No abstract

Background: Organophosphorus poisoning occurs as a result of accidental exposure, suicidal and homicidal attempts. Organophosphorus compounds are known to cause selective release of liver microsomal ß-glucuronidase (BG) into serum. Dissociation of the egasyn -ß-glucuronidase complex in the liver by organophosphorus compounds was followed by a massive release of ß-glucuronidase from liver into the serum. Objectives: There are few papers suggesting increase in activity of ß-glucuronidase (BG) in serum of experimental animals subjected to organophosphorus poisoning. But, still there is less or no such study in human beings having organophosphorus poisoning. Thus, aim of our this research was to estimate and correlate activity of ß-glucuronidase (BG) in different stages of organophosphorus poisoning. Methods: ß-glucuronidase (BG) activity was determined by Goldstein method. Results and Conclusions:We found that the serum activity of β -glucuronidase (BG) proportionally increases (p < 0.01) and correlates with severity of organophosphorus poisoning. Further, there was found a significant increase in β -glucuronidase (BG) activity in low dose (mild) poisoning also. Thus, β -glucuronidase (BG) can be used as a potent biochemical marker in the diagnosis and prognosis of organophosphorus poisoning along with acetylcholinesterase or may also without acetylcholinesterase.

The aim of our research was to correlate blood glucose and serum lipid profile parameters with risk of coronary heart disease associated with organophosphorus pesticide poisoning. For the purpose of this, 50 patients of organophosphorus poisoning and 50 healthy controls were selected. Blood glucose and serum lipid profiles were estimated by using commercially available diagnostic kits. We found a significant decrease (p < 0.05) in serum TAG, serum HDL cholesterol and serum VLDL cholesterol. On other hand we found a significant increase (p < 0.05) in blood glucose, serum total cholesterol and serum VLDL cholesterol. Organophosphorus poisoning is also associated with increased free radical production. Free radicals oxidize LDL cholesterol and oxidized cholesterol is taken by macrophages to form foam cells. Foam cells are responsible for formation of atherosclerotic plaques. Such plaques reduce coronary artery lumen and thus blood supply to heart get reduced which enhances the chances of myocardial infarction. Here, decreased HDL and VLDL and increased LDL cholesterol in organophosphorus poisoning is associated with increased risk of coronary heart diseases. Hence, estimation of blood glucose and lipid profile play important role in the diagnosis of risk of coronary heart diseases in organophosphorus poisoning.

Abstract-

Organophosphorus compounds were first developed by scientist Schrader shortly before and during Second World War. They were first used as agricultural insecticides and later as potential chemical warfare agent. A great proportion of acute poisoning cases are caused by exposure to these pesticides. Pesticides can enter the body through the skin (dermal), mouth (oral), lungs (breathing), and eyes (ocular) and due to accidental ingestion. It is found that the Organophosphorus compound, dimethoate is more commonly used to attempt suicide as it is easily available and cheap. 54 % poisoning cases were observed only due to dimethoate. The poisoning due to warfarin, tick-20, chlorpyrifos, fenthion, thymate and lice powder is less common. Acute Organophosphorus poisoning leads to paralysis of skeletal muscles. Paralysis generally occurs in between 48 to 72 hours after poisoning and is associated with cranial and proximal limb muscle weakness. Inability to lift the neck, inability to sit up, opthalmoparesis, slow eye movements, facial weakness, difficulty in swallowing, limb weakness (proximal is more than distal), areflexia, respiratory failure etc. are clinical features of paralysis. These features together are called as intermediate syndrome. On other hand, organophosphorus poisoning is also associated with respiratory failure. Respiratory failure occurs due to many reasons, such as central respiratory depression, respiratory muscle weakness, bronchospasm, bronchorrhea, aspiration of gastric contents, anorexic brain damage etc. This togetherly is associated with Acute Respiratory Distress Syndrome (ARDS). Identification of poisoning is done on the basis of symptoms shown by patients while perfect diagnosis requires biochemical analysis. Symptoms such as hyper-salivation, convulsions, respiratory failure, ataxia, slurred speech, miosis, muscle cramping suggest about poisoning. To access Organophosphorus poisoning, it is necessary to analyze biological samples mostly blood and urine. Organophosphorus compounds can be detected in urine however, their degradation is rapid and hence their detection in urine is possible for short time. The detection of metabolites of Organophosphorus compounds is another way to detect Organophosphorus poisoning. Metabolites circulate for longer time and mostly excreted in urine. Detection of metabolites of Organophosphorus compounds is always better than detection of parent compound in blood or urine. This is because parent compound has short life time and its detection is not possible for more than hours after poisoning. For some Organophosphorus compounds (e.g. Parathion, Paraoxon), detection of P-nitrophenol in urine is an indicator of Organophosphorus poisoning. Recently, antibodies against Organophosphorus compounds in blood are also detected. Thus, blood and urine remains main source for biological and biochemical examination in Organophosphorus poisoning. Most commonly, detection of Organophosphorus poisoning is done by estimating activities of enzymes namely Acetyl Cholineste...