Copyright 2007 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2007
Biologic therapies such as tumor necrosis factor α (TNF-α) inhibitors have revolutionized the therapeutic approach to rheumatologic diseases. Although these agents have also proven useful in the treatment of psoriasis, paradoxically, there have been reports of TNF-α inhibitors triggering or worsening psoriasis. In this case series, de Gannes et al demonstrate clinical and histopathologic evidence of psoriasis in 15 patients treated with TNF-α inhibitors for a variety of rheumatologic conditions. These data suggest that these therapies may induce interferon α expression in lesional dermal vasculature in predisposed individuals, thus promoting the development of psoriasis lesions in a manner similar to infection or injury.
Dermoscopy is a noninvasive technique that allows for visualization of subsurface skin structures by decreasing reflection at the stratum corneum–air interface. The accurate interpretation of dermoscopy is essential for differentiating benign from malignant lesions, and histopathologic analysis has been used to better understand the basis of dermoscopically revealed structures. The perpendicular plane of section of a pathologic specimen hinders precise correlation with the horizontal plane view of dermoscopy. In this study, Scope et al demonstrate that in vivo reflectance confocal microscopy is a noninvasive imaging technique that allows for en face visualization of microscopic structures and correlation of these structures with dermoscopic data. Used jointly, these techniques may offer improved diagnostic accuracy in the evaluation of melanocytic neoplasms.
Epidermolysis bullosa acquisita is a chronic subepidermal bullous disease of the skin and mucous membranes that is characterized by the presence of autoantibodies directed against type VII collagen, a major component of anchoring fibrils. At least 5 clinical subtypes have been identified, and owing to the rarity of the disease, controlled clinical trials to identify the most appropriate therapies are lacking. In this case report, Niedermeier et al describe 2 patients with severe, refractory, mechanobullous epidermolysis bullosa acquisita who were successfully treated with a combination of immunoadsorption followed by rituximab, a genetically engineered chimeric monoclonal antibody directed against CD20.
Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease that typically affects elderly patients. Reports of BP in children are quite rare and typically occur after age 8 years. As in adult BP, antibodies directed against the 180-kDa bullous pemphigoid antigen seem to be involved in the pathogenesis of the disease, but the clinical manifestations differ. In this case series, Martinez-De Pablo et al describe 4 infants with characteristic clinical, histopathologic, and immunologic features of BP. All had blisters predominantly on the hands and feet, and autoantibodies of both the IgA and IgG class to the NC16A domain of BP180 were demonstrated in these patients.
Pompholyxlike appearance at presentation with tense vesicles and blisters on the hands (A) and feet (B).
Injectable dermal fillers are becoming increasingly popular for improving skin contour defects. Nonanimal stabilized hyaluronic acid (NASHA) is among the most widely used temporary fillers in the United States. The long-lasting effect of this filler has been attributed not only to the stabilizing crosslinks, but also to the observation that NASHA absorbs increasing amounts of water while being slowly degraded. This hydration may help maintain dermal volume even as the injected material is being broken down. Wang et al demonstrate that NASHA also induces robust neocollagenesis, thus partially restoring the dermal matrix that is diminished in photodamaged skin. This suggests that collagen accumulation from multiple NASHA injections over time may yield durable cosmetic effects.
This Month in Archives of Dermatology. Arch Dermatol. 2007;143(2):146. doi:10.1001/archderm.143.2.146