Observations on the Pathogenesis of Carcinoid Heart Disease and the Tanning of Fluorescent Fibrin by 5-Hydroxytryptamine and Ceruloplasmin

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Abstract
A theory is suggested to explain the pathogenesis of carcinoid heart disease. The process occurs in several stages. Subendocardial edema and damage to tissue result from the direct action of circulating 5-HT on tissue mast cells; reactive fibrosis occurs in subendocardial tissue and fibrin is deposited onto the injured endothelium. The fibrin is tanned as a result of the interaction of 5-HT and ceruloplasmin and resists fibrinolysis. The deposit of tanned fibrin grows by accretion, and becomes organized and transformed to dense connective tissue. Autopsy data are summarized from a patient who manifested functioning carcinoid syndrome. The results of an experimental biochemical model are presented in which in vitro fibrin-tanning resulted from the interaction of 5-HT and ceruloplasmin. The frequent occurrence of connective tissue fibrosis in this syndrome is emphasized; its pathogenesis is thought to be similar to that of the initial endo-cardial lesion, with edema of connective tissue and injury acting as the stimulus for reactive fibrosis.

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