Faculty Bibliography

Atopic dermatitis is a chronic inflammatory skin disease that is frequently associated with respiratory allergies. Atopic dermatitis develops as a result of a complex interrelationship of environmental, immunologic, genetic, and pharmacologic factors. Efforts to understand the relative contributions of these factors have led to research seeking to identify the relevant effector cells and mediators involved in the pathogenesis of atopic dermatitis. These factors include the pattern of local cytokine release, the differentiation of helper T cells, multiple roles of IgE, skin-directed cell responses, infectious agents, and superantigens. This article reviews these cellular and immunologic mechanisms underlying atopic dermatitis and discusses how an understanding of their role in the inflammatory process may lead to improved treatments for atopic dermatitis

In two randomized, double-blind, multicenter studies, a total of 631 adult patients with moderate to severe atopic dermatitis applied tacrolimus ointment (0.03% or 0.1%) or vehicle twice daily for up to 12 weeks. The mean percent body surface area (%BSA) affected at baseline was 45%, and 56% of patients had severe atopic dermatitis. As previously reported, these studies showed that tacrolimus ointment was superior to vehicle for all efficacy parameters measured. This report focuses on the safety of tacrolimus ointment in these studies. The most common adverse events were the sensation of skin burning, pruritus, flu-like symptoms, skin erythema, and headache. Skin burning and pruritus were more common among patients with severe or extensive disease; these events were usually brief and were resolved during the first few days of treatment. Common adverse events with a significantly higher incidence in one or both of the tacrolimus ointment groups than in the vehicle group included skin burning, flu-like symptoms, and headache. More patients in the vehicle group discontinued the study because of an adverse event than in either of the tacrolimus ointment groups. There were no notable or consistent changes in any laboratory variables. Tacrolimus was not detected in 80% of blood samples collected. Measurable concentrations of tacrolimus were transitory and were not associated with adverse events. Tacrolimus ointment is a safe therapy for the treatment of adult patients with atopic dermatitis on the face, neck, or other body regions

Episodes of recurrent urticaria and angioedema may be a clinical manifestation of cutaneous necrotizing venulitis. Known as urticarial vasculitis, this edematous form of necrotizing venulitis occurs in patients with serum sickness, connective tissue disorders, hematologic malignant conditions, an IgM?M component, infections, or physical urticarias after the administration of therapeutic agents, and as an idiopathic disorder. The skin lesions appear as erythematous, occasionally indurated wheals which may contain foci of purpura. Although the individual urticarial lesions may last for less than 24 hours, they often persist up to 3-5 days. The episodes of urticaria are chronic; approximately 70% of the afflicted individuals are women. General features include fever, malaise, and myalgia. Specific organ involvement includes enlargement of the lymph nodes, liver, and spleen and involvement of the synovia, kidneys, gastrointestinal tract, respiratory tract, eyes, and central nervous system. In the treatment of urticarial vasculitis there are no double-blind, placebo-controlled trials. Reports exist of the treatment of patients with H1 antihistamines, nonsteroidal anti-inflammatory agents, colchicine, hydroxychloroquine, dapsone, prednisone, azathioprine, methotrexate, cyclophosphamide, and intramuscular gold therapy

The most frequent site of organ involvement in individuals with any form of mastocytosis is the skin. Cutaneous lesions include urticaria pigmentosa, mastocytoma, diffuse and erythematous cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans. The major histologic feature is an increase in the number of mast cells in the dermis. Treatment depends on the type of skin lesions