Introduction: Zinc deficiency is of high magnitude in developing countries such as the Philippines. Zinc deficiency dermatitis is recognized through characteristic cutaneous presentation supported by diagnostic workups which may not be feasible or practical in low-resource settings. Case report: A three-month-old Filipino male was brought in for erosions of three (3) weeks duration that were unrespon- sive to topical and systemic antimicrobial treatment. On examination, he had multiple erythematous erosions with yellowish to brownish, crusted borders with predilection on the face, inguinal and gluteal areas, flexures of the extremities, and digits. Workup revealed normal zinc levels, decreased alkaline phosphatase, and bacterial growth in cultures. Histopathology revealed intraepidermal vesiculobullous dermatitis. Given the clinicopathologic presentation, a diagnosis of zinc deficiency-associated dermatitis was made. Along with antimicrobials and topical care, oral zinc sulfate with elemental zinc at 3 mg/kg/day was started, with remarkable improvement within three (3) days and near-resolution after eight (8) days of zinc therapy. Zinc supplementation was administered for three (3) months with gradual tapering. The skin remained clear despite the withdrawal of zinc supplemen- tation. Response to treatment supported the impression of zinc deficiency, while sustained skin clearance upon withdrawal verified an acquired etiology. Conclusion Zinc deficiency-associated dermatitis is more common in areas where costly diagnostic modalities are not readily available. In clinically suspected zinc deficiency, response to treatment can serve as a retrospective diagnostic feature, and sus- tained clearance upon withdrawal may aid in identifying etiology. Trial of therapy may then be considered in optimizing the cost-ef- fective management of zinc deficiency-associated dermatitis.
Malnutrition

Bullous pemphigoid (BP) is the most common autoimmune blistering disease primarily characterized by tense blisters and occasionally with urticarial plaques, affecting the skin and mucous membranes. These are caused by autoantibodies against BP180 and BP230 which target antigens on the basement membrane zone. The diagnosis relies on the integration of clinical, histopathological, immunopathological, and serological findings. The management depends on the clinical extent and severity. We present in this article a literature review and the clinical consensus guidelines of the Immunodermatology Subspecialty Core Group of the Philippine Dermatological Society in the management of BP.
Pemphigoid, Bullous