PSORIATIC LESIONS IN PATIENTS WITH CHRONIC LIVER-DISEASE ARE DISTINCTFROM PSORIASIS-VULGARIS LESIONS, AS JUDGED ON BASIS OF INTEGRIN ADHESION RECEPTORS
G. Giannelli et al., PSORIATIC LESIONS IN PATIENTS WITH CHRONIC LIVER-DISEASE ARE DISTINCTFROM PSORIASIS-VULGARIS LESIONS, AS JUDGED ON BASIS OF INTEGRIN ADHESION RECEPTORS, Hepatology, 20(1), 1994, pp. 56-65
Psoriatic lesions are relatively frequent in patients with chronic liv
er disease. Furthermore, therapy with interferons tends to exacerbate
the symptoms. The pathogenesis of psoriatic lesions is unclear. An imp
ortant question is whether such lesions may be linked to the underlyin
g chronic liver disease in these patients, or whether they are inciden
tal manifestations of psoriasis vulgaris. We collected biopsy specimen
s from involved and uninvolved skin areas of chronic liver disease pat
ients with psoriatic manifestations, as well as from psoriasis vulgari
s patients, and investigated the patterns of integrin adhesion recepto
rs by means of immunohistochemical methods. Integrin expression is kno
wn to be characteristically altered in psoriasis vulgaris. We found so
me of these changes in chronic liver disease psoriatic lesions - namel
y pericellular redistribution and suprabasal expression of the basemen
t membrane receptor alpha 6 beta 4 and of the intercellular integrins
alpha 2 beta 1 and alpha 3 beta 1. However, psoriasis vulgaris causes
two other typical changes: One is the induction of the prototype fibro
nectin receptor alpha 5 beta 1, and the other is the alteration of int
egrin expression in areas of the epidermis that are macroscopically no
rmal. These two changes were not found in chronic liver disease psoria
sis biopsy specimens in 14 patients investigated. Thus integrin expres
sion may be useful in differentiating chronic liver disease psoriatic
lesions from psoriasis vulgaris lesions. Even though the two types of
lesions are indistinguishable on inspection or by their histological f
eatures, they may be caused by distinct pathogenetic mechanisms. It re
mains to be seen whether the underlying chronic liver disease has a ro
le, albeit indirect, in such mechanisms.