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BACKGROUND: Hypoglycemic coma is a continuous threat for diabetic patients treated with insulin and/or oral hypoglycemic agents; it may be associated with substantial morbidity and mortality. METHODS: We retrospectively reviewed our clinical experience with drug-induced hypoglycemic coma during a 7-year period. RESULTS: The study consisted of 102 patients and included 61 females and 41 males. The median age was 72 years. Ninety-two patients suffered from type 2 diabetes mellitus; 10 patients had type 1 diabetes mellitus. The median lowest blood glucose level was 1.77 mmol/L (32 mg/dL). Drug-induced hypoglycemic coma occurred in 99 patients out of the hospital, while 3 patients developed it during hospitalization. Drug-induced hypoglycemic coma occurred in patients undergoing treatment with insulin, glyburide, and combined therapy with insulin and glyburide, insulin and metformin, or glyburide and metformin. Ninety-three patients had at least 1 of the following risk factors: age older than 60 years, renal dysfunction, decreased intake of energy, and infection. Fourteen patients concomitantly received drugs that potentiated hypoglycemia. Forty patients responded to treatment within the first 12 hours, while 62 patients had protracted hypoglycemia of 12 to 72 hours' duration. Morbidity included physical injuries in 7 patients, myocardial ischemia in 2 patients, and stroke in 1 patient. Death occurred in 5 patients. CONCLUSIONS: Hypoglycemic coma is a serious and not an uncommon problem among elderly patients with diabetes mellitus and treated with insulin and/or oral hypoglycemic drugs. Risk factors contribute substantially to the morbidity and mortality of patients with drug-induced hypoglycemic coma. Enhanced therapeutic monitoring may be warranted when hypoglycemic drugs are administered to an elderly patient with the above predisposing factors and potentiating drugs for hypoglycemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9989540&dopt=Abstract
Acta Pharmacol Toxicol (Copenh). 1984 May;54(5):327-32.
The effects of metformin compared to the effects of phenformin on the lactate production and the metabolism of isolated parenchymal rat liver cell.
Jalling O, Olsen C.
The metabolic effects of metformin were compared to the effects of phenformin on isolated parenchymal liver cells from fed and fasted rats with ethanol or glycerol as the only substrate. Both biguanides caused a fall in the hepatic oxygen-consumption, in the cellular ATP-content and in the ATP/ADP-ratio. The lactate production and the concentration-ratios of lactate/pyruvate and of beta-hydroxybutyrate/acetoacetate rose. The production rate of ketone bodies remained unchanged. This response was the same whether the hepatocytes were from fed or fasted rats and whether glycerol or ethanol was substrate. Only quantitative differences in the response on the biguanides were detected. The effects of the biguanides were dose dependent. Phenformin was ten times more potent than metformin. The same holds for their therapeutical potency. The findings indicate inhibition of the oxidative phosphorylation by both biguanides resulting in reduction of the cytoplasmic and the mitochondrial redox potentials causing enhanced lactate production. It is concluded that metformin excerts the same effects as phenformin on the hepatic metabolism, when the concentration ratio is about ten to one. Both biguanides give rise to elevated lactate production. This effect is highly increased when ethanol is present.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6431751&dopt=Abstract
Diabete Metab. 1991 May;17(1 Pt 2):164-7.
Erythrocyte glucose consumption in insulin-dependent diabetes: effect of metformin in vitro.
Rapin JR, Lespinasse C, Yoa R, Wiernsperger N.
Laboratory of Clinical Pharmacy, Faculty of Medicine and Pharmacy, Dijon, France.
Erythrocyte glucose consumption in red blood cells from healthy donors or insulin-dependent diabetics with stable glycemia was measured using the 2-deoxyglucose technique. Data showed that the formation of glucose-6P was severely impaired in diabetic red blood cells in both normo- and hyperglycemic incubation conditions. This defect seems to be inherent to the disease. Coincubation with Metformin (6.4 ug/ml) did not modify the G6P levels in RBCs from healthy donors and in RBCs from diabetics when incubated in normoglycemic conditions. However, when diabetics RBCs were incubated in a hyperglycemic medium, addition of Metformin strongly improved the intracellular levels of G6P. The underlying mechanism for the defect and the correction by Metformin remains to be determined. This study shows that also red blood cells may be involved in the failure of glucose homeostasis in diabetes and thus this may represent an additional target for therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1936470&dopt=Abstract
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