• schistosomiasis;
  • somatostatin;
  • fibrosis

This review explores the possible modulatory role of the neuropeptide somatostatin in the outcome of Schistosoma-caused morbidity in man. Somatostatin could play an important role in Schistosoma mansoni–man interactions via its influence on intersystem signalling; therapeutically, via its direct effect on Schistosoma-caused morbidity (fibrosis, granuloma size, portal hypertension, variceal bleeding); and via immunomodulation of Schistosoma-induced inflammatory responses in the liver and intestines. In schistosomiasis-endemic regions two interesting patterns of infection emerge. First, the intensity of infection is higher in children than in adults; secondly, at any given time, only a fraction of Schistosoma-infected individuals develop Symmer’s pipe-stem fibrosis. These morbidity patterns cannot be explained on the basis of acquired immunity alone. Somatostatin has an inhibitory effect on hormone, immune and physiological body functions like growth hormone secretion, Interferon (IFN) γ production, collagen I and III formation and hepatic stellate cell activation. Levels of somatostatin secreted endogenously by man upon the onset of Schistosoma infection may be one factor regulating the activity of the above, and thereby fibrosis in the host. The neuropeptide hormone somatostatin may determine pre-disposition to Schistosoma-caused morbidity.