Transforming growth factor beta 1 in essential hypertension and glomerulonephritis: the effects of inhibition of the renin angiotensin system on its serum level in glomerulonephritis

This study was carried out on 12 patients with essential hypertension without micro or macroalbuminuria [group I] and 15 patients with chronic glomerulonephritis with mean 24-hour urinary protein = 4.3 + 3.l g/24 hours, [group II], 7 patients had hypertension [group IIa] and 8 patients had normal blood pressure [group IIb]. Ten healthy subjects were taken as controls. Blood urea, serum creatinine, fasting and 2-hour postprandial plasma glucose, urine analysis, 24-hour urinary protein and serum TGF-beta 1 were measured in diseased groups and controls. TGF-beta 1 was significantly higher in group I with essential hypertension [mean +/- SD 80.4 +/- 18.2 ng/dl] and group II with glomerulonephritis. [387.2 +/- 89.0 ng/dl], compared to control group [36.3 +/- 12.9 ng/dl]. In group II, patients with glomerulonephritis mean serum TGF-beta 1 was significantly higher than group I patients with essential hypertension [p <0.001]. In group II, TGF-beta 1 was not significantly different in hypertensive [group IIa] or normotensive patients [group IIb] [mean serum TGF-beta l = 393.3 +/- 92.0 and 379.0 +/- 84.l ng/dl, respectively]. Patients with glomerulonephritis received the angiotensin converting enzyme inhibitor ACE-I [captopril 25-75 mg/day] for four weeks then blood urea, serum creatinine, 24-hour urinary protein and serum TGF-beta 1 were re-estimated. There was significant reduction in both 24-hour urinary protein and TGF-beta 1 after captopril with no significant changes in urea and creatinine. It might be concluded that serum TGF-beta 1is elevated in patients with essential hypertension and glomerulonephritis. In patients with glomerulonephritis the use of ACE-I may reduce proteinuria and serum TGF-beta 1. Reduction of TGF-beta 1 might be a possible mechanism in the reduction of proteinuria in patients with glomerulonephritis, however, other mechanisms cannot be ruled out

Plasma level of soluble thrombomodulin in acute myocardial infarction and acute ischemic stroke in type 2 diabetes mellitus

The present study was carried out on 40 patients with acute myocardial infarction [AMI] or acute ischemic stroke [AIS]. The patients were divided into four groups [each group comprised ten patients]: Group I included nondiabetic patients with AMI, group II included diabetic patients with AMI, group III included nondiabetic patients with AIS and group IV included diabetic patients with AIS. In addition, ten healthy subjects were taken as a control group. Mean plasma soluble thrombomodulin [sTM] level was significantly lower in patients with AMI [group I + group II] [3.88 ng/ml + 3.8] and in patients with AIS [group III + IV] [3.75 ng/ml + 2.8] compared with the control group [6.64 ng/ml + 2.33] with no significant difference between patients with AMI and AIS. Acute myocardial infarction [AMI] and acute ischemic stroke [AIS] were associated with decreased plasma sTM, reflecting the decreased expression of endothelial TM, thus disturbing the balance between procoagulant and anticoagulant factors towards a pro-coagulant state. In patients with AIS, diabetics have lower plasma sTM than non-diabetics

Von Willebrand factor as marker of endothelial dysfunction in non - insulin - dependent diabetes mellitus.

This study evaluated the plasma level of von Willebrand factor [vWF] in non-insulin-dependent diabetes mellitus [NIDDM] patients with and without microalbuminuria [MA] to elucidate whether MA is a consequent of endothelial injury. This work was enrolled on 30 NIDDM patients classified into three groups, each including 10 age matched subjects. Group I included normoalbuminuric patients, group II included microalbuminuric patients and group III included microalbuminuric patients complicated by coronary artery disease [CAD], in addition to 10 healthy normoalbuminuric age matched control subjects. Von Willebrand factor, malondialdehyde [MDA], vitamin C, erythrocyte reduced glutathione [GSH], albumin execration rate [AER], total cholesterol, LDL and HDL cholesterol, urea and creatinine were measured in all patients groups and control group. It can be concluded that NIDDM is characterized by many metabolic disorders including excessive oxidative stress, deficiency of antioxidants and dyslipidemia, resulting in endothelial injury, which can be marked by an elevation of vWF level even before the development of microalbuminuria. Thus, microalbuminuria might be considered a consequence of endothelial dysfunction

Nonalcoholic steatohepatities in type 2 diabetes mellitus

The present study was conducted on 22 females with type 2 diabetes mellitus and hepatomegaly in whom ultrasonography showed bright hepatomegaly, in addition to 20 healthy controls of comparable age and sex. Patients with evidence of hepatitis C, B, metabolic liver disease or autoimmune hepatitis were excluded. None of the patients and controls was alcohol drinker. In all patients and controls, fasting and two-hour postprandial plasma glucose, HbA1c, bilirubin, aspartate aminotransferase [AST], alanine aminotransferase [ALT], alkaline phosphatase, cholesterol and triglyceride were done. Liver biopsy using Baxter cut needle [G14] was done in patients only. It can be concluded that nonalcoholic steatohepatitis [macrovesicular steatosis and lobular inflammation alone] occurs in 31.8% of patients with hepatic steatosis in type 2 diabetes mellitus. Hepatocyte necrosis and progression to hepatic fibrosis may occur in some cases. Progression to fibrosis may occur in patients with inadequate glycemic control

Growth hormone and insulin like growth factor-1 in patients with heart failure due to dilated cardiomyopathy

The aim of this study was to evaluate the level of growth hormone [GH] and insulin like growth factor-1 [IGF-1] in patients with heart failure due to idiopathic dilated cardiomyopathy to find out if the development or progression of heart failure is associated with a derangement of GH and IGF-1. The study was conducted on 30 patients with congestive heart failure due to dilated cardiomyopathy and 7 normal healthy subjects as a control group. The results revealed a significant increase in the serum levels of GH and a significant low serum IGF-1 and albumin in the patients as compared with the control group. Then, the patients were classified according to the NYHA functional classes into four classes [I, II, III and IV]. Sixteen patients were found in functional class IV. There were no differences in the results of this class and the whole patients group, suggesting that class IV represented the whole patient group studied. The study concluded that the serum levels of GH were increased and the serum levels of IGF-1 were diminished in patients with heart failure due to dilated cardiomyopathy. These abnormalities in GH and IGF-1 may have many etiological factors. Abnormalities of GH/IGF-1 axis might have a role either in the development or the progression of heart failure in dilated cardiomyopathy