Acute fenitrothion poisoning.

A technician was accidentally exposed to the organophosphorus insecticide fenitrothion and subsequently treated with pralidoxime for the autonomic, somatic and psychiatric manifestations of intoxication. Although long-term therapy with pralidoxime is not recommended, this patient required and obtained symptomatic benefit from its prolonged use. Erythrocytic and plasma cholinesterase activities had been monitored prior to exposure and were monitored throughout treatment and following recovery. Continual monitoring of cholinesterase activities of individuals occupationally exposed to organophosphorus ester insecticides and early diagnosis are essential.     

Acute poisoning: an update.

Treatment of the patient who has taken an overdose of a harmful substance includes support of vital functions and toxicologic analysis. Early recognition of signs and symptoms indicating poisoning by a specific agent or group of related chemicals is essential since specific antidotes may be lifesaving. Activated charcoal is an effective gastrointestinal decontaminant that adsorbs many common drugs. Administration of weak acids as an antidote to alkali ingestion is to be condemned; the only treatment should be dilution with water. The use of physostigmine as a specific antidote for the anticholinergic syndrome has been very successful; the incidence of this syndrome as a result of poisoning by tricyclic antidepressants is increasing. Effective therapy for acetaminophen overdose is still being investigated, but activated charcoal and methionine, if given early enough, seem to be effective.     

Formation of gamma-hydroxybutyrate in brain.

Abstract— Gamma-hydroxybutyric acid is a neuroactive compound which has been found to be a normal constituent of mammalian brain. The present report characterized enzymatic activity in brain forming gamma-hydroxybutyrate (GHB) from succinic semialdehyde (SSA). When NADPH served as cofactor, whole brain homogenate was capable of forming nearly 300 nmol GHB/min/g brain when enzyme activity was measured at 37°C. GHB production was significantly less (50%) when NADH was the cofactor. A regional localization of these activities indicated that the cerebellum and septal area contained the highest capacity to form GHB in the presence of NADPH; intermediate to high activity was found in the cortex, medulla, superior colliculus and corpus striatum; low activity was present in the inferior colliculus, thalamus, pons, hippocampus, substantia nigra and hypothalamus. Activity in the presence of NADH was rather evenly distributed with the exceptions of the cerebellum and inferior colliculus, which contained high and low activity respectively. Both NADPH- and NADH-dependent activities were found primarily in the cytosol. Pentobarbital inhibited enzyme activity and enzyme activity was differentiated from lactic dehydrogenase and alcohol dehydrogenase by use of specific inhibitors. In addition, mixed substrate experiments and kinetic analysis provided evidence for the presence of two reversible NADPH-dependent enzymes capable of producing GHB from SSA.     

Acute zincteral oral poisoning

Zinc vapour poisoning by inhalation in the form of zinc fever is more frequent than oral zinc product poisoning, the product used in therapy. The main aim of the study was the evaluation of clinical manifestation present after Zincteral ingestion as well as attempt to find the relationship between the presence and aggravation of the clinical manifestation and zinc level in the blood. The course of acute clinical suicidal poisoning by ingestion of Zincteral 50 tablets (10.0 g) and 100 tablets (20.0 g) is presented. The clinical picture revealed the following symptoms and signs: tachycardia, changes of arterial BP, vascular shock; dyspeptic nausea, vomiting cramps in abdominal region, diarrhoea. Damage of the parenchymatous organs, mainly liver was evident. In pregnant woman (9-week-pregnancy) on the 12-th day of her stay in the Clinic complete miscarriage took place accompanied by haemorrhage from reproductive organs. The kind and exacerbation of the clinical manifestations in relation to the zinc level in body fluid were analysed.