Vitamin D has been used in a gamut of medical conditions, including dermatology. Intralesional Vitamin D, however, is not a common therapeutic option in dermatological disorders. This review is an attempt to summarise the evidence available for using intralesional vitamin D in warts, molluscum, keloids, and vitiligo.

Background:There has been a significant increase in the incidence of recurrent, resistant, and extensive dermatophyte infections worldwide recently. This menace has spurred the need for more well-designed randomized controlled trials to optimize the treatment of dermatophyte skin infections. One of the limitations in designing such studies is the limited availability of standard and validated score, to measure the severity of dermatophyte infections. Aims:To create a severity score for the evaluation of dermatophyte infections. Materials and Methods:A Delphi consensus model was used to frame a severity scoring tool for superficial dermatophyte skin infections. Fourteen experts participated in the first round and twelve experts participated in the second round. Results:Based on the expert consensus, a final scoring system proposed was: Final Severity Score (FSS) = Sum total of Body Surface Area (BSA) in hand units for each patch multiplied by the sum of the scores for pruritis (P), lichenification (L), and actively raised borders (A) for each patch (FSS = BSA in hand units × (P + E + L + A) of patch 1 + BSA in hand units × (P + E + A) of patch 2 …etc.). For measuring hand units more accurately fractional values of 0.25 can be used (0.25 corresponding to an approximate 1/4th of a hand unit). A score of +1 will be added in case of the following - 1) Close contact/family member affected, 2) History of at least one recurrence in the previous 6 months after a course of oral antifungals, 3) History of immunosuppression (on immunosuppressive medication or having underlying immunosuppressive disease). The scores will be valid only if the patient has not used any treatment topical or systemic, for at least 2 weeks before enrolment. Conclusion:The proposed Dermatophytosis Area and Severity Index (DeASI) score will help the physicians and researchers standardize the treatment protocol for dermatophytosis, henceforth, assessing the response to therapy. This will also help to standardize the parameters of effectiveness while designing any clinical trial.

Macrodystrophia lipomatosa (MDL) is a rare congenital nonhereditary anomaly, in which progressive overgrowth of mesenchymal tissue leads to disproportionate enlargement of the digits of the hands and feet. We discuss the case of a 5-year-old girl who presented with progressive disproportionate enlargement of the third and fourth toes of the right foot since birth. A diagnosis of MDL was made on the basis of clinical and radiological findings.

CRC Press is a well organized and illustrated resource of value to practicing clinicians, residents 16 and students.The most obvious problem for North American readers is the title, given the 17 pejorative and offensive nature of the term "colored" in North

A 5-year-old female child born out of nonconsanguineous marriage presented to the dermatology clinic with red raised linear lesion over the right lower limb. This asymptomatic lesion was present since birth albeit of a smaller size which gradually progressed to the present state. On examination, there were multiple nodules and plaques coalescing at places in a reticulate pattern and extending from the dorsum of the foot to the knee. The lesion was of varied colors ranging from pink to violaceous and had a verrucous surface. At one place, it had a small ulcer with overlying crust. This lesion which followed a blaschkoid distribution was nontender and normothermic on palpation. There was no difference in limb girth between both limbs. Dermoscopy of the lesion revealed hyperkeratosis over a bluish background and reddish-blue lacunae. Hyperkeratosis correlated with verrucous nature of the lesion and reddish-blue lacunae pointed toward the vascular lesion. Based on clinico-dermoscopic correlation a differential diagnosis of verrucous hemangioma (VH) and angiokeratoma circumscriptum neviforme (ACN) were contemplated [Figures 1 and 2]. A punch biopsy was performed which revealed widely dilated thin-walled vessels in the papillary and upper reticular dermis. Capillary-sized vessels were also distributed in the lower reticular dermis and upper subcutis. The epidermis showed mild hyperplasia and hyperkeratosis. Based on clinico-dermoscopic-pathological correlation a final diagnosis of VH was rendered [Figure 3]. The patient was recommended surgery; however, she was lost to follow-up.Figure 1: Multiple well-defined erythematous to violaceous plaques with verrucous surface over the right lower limbFigure 2: Dermoscopy from the peripheral area showing hyperkeratosis over bluish background (black circle) and reddish blue lacunae (DermLite DL4, polarized light, ×10)Figure 3: Multiple dilated erythrocyte-filled capillaries in papillary dermis with similar vessels also seen in the mid and deep reticular dermis. The epidermis shows acanthosis and hyperkeratosis (H and E, ×40)The international society for the study of vascular anomalies categorizes VH into “provisionally unclassified vascular anomalies” because its clinicopathologic characteristics are not still fully understood.[1,2] Immunohistochemically, VH is GLUT1 positive in the majority of cases but staining is inconsistent. WT1, D2-40, and Prox1 staining are negative. An important differential diagnosis for this case was ACN which was ruled out by vessel proliferation in the deep dermis and upper subcutis on histopathology.[3] There are various surgical and nonsurgical ablative modalities for the treatment of VH, but surgery is considered more effective.[4] Oral sirolimus may be considered in the management of widespread or extensive lesions, where surgery is not feasible.[5] Declaration of consent The authors certify that they have obtained all appropriate consent forms, duly signed by the parent(s)/guardian(s) of the patient. In the form, the parent(s)/guardian(s) has/have given his/her/their consent for the images and other clinical information of their child to be reported in the journal. The parents understand that the names and initials of their child/children will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Blue light has garnered attention because of its ability to penetrate more deeply into the skin layers, and induce cellular dysfunction and DNA damage. Photoageing, hyperpigmentation and melasma are some of the cutaneous changes that develop on exposure to blue light. To date, the therapeutic roles of blue light have been evaluated in dermatological conditions like psoriasis, eczema, acne vulgaris, actinic keratosis and cutaneous malignancies, among others. In this review, we have attempted to present an evidence-based compilation of the effects of blue light on the skin.

