Patients with schistosomiasis and portal hypertension have significant
ly lower levels of hydroxyproline in their saphenous veins and anterio
r rectus sheaths than do individuals without schistosomal hepatic fibr
osis. The stomach of patients with schistosomal portal hypertension de
monstrates 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 th
e gastric lymphatics. These histological and lymphangiographic finding
s could be attributed to the effect of venous and lymphatic hypertensi
on. A postmortem histological examination of the esophagus of patients
with decompensated schistosomal portal hypertension revealed edema of
the entire esophageal wall with lymphatic dilation and tortuosity. Ba
sed upon these data, we suggest that the varices that develop in patie
nts with schistosomal portal hypertension occur as a consequence of an
increased portal venous pressure together with acquired lymphangectas
ia as well as an intrinsic weakness of the walls of the portosystemic
venous channels.