Increased Brain Serotonin Rather Than Increased Blood Acetaldehyde as a Common Denominator Behind Alleged Disulfiram-Like Reactions.

Several pharmaceutical agents are known to produce ethanol intolerance, which is often depicted as disulfiram-like reaction. As in the case with disulfiram, the underlying mechanism is believed to be the accumulation of acetaldehyde in the blood, due to inhibition of the hepatic aldehyde dehydrogenases, albeit this has not been confirmed in all cases by blood acetaldehyde measurements. Herein, cefamandole, cotrimoxazole, griseofulvin, procarbazine, and propranolol, which are reported to produce a disulfiram-like reaction, as well as disulfiram, were administered to Wistar rats and the hepatic activities of ethanol metabolizing enzymes along with the levels of brain monoamines were determined.

Evidence for the efficacy of disulfiram and copper combination in glioblastoma multiforme - A propos of a case.

Glioblastoma multiforme (GBM) is the most common and aggressive malignancy of the central nervous system. Treatment usually involves a combination of surgical resection, chemotherapy, and radiotherapy, but ultimately this condition is incurable. Besides the dismal prognosis of GBM, financial factors have also presented challenges for advancing treatments.

The Alcohol Intolerance Produced by Isoniazid Is Not Due to a Disulfiram-Like Reaction Despite Aldehyde Dehydrogenase Inhibition.

Background/aims: Isoniazid (ISO) has been reported to inhibit the hepatic aldehyde dehydrogenase (ALDH) and to cause a disulfiram (DIS)-like reaction, albeit there are no reports demonstrating increased blood acetaldehyde levels after co-administration of ISO with alcohol. The aim of our study was to clarify whether the alcohol intolerance produced by ISO is indeed due to a typical DIS-like reaction.

Methods: DIS and ISO were administered to Wistar rats and the hepatic ethanol (ETH) metabolizing enzyme activities along with the levels of brain monoamines were determined.

Risk factors for three phases of 12-month mortality in 1657 patients from a defined population after acute aneurysmal subarachnoid hemorrhage.

Objective: To analyze the impact of factors known after admission on mortality attributable to aneurysmal subarachnoid hemorrhage (SAH) resulting from saccular intracranial aneurysm (IA).

Methods: Data of 1657 consecutive patients admitted alive within 24 hours after aneurysmal SAH to Kuopio Neurosurgery during the years 1980-2007 from a defined population were analyzed.

Results: Aneurysmal SAH caused excess mortality for 12 months, after which other causes of death became dominant.

A randomized outcome study of enteral versus intravenous nimodipine in 171 patients after acute aneurysmal subarachnoid hemorrhage.

Background: Delayed ischemic neurologic deficit (DIND) is a serious complication of acute aneurysmal subarachnoid hemorrhage (aSAH). Although oral nimodipine is accepted as standard care for the prevention of DIND, the intravenous route is preferred by several centers. In the present study we compared the clinical efficacy between enteral and intravenous nimodipine after aSAH.

The impact of endovascular management on the outcome of aneurysmal subarachnoid hemorrhage in the elderly in eastern Finland.

Background: The International Subarachnoid Aneurysm Trial (ISAT) concluded that "there is currently no reason to doubt that the reduction of dependent survival or death after endovascular coiling seen in all patients in the ISAT cohort should not be valid in the elderly". We feel that this generalization requires further investigation to assess its validity.

Methods: We studied the impact of treatment era and independent risk factors for outcome in 179 consecutive elderly (> or =70 years) aneurysmal subarachnoid hemorrhage (aSAH) patients admitted to Kuopio University Hospital either between 1983 and 1992 (Era I, n = 56), prior to the introduction of endovascular management, or between 1995 and 2004 (Era II, n = 123) when the endovascular treatment was established at our institute.

Malignant giant cell tumor in the posterior fossa of a neonate.

Giant cell tumors (GCTs) of the bone are rare, usually benign but locally aggressive neoplasms that primarily occur in the epiphyses of long bones. They seldom develop in the cranium; when they do, they involve principally the sphenoid and temporal bones. These tumors usually affect young adults, and few reports in children have been published.

CYP2E1 and risk of chemically mediated cancers.

Importance Of The Field: Among various human CYPs, CYP2E1 is of particular interest because of its involvement in the metabolic activation of many low molecular mass procarcinogens. CYP2E1 induction, which may be a consequence of genetic polymorphism or/and gene induction by xenobiotics, is the first step leading to the development of certain chemically-mediated cancers. The aim of this review is to outline the current knowledge on chemically-induced cancers through activation by CYP2E1, with emphasis on the association between polymorphisms of the CYP2E1 gene and incidence of different neoplasias.

Inhibition of rat hepatic CYP2E1 by quinacrine: molecular modeling investigation and effects on 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced mutagenicity.

Increased activity of CYP2E1 has been associated with increased risk of chemically-mediated cancers, through enhanced activation of a variety of procarcinogens. In this context, inhibition of CYP2E1 is potentially of significance in xenobiotic toxicity. The aim of the present study was to test the hypothesis that quinacrine inhibits hepatic CYP2E1.

Pharmaceutical agents known to produce disulfiram-like reaction: effects on hepatic ethanol metabolism and brain monoamines.

Several pharmaceutical agents produce ethanol intolerance, which is often depicted as disulfiram-like reaction. As in the case with disulfiram, the underlying mechanism is believed to be the accumulation of acetaldehyde in the blood, due to inhibition of the hepatic aldehyde dehydrogenases. In the present study, chloramphenicol, furazolidone, metronidazole, and quinacrine, which are reported to produce a disulfiram-like reaction, as well as disulfiram, were administered to Wistar rats and the hepatic activities of alcohol and aldehyde dehydrogenases (1A1 and 2) were determined.