Gamma-Aminobutyric Acid (GABA) inhibitory neurotransmitter departs an energetic role in brain signalling system. Levels of GABA in the brain influence human behaviour, diminishes in the degree of GABA can cause seizures, depression, Parkinson's. To put it plainly, it plays a basic part in the significant issues of mind. It is exceptionally important to cure the issues linked to GABA. Writing overview proposed that nipecotic acid is an intense GABA reuptake inhibitor. This scaffold is likewise present in one of the promoted anticonvulsant drugs 'Tiagabine'. Tiagabine is only drug in the market which works through this mechanism however the medication is regulated with one more prescription for the synergistic impact. Nipecotic acid has several disadvantages such as it can't cross the blood-brain barrier because of its hydrophilic and zwitterionic nature. To avoid this problem nipecotic acid scaffold hybrids with the different aromatic groups can enhance the physical (lipophilicity) as well as biological properties of the resultant compound. So, there is a dire requirement for compounds that work through this mechanism. Several medicinal chemists and researchers are already working in this field and developed outstanding newer molecules. This review article compiles these developed new hybrids along with design strategies, structure-activity relationship, and biological activity as well as in silico studies. This review also demonstrates the synthesis of nipecotic acid and the core mechanism through which nipecotic acid acts as a GABA reuptake inhibitor.

An elderly male presented with asymptomatic nodules on the hands and feet of 1 year duration. A few similar lesions were noted on the chest too. There was symmetrical and bilateral loss of sensation over the hands and feet, up to mid-forearm and mid-calf level. However, there were no facial lesions, ear lobe infiltration, or madarosis. Histoid leprosy and lepromatous leprosy were considered as clinical differentials, and biopsy from the nodule on the hand was done. Biopsy showed dense nodular monomorphous infiltrate of foamy histiocytes involving the reticular dermis and sparing the upper dermis. Slit skin smear from the lesion showed acid-fast bacilli in clumps with BI >5+. On clinicopathological correlation, diagnosis of lepromatous leprosy was made.KeywordsLeprosyLepromatous leprosyHistoid leprosyAcid-fast bacilliAcral nodules

Chronic venous disease (CVD) is a commonly encountered condition in the dermatology outpatient department. If untreated, CVD may progress to chronic leg ulcer causing serious morbidity to the patient. It also affects the quality of life of the affected patient and contributes to loss of work productivity. The spectrum of clinical manifestations for CVD is myriad, ranging from asymptomatic varicose veins and pigmentation to ulceration and scarring. Awareness of spectrum of clinical presentations is required to identify, diagnose and manage CVD. Long-standing cases may develop ankle joint stiffness, fixed flexion deformity, periostitis and even Marjolin ulcer. Increased venous hypertension, thought to result from valve incompetence and failure of the calf muscle pump, is central to the pathophysiology of the development of CVD. Tissue oedema, hypoxia and subsequent fibrosis are major immediate contributing factors responsible for the clinical manifestations of CVD. Localized, chronic inflammation is now increasingly being recognized as a key player, directly responsible for stasis dermatitis and hypercoagulable state. The complete ramifications of persistent inflammation in CVD are yet to be understood and serious systemic morbidities such as arterial and cardiac disease are increasingly being recognized in association with CVD.

