[Clinical studies on a new preparation for the probeless determination of gastric acidity].
Explore the source record for details and available documents.
Gastric Acidity Determination↗
Biomedical subjects
M Hanefeld
Publications and source records attributed to M Hanefeld.
Hyperinsulinemia in patients with low fractional catabolic rate of triglycerides.
In non-diabetic persons whose serum triglyceride (TG) concentrations ranged from normal to very high levels, endogenous TG turnover was measured using the radioglycerol method of Farquhar and coworkers. Insulin, FFA, and glucose concentrations were estimated during an oral glucose tolerance test. Stimulated insulin levels were correlated positively to TG concentrations and absolute TG turnover rates, and negatively to fractional TG catabolic rates. FFA concentrations had similar relationships, also in non-insulin-dependent diabetics. A more detailed analysis showed that elevated insulin and FFA levels - as an expression of peripheral insulin resistance - are typical finding in the kind of patients whose fractional TG catabolic rate is low [less than or equal to 0.210 (h-1)], irrespective of actual serum TG concentration. Our data do not suggest a stimulatory role of insulin for TG production.
Adult↗
The role of acarbose in the treatment of non-insulin-dependent diabetes mellitus.
Acarbose is the first of a new class of antidiabetic agents, the alpha-glucosidase inhibitors. Acarbose has proven effectiveness as a first-line drug in type 2 diabetes insufficiently controlled by diet alone. In addition to providing short-term glycemic control, acarbose also reduces HbA1c levels. This effect is greatest when therapy is initiated early in the disease and when baseline HbA1c levels are high. Depending on the baseline HbA1c value, therapeutic doses of acarbose lead to a HbA1c reduction of 0.5%-1.2%. Acarbose may be safely combined with all oral hypoglycemic agents, and has been found to have utility as an adjunct to sulfonylurea and metformin therapy. It also improves control of insulin-treated type 2 diabetes and enables a reduction of exogenous insulin requirements of up to 30%. Acarbose also has beneficial effects on the coronary risk factors, e.g. postprandial triglyceride levels, elevated cholesterol, and hyperinsulinemia. The early phase of acarbose therapy may be associated with side effects such as meteorism, flatulence, and diarrhea. These result from the local effect of the drug and decline with time. To date, there have been no reports of systemic toxicity. Acarbose does not cause hypoglycemias or weight gain.
Acarbose↗
Elimination of lipofundin S during the intravenous fat tolerance test in patients with low, medium, and high fasting triglyceride concentrations.
The intravenous fat tolerance test with Lipofundin S (0.5 ml of 20% emulsion/kg body weight) was performed in 22 male nondiabetic patients. According to their fasting triglycerides (TG), the patients were arranged into three groups: low (less than 2.8 mmol/liter), medium (2.8-5.7 mmol/liter), and high (greater than 5.7 mmol/liter) concentrations. Fractional elimination rates of injected Lipofundin S decreased from 11.08 in low TG to 4.57%/min in high TG; they were positively correlated with fasting levels of high-density lipoprotein cholesterol but negatively with those of TG. The same pattern of correlations was observed with fractional catabolic rates of endogenous TG as measured after injection of tritium-labeled glycerol. The intravenous Lipofundin S load effected transient TG and free fatty acid elevations which were delayed in high TG. The elimination mechanisms of injected Lipofundin S and of endogenous TG are compared.
Adult↗
Efficacy and safety of 300 micrograms and 400 micrograms cerivastatin once daily in patients with primary hypercholesterolaemia: a multicentre, randomized, double-blind, placebo-controlled study.
