Drugs online research references
Rev Invest Clin. 1991 Oct-Dec;43(4):305-14.
[Postprandial lipemia in the non-insulin-dependent diabetes mellitus patient. Effect of gemfibrozil]
[Article in Spanish]
Lerman Garber I, Ahumada Ayala M, Cardoso Saldana G, Zamora Gonzalez J, Ichazo Cerro S, Posadas Romero C.
Departamento de Endocrinologia, Instituto Nacional de Cardiologia Ignacio Chavez, Mexico, D.F.
The postprandial (PP) elevations in triglyceride rich lipoproteins are potentially atherogenic. To describe the characteristics of PP lipemia after a fat load in non insulin dependent diabetes mellitus (NIDDM) and evaluate the response to a fibric acid derivative, seven males with NIDDM were studied for 12 hours after the ingestion of a fat load (65 g of fat/square meter of body surface). Plasma glucose, and triglycerides and cholesterol levels were measured in total plasma and in the different lipoprotein fractions. The fat load study was repeated after four weeks of treatment with gemfibrozil (GEM) 600 mg x 2. PP triglyceridemia correlated significantly with the fasting triglyceride concentrations. Basal triglyceride levels diminished significantly with the use of gemfibrozil and so did the magnitude of the PP triglyceridemia. Otherwise the curve patterns of lipemia were similar before and after the use of the fibrate; only the triglyceridemia persisted for a longer period of time. Patients with NIDDM may have a significant PP lipemia which is not likely related to the diabetes per se as to the increased triglyceride levels frequently observed in these patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1798863&dopt=Abstract
Atherosclerosis. 1991 Jul;89(1):59-67.
Lipoprotein (a) and coronary heart disease risk: a nested case-control study of the Helsinki Heart Study participants.
Jauhiainen M, Koskinen P, Ehnholm C, Frick MH, Manttari M, Manninen V, Huttunen JK.
National Public Health Institute, Helsinki, Finland.
To prospectively assess the role of lipoprotein(a) (Lp(a)) as a risk factor for coronary heart disease, the serum Lp(a) concentration was determined in 130 subjects without coronary events and in 138 patients in whom coronary events (i.e. fatal and non-fatal myocardial infarction and cardiac death) occurred during the 5-year Helsinki Heart Study. The participants of this study (n = 4081) were 40-55-year-old men who were devoid of coronary heart disease at the beginning of the trial; half were randomized to gemfibrozil and the other half to placebo treatment. In patients with coronary events blood pressure and total cholesterol were not significant predictors of the events but their LDL cholesterol was higher than compared to the control group in this cohort (P less than 0.05). The serum Lp(a) concentration was determined by immunoassay from samples obtained 3 months after the beginning of the trial and then stored at -20 degrees C until analysed. Studies on the effect of long term storage at -20 degrees C on serum Lp(a) levels did not reveal significant changes in Lp(a) concentration in sera stored for up to 8.5 years. The distribution of Lp(a) concentrations were similar in the men with coronary events and the controls. Nor did the mean or median levels of Lp(a) differ significantly between the two groups. Measurements of Lp(a) levels in fresh samples using 2 different immunoassays did not reveal any significant difference between the participants who had survived a myocardial infarction or participants without cardiac events. Thus, we conclude that in the Helsinki Heart Study cohort the serum Lp(a) level was not a predictor of future coronary events.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1837713&dopt=Abstract
Proc R Soc Med. 1976;69 Suppl 2:58-63.
Gemfibrozil: effect on serum lipids, lipoproteins, postheparin plasma lipase activities and glucose tolerance in primary hypertriglyceridaemia.
Nikkila EA, Ylikahri R, Huttunen JK.
The hypolipidaemic effect of a new drug, gemfibrozil (CI-719), was studied for 20 weeks in 20 patients with primary type IIb, III, IV or V hyperlipoproteinaemia. Baseline recordings of serum cholesterol (9.1 mmol/l), triglyceride (3.79 mmol/l) and ultra-centrifugally isolated lipoproteins were obtained during a six-week pretreatment period with stable diet and body weight. With 800 mg of gemfibrozil per day given in two divided doses, the mean serum triglyceride and cholesterol levels were decreased by 44.6% and 10.5% respectively, during 20 treatment weeks. Only 2 patients were completely resistant to the hypolipidaemic action of the drug. Serum triglyceride was brought down to normal levels in 9 subjects. After 12 weeks of treatment the mean VLDL-triglyceride, VLDL-cholesterol, and LDL-triglyceride were reduced by 48.5%, 57.6%, and 22.7% respectively, while the HDL-cholesterol rose by 16%. The LDL-cholesterol increased slightly but significantly during treatment in type IV patients and decreased in type IIb patients. The change of LDL-cholesterol showed an inverse correlation with the initial LDL-cholesterol level (r=-0.87). The postheparin plasma lipoprotein lipase and hepatic lipase activities, determined separately by an immunochemical method, increased during four weeks of gemfibrozil treatment (+18.1% and +20.6% respectively), but neither of these changes was significantly correlated with the changes in any of the serum lipid or lipoprotein levels. Oral glucose tolerance was not influenced by the treatment, but one-hour plasma insulin increased slightly during administration of the drug. One patient discontinued the drug after eight weeks because of generalized allergic eczema, but no other side effects were recorded. It is concluded that gemfibrozil is highly effective in reducing elevated serum VLDL levels. The simultaneous elevation of LDL in type IV patients needs more attention and study. The mechanism of the hypolipidaemic action of the drug is so far obscure, but it might partly be due to an increased efficiency in VLDL removal by an increased activity of lipoprotein lipase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=190608&dopt=Abstract
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