Postinflammatory hyperpigmentation (PIH) is very likely the most common adverse effect of laser treatment in dark-skinned individuals. Treatment of PIH is difficult, thus emphasizing the need for prevention strategies. Acquired bilateral nevus of Ota–like macules (ABNOMs) are clinically characterized by blue-brown macules on periocular and nasal skin, and Q-switched lasers represent an excellent therapeutic modality. In this randomized, controlled, split-face study, Manuskiatti et al sought to evaluate the benefit of epidermal cooling on reducing the occurrence of PIH after Q-switched Nd:YAG laser treatment of ABNOMs. Unexpectedly, cold air cooling was associated with an increased risk of PIH after laser treatment, through an unknown mechanism.
Herpes gestationis (HG) is a rare, autoimmune, bullous disease that affects women in the second or third trimester of pregnancy. Immunologically, HG is characterized by linear deposition of C3 with or without associated IgG at the basement membrane zone on direct immunofluorescence and by the presence of serum antibodies directed against the 180-kDa bullous pemphigoid antigen (BP180). In this case report, Aoyama et al describe a mother and neonate with cutaneous manifestations of HG. The BP180 enzyme-linked immunosorbent assay indexes were observed in both patients and clearly demonstrated that the vesicular lesions in the neonate were caused by transplacental passage of pathogenic BP180 antibodies.
Graft-vs-host disease (GVHD) is a multisystem disease initiated by allogeneic T lymphocytes that recognize foreign tissue antigens in the host. In the chronic form, GVHD demonstrates cutaneous manifestations that may be classified as lichenoid or sclerodermatous in nature. In this case series of patients who developed cutaneous GVHD after hematopoietic stem cell transplantation, Creamer et al identified a novel, distinct group of 10 who were characterized by persistent, widespread, chronic eczematous dermatitis. Histopathologically, these eczematous features strikingly coexisted with changes of GVHD. The factors provoking the expression of an eczematous phenotype in these patients remain unclear.
Erythropoietic protoporphyria (EPP) is an inherited disorder of porphyrin metabolism caused by a partial deficiency of the ferrochelatase gene (FECH). Clinical expression of the disease commonly results from the coinheritance of a null FECH mutation plus a wild-type low-expressed allele, which further reduces ferrochelatase activity to below a critical threshold of about 35%. The low-expression allele IVS3-48C is relatively common among European populations, such that overt EPP is typically inherited in such a way that it resembles an autosomal dominant disease with low clinical penetrance. In this case series, Herrero et al confirm the common view that clinically overt EPP is most typically associated with inheritance of the low-expression IVS3-48C allele in trans to a severe FECH mutation. One rare homozygous mutation was identified in a patient showing early signs of liver involvement.
Psoriasis is a common, chronic, inflammatory, hyperproliferative skin disease. Therapeutic options for psoriasis vary widely in terms of efficacy and toxic effects. In this discrete choice experiment, Seston et al explore the extent to which different attributes of a treatment affect a patient's choice of therapy and the hierarchical importance of these attributes. Most respondents were willing to trade among different attributes of a treatment to achieve an improvement in their psoriasis with minimal adverse effects. For example, patients indicated that they would wait longer for therapy to work if the chance of a severe adverse effect could be reduced. Long-term risks (such as skin cancer or liver damage) were prioritized over short-term risks (such as skin irritation). Only one-quarter of the sample patients were unwilling to trade among attributes and always chose the therapy with a particular level of their chosen attribute, most often no risk of skin cancer.
This Month in Archives of Dermatology. Arch Dermatol. 2007;143(9):1107. doi:10.1001/archderm.143.9.1107