Study of endothelin in portal hypertension

The aim of this study was to evaluate the plasma level of endothelin -1 in portal hypertension in patients with hepatic cirrhosis. Thirty patients with portal hypertension due to cirrhotic liver were studied at the Critical Care Medicine and Internal Medicine departments at Alexandria Main University Hospital. Clinical evaluation of the severity of illness was done using Modified Child- Pugh Score and portal hypertension was assessed by doing Duplex Doppler ultrasonogram. Plasma levels of endothelin-1 [ET-1] were estimated by radioimmunoassay. Plasma levels of endothelin-1 [ET-1] were significantly higher in patients with portal hypertension than control group [mean +/- SD was 94.3 +/- 14.91, 33.8 +/- 5.39 ng/ml respectively, p=.000]. Also, the study showed that plasma levels of ET-1 were significantly higher in patients with ascites than without [mean +/- SD was 104.15 +/- 11.71, 86.77 +/- 12.68 ng/ml respectively, p= .001]. The levels of ET-1 were significantly higher with the increased severity of liver disease according to modified Child -Pugh score [F = 10.25, p = .005]. Plasma ET-1 concentrations were increased in patients with portal hypertension with or without ascites, compared with controls. Patients with cirrhosis and ascites have increased ET-1 concentrations compared with those without ascites. The degree of increasing of plasma levels of endothelin was related to the severity of liver disease. The result of the present work may be of help in understanding the mechanism and may open a new field in the management of portal hypertension

IL-6 and thyroid hormones in critically ill patients with sepsis

The aim of this study was to investigate whether the activation of the cytokine system, in particular, activation of interleukin-6 production, has a role in pathogenesis of thyroid hormones changes in critically ill patients with sepsis. Thirty one patients with sepsis were studied at the Critical Care Medicine department at Alexandria Main University Hospital. Clinical evaluation of the severity of illness was done using sepsis related organ failure score [SOFA score]. Blood samples were obtained within 6 hours after admission and were collected with EDTA. Plasma was separated by centrifugation at 3000rPM for 10 minutes and stored at -80°C until assayed. 10 blood samples were obtained from healthy volunteers [5 males and 5 females] as control group. These plasma samples were used for measurement of inerleukin-6 [IL-6], free thyroxine [fT4], free triiodothyronine [f T[3]] and thyroid stimulating hormone [TSH]. Serum interleukin-6 level was significantly higher in patients with sepsis than control group [mean +/- SD was 100.904 +/- 10.941 pg/ml versus 26.652 +/- 5.125 pg/ml respectively, P = 0.0001*]. The patients were divided into 4 groups according to SOFA score. It was found that fT3 and FT4 levels were significantly decreased with increased severity of sepsis [F= 20.306, P=.000* and F= 7.025, P= .001* respectively], while serum levels of IL-6 were increased significantly with the increased severity of sepsis [F =18.55, p =.000*]. A significantly positive correlation was found between IL-6 and SOFA score, [r = .823, P .000*] while significantly negative correlation was found between levels of fT3 and serum IL-6 levels and SOFA score, [r= -.887, P = .000* and r = -.866, P= .000* respectively]. Also, a significant negative correlation was found between levels of fT4 and serum IL-6 levels and SOFA score [r= -.597. P =.000* and r= -.579, P = .000* respectively]. Also, there was a negative correlation between TSH, IL-6 and SOFA score levels but significant only with IL-6 levels [r= -0.407, P= .023* and r= -.0085, P= 0.649 respectively.] This study demonstrated that there is a positive correlation between serum level of IL-6 and severity of sepsis as it was significantly increased with increased SOFA score. While fT3, fT4 and TSH levels are significantly decreased with increased levels of IL-6. So, these suggest that the activation of the cytokine system, in particular, activation of interleukin-6 production, has a role in pathogenesis of thyroid hormones changes in critically ill patients with sepsis

Soluble tumor necrosis factor receptor -2 in acute coronary heart diseases

The aim of this study was to evaluate the impact of soluble tumor necrosis factor receptor -2 in acute coronary heart diseases. This prospective study had been carried on 30 patients with acute coronary heart diseases [group I] admitted consecutively in the critical care medicine department at Alexandria main university hospital. Demographic data and medical history had been taken. Thorough clinical examination, Troponin, CKMB, ECG, x ray chest and echocardiography had been done for each patient on admission. In addition, samples of plasma had been taken from each patient and also, from 10 healthy volunteers of matched age and sex [control group] [group II] to determine plasma level of soluble tumor necrosis factor receptor -2 [sTNFR-2] by ELISA test. Plasma level of sTNFR-2 in group [I] was significantly higher than the group [II], [mean +/- SD was 15.315 +/- 8.909 versus 5.03 +/- 2.01ng/ml respectively, t=5.22. p = 0.0001*]. It was found non significant positive correlation between both ejection fraction [EF] and fraction shorting [FS] [left ventricular systolic function] and sTNFR-2, [r=0.121, p=0.526, r=0.293 and p=0.116 respectively]. Non significant, negative correlation was found between both early filling left ventricle/late filling left ventricle [E/A ratio] [left ventricular diastolic function] and mitral valve regurgitation [MR] and sTNFR-2 [r=- 0.108, p=0.569, r=-0.320 and p=0.085 respectively]. A negative significant correlation was found between wall motion score index [WMSI] and sTNFR-2 [r=-0.419, p=0.021*]. Measurement of sTNFR-2 may be of value in evaluation of the TNF system in acute coronary heart diseases. sTNFR-2 is increased in acute coronary heart diseases and may modulate the in vitro cytotoxicity of TNF. In this work, it is not clear whether the elevation of sTNFR-2 in acute coronary heart diseases is due to an actual increase or to a reduced breakdown or elimination of these receptors. Further explorations are needed to more precisely define the meaning, molecular basis, and interaction ofsTNFR-2 and TNF