PubMed1991
We report a patient with serious organophosphorus-induced delayed neurotoxicity due to malathion. The patient was a 49-year-old male with a history of habitual alcohol drinking, who ingested approximately 100 ml of 50% malathion [S-1,2-bis(ethoxycarbonyl)-ethyl-0,0-dimethyl phosphorodithioate solution], with a large amount of alcohol in a suicide attempt. Following recovery from an acute cholinergic phase 36 hours after ingestion, respiratory muscle weakness, consciousness disturbance and diffuse weakness of the limb muscles occurred, necessitating mechanical ventilation. On the 7th hospital day, glove and stocking type sensory disturbance was observed and weakness of the limbs had progressed to distal dominant flaccid quadriparalysis with moderate muscle atrophy. Two months after onset, neurogenic bladder and spinal automatism became obvious. After 7 months, spasticity of the lower limbs developed, while the weakness of the upper limbs improved. Sural nerve biopsy showed axonal degeneration, loss of large myelinated fibers and increases in Schwann cell clusters. These findings were similar to those seen in patient with triorthocresyl phosphate (TOCP) intoxication. The symptoms of this patient seemed to correspond to Senanayake's "intermediate syndrome". The final clinical features and sural nerve biopsy findings were in close agreement with those in patients with serious organophosphorus compounds induced delayed neurotoxicity due to TOCP intoxication. However, this patient exhibited more severe neuropathy than seen in previously reported cases of organophosphorus compounds induced delayed neurotoxicity caused by less toxic organophosphorus compounds, such as Dipterex. This suggests that alcohol might have been an etiological factor in damage of nervous tissue in this rare case. This is the first case of organophosphorus compounds induced delayed neurotoxicity due to malathion to be reported in Japan.