A comprehensive review on experimental and clinical findings in intermediate syndrome caused by organophosphate poisoning

Abstract

Acute organophosphate (OP) intoxication is important because of its high morbidity and mortality and occurrence of muscular paralysis associated by inhibition of acetylcholinesterase (AChE) activity at the neuromuscular junction. Cholinergic crisis, intermediate syndrome (IMS), and OP-induced delayed neuropathy (OPIDN) are the evidences that can be observed in OP intoxication. The main cause of morbidity due to OP poisoning is IMS that occurs 24-96 h after poisoning. Mechanisms underlying the IMS are not fully known. Although the electrophysiological aspects of delayed neuropathy are best characterized, the IMS remain very little studied. The aim of this study was to revisit current knowledge related to OP and the IMS. For this purpose, a systematic review without date limitation was performed. A total of 599 relevant articles were found and reviewed. Data were categorized according to experimental and clinical studies. Occurrences of persistent AChE inhibition, electromyography changes, muscle cell injury, and oxidative stress are the most important pieces of evidence for involvement of IMS in OP toxicity. Delayed AChE inhibition, muscle necrosis, down regulation or desensitization of postsynaptic ACh receptors, failure of postsynaptic ACh release, and oxidative stress-related myopathy are involved in IMS. Toxicokinetic factors, such as a high lipid-solubility, duration of AChE inhibition and metabolite excretion, evolution of alterations on repetitive nerve stimulation (RNS), type and frequency of muscle lesions can estimate the probability of the IMS. Plasma AChE of less than 200 units is a predictor and the 30 Hz RNS decremental response could be a useful marker for the IMS.

Neurocognitive, Mental Health, and Glucose Disorders in Farmers Exposed to Organophosphorus Pesticides

“…Many studies corroborate that OP exposure might contribute to type 2 diabetes (17)(18)(19)(20)(21)(22)(23)(24)(25). Although the overall evidence of neurological and neurobehavioral effects of long-term OP exposure is thought to be small, it is not that diffi cult to fi nd some (26,27). Environmental agents which have neurotoxic effects may cause a wide variety of problems, including mental retardation and disability as well as subtle changes in performance, which are mainly related to exposure time and the amount of the chemical agent (28).…”

“…Moreover, OPs can inhibit neuropathy target esterase (NTE) to cause paralysis of lower-limbs and a distal injury to long nerve axons (34). Main neurotoxic effects in humans caused by OPs include the cholinergic syndrome, the intermediate syndrome, delayed polyneuropathy, and chronic neuropsychiatric disorder (27,35).…”

Acetamiprid Poisoning Followed By Prolonged Muscle Weakness

“…Possible mechanisms include prolonged acetylcholinesterase inhibition, downregulation or desensitization of acetylcholine receptors, muscle necrosis, oxidative injury-associated myopathy, and inadequate oxime treatment. Complete recovery can be achieved with appropriate treatment including respiratory support within 5 to 18 days (5,6).…”

Utility of Red Blood Cell Acetylcholinesterase Measurement in Mechanically Ventilated Subjects After Organophosphate Poisoning

“…23,24 With AChE inhibition, muscle necrosis, down-regulation or desensitization of the acetylcholine receptor, and oxidative stress together contribute to development of respiratory muscle weakness. 25 These mechanisms may also lead to the fact Table 6. RBC AChE Activity at Weaning According to Weaning Outcome…”