重症の遅発性神経障害を呈したマラチオン中毒の一症例

A Case of Delayed Myeloneuropathy Due to Malathion Intoxication

　低毒性有機燐剤マラチオンを服用後約36時間の間欠期をおいて呼吸筋，体幹筋に及ぶ四肢麻痺が出現，やがて高度の感覚障害，膀胱直腸障害を伴う重篤な運動神経優位のmyeloneuropathyを呈したorgano—phosphorus compounds induced delayed neurotoxicityの1例を報告した。臨床像および腓腹神経生検所見より本症例は燐酸トリオルトクレジル中毒に代表される有機燐剤性遅発性神経障害に等しい病態であると考えられたが，発症までの期間が短く，近位筋に初発したことからSenanayakeらの"intermediate syndrome"に相当するものと考えられた。また，有機燐剤性遅発性神経障害の発症にアルコールなどのなんらかの宿主側の要因を考慮すべきことを指摘した。

We report a patient with serious organophosphor-us-induced delayed neurotoxicity due to malathion. The patient was a 49-year-old male with a history of habitual alcohol drinking, who ingested approxi-mately 100ml of 50% malathion [S-1, 2-bis (ethox-ycarbonyl) -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 injestion, respiratory muscle weakness, consiousness disturbance and diffuse weakness of the limb muscles occurred, necessitat-ing 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 phos-phate (TOCP) intoxication.

The symptoms of this patient seemed to corres-pond 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 neurotoxity due to TOCP intoxica-tion. However, this patient exhibited more severe neuropathy than seen in previously reported cases of organophosphorus compounds induced delayed neurotoxity 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 com-pounds induced delayed neurotoxity due to malath-ion to be reported in Japan.