The temporal profile of butyrylcholinesterase (BuChE) and in vitro pralidoxime-reactivated BuChE was studied in a cohort of 25 organophosphate-poisoned patients to examine their relationship to the development of intermediate syndrome and to understand reasons for lack of efficacy of oxime treatment. The clinical severity of poisoning (assessed by the Namba Scale) correlated significantly with the severity of intermediate syndrome. BuChE activity increased significantly over time and showed significant relationship to muscle power. The temporal profile of the enzyme was correlated to the clinical severity of poisoning. Reactivation potentials of BuChE (the difference between oxime-reactivated and-unreactivated enzyme activity) declined significantly with time after organophosphate ingestion. The reactivation potential of the enzyme at admission decreased significantly with increasing severity of poisoning and was lower in patients who developed intermediate syndrome. Patients who received oxime prior to hospitalization had a higher rate of intermediate syndrome and lower levels of BuChE at admission than those who had not. The study suggests that (i) BuChE reflects the clinical course of poisoning, confirming earlier studies; (ii) intermediate syndrome may be associated with a persistent inhibition of BuChE; and (iii) the lack of oxime efficacy in our patients maybe due to their severity of poisoning and the timing of oxime treatment.

INTRODUCTION: Organophosphorus poisoning (OPP) is a major public health problem in developing countries like India. Leukocyte count is a simple and inexpensive test, and elevated count is associated with acute inflammation and increased oxidative stress-like OPP. This study was done to correlate the severity of acute OPP with leukocyte count and also to assess the prognosis. MATERIALS AND METHODS: A prospective, observational clinical study was done on 80 patients suspected of OPP of age >15 years admitted to emergency unit at a tertiary rural teaching health-care center of Central India. Serum cholinesterase level and leukocyte count were estimated at the time of admission in all patients and severity of OPP was assessed according to Peradeniya organophosphorus poisoning (POP) scale. RESULTS: The mean age of the patients was 33.52 years (standard deviation [SD] 11.62) in males and 27.30 years (SD 7.33) in females. Among them, 57 (71.25%) were males and 23 (28.75%) were females. The severity of poisoning was directly correlated with serum cholinesterase level (P = 0.0001). Leukocyte count had a sensitivity of 60%, specificity of 76%, and negative predictive value of 85% if counts were more than 12,000 and 30% sensitivity, 95% specificity, and 80% negative predictive value if counts were more than 15,000 in predicting mortality in patients with OPP. CONCLUSION: Leukocyte count levels on admission can be used a prognostic marker in patients with OP poisoning.

Treatment with diazinon resulted in hyperglycaemia and depletion of glycogen from cerebral and peripheral tissues 2 h after its administration in rats; the changes were maximal after 40 mg/kg diazinon, administered intraperitoneally. The activities of glycogen phosphorylase and phosphoglucomutase were significantly increased in brain and liver, while that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in brain. The cholinesterase activity of the brain was reduced by treatment with diazinon. The activities of hepatic gluconeogenic enzymes (fructose 1,6 diphosphatase and phosphoenolpyruvate carboxykinase) were also significantly increased in diazinon-treated animals. The level of lactate was increased in brain and blood while that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not significantly changed. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. Adrenalectomy abolished the hyperglycaemia and changes in carbohydrate metabolism, suggesting the possible involvement of adrenals in the induced changes in diazinon-treated animals.

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