Characterization of cAMP‐phosphodiesterase as a possible laboratory marker of atopic dermatitis

Atopic dermatitis (AD) is a chronically recurrent cutaneous inflammatory disease which may affect up to 10% of the population. The condition is part of the atopic triad which also includes asthma and allergic rhinitis. These diseases have strong hereditary patterns but the genetics is unclear. AD is characterized by a variety of immunologic and pharmacologic abnormalities, and evidence from transplant studies indicates that the basic abnormality is expressed in bone marrow cells. Defects such as increased basophil histamine release and high spontaneous IgE production by B lymphocytes imply defective cellular regulation. Abnormalities of cyclic nucleotide metabolism have been demonstrated in AD, and elevated cAMP-phosphodiesterase (PDE) with resultant low intracellular cAMP levels may have a net permissive effect on immune and inflammatory responses. Biochemical characterization studies of abnormal PDE in mononuclear leukocytes from patients with AD have demonstrated two distinctly abnormal cytosolic fractions of PDE activity. These probably represent different enzyme forms in monocytes and lymphocytes; the consequent dysregulation of these immunologically important cells may explain many of the immune abnormalities associated with AD, and may provide a much needed biochemical marker for epidemiologic, genetic and clinical studies.