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Severe lactic acidosis and acute renal failure following ingestion of metformin and kerosene oil: a case report.

ABSTRACT: INTRODUCTION: Kerosene is a freely accessible hydrocarbon used in Sri Lankan (and other Asian) households for cooking and for lighting lamps. Kerosene poisoning is rarely reported among adults and its toxicological effects are not well known. Metformin is a commonly used oral hypoglycemic drug and its overdose leads primarily to lactic acidosis. Combined poisoning of metformin and kerosene and their interactions have not been reported. CASE PRESENTATION: An 18-year-old, previously healthy, unmarried Sinhalese woman was referred following ingestion of 17.5 g of metformin and approximately 200 mL of kerosene oil in a suicide attempt. She had vomiting, burning epigastric pain, and a hypoglycemic seizure (capillary blood glucose of 42 mg/dL). Subsequently, she developed severe lactic acidosis followed by acute renal insufficiency, was treated with sodium bicarbonate, and underwent intermittent hemodialysis with bicarbonate. She recovered completely. CONCLUSIONS: This report proposes possible interactions that occur between metformin and kerosene that augment toxicity when the two are ingested together. It also stresses the importance of early treatment with intermittent hemodialysis in severe lactic acidosis with maintenance of blood glucose.

SUBMITTER: Rathnapala A

PROVIDER: S-EPMC3292833 | biostudies-other | 2012

REPOSITORIES: biostudies-other

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Severe lactic acidosis and acute renal failure following ingestion of metformin and kerosene oil: a case report.

Rathnapala Amila A Matthias Thushara T Jayasinghe Saroj S

Journal of medical case reports 20120117

<h4>Introduction</h4>Kerosene is a freely accessible hydrocarbon used in Sri Lankan (and other Asian) households for cooking and for lighting lamps. Kerosene poisoning is rarely reported among adults and its toxicological effects are not well known. Metformin is a commonly used oral hypoglycemic drug and its overdose leads primarily to lactic acidosis. Combined poisoning of metformin and kerosene and their interactions have not been reported.<h4>Case presentation</h4>An 18-year-old, previously h ...[more]

PMID: 22251748

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Project description:BackgroundDespite strong recommendations to use metformin as first-line therapy for type 2 diabetes (T2DM), its use has been suboptimal, likely due to concerns of lactic acidosis. This study compared the association of acidosis in patients with T2DM prescribed metformin with those prescribed other antihyperglycemic medications or no medications.MethodsThis was a retrospective cohort study of patients with newly diagnosed T2DM utilizing an administrative database, which includes medical and prescription claims. Eligible patients had a diagnosis of T2DM, had continuous health plan enrollment 3 months prior to study enrollment and during the study period, and were at least 18 years of age. Mutually exclusive exposure groups were metformin only, other antihyperglycemic medications, and no medication. Acidosis cases were stratified by exposure group and risk factors for lactic acidosis (chronic obstructive pulmonary disease, hepatic dysfunction, alcohol abuse, heart failure, renal insufficiency, age of 80 years or older, and a history of acidosis). Degree of renal insufficiency was not available. Associations between exposure and acidosis were estimated, and risk factors evaluated.ResultsA total of 132,780 patients met inclusion criteria: 24,936 (20%) metformin only group, 15,059 (11%) other antihyperglycemic medication group, and 92,785 (70%) no medication group. Acidosis was observed in 1.45 per 10,000 patient months (0.78 metformin, 1.59 other antihyperglycemic medication, 1.51 no medication). The unadjusted relative risk of acidosis was 0.5 for patients prescribed metformin only compared with the other exposure groups (95% confidence interval = 0.2-1.2). There was no significant difference in risk of acidosis between exposure groups, irrespective of risk factors for lactic acidosis.ConclusionsRisk of acidosis was similar with metformin only compared with those prescribed other antihyperglycemic medications or no medication. These results support expanded use of metformin for T2DM. Additional studies are needed to understand the impact of risk factor severity on risk of lactic acidosis.

Project description:IntroductionHepatic mitochondrial dysfunction may play a critical role in the pathogenesis of metformin-induced lactic acidosis. However, patients with severe metformin intoxication may have a 30 to 60% decrease in their global oxygen consumption, as for generalized inhibition of mitochondrial respiration. We developed a pig model of severe metformin intoxication to validate this clinical finding and assess mitochondrial function in liver and other tissues.MethodsTwenty healthy pigs were sedated and mechanically ventilated. Ten were infused with a large dose of metformin (4 to 8 g) and five were not (sham controls). Five others were infused with lactic acid to clarify whether lactic acidosis per se diminishes global oxygen use. Arterial pH, lactatemia, global oxygen consumption (VO2) (metabolic module) and delivery (DO2) (cardiac output by thermodilution) were monitored for nine hours. Oxygen extraction was computed as VO2/DO2. Activities of the main components of the mitochondrial respiratory chain (complex I, II and III, and IV) were measured with spectrophotometry (and expressed relative to citrate synthase activity) in heart, kidney, liver, skeletal muscle and platelets taken at the end of the study.ResultsPigs infused with metformin (6 ± 2 g; final serum drug level 77 ± 45 mg/L) progressively developed lactic acidosis (final arterial pH 6.93 ± 0.24 and lactate 18 ± 7 mmol/L, P < 0.001 for both). Their VO2 declined over time (from 115 ± 34 to 71 ± 30 ml/min, P < 0.001) despite grossly preserved DO2 (from 269 ± 68 to 239 ± 51 ml/min, P = 0.58). Oxygen extraction accordingly fell from 43 ± 10 to 30 ± 10% (P = 0.008). None of these changes occurred in either sham controls or pigs infused with lactic acid (final arterial pH 6.86 ± 0.16 and lactate 22 ± 3 mmol/L). Metformin intoxication was associated with inhibition of complex I in the liver (P < 0.001), heart (P < 0.001), kidney (P = 0.003), skeletal muscle (P = 0.012) and platelets (P = 0.053). The activity of complex II and III diminished in the liver (P < 0.001), heart (P < 0.001) and kidney (P < 0.005) while that of complex IV declined in the heart (P < 0.001).ConclusionsMetformin intoxication induces lactic acidosis, inhibits global oxygen consumption and causes mitochondrial dysfunction in liver and other tissues. Lactic acidosis per se does not decrease whole-body respiration.

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Severe lactic acidosis and acute renal failure following ingestion of metformin and kerosene oil: a case report.

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Severe lactic acidosis and acute renal failure following ingestion of metformin and kerosene oil: a case report.

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