Drugs online research references
Am J Manag Care. 1999 Jan;5(1):62-8.
Safety and efficacy of metformin in a restricted formulary.
Swislocki AL, Khuu Q, Liao E, Wu E, Beza F, Lopez J, Kwan G, Noth RH.
VA Northern California Health Care System (VANCHCS), Martinez, USA.
OBJECTIVE: To assess the efficacy and safety of metformin (MET) in the Veterans' Administration Northern California Health Care System during the period from June 1995 through April 1996 when its use required approval by Endocrinology. STUDY DESIGN: A retrospective review of patient charts and computerized pharmacy and laboratory records. Patients served as their own historical controls. PATIENTS AND METHODS: Patients receiving MET (n = 251) were identified from the pharmacy database. On-line laboratory data, including the intermediate outcome variable HbA1c, were retrieved by computer for the interval 4 months prior to the initial prescription to May 1996. Clinical data including weight and blood pressure were obtained from chart review. RESULTS: Of 228 patients whose charts were available for review, 29 reported side effects, and 12 discontinued use due to these side effects. No patients were identified with lactic acidosis. Both baseline and treatment data on HbA1c were available on 164 patients. Mean HbA1c (%) data (unpaired), expressed as mean +/- SE, were as follows: between 4 months pretreatment and 1 month pretreatment, 9.41 +/- 0.19 (n = 103 tests); between 1 month pretreatment and baseline, 9.41 +/- 0.19 (n = 110 tests); 3 months of treatment, 8.79 +/- 0.16 (n = 157 tests, P < 0.05); 6 months of treatment, 8.30 +/- 0.17 (n = 79 tests, P < 0.0001); 9 months of treatment, 8.72 +/- 0.24 (n = 70 tests, P < 0.05), compared to pretreatment values. Similar analysis of unpaired weight and blood pressure data in 152 patients did not reveal any reduction in these clinical parameters over this treatment period. Serum lipids were unchanged on treatment (by paired analysis), but the number of tests was limited. CONCLUSION: In this setting, MET provided sustained beneficial effects on glycemic control and was well tolerated. Any effects on weight, blood pressure, and serum lipids were not demonstrable in this analysis. We conclude that MET can substantially improve outcome of diabetes care.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10345968&dopt=Abstract
Metabolism. 1999 Nov;48(11):1357-60.
Effects of insulin and metformin on glucose metabolism in rat vascular smooth muscle.
Ofenstein JP, Dominguez LJ, Sowers JR, Sarnaik AP.
Department of Pediatrics, Wayne State University School of Medicine, Detroit, MI, USA.
Glucose metabolism in vascular smooth muscle cells (VSMCs) is characterized by substantial lactate production even in fully oxygenated conditions. Insulin and metformin, an insulin-sensitizing agent, have direct effects on the vascular tissue metabolism. We investigated whether insulin or metformin can induce a switch in VSMC glucose metabolism from lactate production to pyruvate oxidation, by measuring lactate oxidation as determined by the conversion of [1-14C]-D,L-lactate to [1-14C]-pyruvate and subsequent oxidation to acetyl coenzyme A and 14CO2 by pyruvate dehydrogenase (PDH). Lactate oxidation was measured in control rat aortic cultured VSMCs incubated for 30 minutes in media with and without additional glucose compared with VSMCs cultured in the presence of insulin or metformin. The addition of glucose to VSMCs decreased lactate oxidation (4.6+/-1.7 v 9.6+/-2.4 pmol/cell/min, P < .001). In the absence of additional glucose, metformin decreased lactate oxidation in VSMCs compared with controls (4.9+/-1.4 v 9.6+/-2.4 pmol/cell/min, P < .01). Metformin in the presence of glucose caused the greatest decline in lactate oxidation (2.5+/-0.4 pmol/cell/min, P < .001). In contrast to the effects of metformin, insulin increased lactate oxidation both with (12.9+/-1.5 pmol/cell/min, P < .001) and without (17.9+/-4.4, P < .01) additional glucose. This suggests that insulin facilitates VSMC utilization of lactate as a source of pyruvate and energy production even during noncontractile periods.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10582541&dopt=Abstract
Diabetes Res Clin Pract. 1989 Jan 3;6(1):61-7.
Study of the effect of metformin on platelet aggregation in insulin-dependent diabetics.
Gin H, Freyburger G, Boisseau M, Aubertin J.
Clinique Medicale et des Maladies Infectieuses, Hopital Pellegrin, Bordeaux, France.
The role of metformin on platelet aggregation was studied in subjects affected by relatively well controlled type 1 diabetes. 1700 mg of metformin were added to their usual daily treatment; nothing else was changed. Patients were trained to monitor their own glycaemia and presence of degenerative retinopathy was proved. Before the administration of metformin and on day 21, the platelet induced by 1.25, 2.5 and 5 mumol of ADP and by collagen was studied. Fibrinogen, cholesterol, triglycerides, glycosylated haemoglobin and mean blood glucose levels did not show any significant modification after treatment but the maximum aggregation induced by ADP was significantly decreased; the inhibition of aggregation was particularly sensitive for low doses of ADP. No significant correlation was found between the variations in metabolism data and the reduction of the amplitude of platelet aggregation. Metformin, added to the usual treatment undergone by a diabetic treated with insulin, seems to affect platelet aggregation independently of other metabolic factors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2702918&dopt=Abstract
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