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Abstract Chronic liver diseases constitute one of the most common health problems in Egypt. This is simply due to ,I ’: I’ endemicity of schistosomiasis and viral hepatitis. The: end result of these disorders, is usually the development of fibrosis or cirrhosis with its major sequel,portal hypertension. Indeed, portal hypertension and its complications constitute a major health hazard in Egypt and their management remains a challenging problem even allover the world. The incidence of bleeding from oeso~ phageal varices in patients with schistosomal hepatic fibrosis was reported to be 28.3%. Nowadays, there is much interest in the use of beta blockers for the treatment of portal hypertension. In this work, efforts were made to study the effects of both propranolol, a non-cardioselective beta blocker and labetalol, an alpha and beta blocker on portal venous pressure in patients with hepatosplenomegaly and portal hypertension associated with schistosomiasis and on the rate constant (K) as indicator for effective hepatic blood flow. 25 male patients with hepatosplenomegaly were the sUbject of this study and they were subjected to full I58 clinical examination, routine laboratory investigations, E.C.G. tracing, proctosigmoidoscopy, upper gastrointestinal endoscopy, abdominal ultrasonography and liver biopsy. Measurements of the portal venous pressure and estimated hepatic blood flow were made by the intra splenic pulp manometry and radiogold uptake technique respectively. All patients came from endemic areas of sch Lst oeu-, miasis, their age ranged between 12-43 years old, most: of them had past history of schistosomiasis and or antischistosomal treatment and according to Child-Turcotte classification, all were Child-A. They were included in the present study according to good hepatic and renal functions with no previous history of airway obstruction, heart failure or diabetes • Patients then were divided into three groups:- A) Propranolol group (la-patients): Patients were given propranolol orally in doses ranging from 40-160 mg. daily aiming at the reduction of resting heart rate by almost 25%. Each patient was then maintained on the appropriate dose for eight weeks. B) Labetalol group (5-patients): Patients were given labetalol 100 mg. orally twice daily for eight weeks(maximum 159 dose tolerated by the patients and producing less untoward side effects e.g. postural dizzness and easy fatigability. , , placebo (Starch tab.) for eight weeks.” c) Placebo group (iO-patients): PIlt1eiHswere given ,”i~I! ! I I Liver function tests, E.C.G. tracing, measuremente of portal pressure and hepatic blood flow we~ uated in the three groups after eight weeks of re-eval-i I therapy. ’,’ ! , Schistosomiasis represents the mos,t common unde~-’: lying hepatic pathology in the atudied groups as it waS present in 50%, 60% and 50% of cases of the propranolol, labetalol and placebo groups respectively. Schistosomiasis was associated ,with chronic persistent hepatitis in 20% of cases in each group. In placebo group schistosomi iasis was associated with chronic active hepatitis in 10% , and with cirrhosis in another 10%. Meanwhile it was assOciated with cirrhosis in 20% of cases of the propranolol group. Chronic active hepatitia waS found in one patient of propranolol and labetalol groups. Continuous oral administration of propranolol produced significant reduction in portal pressure after eight weeks. This was attributed to the decrease in splanchnic TGO blood flow as consequences of the reduction in cardiac output (due to blockade of BI receptors) and vasoconstriction in the splanchnic vessels due to unopposed alpha receptor activity. Simi1arl~tth~ unopposed al;p~: receptor activity on the hepatic artery producing vasoi, constriction may, by the principal of reciprocity , reduce portal vascular resistance. The significant re-’ duction in the estimated hepatic blood flow observedi, the present study ,after propranolol ,therapy confirmed i this explanstion as long as, the problem of portal vas~ cular resistance had not been solved. No direct correlation waS observed between the, fall in estimated hepatic blood flow and the reduction in portal pressure in those recievingpropranolol. In both labetalol and placebo groups, there was no change in portal pressure and estimated hepatic blood flow after eight weeks of therapy. The less potent effect of labetalol on cardiac output besides its blockade to alpha receptors can explain its effect on portal pressure and hepatic blood flow. Neither propranolol nor labetalol had detrimental effects on liver function tests in both groups. 161 Propranolol, can thus be considered as an effective portal hypotensive drug, though the associated marked reduction in hepatic blood flow may have long term deleterious .. effects on liver. funqtlons.Still ,the role of propranolol in prevention of bleeding oesophageal varices, a matter of controversy. It is concluded therefore that, the use of propranolol in the treatment ’r of portal hypertensioa and bleeding varices should for I’ the time being limited to prolonged randomized contro~ lIed studies only. ” |