Background Melasma is a hypermelanosis which is difficult to treat. There are several treatment options for melasma and one of them is topical therapy using 10% L-Ascorbic acid and 10% Zinc sulfate. Aim To compare the efficacy and side effects of 8 weeks 10% L-Ascorbic acid solution with 10% Zinc sulfate on melasma. Methods This is an observational study with cross sectional design and single-blind, comparing the left and right side of the faces sequentially (right-left comparison study) with each treatment 10% L-Ascorbic acid and 10% Zinc sulfate applied at night. In the morning and afternoon patients uses sunscreen SPF 30. Only new patients with melasma seen at Dermatology Polyclinic Dr M Djamil Hospital Padang from March 2012 to May 2012 were included in this study. Results 20 melasma patients were studied. Their ages range from 25-54 years. 12 (60%) had combination triggering factors. All patients had epidermal type of melasma with 65% located over the centrofacial and 35% on the malar zones. After 2 months of treatment there was significant improvement of melasma treated with 10% Zinc sulfate and 10% L-Ascorbic acid with a P value of <0.05. Minimal side effects were found with Zinc sulfate. Conclusion Improvement of melasma was noted with both topical 10% L-Ascorbic acid and 10% Zinc sulfate but minimal side effects were noted with the use of 10% Zinc sulfate.

Inherited epidermolysis bullosa (EB) encompasses over 30 phenotypes or genotypes. A characteristic feature of all types of EB is the presence of recurrent blistering or erosions, the result of even minor traction to this tissues. There are four major types of inherited EB: EB simplex (EBS), junctional EB (JEB), dystrophic EB (DEB), and Kindler syndrome. These differ not only phenotypically and genotypically but more importantly by the site of ultrastructural disruption or cleavage. Dystrophic epidermolysis bullosa (DEB) is a rare mechanobullous genodermatosis inherited either with autosomal dominant or recessive pattern and characterized by fragility, blistering and scarring of the skin and mucous membranes. Blistering is due to abnormalities in anchoring fibrils (AF), microstructures mainly composed of type VII collagen (COLLVII), which contributes to the maintaining of dermal-epidermal adhesion. Most cases are sporadic, but a few show autosomal dominant or autosomal recessive pattern of inheritance. Microscopic studies of EB pruriginosa show typical findings of dystrophic EB, and it has been postulated that itching lesions of EB pruriginosa could represent an abnormal dermal reactivity of some subjects to their inherited bullous disorder. The study of the molecular basis of dominant dystrophic EB (classical) and EB pruriginosa shows that both diseases are caused by a missense glycine substitution mutation by different amino acids in the same codon of COL 7A (G2028R and G2028A)