Pathogenesis of varices in schistosomal portal hypertension

Patients with schistosomiasis and portal hypertension have significantly lower levels of hydroxyproline in their saphenous veins and anterior rectus sheaths than do individuals without schistosomal hepatic fibrosis. The stomach of patients with schistosomal portal hypertension demonstrates an increased number of lymphatics by lymphangiography. The disrupted lymph node architecture in these patients could be partially responsible for dilation, tortuosity, and retrograde lymph flow in the gastric lymphatics. These histological and lymphangiographic findings could be attributed to the effect of venous and patients with decompensated schistosomal portal hypertension revealed edema of the entire esophageal wall with lymphatic dilation and tortuosity. Based upon these data, we suggest that the varices that develop in patients with schistosomal portal hypertension occur as a consequence of an increased portal venous pressure together with acquired lymphangiectasia as well as an intrinsic weakness of the walls of the portosystemic venous channels.