Study of the prognostic value of early echocardiographic assessment of left ventricular function in acute variceal bleeding

To determine the prognostic value of early echocardiographic assessment in patients with acute variceal bleeding. The study was conducted on 80 patients with portal hypertension, admitted to the emergency hematemesis and tropical medicine units at the Alexandria University main Hospital. They were divided into two groups; group I: included 40 patients with acute variceal hemorrhage and group II: included 40 patients without active bleeding. Transthoracic echocardiography was used to measure and calculate left ventricular fractional shorting, left ventricular ejection fraction, stroke volume, cardiac output, total peripheral vascular resistance and the left venticular stoke work. According to the inhospital course; the bleeders [group I] were further subdivided into two subgroups: group la included 16 [40%] patients who had a poor evolution [inhospital mortality or early variceal rebleeding], and group Ib included 24 [60%] patients were discharged uneventfully. Using standard univariate analysis, the poorly evoluted patients had lower stroke volume [64.44 +/- 13.25vs. 82.33 +/- 15.88ml/beat, p=0.017], lesser cardiac index [3.10 +/- 0.66vs. 4.48 +/- 0.69L/min/[m]2, p=0.007], higher systemic vascular resistance [1387 +/- 379vs. 990 +/- 239dynes/sec/[cm]-5,p=0.010] and lower left ventricular stroke work [77.94 +/- 13.34vs. 104.18 +/- 23gram-m; p=0.007]. The prognostic value of such four variables was tested by running a stepwise logistic regression analysis. The cardiac index was the only significant predictor factor for poor evolution among our patients [chi square = 13.78, P=0.002]. The resting cardiac index is a useful predictor for inhospital mortality among patients with portal hypertension and acute variceal bleeding. Echocardiographic measurement of the cardiac index and the systemic vascular resistance may help to identify the high risk bleeders to optimise their management

Effect of progesterone hormone on liver fibrosis in experimental schistosomiasis in mice

The present work aimed at studying the effect of progesterone on liver fibrosis in experimental schistosomiasis mansoni in mice. One hundred fifty female albino mice were used. Each animal was infected with 100 cercariae of S. mansoni using the partial immersion method. Animals were divided into 3 equal groups. Group I was infected with S. mansoni only, in group II progesterone was given for 8 weeks after infection and in group III progesterone was given for 4 weeks after the 8th week of infection. Two animals from each group were sacrificed weekly, dissected and biopsies were taken from liver to be stained by hematoxylin and eosin, Van-Gieson and silver stains. It was found that progesterone decreased cellular infiltration, reticular and fibrous tissue formation in liver specimens. This was especially when progesterone was given for a long period from the start of infection [group 1]

study of the pathology of pulmonary schistosomiasis in hamsters experimentally infected with schistosoma mansoni

The present work aimed to study the pathological features of pulmonary schistosomiasis in 25 hamsters. Twenty were infected with S. mansoni and five were used as controls. Fifty days after infection, the animals were sacrificed, dissected and their lungs were processed for staining by haematoxylin and eosin as well as Verhoef Van Gieson stains. Results showed that 6 animals died during the third week of infection. Ten animals showed signs of s. pulmonary infection [71.31%]. Adult worms and s. ova were detected in the lungs prior to the development of portosystemic collaterals, which suggested that liver sinusoids may be the direct route through which worms and ova travel to the lungs. The majority of lesions observed simulated those reported in man. Ova were present in alveoli in some sections verifying their possible detection in sputum. Parenchymal lung granulomata were found in 8 animals [57.12%]. These granulomas showed minimal necrosis and fibrosis compared to what was described in the liver. The prominent vascular changes observed in the lungs of infected hamsters were end arteritis, intimal thickening and medial arterial hypertrophy. Secondary pneumonia was observed in all infected hamsters due to the lowered resistance secondary to S. infection

Acute phase reactant proteins in typhoid fever

The level of the acute phase reactant proteins alpha-1 antitrypsin, alpha-1 acid glycoprotein, haptoglobulin and c-1 complement component together with IgG and IgG were determined in 30 blood culture positive acute typhoid patients and 10 healthy controls. Results showed that the levels of IgG and the acute phase reactants [APR] studied were significantly increased in patients with acute typhoid fever than in healthy controls. This increased level is a response to tissue damage by the infectious agent and could be attributed to an increased rate of synthesis of acute phase reactants by the liver. It is related to the host immune responses and antimicrobial defenses

Plasma fibronectin in patients with hepatic schistosomiasis mansoni

The present study was designed to determine the concentration of plasma fibronectin in patients with hepatic Schistosomiasis mansoni in different stages and to examine the relation of the fibronectin level to the pathogenesis of schistosomal liver fibrosis. The study included 20 male patients and 10 matched controls. Ten patients were in the hepatomegalic stage [group I] and 10 were in the late stage of hepatic fibrosis with splenomegaly [group II]. Results showed that the mean fibronectin concentration in group I [47.75 mg/dl] was significantly higher than that of controls [20.9 mg/dl] or group II [19.17 mg/dl]. This is most probably secondary to an increase in the secretion of fibronectin from the macrophages in the secretion of fibronectin from the macrophages in the schistosomal hepatic granulomas in the hepatomegalic stage. With the development of liver fibrosis, granulomas shrink and macrophages may disappear leading to low fibronectin plasma level in the late fibrotic stage. Plasma fibronectin shares in the formation of tissue matrix fibronectin. Modulation of the sequence of deposition of plasma fibronectin into tissue fibronectin may possibly delay the development of end stage liver fibrosis