TXA appears to be an effective and safe treatment for melasma, irrespective of its route of administration.

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors and comprise three different isoforms namely PPARα, PPARγ, and PPARβ/δ with PPARβ/δ being the predominant subtype in human keratinocytes. After binding with specific ligands, PPARs regulate gene expression, cell growth and differentiation, apoptosis, inflammatory responses, and tumorogenesis. PPARs also modulate a wide variety of skin functions including keratinocyte proliferation, epidermal barrier formation, wound healing, melanocyte proliferation, and sebum production. Recent studies have shown the importance of PPARs in the pathogenesis of many dermatological disorders. Clinical trials have suggested possible role of PPAR agonists in the management of various dermatoses ranging from acne vulgaris, psoriasis, hirsutism, and lipodystrophy to cutaneous malignancies including melanoma. This article is intended to be a primer for dermatologists in their understanding of clinical relevance of PPARs and PPAR agonists in dermatology therapeutics.

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AIMTo evaluate the utility of patch test and cross-sensitivity patterns in patients with adverse cutaneous drug reactions (ACDR) from common anticonvulsants.METHODSTwenty-four (M:F = 13:11) patients aged 18-75 years with ACDR from anticonvulsants were patch tested 3-27 mo after complete recovery using carbamazepine, phenytoin, phenobarbitone, lamotrigine, and sodium valproate in 10%, 20% and 30% conc. in pet. after informed consent. Positive reactions persisting on D3 and D4 were considered significant.RESULTSClinical patterns were exanthematous drug rash with or without systemic involvement (DRESS) in 18 (75%), Stevens-Johnsons syndrome/toxic epidermal necrolysis (SJS/TEN) overlap and TEN in 2 (8.3%) patients each, SJS and lichenoid drug eruption in 1 (4.2%) patient each, respectively. The implicated drugs were phenytoin in 14 (58.3%), carbamazepine in 9 (37.5%), phenobarbitone in 2 (8.3%), and lamotrigine in 1 (4.7%) patients, respectively. Twelve (50%) patients elicited positive reactions to implicated drugs; carbamazepine in 6 (50%), phenytoin alone in 4 (33.3%), phenobarbitone alone in 1 (8.3%), and both phenytoin and phenobarbitone in 1 (8.33%) patients, respectively. Cross-reactions occurred in 11 (92%) patients. Six patients with carbamazepine positive patch test reaction showed cross sensitivity with phenobarbitone, sodium valproate and/or lamotrigine. Three (75%) patients among positive phenytoin patch test reactions had cross reactions with phenobarbitone, lamotrigine, and/or valproate.CONCLUSIONCarbamazepine remains the commonest anticonvulsant causing ACDRs and cross-reactions with other anticonvulsants are possible. Drug patch testing appears useful in DRESS for drug imputability and cross-reactions established clinically.

Background: Idiopathic hypereosinophilic syndrome (HES) is a rare and potentially lethal disorder characterized by persistently elevated eosinophil counts without any underlying causes. Two variants, the myeloproliferative and lymphocytic hypereosinophilic syndrome, have been identified. The symptoms are variable and related to the organs involved (cardiovascular system, skin, central and peripheral nervous system, gastrointestinal tract, eyes). Skin lesions can be the dominating and/or presenting symptom in about 50% of patients. Main observations:We describe a 54-year-old man with a 12-year history of skin lesions, clinically consistent with psoriasis and psoriatic erythroderma. The patient was treated with methotrexate with no response. He experienced intense pruritus, dry/coarse skin and palmoplantar hyperkeratosis. Histopathology showed spongiotic dermatitis with no epidermotropism. Inflammatory infiltrates in upper dermis consisted predominantly of lymphocytes and eosinophils. Peripheral and tissue eosinophilia, immunophenotyping, and results of FIP1L1-PDGFRA gene analysis were suggestive of lymphocytic HES. The patient was treated with hydroxycarbamide (1 g/day), prednisolone (40 mg/day) and antihistamines with improvement.Conclusions: HES requires early treatment to prevent severe damage of targeted organs. The pleomorphic dermatological manifestations may delay the diagnosis. This case shows the importance of wide differential diagnosis of erythroderma. In this article we discuss the diagnostic criteria, the recommended work-up and management of idiopathic hypereosinophilic syndrome variants. (J Dermatol Case Rep.