ABSTRACT
The role of the cyclic nucleotide phosphodiesterases (PDE) in the pathogenesis of atopic dermatitis (AD) was proposed more than 20 years ago as a possible explanation for the rapid enzymatic breakdown of cAMP found in leukocytes from atopic dermatitis patients when compared to leukocytes from healthy controls (1). Based on these findings, inhibition of PDE enzymes was proposed as an approach to correct the biochemical abnormality found in AD.
