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PubMed1981

Metformin-induced lactic acidosis: potentiation by ethanol.

Although lactic acidosis has been recognized as a potential hazard in biguanide therapy, this complication has been claimed to be extremely rare with dimethylbiguanide (DMBG) (metformin). In the present studies, using the fasted guinea pig, DMBG (125-500 mg/kg i.p.) caused marked dose-related changes in both plasma glucose (43-88% reduction) and blood lactate (3.5-13 fold increase). Lactate/pyruvate ratios were substantially increased. While i.p. doses of 100 mg/kg of DMBG or of 1 g/kg of ethanol produced no changes in plasma glucose, lactate or pyruvate, the two drugs administered conjointly at the indicated doses produced a 53% decrease in plasma glucose and 2 and 10-fold increases in pyruvate and lactate levels respectively, and correspondingly, an increase in the lactate/pyruvate ratio. Ethanol decay curves indicated that DMBG did not significantly influence the disappearance of ethanol from the blood. These results indicate that: (1) doses of DMBG which produce hypoglycemia are associated with lactic acidosis, and (2) this effect of DMBG can be markedly potentiated by ethanol.

Acidosis↗
PubMed1995

[Mitochondrial encephalomyopathies: 3243 mutation as a central matter].

Molecular diagnosis for mitochondrial diseases offers a powerful means to clarify that mitochondrial DNA (mtDNA) defects have different characteristics from those of nuclear DNA. Regarding the relationship between genotype and phenotype, there is a dual heterogeneity. It means that one mutation, for example, a 3243 mutation, has several clinical phenotypes, including MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes), myopathy only, diabetes and/or deafness and even CPEO (chronic progressive external ophthalmoplegia). Conversely, one phenotype, for instance, MELAS has several genetypes; 3243, 3271, and 3291 mutations. The second unique event in mitochondrial DNA mutation is heterogenous distribution of mutant mtDNA in a mitochondrion or a cell that is called heteroplasmy. The extend of heteroplasmy seems different from tissue to tissue providing clues to explain the variability of tissue impairment and heterogenous clinical symptoms. The above evidence suggests that we should take care in selecting tissues to be tested. The third problem remained is on maternal inheritance. It makes the genetic counselling on mitochondrial diseases at clinics difficult and laborious. In conclusion, mtDNA analysis must be used as a last resort to get final diagnosis.

Animals↗
PubMed1997

Metformin: a safe and effective treatment in the management of NIDDM.

The oral antihyperglycemic drug metformin has a unique mechanism of action and controls glycemia in both obese and normal-weight NIDDM patients without inducing hypoglycemia, insulin stimulation or hyperinsulinemia. Metformin used in combination with sulfonylureas has a synergistic effect in lowering fasting and postprandial glucose and hemoglobin A1c levels, and improving the lipid profile. Metformin does not increase lactate production from skeletal muscle and has little clinically significant effect on vitamin B12 and folic acid absorption. Lactic acidosis associated with metformin use is extremely rare (reported incidence of 0.03/1,000 patient-years exposure) and has occurred predominantly in patients for whom the drug was contraindicated. Observance of prescribing guidelines will greatly minimize risk, since risk factors have been identified. Metformin can be safely used in the elderly, provided prescribing precautions are followed. Dosing in the elderly should be conservative, with dose adjustment designed to achieve normal blood sugar levels.

Acidosis, Lactic↗
PubMed1989

Diabetic ketoacidosis.

The classic presentation of DKA, consisting of hyperglycemia, anion gap acidosis, and ketonuria, is readily recognized. The diagnosis may be missed, however, in the patient who is euglycemic, has a negative nitroprusside test for ketones, or has a nonanion gap metabolic acidosis. Treatment includes replacement of fluid and electrolytes lost through osmotic diuresis. Failure to recognize the magnitude of total-body potassium depletion and to begin replacement despite an initially normal serum potassium level may lead to fatal cardiac arrhythmia. Serum glucose must be monitored closely to avoid hypoglycemia; dextrose should be added to the infusion once the serum glucose falls to 250 mg per dl. Insulin is required to reverse ketoacid production by the liver; low-dose therapy is recommended. Ketogenesis may be reversed inadequately unless insulin treatment is continued until the anion gap has normalized. Failure to recognize precipitating causes may result in increased morbidity and mortality from underlying infection or myocardial infarction as well as rapid relapse of ketoacidosis.

Diabetic Ketoacidosis↗
PubMed2001

[Metabolic disorders and lipodystrophy. Adverse effects of antiretroviral therapy].

Lipodystrophy resp. lipoatrophy and metabolic disorders under antiretroviral therapy are mainly imputed to protease inhibitors. Nucleoside-analogues are suspected to cause lactatea-cidosis as well. The treatment does not pursue standardized concepts. The lipodystrophic alterations which are not endangering the patient but are often cumbersome for him, can be met by PI-saving therapy in a few cases. Against hyperlipidemia cholesterol-synthesis inhibitors are currently debated. Diabetes-therapy follows the conventional concepts. In case of lactate-acidosis antiretroviral therapy must be discontinued temporarily.

Anti-HIV Agents↗
PubMedDate not supplied

Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: case report.

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA1c) 8%, C peptide <0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.

Adult↗
PubMed1999

Prevalence of macular pattern dystrophy in maternally inherited diabetes and deafness. GEDIAM Group.

OBJECTIVE: To evaluate the prevalence of macular pattern dystrophy (MPD) in maternally inherited diabetes and deafness (MIDD), a new subtype of diabetes mellitus that cosegregates with a mutation of mitochondrial DNA (i.e., the substitution of guanine for adenine at position 3243 of leucine transfer RNA) and to report the clinical characteristics of MPD. DESIGN: Prospective cohort study. PARTICIPANTS: Forty-six patients from 29 families with an adenine-to-guanine mutation of mitochondrial DNA were recruited from a French collaborative multicenter study. Thirty-five patients had MIDD, 8 were asymptomatic children of MIDD patients, and 3 had MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes). The 33 MIDD patients with diabetes were matched for diabetes duration and gender with 33 patients with "common" type-2 diabetes to compare the prevalence of diabetic retinopathy (DR) in both series. METHODS: All patients had a full ophthalmologic examination and fundus photographs. MAIN OUTCOME MEASURES: The presence and severity of MPD and DR were assessed in each patient. RESULTS: Thirty MIDD patients (85.7%) of 35 exhibited bilateral MPD characterized by linear pigmentation surrounding the macula and optic disc. In 24 of these 30 patients, visual acuity was 20/25 or more in both eyes. The prevalence of DR was 6% in MIDD patients with diabetes versus 15% for patients with common type-2 diabetes (a difference that was not significant, P = 0.23). The fundus of each of the eight asymptomatic children was normal. MPD was present in one of the three cases of MELAS. CONCLUSION: The prevalence of MPD in MIDD is high. Its detection may be helpful for the diagnosis of this new subtype of diabetes, for which specific treatments may be proposed.

Adult↗