This study examined the action of cerivastatin, a new statin, in subjects with primary hypercholesterolaemia. The effects of two oral doses of cerivastatin (400 micrograms/day or 300 micrograms/day) were compared with placebo in 349 patients using a multicentre, randomized, double-blind, placebo-controlled study design. Cerivastatin treatment lasted 8 weeks and produced significant reductions in low density lipoprotein-cholesterol (LDL-C) levels from baseline compared with placebo. The reduction in LDL-C was significantly greater with 400 micrograms than with 300 micrograms cerivastatin. When responder rates were examined, the higher (400 micrograms/day) cerivastatin dose was found to be more effective in producing larger (> 40%) reductions in LDL-C levels. Cerivastatin treatment was well tolerated. Only two withdrawals due to adverse events during active treatment occurred, neither of which was considered to be due to the study medication. In addition, no clinically relevant increases in the levels of creatine phosphokinase and hepatic transaminases (alanine transaminase and aspartate transaminase) compared with placebo were seen in this study. In conclusion, cerivastatin treatment produced a significant lowering of LDL-C levels, with the higher dose providing the greatest benefit.
Administration, Oral↗
Effect of the angiotensin II receptor antagonist valsartan on lipid profile and glucose metabolism in patients with hypertension.
The beneficial effects of anti-hypertensive agents on the cardiovascular system can be counterbalanced by the induction of metabolic disorders, such as hyperlipidaemia. The present trial evaluated the effect of the angiotensin II receptor antagonist, valsartan, on the lipid profile and glucose metabolism in patients with mild-to-moderate hypertension. This was a multicentre, randomized, double-blind, placebo-controlled study with a 3-week dietary run-in period under placebo; thereafter, patients received either valsartan 80 mg orally once daily or placebo for 12 weeks. A total of 123 patients were randomized, of whom 112 patients completed the study. Valsartan significantly lowered systolic blood pressure by 14.1 +/- 12.8 mmHg and diastolic blood pressure by 9.0 +/- 6.6 mmHg. In the placebo group, the corresponding values were 7.8 +/- 14.9 mmHg and 6.2 +/- 7.3 mmHg, respectively. Additionally, in the valsartan group, there was a significant decrease in levels of both low-density lipoprotein (LDL) cholesterol (valsartan, -6.3 +/- 24.9 mg/dl; placebo, +4.2 +/- 27.0 mg/dl) and total cholesterol (valsartan, -7.1 +/- 28.1 mg/dl; placebo, +6.0 +/- 29.4 mg/dl) in comparison with placebo. No significant changes were observed in the levels of triglycerides, high-density lipoprotein cholesterol, very low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol and apolipoprotein B after valsartan treatment. No effect of valsartan was found with respect to fasting plasma glucose and glycosylated haemoglobin levels. Valsartan therapy was safe and well tolerated in our patient population. In conclusion, in addition to the marked decrease in blood pressure, valsartan significantly reduces total and LDL cholesterol levels and is neutral on glucose metabolism.
Adult↗
Clinical rationale for rosuvastatin, a potent new HMG-CoA reductase inhibitor.
Coronary heart disease (CHD) is the leading cause of death worldwide, and effective treatment of hyperlipidaemia can prevent development of CHD and significantly reduce the risk for cardiovascular events and mortality in this disease. The advent of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) has revolutionised the treatment of hyperlipidaemia, but many patients receiving these drugs still do not achieve their therapeutic goals. Rosuvastatin (Crestor; formerly ZD4522) is a new, potent and long-lasting inhibitor of HMG-CoA reductase that is highly selective for hepatocytes. Its pharmacokinetics permit once-daily dosing, and a lack of oxidative hepatic metabolism results in a reduced potential for drug-drug interactions. Preliminary clinical results indicate that it produces rapid dose-related reductions in total cholesterol, low-density lipoprotein cholesterol, triglycerides, and apolipoprotein B that may exceed those achieved with other currently available statins. Increases in high-density lipoprotein cholesterol have also been observed. Rosuvastatin is also well tolerated, with no evidence of either hepato- or myotoxicity. It is hoped that new agents such as rosuvastatin may help to reduce the high global morbidity, mortality and associated costs of CHD and related vascular disorders.
Coronary Disease↗