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.
[Show abstract][Hide abstract] ABSTRACT: The case is presented of a 34-year-old man, an insulin-dependent diabetic, who was found decomposed in his apartment. The victim had been recently discharged from a mental hospital and was to be monitored by the community's mental health personnel. While the autopsy revealed little in the way of disease, toxicological studies yielded a blood acetone level of 0.070 g/dl and a urine acetone level of 0.086 g/dl. The medical examiner ruled the cause of death diabetic ketoacidosis. To support this conclusion in the absence of a vitreous humor glucose concentration, 18 well-documented cases of diabetic ketoacidosis were reviewed, and acetone concentrations were compared with the acetone concentrations found in the presented case.
American Journal of Forensic Medicine & Pathology 03/1998; 19(1):98-101. · 0.70 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A 29-year-old man presented to the Emergency Department with acute mental status changes. He was unable to give a history. He was found to be in diabetic ketoacidosis, although his family reported no prior history of diabetes. A toxic exposure work-up revealed the presence of isopropyl alcohol in the patient’s blood. His condition improved with treatment of the ketoacidosis, and he subsequently denied any exposure to isopropyl alcohol prior to presentation to the hospital. This case provides further support to a growing body of evidence that the detection of isopropyl alcohol may not represent an acute ingestion but, rather, a byproduct of acetone metabolism in certain disease states.
Journal of Emergency Medicine 09/2000; 19(2-19):165-168. DOI:10.1016/S0736-4679(00)00203-1 · 0.97 Impact Factor
[Show abstract][Hide abstract] 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. · 1.43 Impact Factor
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