Editorial: Hepatosplenic schistosomiasis: a tropical noncirrhosis.

In his clinical vignette on schistosomiasis in this issue of The Yale Journal Dr. Gil-berto Reboucas shows us that the art of medicine is not yet dead. As he compares and contrasts schistosomiasis with cirrhosis, he opens our eyes to a number of fascinating and exciting aspects of schistosomiasis. More important, he exposes the myopic provincialism of some of our concepts of schistosomiasis as a variant of cir-rhosis. Clearly, hepatosplenic schistosomiasis (HSS) is not the tropical equivalent of cirrhosis. The approach to schistosomiasis in Bahia, where medical facilities by our standards are primitive, is simple and direct and, above all, clinical. Although there is great frustration about the overwhelming magnitude of the problem and their inability to prevent schistosomiasis, physicians view the situation pragmatically. In an endemic area schistosomiasis is never overlooked. Cirrhosis may occasionally be missed, however. The diagnosis is established by the microscopic demonstration of the ova in the stools and not by more sophisticated, indirect, inferential, immu-nologic methods. The management of schistosomiasis and, indeed, the whole practice of medicine in Bahia, is carried out with overtones of condomble in a unique blend of voodoo, macumba, and Catholicism. Since we encounter cirrhosis frequently and schistosomiasis rarely in the overde-veloped nations, we lose sight of the fact that in the global sense schistosomiasis is by far the greater problem. We frequently fail to consider schistosomiasis in our differential diagnoses. If one accepts that 2.5% of Americans are seriously alcoholic and that 10% of that population may eventually develop cirrhosis, then up to 500,-000 cases of cirrhosis will emerge in the United States. By contrast, if 10% of the patients with schistosomiasis develop HSS, then we are faced with 20,000,000 patients worldwide. The primary clinical manifestation of HSS is hemorrhage from varices, which is also the most formidable complication of cirrhosis. Actually, however, the clinical behavior of bleeding varices in HSS is much more like hemorrhage following portal vein thrombosis than it is that of cirrhosis. In HSS, as in portal vein thrombosis, and unlike cirrhosis, the total hepatic blood flow is maintained at normal levels by a compensatory increase in hepatic arterial blood flow. Thus, the liver remains functionally normal. Hepatic parenchymal decompensation does not precede nor follow variceal hemorrhage. Clotting function is normal, and bleeding tends to stop spontaneously or easily with therapy. The liver retains the capacity to extract large loads of ammonia and other nitrogenous breakdown …