Basic and clinical aspects of atopic dermatitis.

The history of atopic dermatitis is replete with many disparate theories. The most enduring is the allergic causation theory but definitive, convincing evidence remains elusive. Elevated IgE synthesis is well established and reflects abnormal immune regulation. The basic mechanism for the regulatory defect remains conjectural. Cellular immune functions, including delayed cutaneous hypersensitivity, in vitro lymphocyte transformation and chemotaxis are reduced in atopic dermatitis. However, these abnormalities fluctuate with the clinical condition and may be secondary phenomena. A number of physiologic and pharmacologic abnormalities in atopic dermatitis are not clearly understood. Recent studies of patients leukocytes have shown that the diminished cyclic AMP responses are a consequence of increased catabolism by elevated cyclic AMP-specific phosphodiesterase. This high enzyme activity correlates well with elevated IgE synthesis and histamine release by cultured leukocytes. Both of these functions can be reduced by phosphodiesterase inhibitors in vitro. These new investigations provide fresh insight into the pathogenesis of atopic dermatitis and offer possible new therapeutic approaches. Basic studies of biochemical abnormalities may help define the defective molecular site that accounts for the many immune and physiologic abnormalities that have been described in atopic dermatitis and the other atopic conditions.