A cyclic
adenosine monophosphate binding abnormality in psoriatic erythrocytes that could be corrected by
retinoid treatment has been reported. It was tested whether this binding abnormality is specific for
psoriasis and the effects of treatment were compared with
etretinate,
cyclosporine A, or
anthralin on 2-(3)H-8-N(3)-cyclic
adenosine monophosphate binding to the regulatory subunit of
protein kinase A in erythrocyte membranes. One hundred and fifteen individuals were evaluated, including: (i) 34 healthy persons; (ii) 15 patients with nonatopic inflammatory
skin diseases (
eczema,
erythroderma,
tinea,
Grover's disease,
erysipelas,
urticaria); (iii) eight with other
dermatoses mediated by immune mechanisms (
systemic lupus erythematosus,
lichen planus, necrotizing
vasculitis,
erythema nodosum,
systemic sclerosis); (iv) 14 with generalized
atopic dermatitis; and (v) 44 with
psoriasis vulgaris clinically assessed by
Psoriasis Area and Severity Index. In
psoriasis, the course of the binding of 2-(3)H-8-N(3)-cyclic
adenosine monophosphate to erythrocytes was measured in nine patients during
a 10 wk treatment with
etretinate, in 21 patients during
a 10 wk treatment with
cyclosporine A, and one patient under topical treatment with
anthralin for 4 wk. We found the following femtomolar binding per mg
protein: (i) healthy persons (1064 +/- 124, mean +/- SD); (ii) nonatopic inflammatory
skin diseases (995 +/- 103); (iii) immune
dermatoses (961 +/- 92); (iv)
atopic dermatitis (960 +/- 110); and (v)
psoriasis (645 +/- 159; p < 0.0001 compared with nonpsoriatics, Mann-Whitney U test). Treatment of
psoriasis with
etretinate,
cyclosporine A, or
anthralin normalized the binding of cyclic
adenosine monophosphate, which was inversely correlated to the
Psoriasis Area and Severity Index score. It was concluded that the decreased binding of cyclic
adenosine monophosphate to
protein kinase A in erythrocytes is specific for
psoriasis and normalizes after successful treatment.