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At least 685 records · Page 38Linked to original sources
PubMed2003

Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus: systematic review and meta-analysis.

BACKGROUND: Metformin therapy for type 2 diabetes mellitus has been shown to reduce total mortality rates compared with other antihyperglycemic treatments but is thought to increase the risk of lactic acidosis. The true incidence of fatal and nonfatal lactic acidosis associated with metformin use is not known. METHODS: A comprehensive search was performed to identify all comparative trials or observational cohort studies published between January 1, 1959, and March 31, 2002, that evaluated metformin therapy, alone or in combination with other treatments, for at least 1 month. The incidence of fatal and nonfatal lactic acidosis was recorded as cases per patient-years for metformin treatment and for placebo or other treatments. In a second analysis, lactate levels were measured as a net change from baseline or as mean treatment values for metformin and comparison groups. RESULTS: Pooled data from 194 studies revealed no cases of fatal or nonfatal lactic acidosis in 36 893 patient-years in the metformin group or in 30 109 patients-years in the nonmetformin group. Using Poisson statistics with 95% confidence intervals, the probable upper limit for the true incidence of lactic acidosis in the metformin and nonmetformin groups was 8.1 and 9.9 cases per 100 000 patient-years, respectively. There was no difference in lactate levels for metformin compared with placebo or other nonbiguanide therapies. CONCLUSION: There is no evidence to date that metformin therapy is associated with an increased risk of lactic acidosis or with increased levels of lactate compared with other antihyperglycemic treatments if the drugs are prescribed under study conditions, taking into account contraindications.

Acidosis, Lactic↗
PubMed2004

Test and teach. Number Fifty-three. Diagnosis: Diabetes-related dyslipidaemia.

Mixed dyslipidaemia is common in people with diabetes and occurs in up to 20% of cases. Diabetes keto-acidosis can occur in patients with type 2 diabetes. Hypertriglyceridaemia is a well-recognised cause of pancreatitis. Other common causes of pancreatitis include gall stones, alcohol, drugs (azathioprine and dideoxyinosine) and post-endoscopic retrograde cholangiopancreatography (ERCP). Therapeutic options for acute and severe dyslipidaemia include insulin therapy, fibric acid derivatives, fish oils and, rarely, nicotinic acids. Hospitalisation may be required for plasmapheresis in specialised centres.

Adult↗
PubMed2000

[Diabetic coma].

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Acidosis, Lactic↗
PubMed1994

[Metabolic acidosis in the 32nd week of pregnancy--uncontrolled diabetes in pregnancy, dehydration or sequela of tocolysis?].

We describe a case of keto- and lactic acidosis in a 22 year old, healthy woman hospitalized for preterm labor at week 32 of gestation. One former pregnancy was normal. Blood glucose level at admission was 115 mg/dl after 8 mg of betamethasone. Continuous salbutamol infusion was used for management of preterm labour. 18 hours later, the patient complained about nausea and dyspnoea followed by tachypnoea and hyperventilation. Blood gas analysis showed severe metabolic acidosis (ph 7.25, BE-17.5, pO2 114 mm Hg, pCO2 15.5 mm Hg). At this moment blood glucose level was 178 mg/dl. Ketone bodies in urine were positive, serum lactate level was also elevated at 8.6 mmol/l. Cesarean section was performed because of prolonged fetal bradycardia. 6 months post partum type-I-diabetes could be excluded. We conclude that this case of acidosis was due to both, beta-2-adrenergic treatment and beginning gestational diabetes.

Acidosis, Lactic↗
PubMed2004

[The short term prognosis in alcoholic liver disease with metabolic acidosis].

BACKGROUND/AIMS: Alcoholic liver disease with metabolic acidosis may have possible causes such as alcoholic ketoacidosis, diabetic ketoacidosis, lactic acidosis. Salicylate, methanol, and ethylene glycol intoxication should also be considered. The aim of this study was to investigate the short-term prognostic factors in patients with alcoholic liver disease with metabolic acidosis. METHODS: Clinical data related to twenty-nine patients with alcoholic liver disease and metabolic acidosis was analysed retrospectively. Patients were divided into two groups according to the outcome (survival or death). Past medical history, and physical, laboratory and radiologic data at admission were compared. RESULTS: The amount of daily alcohol intake differed significantly between the two groups (P=0.034), but duration and total amount of alcohol intake did not differ significantly between the two groups (P=0.128; P=0.360). The presence of ascites differed significantly between two the groups (P=0.019). On laboratory testing, the following differed significantly: base excess (P=0.038), hemoglobin (P=0.019), platelet (P=0.040), total bilirubin (P=0.007), albumin (P=0.012), creatinine (P=0.014), phosphorus (P=0.021), chloride (P=0.010), ammonia (P=0.003), prothrombin time (P=0.033), fibrinogen (P=0.011) and D-dimer (P=0.024). Review of the medical history of the patients showed diabetes (10/29), cirrhosis (10/29), and hepatocellular carcinoma (1/29). Combined conditions at admission were sepsis (8/29), pneumonia (7/29), acute renal failure (6/29), rhabdomyolysis (5/29), gastrointestinal hemorrhage (4/29), acute pancreatitis (3/29), acute respiratory distress syndrome (2/29), and acute myocardial infarction (1/29). CONCLUSIONS: The amount of daily alcohol intake, base excess, hemoglobin, platelet, total bilirubin, albumin, creatinine, phosphorus, chloride, ammonia, prothrombin time, fibrinogen and D-dimer seemed to be useful parameters in predicting short-term prognosis of patients with alcoholic liver disease with metabolic acidosis. Further study is needed to define the significance of these factors.

Acidosis↗
PubMed1979

[Autoradiographic studies on protein metabolism and histochemical demonstration of the brain zinc content in diabetes mellitus. 1. Comparison in experimental streptozotocin-induced diabetes].

By application of streptozotocin diabetes mellitus is induced in rats: 40 mg/kg body weight streptozotocin produce a fairly serious diabetes with minimal ketosis, 125 mg/kg body weight streptozotocin cause a severe diabetic keto-acidosis. After 72 hours these animals and also a group of control animals receive 8.33 mCi/animal 3H-leucine intraperitoneally. By means of stripping film autoradiograms the rates of uptake of 3H-leucine in different areas of the rat brain are measured. The values of the control animals are compared with those of a fairly serious diabetes and those of a severe diabetic keto-acidosis. In the regions of the neocortex parietalis and of the thalamus the 3H-leucine values of the diabetic animals are considerably lower in comparison with the controls, and that irrespective of the degree of severity of the diabetic disease. Compared with the control animals the 3H-leucine values of diabetic animals decrease according to the degree of severity of the disease within the Ammon's horn and the dentate fascia. Within the Ammon's horn and dentate fascia also the zinc contents change very specifically in different areas with the degree of severity of diabetes mellitus. The zinc is identified on H2S-alcohol fixed brains by means of a photographic development. The particular significance of the Ammon's horn and the dentate fascia concerning diabetic metabolic conditions is discussed.

Animals↗