Could beta blockers be used in th treatment of cirrhotic ascites? the role of serum-ascites albumin gradient estimation

This study included 30 portal hypertensive cirrhotic ascitic patients assigned into 3 groups of 10 patients each, well matched as regards age and sex. Groups I, II and III were put on diuretics, beta blocker propranolol, and both, respectively, and restudied 1 month latter. Serum-ascites albumin gradient [S-AAG] was found to correlate positively with grade of esophageal varices and portal vein diameter [P <0.001] and the reduction of portal blood flow [P <0.05]. Diuretics with or without beta blockers propranolol gave a good therapeutic response as regards body weight [P <0.001], 24-hour urine output [P <0.001] and sodium excretion [P <0.05], whereas propranolol alone was found to have deleterious effect on ascites. There was a decrease in renal blood flow in the 3 groups which was more by the use of propranolol. It was concluded that S-AAG is a good predictor of portal hypertension and its response to beta blockers. The portal hypotensive effect of beta blockers showed no beneficial effect on ascites for renal hemodynamic changes resulting in less water and sodium excretion

Effect of autonomic dysfunction on anginal perceptual threshold in diabetes mellitus

In diabetes anginal perceptual threshold may be delayed. To investigate the pathogenesis of delayed anginal perceptual threshold we examined 80 subjects classified into a control group [n = 24] not diabetics but with other risk factors and a diabetic group [n = 56]. Diabetic patients were subdivided according to prior autonomic function testing into a group with normal autonomic functions [n = 30] and a group with autonomic neuropathy [n = 26]. All subjects underwent treadmill exercise after assessment of their autonomic functions. Anginal perceptual threshold, defined as the time from onset of exertional >/= 1 mm ST-segment depression to onset of chest pain, was measured in all cases with exercise-induced angina. Silent myocardial ischemia was encountered in 14.3% of diabetic patients vs 0% in nondiabetic control subjects. This percentage was significantly higher in diabetics with than in diabetics without autonomic neuropathy [23.08% vs 6.67% respectively] [P < 0.01]. Exercise-induced angina was significantly higher in diabetics than in non diabetics [32% vs 16.67% respectively] [P < 0.01], with no -significant difference between diabetics with and without autonomic neuropathy. Anginal perceptual threshold was significantly prolonged in diabetics than in non-diabetics [114.4 +/- 6.3 sec vs 45 +/- 7.5 sec]

Cardiac function and its relation to microalbuminuria in type 11 diabetes mellitus: an echocardiographic study

To study the possible changes in cardiac function associating type II diabetes mellitus, echocardiography was performed for 30 non-insulin dependent diabetic patients and 10 normal healthy subjects as control group. The selected diabetic patients were free from risk factors that may affect cardiac function and were further subdivided according to duration of diabetes and presence or absence of microalbuminuria. The results of this study showed a high incidence of impaired left ventricular function [systolic and diastolic] of variable degrees [18/30, 60%]. The mean values of duration of diabetes, fasting and 2 hours post prandial blood glucose for patients with left ventriculardysfurction 9.5 +/- 3.97, 225.11 +/- 66.68 mg/dl and 305.72 +/- 78.85 mg/dl respectively were singnificantly higher [P<0.01, P<0.05 and P<0.01 respectively] than those for diabetics with normal left ventricular function [6.0 +/- 2.45 years, 182.41 +/- 37.01 mg/dl and 239.5 +/- 41.27 mg/dl respectively. Also we found that the degree of cardiac dysfunction was higher in patients with microalbumimuria than that in diabetics without microalbuminuria. We concluded that type II diabetes mellitus may be associated with cardiac dysfunction which may positively correlate with duration of diabetes and degree of hyperglycemia. Also a higher degree of cardiac dysfunction might be expected in the presence of microalbuminura which could be considered as an indicator not only of early diabetic nephropathy but also of early other diabetic microvascular complications including myocardial dysfunction

possible role for deficient vitamin E and selenium antioxidant activity in the pathogenesis of diabetic retinopathy

This study aimed at the delineation of the role possibly played by the two antioxidant synergists, namely vitamin E and selenium in the pathogenesis of diabetic retinopathy. Serum analysis for vitamin E [by a colorimetric reaction] and selenium [using atomic absorption spectrophotometer techniques] was studied in insulin dependent [n = 14] with [n = 7] and without [n = 7] retinopathy [fundus], non insulin dependent diabetics [n = 45] with [n = 14] and without [n = 31] retinopathy matched to 16 control subjects. Serum selenium was significantly lower [P < 0.01] in NIDD patients [6.05 ug/dl] compared to IDD [10.96] and controls [10.67]. Vitamin E serum levels [mg/l] were significantly lower in NIDD patients [46.04] and IDD [38.41] compared to controls [57.71]. Vitamin E was significantly lower [P < 0.01] in IDD patients with retinopathy [27.17 mg/l] in relation to those without [49.64].A significant correlation was found between serum selenium and vitamin E in IDD patients [P < 0. 05] especially those with retinopathy [P <0.01] with a significant decrease of vitamin E in such patients. It can be concluded that age may have a role in decreased serum selenium in diabetic patients while decreased serum tocopherol may be related to diabetes and may have a role in the pathogenesis of retinopathy in IDD patients

Angiotensin converting enzyme[ACE] inhibition versus conventional treatment of cirrhotic ascites: impact of either treatment on the renin angiotensin system

Plasma renin activity [PRA] and serum aldosterone were estimated in 10 healthy males and in 30 males with hepatic ascites before and after either angiotensin converting enzyme, ACE, inhibition by captopril 50 mg/day [n = 10], spironolactone 50 mg + Furosemide 40 mg/day [n = 10] or restriction of salt and water [n = 10]. Body weight [Wt] and abdominal girth [Gth], serum sodium, potassium and liver function tests [LFT's] were also checked before and after treatment for 3 weeks. Ascetics had higher PRA and aldosterone compared with controls [P < 0.01]. After captopril, PRA increased and aldosterone decreased [P < 0.05 and P < 0.01] with a significant decrease in Wt and Gth [P < 0.01]. After diuretics, PRA and oldosterone significantly increased [P < 0.05] with non-significant decrease in wt and Gth. Restriction of salt and water caused nonsignificant increase in PRA and a significant increase in aldosterone [P < 0.05] with non-significant increase in Wt and Gthd. Electrolytes and LFT's were not significantly affected by the 3 treatment modalities. The antiascitic effect; delta Wt and delta Gth; by captopril was significantly more than the diuretic effect [P < 0.05]. It is concluded that suppression of renin-angiotensin aldosterone system by captopril, has a significant antiascitic effect in patients with hepatic ascites. In addition, the diuretic induced hyperaldosteronism, a potential risk for failed diuresis on the long term, might be prevented by the addition of an ACE inhibition