercellular adhesion caused by the loss of Dsg1 at the surface of cells in the epidermis. IL-17 is secreted by T-cells involved in the body's inflammatory response. This inflammatory signature was also similar to that seen in patients with psoriasis. Further demonstrating the relevance of their findings in vivo, two Dsg1-deficient patients with SAM syndrome were treated with ustekinumab, an immunosuppressive drug commonly prescribed to treat psoriasis. The drug inhibits IL-12/IL-23 cytokine activity, which is involved in the body's inflammatory response. After 10 months of treatment, both patients experienced significant improvement of pre-existing skin lesions.Immunostaining of protein constituents of the cell-cell adhesive junction in the desmosome in skin biopsies taken from a patient with SAM syndrome harboring a genetic mutation in Dsg1. The levels of Dsg1 and its associated partner protein plakoglobin (PG) are restored at cell borders following ustekinumab treatment. At the very least, Dsg1 expression could serve as a biomarker that can be used to improve treatment of genetic skin diseases. Furthermore, a topical treatment that can help increase the expression of Dsg1 in the skin would be a game changer in treating these diseases.If we can actually improve Dsg1 expression, we might be able to target all these diseases that have a Dsg1 decrease. February 2022

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