Sir, Pemphigus vulgaris (PV) is an autoimmune bullous dermatosis, developing due to autoantibodies against desmogleins 1 and 3.[1] Clinically, it manifests with painful mucosal erosions and flaccid bullae with erosions distributed mostly over the trunk, groin, armpits, scalp, and face.[2] We hereby present an unusual case of PV where the patient presented with multiple pustules having a targetoid appearance. A 32-year-old lady presented with pustules on the extremities of 1-month duration and recurrent oral erosions for 6 months. She had consulted dentists, ear-nose-throat specialists, and physicians for oral lesions; however, the erosions kept recurring. Recently, she developed multiple pustules on the extremities, which healed in around 10–14 days with post-inflammatory hyperpigmentation, but newer lesions kept appearing. There was no history of weight loss or changes in bowel or bladder habits. An examination showed a well-built lady with palatal erosions and targetoid lesions (pustules on an erythematous base) over the extremities. [Figures 1a, b and 2] Nikolsky sign was negative. We kept clinical differentials of IgA pemphigus, paraneoplastic pemphigus, PV, erythema multiforme, Rowell syndrome and subcorneal pustular dermatosis. Histopathology showed intra-epidermal blisters in suprabasal location, with acantholytic cells within the blister cavity. [Figure 3a] Direct immunofluorescence (DIF) showed epidermal deposition of IgG in the intercellular spaces in a "fishnet" pattern. [Figure 3b] Considering histopathology and DIF, the case was diagnosed as PV. Assessment of autoantibodies against desmoglein 1 and 3 could not be done. Gram stain and culture from the pus did not show any organism. Routine blood investigations, lactate dehydrogenase, and protein electrophoresis were within normal limits. Serology for antinuclear antibody, computed tomography of the chest, abdomen and pelvis and mammogram were negative. She was treated with prednisolone (1 mg/kg/day for 6 weeks followed by tapering over 3 months) and azathioprine (50 mg twice daily). The lesions have healed with post-inflammatory hyperpigmentation [Figure 4], and new lesions have stopped appearing.Figure 1: (a and b) Targetoid lesions on an erythematous base over the extremitiesFigure 2: Multiple erosions on the palateFigure 3: Photomicrograph showing suprabasal blister and acantholytic cells in the blister cavity (a) [hematoxylin and eosin, 400 ×] and direct immunofluorescence showing intercellular deposits of IgG (b) [100 ×]Figure 4: Post-treatment resolution of the lesions with hyperpigmentationPV can present with atypical and rare manifestations like crusted plaques on the face and scalp, foot ulcers, dyshidrosiform dermatitis, macroglossia, nail dystrophy, paronychia, subungual hematomas and targetoid pustules (consistent with our case). There have been isolated reports of patients with PV presenting with pustules as reported by Rimal et al.[3] and Yang et al.[4] Another case of PV presenting with true target lesions coalescing into an annular configuration has also been reported.[5] Our case was unique because of targetoid pustules as predominant lesions, localization of the pustules on the extremities, pustules having no tendency to spread and form bigger erosions (unlike classical PV), and negative Nikolsky sign. These unusual features make the presentation unique; however, it is not clear if such a presentation represents a subset of PV with a different course and prognosis. Similar pustules predominant presentation has been described in pemphigus foliaceous too.[6] Treatment of PV should be initiated as early as possible in order to achieve and maintain disease remission and prevent complications.[7] Corticosteroids form the mainstay of therapy in developing and resource-poor countries. It is prudent to start oral prednisolone at a dose of 1 to 2 mg/kg/day, followed by gradual tapering when remission has been achieved. Steroid-sparing immunosuppressives like azathioprine, mycophenolate mofetil, and cyclophosphamide are almost universally used. Rituximab appears to be the most preferred treatment for PV, and both lymphoma protocol and the protocol for rheumatoid arthritis have been used successfully.[7] Other therapeutic options include cyclophosphamide 1 to 3 mg/kg/day orally or intravenously, dexamethasone-cyclophosphamide pulse therapy, methotrexate (10–20 mg/week), dapsone (50–200 mg/day), cyclosporine (3–5 mg/kg/day), intravenous immunoglobulins (0.4 g/kg/day for 5 days), plasmapheresis and immunoadsorption.[8] With updates in the understanding of the pathomechanism of the disease, future therapeutic options are being investigated systematically. Some of them include modified chimeric antigen receptor (CAR) therapy to target Dsg3-specific B-cells, anti-CD154 monoclonal antibody to prevent the production of anti-Dsg3 IgG, B-cell activating factor (BAFF) inhibitor, A proliferation-inducing ligand (APRIL) inhibitor, p38 mitogen-activated protein kinase signaling pathway inhibitor, c-Myc and epidermal growth factor receptor inhibitors and Bruton's tyrosine kinase (BTK). To conclude, as we delve deep into the molecular targets for the management of PV, dermatologists should be aware of the atypical clinical presentations of this elusive immunobullous disorder. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Chronic venous disease (CVD) is a common medical condition that results from venous hypertension of the limbs, leading to significant morbidity. The diagnosis is quite straightforward from patient history and obvious clinical manifestations. In the recent past, the availability of various invasive and noninvasive treatments has assisted in evaluation of such cases. Although compression therapy is the mainstay of management, newer surgical and other interventional techniques are now being considered for patients who do not respond to conventional medical management. The second part of this two-part review article will outline a diagnostic approach in cases of CVD and discuss the management principles encompassing conservative, pharmacological and interventional options.