Drugs online research references
Ann Fr Anesth Reanim. 1987;6(2):88-94.
[Physiopathological approach to pathological hyperlactatemia in the diabetic patient. Value of blood metformin]
[Article in French]
Lambert H, Isnard F, Delorme N, Claude D, Bollaert PE, Straczek J, Larcan A.
Type B lactic acidosis, or pathological hyperlactatemia (PHL), is defined by an arterial lactate level greater than 5 mmol X l-1. It is a known and severe complication of diabetes mellitus treated with biguanide hypoglycaemic agents, particularly phenformin which was taken off the French pharmaceutical market in 1977. Metformin, which remains the only biguanide hypoglycaemic agent currently prescribed in France, may also lead to this complication. However it does so less frequently and mostly in the diabetic presenting with renal failure. A few well studied cases showed that PHL could be correlated with excessive metformin blood levels, i.e. a toxic mechanism. In order to find out whether this toxic mechanism was the real cause of PHL in diabetics treated with metformin, a systematic study of metformin blood levels was carried out in 20 such patients. They had all been admitted to a critical care unit presenting with PHL. The results of this study led us to distinguish between two groups of patients. The seven patients of the first group had high metformin blood levels (4.3 to 65.8 micrograms X l-1). In these, renal excretion or extrarenal dialysis lowered or normalized their hyperlactatemia, and six of the seven recovered from PHL. In the second group, with thirteen patients, metformin blood levels were within the normal therapeutic range (0.225 to 3 micrograms X l-1) for seven patients and close to zero for the other six. This second group received the same treatment as the first one. Only three patients recovered, the others all died.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3109285&dopt=Abstract
Acta Diabetol Lat. 1988 Jul-Sep;25(3):205-14.
Rapid improvement in insulin binding to erythrocyte insulin receptors in non-insulin-dependent diabetes mellitus during therapy.
Ramachandran A, Susheela L, Mohan V, Kuzhali DA, Viswanathan M.
Diabetes Research Centre, Royapuram, Madras, India.
Insulin binding to erythrocyte receptors was studied in 36 newly diagnosed male subjects with NIDDM, treated with diet alone (Group I; n = 10) or diet + glibenclamide (Group II; n = 12) or diet + glibenclamide + metformin (Group III; n = 14). Fourteen matched non-diabetic subjects were also studied as controls. Initially, mean (+/- SD) specific insulin binding was lower in NIDDM patients than in controls (p less than 0.001), due to decreased receptor number and affinity. Control of diabetes with short-term therapy (10 +/- 2 days) resulted in significantly increased specific insulin binding in Groups II and III (p less than 0.001). A marginal increase was observed in Group I (p less than 0.01). The improved insulin binding observed in Group II and III patients after short-term therapy was maintained even after long-term therapy (9 +/- 1 months). Analysis of the insulin binding data by Scatchard plots and average affinity profiles indicated increased receptor number and affinity after short-term therapy. However, changes in affinity were reversed with long-term therapy in Groups II and III and the predominant effect appeared to be an increase in the number of binding sites.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3149105&dopt=Abstract
Metabolism. 1997 Apr;46(4):454-7.
Metformin therapy is associated with a decrease in plasma plasminogen activator inhibitor-1, lipoprotein(a), and immunoreactive insulin levels in patients with the polycystic ovary syndrome.
Velazquez EM, Mendoza SG, Wang P, Glueck CJ.
University of Los Andes, Merida, Venezuela.
Sixteen nondiabetic women with polycystic ovary syndrome (PCOS) aged 18 to 33 years were studied before and after 8 weeks on metformin (1.5 g/d) therapy to assess whether reducing hyperinsulinemia would reduce the levels of the major inhibitor of fibrinolysis, antigenic plasminogen activator inhibitor type 1 (PAI-1). Compared with six normal control women, PCOS women had a higher body mass index (BMI), waist to hip ratio, fasting insulin (Izero), insulin area under the curve during oral glucose tolerance testing (IA), glucose area under the curve during oral glucose tolerance testing (GA), IA/GA ratio, PAI-1, luteinizing hormone (LH) and ratio of LH to follicle-stimulating hormone (FSH), and free testosterone, and lower high-density lipoprotein (HDL) cholesterol (all P < .025). On metformin, BMI decreased 1.3% (P = .04), Izero 43% (P = .002), IA 31% (P = .03), GA 11% (P = .02), PAI-1 16% (P = .01), lipoprotein(a) [Lp(a)] 42% (P = .004), free testosterone 46% (P = .0006), LH 44% (P = .004), and the LH/FSH ratio 41% (P = .0001). On metformin, absolute and percent reductions in Izero correlated with absolute and percent reductions in PAI-1 (r = .60, P = .015 and r = .64, P = .008). On metformin, by stepwise multiple regression, the absolute reduction in Izero was a significant determinant of the absolute reduction in PAI-1 (partial R2 = 35%, P = .02), and the percent reduction in Izero was a significant determinant of the percent reduction in PAI-1 (partial R2 = 52%, P = .003). Metformin decreases Izero in hyperinsulinemic PCOS patients, reverses the hyperinsulinemia-driven endocrinopathy, decreases PAI-1, and decreases Lp(a), and should thus reduce the increased risk of atherothrombosis in PCOS.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9109854&dopt=Abstract
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