Cutaneous tuberculosis in children continues to be an important cause of morbidity, there is a high likelihood of internal involvement, especially in patients with scrofuloderma. A search is required for more sensitive, economic diagnostic tools. Response to treatment at 4 weeks often helps in substantiating the diagnosis of tuberculosis in doubtful cases.

Lichen planus (LP) is infrequently seen in children and the clinical presentation is often atypical. We conducted a retrospective analysis of clinical features and treatment response in childhood LP to date. The clinical profile and treatment response data of patients younger than 14 years old with LP (entered in a predesigned pro forma study) from January 1997 to June 2011 were analyzed. The treatment was administered according to a predetermined departmental protocol and was comprised of topical steroids with or without oral dapsone or corticosteroids. Patients were evaluated for response, adverse effects, and relapse. The study population consisted of 316 children (166 boys, 150 girls), or 18.7% of the total registered patients in the LP clinic. The mean age was 10.28 years (range 2-14 years). Cutaneous lesions were seen in 96.2%. Involvement of the oral mucosa was detected in 18%, nails in 13.9%, scalp in 8.2%, and genitalia in 4.4%. Classic LP was most prevalent (53.8%), followed by eruptive (16.5%), hypertrophic (8.2%), linear (6.9%), and lichen planopilaris (6.3%). LP pigmentosus, annular, and atrophic variants were encountered infrequently. Topical corticosteroids were the most common treatment used in 69.5% of patients, 28.8% of whom had excellent response at 6 months, although 38.8% failed to follow up. Dapsone was prescribed in 20% and systemic steroids in 9.8% of patients. We report the largest series to date of LP in childhood, with a more varied clinical presentation than in previous series. The course and response to treatment were similar to those in adults.

Premature graying is an important cause of low self-esteem, often interfering with socio-cultural adjustment. The onset and progression of graying or canities correlate very closely with chronological aging, and occur in varying degrees in all individuals eventually, regardless of gender or race. Premature canities may occur alone as an autosomal dominant condition or in association with various autoimmune or premature aging syndromes. It needs to be differentiated from various genetic hypomelanotic hair disorders. Reduction in melanogenically active melanocytes in the hair bulb of gray anagen hair follicles with resultant pigment loss is central to the pathogenesis of graying. Defective melanosomal transfers to cortical keratinocytes and melanin incontinence due to melanocyte degeneration are also believed to contribute to this. The white color of canities is an optical effect; the reflection of incident light masks the intrinsic pale yellow color of hair keratin. Full range of color from normal to white can be seen both along individual hair and from hair to hair, and admixture of pigmented and white hair is believed to give the appearance of gray. Graying of hair is usually progressive and permanent, but there are occasional reports of spontaneous repigmentation of gray hair. Studies evaluating the association of canities with osteopenia and cardiovascular disease have revealed mixed results. Despite the extensive molecular research being carried out to understand the pathogenesis of canities, there is paucity of effective evidence-based treatment options. Reports of repigmentation of previously white hair following certain inflammatory processes and use of drugs have suggested the possibility of cytokine-induced recruitment of outer sheath melanocytes to the hair bulb and rekindled the hope for finding an effective drug for treatment of premature canities. In the end, camouflage techniques using hair colorants are outlined.