Beta-adrenoceptor antagonist-induced psoriasiform eruption. Clinical and pathogenetic aspects

A number of beta-adrenoceptor blocking drugs have been reported to induce a papulosquamous eruption which resembles psoriasis. We report distinctive clinical, histopathologic, immunocytochemical, and electron microscopic features in beta-blocker-induced psoriasiform eruptions that differentiate this syndrome from psoriasis. Preliminary data suggest that biopsy specimens from eruptions caused by beta 1-selective adrenoceptor blocking agents (metoprolol and atenolol) were characterized by excessive degranulation of the neutrophils in the dermis, while the nonselective beta blockers (propranolol, nadolol, and sotalol) were marked by excessive release of proteolytic enzymes from macrophages, which are thought to possess beta 2-adrenergic receptors. Surprisingly, excessive release of enzymes by lymphocytes were noted in both the beta 1-selective and in the nonselective induced syndromes. It is believed that excessive lysosomal enzyme release by neutrophils, lymphocytes, and macrophages is responsible for the presence of basal keratinocyte herniations, which have previously been shown to correlate with hyperproliferation and psoriasiform changes, as well as with the presence of excessive proteolytic enzymes in the skin. It is postulated that the beta-blocker-induced syndrome may result from enhanced proliferation, motility, and activity of lymphocytes, neutrophils, and cells of the macrophage-Langerhans cell series, stemming from depressed intracellular cyclic adenosine monophosphate levels caused by the beta blockade.