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John J. Voorhees, MD; Elizabeth A. Duell, PhD; Lawrence J. Bass, MD; John A. Powell, MD; E. Richard Harrell, MD

Arch Dermatol. 1972;105(5):695-701.

Abstract
Previously we suggested that incomplete differentiation, accelerated proliferation and glycogen accumulation in epidermis of psoriatic lesions might be due to deficient adenosine 3',5'-monophosphate (cyclic AMP) in epidermis of the lesion. Therefore, we measured endogenous cyclic AMP in involved and uninvolved epidermis of 25 psoriasis patients and normal epidermis of 25 control subjects. A statistically significant decrease in cyclic AMP was found in involved psoriatic epidermis when compared with uninvolved psoriatic and control epidermis. Because cyclic AMP regulates glycogen metabolism and promotes differentiation of cancer cells in culture while limiting their proliferation, the cyclic AMP deficiency may play a pathophysiological role in the rapid epidermal cell cycle kinetics of psoriasis. Therefore, topical application of cyclic AMP analogues or agents which promote cyclic AMP synthesis or retard its hydrolysis might be used therapeutically to either normalize psoriatic differentiation or prevent psoriasis from occurring.

Author Affiliations
Ann Arbor, Mich

From the Department of Dermatology, University of Michigan Medical School, Ann Arbor.

Footnotes
Accepted for publication Feb 22, 1972.

Read in part before the Workshop on Cell Controls in Psoriasis, National Institutes of Health, Bethesda, Md, 1971; and in part before the American Society for Experimental Pathology at the 56th FASEB annual meeting, Atlantic City, NJ, 1972.

Reprint requests to Department of Dermatology, University of Michigan Medical School, R6558 Kresge Medical Research Bldg, Ann Arbor, Mich 48104 (Dr. Voorhees).

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