Detection of isopropanol in acetonemic patients not exposed to isopropanol.
ABSTRACT Isopropanol has been identified in five acetonemic patients not exposed to this compound. Serum concentrations ranged up to 297 mg/L for IPA and up to 321 mg/L for acetone. Concentration ratios (isopropanol:acetone) ranged up to 5.12. All five patients had Type I diabetes mellitus and were insulin-dependent. At the time isopropanol was detected each patient was hyperglycemic, and four patients were acidotic. These findings tend to corroborate clinically some earlier autopsy reports that acetone may be converted to isopropanol in physiological conditions in which reduced nicotinamide adenine dinucleotide is elevated. The conversion of acetone to isopropanol in vivo has significant clinical and forensic toxicological implications.
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ABSTRACT: A 19-year-old non-diabetic female suffering from irritable bowel syndrome was found unconscious outdoors in the month of October. She was severely hypothermic and rushed to hospital for life-saving treatment. Evidence emerged that the victim had attempted suicide by drinking denatured alcohol (T-Red). According to the manufacturer of this product, it contains > 85% (v/v) ethanol, ~5% (v/v) acetone, 1-2% (v/v) ethyl acetate, and ∼3% (v/v) methyl ethyl ketone (MEK), but no isopropanol. A venous blood sample taken on admission to hospital contained ethanol (660 mg/100 mL), acetone (25 mg/100 mL), isopropanol (78 mg/100 mL), and MEK, although the latter was not quantified. Despite intensive care, the patient died 21 h after admission and postmortem femoral blood contained ethanol (390 mg/100 mL), acetone (14 mg/100 mL), isopropanol (53 mg/100 mL), and MEK. During oxidative metabolism of ethanol, there is a shift in the redox state of the liver to a more reduced potential as reflected in a raised NADH/NAD(+) ratio, which impacts on other NAD-dependent biochemical reactions, including reduction of acetone to isopropanol. The lower concentrations of ethanol, acetone, and isopropanol in postmortem blood compared with antemortem blood indicate the metabolism of these substances during the 21-h survival period when the patient received emergency hospital treatment.Journal of analytical toxicology 01/2011; 35(5):316-8. · 2.11 Impact Factor
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ABSTRACT: The mechanism of action of the ketogenic diet, a therapy for refractory epilepsy, is unknown. Our hypothesis is that acetone, one of three ketones elevated by the ketogenic diet, is directly responsible for the diet's anticonvulsant effects. This study examined the basic concepts of this hypothesis. Rats were acutely injected with acetone intraperitoneally at doses of 1 or 10 mmol/kg, or received acetone chronically in drinking water (1% v/v) for 10 days before being injected with a 1 mmol/kg dose of acetone. Controls consumed regular water and were injected with vehicle. A pentylenetetrazole seizure test was administered 15 min after the injections. Following the test, acetone was measured in the cerebrospinal fluid. A 10 mmol/kg injection of acetone suppressed seizures in 60% of rats (P<0.05). A chronic administration of acetone followed by a 1 mmol/kg injection suppressed seizures in 47% of rats (P<0.05). The acetone concentrations in these rats were 10.3I2.3 and 1.0I0.2 mmol/L, respectively. The effect of the acute 1 mmol/kg injection (without acetone pretreatment) was not statistically significant. This dose elevated acetone to 1.1I0.1 mmol/L in the cerebrospinal fluid. Our findings suggest that acetone is an anticonvulsant and that chronic administration may enhance its action. Linking acetone to the effects of the ketogenic diet requires further research. In particular, it will be important to confirm that the ketogenic diet generates relevant concentrations of acetone.Medical science monitor: international medical journal of experimental and clinical research 08/2002; 8(8):HY19-24. · 1.22 Impact Factor
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ABSTRACT: Isopropanol is an important chemical to forensic pathologists in that intoxication can result in death yet presence does not necessarily indicate intoxication. Several reports have been published, which indicate that isopropanol can be created endogenously in certain situations including diabetes mellitus, starvation, dehydration, and chronic ethanol use; however, a large-scale analysis addressing all of the possible causes of postmortem isopropanol detection has not been performed. A retrospective review of all cases examined at the Bexar County Medical Examiner's Office between 1993 and 2008 in which isopropanol was detected in routine alcohol screening was undertaken. The cases were categorized by the source of the isopropanol, and the concentrations of isopropanol and acetone were analyzed. Analysis revealed isopropanol concentrations to be low (<100 mg/dL) in cases of antemortem and postmortem creation and in postmortem contamination and high (>100 mg/dL) in cases of antemortem exposure. These results are consistent with other published reports.Journal of Forensic Sciences 04/2010; 55(4):998-1002. · 1.24 Impact Factor