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Abstract SUMMARY AND CONCLUSION In Egypt approximately 20 million individuals, nearly half of the population, are infected with schistosomal hepatic fibrosis. Hepatosplenomegaly is one of the main constant manifestations of schistosoma mansoni infection. Schistosomiasis is the main cause of portal hypertension in Egypt. Its subsequent complication of variceal haemorrhage threatens the life of the patient. The main factor producing portal hypertension is the pre-sinusoidal periportal fibrosis. Hypervolaemia was suggested as a contributing factor for the production of portal hypertension which was mainly attributed to salt and water retension resulting from an increase in plasma aldosterone. Another contributing factor is portal venospasm. Until1 now management of portal hypertension is puzzling. A portocaval shunt does not appear to prolong survival and may be followed by encephalopathy and neuropsychiatric syndromes, even in those patients with good liver function. The complications of sclerotherapy include precipitation or worsening of haemorrhage,oesophageal necrosis, perforation or stenosing. Chest complications, dysphagia, fever and pains are also reported. Medical management included the use of drugs aiming at lowering portal hypertension and thus reducing the possibility of bleeding or recurences. The aim of the present study was to evaluate the different specific-Vasopressin, glyperssin, propranolol and captopril - chemotherapeutic agents as regard to their effects in lowering portal hypertension and their effects on the haemostatic mechanisms especially the fibrinolytic system. The study was carried out on patients with schistosomal hepatic fibrosis and past history of bleeding oesophageal varices. The patients were classified into 4 groups each comprising 10 patients. group ( A ) : received vasopressin in a dose of 20 U. in 100 ml. 5% dextrose over a period of 20 minutes. group ( B ) : received 1 mg of glypressin intravenously group ( C ) : received oral propranolol in a doses which reduced heart rate by 25% (40 to 80 mg) twice daily for one week and the investigations were carried out before and after administration of the drug as scheduled with other drugs. group (D) : received captopril in a dose of 25 mg three times daily one hour before meals for one week and the investigations were carried out before and after administration of the drug as scheduled with other drugs. The patients were subjected to the following: 1 - Complete history taking with special references to schistosomiasis and other diseases known to produce portal hypertension. 2- Complete clinical examination with special stress on the liver, spleen, signs of portal hypertension, manifestations of liver insufficiency, pulmonary hypertension, the presence or absence of ascites and or jaundice.. Patients with cardiac disease, pulmonary hypertension, chest diseases and advanced hepatic insufficiency were excluded from the study. 3- The following investigations were carried out: - investigations to confirm the diagnosis of schistomiasis. - investigations to confirm the diagnosis of portal hypertension and oesophageal varices. - blood pictures before and after 2 weeks of therapy - Liver function tests before and after 2 weeks of therapy. - Euglobulin lysis time test before and after administration of each drug then after 2 weeks. - Systolic time Intervals before and after administration of each drug 6 hours later then after 2 weeks. - measurement of portal pressure before and after administration of each drug 6 hours later then after 2 weeks using the percutaneous trans-splenic route. Vasopressin lowers portal pressure for about an hour after its administration may be due to constriction of the splanchnic arterial bed causing an increase in resistance to the inflow of blood to the gut. It controls haemorrhage from oesophageal varices by lowering portal venous pressure and this mechanism may be aided by contraction of the smooth muscle fibres present in the lower third of the oesophagus. In our study vasopressin did not affect the blood pictures and liver functions. It can be given in schistosoma1 hepatic fibrosis where the liver functions remain intact until1 late stages of the disease. Vasopressin was found to decrease pulse rate, to increase the systemic arterial blood pressure and to decrease the portal pressure for about one hour. The three items may be benefit in cases of bleeding varices in patients with schistosomal hepatic fibrosis. Although complications of vasopressin are well known to occur rarely, but could not be confirmed in our study. Abdominal colicky discomfort and evacuation of the bowels, together with facial pallor are usual side effects during our study. These may decrease the incidence of hepatic coma in cases of bleeding oesophageal varices. Our study showed no effect of vasopressin on the left ventricular performance. This may be attributed to our selection of cases. We recommed utilization of vasopressin in patients after doing E.C.G. or ST1.s if available to exclude patients with cardiac lesions. Vasopressin can be given with nitroglycerine to avoid the coronary vasoconstriction as well as nitroglycerine was known to enhance the decrease in the portal pressure. The main disadvantage of vasopressin noticed in our study is its stimulation to the plasminogen activator. Plasminogen activator will accelerate the fibrinolysis process which is not needed in cases of bleeding oesophageal varices. Vasopressin remains a useful initial, simple, cheap emeregency method of controlling variceal bleeding due to portal hypertension in schistosomal hepatic fibrosis. |