Subacute cutaneous lupus erythematosus leukoderma treated with melanocyte‐keratinocyte transplantation procedure

Depigmented lesions may occur as postinflammatory sequelae of subacute cutaneous lupus erythematosus (SCLE), leading to great psychosocial impact. A 53‐year‐old male patient presented with post‐SCLE depigmented facial lesions after five years of disease stability. We proposed surgical treatment with melanocyte‐keratinocyte transplantation procedure (MKTP), and after five months the patient achieved 90% repigmentation, without Koebner phenomenon (KP). In theory, KP is a possible complication of MKTP procedure since the preparation of the receptor area involves the use of dermabrasion. In an attempt to avoid it, we suggest to maintain the treatment of the underlying disease and wait for a minimum period of disease stability before the procedure.     

Successful treatment of hemorrhagic bullous Henoch‐Schonlein purpura with intravenous immunoglobulins

Henoch‐Schonlein purpura (HSP) is the most common systemic vasculitis in childhood. There is no consensus about the management for isolated cutaneous manifestations in HSP. We describe a case of HSP presenting with severe skin lesions that did not respond to standard therapy with corticosteroids. The 11‐year‐old child was treated with intravenous immunoglobulins, which induced rapid and persistent resolution of symptomatology.     

HLA markers in familial Lichen Sclerosus

Background: Lichen sclerosus (LS) has been identified with increased frequency in families,often associated with HLA markers, mainly DQ7. A genetic co‐etiology seems likely in this setting. Moreover, there is an association of LS with autoimmune disorders, such as the presence of anti‐thyroid peroxidase autoantibodies (anti‐TPO), a hallmark of autoimmune thyroid diseases. Patients and Methods: In 3 families affected by LS, we verified their HLA markers, and identified previously undiagnosed cases of LS and autoimmune disorders. 30 individuals were examined with history, skin biopsy, HLA class I and II typing by PCR‐SSP, and measurement of anti‐TPO, free thyroxine and thyroidstimulating hormones (TSH) levels. Results: There were 8 cases of LS, 50 % of them anti‐TPO+. Autoimmune disorders were found in 40 % (total) and in 87.5 % of those affected. Most common HLA markers were B*15, B*57, CW*03, CW*07, CW*18, DRB1*04, DRB1*07, DRB4*. The three latter have been previously associated with LS. Conclusion: New cases of LS and autoimmune disorders can be detected in first degree relatives of patients with LS. The presence of anti‐TPO antibodies strongly suggests autoimmune thyroiditis. There is intra‐familial association between the haplotype HLA‐B*15 ‐DRB1*04 ‐DRB4* and anti‐TPO,emphasizing their link with thyroiditis. New familial approaches might help to make clear the pathogenesis of LS and its association with autoimmune diseases.