Incidents of poisoning in humans caused by the ingestion of the glufosinate ammonium containing herbicides are gradually increasing in Japan. This poisoning is characterized by various neurological symptoms such as disturbances of consciousness, convulsions and apnea which appear after an asymptomatic interval of several hours. We studied the toxicokinetics of glufosinate in a patient with this poisoning successfully treated without extracorporeal hemopurification. A 65-year-old male ingested BASTA, which contains 20% w/v of glufosinate ammonium, about 300 ml, more than the estimated human toxic dose. Four and a half hours after ingestion, he showed speech ataxia and systemic tremor. He was prophylactically intubated before the occurrence of serious respiratory failure. After 5 days of artificial ventilation he was extubated and discharged without any sequelae. We studied the serial change of serum glufosinate concentration every 3-6 h and assessed the urinary excretion of glufosinate every 24 h. The absorbed amount of glufosinate was estimated from the cumulative excreted in urine. Toxicokinetic analysis was performed using the two-compartment model. The changes in serum glufosinate concentration exhibited T1/2α of 1.84 and T1/2α of 9.59 h. The apparent distribution volume at b-phase and the total body clearance were 1.44 l/kg and 86.6 ml/min, respectively. Renal clearance was estimated to be 77.9 ml/ min. The indication for extracorporeal hemopurification for this poisoning has been discussed.

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Two patients with rapidly developing shock, multisystem organ failure, and destructive soft-tissue infection caused by groups G and C streptococci are described. Both patients died rapidly despite aggressive treatment. The clinical characteristics cannot be distinguished from those of toxic shock-like syndrome, but Streptococcus pyogenes was not recovered. These strains did not produce any previously identified type of streptococcal pyrogenic exotoxins. These findings suggest that toxic shock-like syndrome can be caused not only by group A but also groups G and C streptococci. The causative strains of toxic shock-like syndrome may have something in common with unknown virulent factors for this syndrome.

This report describes 7 victims of sodium azide poisoning caused by drinking poisoned water. Ten employees at the poisoning site developed symptoms immediately after ingesting coffee or tea made from hot water contained in a thermos bottle. Symptoms included altered consciousness, faintness, blackout, palpitation, nausea, and paresthesia of both hands and feet. Seven patients were transferred to our institution by ambulance. We assumed symptoms were caused by acute poisoning but the causative agent was unknown. We could not rule out cyanide poisoning because of the rapid emergence of symptoms suggesting circulatory failure, so we administered amyl nitrate, sodium nitrate, and sodium thiosulfate. Symptoms rapidly subsided. The causative agent was identified the next day as sodium azide. While the victims were being treated at the emergency room, 2 doctors, 3 nurses, and 1 pharmacist complained of faintness, headache, nausea, sensations of dyspnea and eye pain. These medical staff members had all either conducted gastric lavage or treated gastric contents. This strongly suggests that symptoms were caused by hydrazoic acid formed in a chemical reaction between sodium azide and gastric acid. Our experience underscores the potential hazard from hydrazoic acid faced by medical staff treating patients with oral sodium azide intoxication.

the tumor or the location of the tumor. Generally speaking, total removal was feasible for the cystic tumors with mural nodule and partial removal or decompressive procedure was suitable for the diffuse solid tumors.Post-operative irradiation for such diffuse solid tumors proved to be effective for the improvement of the clinical symptoms and signs and for the prevention of recurrence.