Effect of free radical scavenger, edaravone, for patients with carbon monoxide poisoning.

OBJECTIVE: Chronic neurological symptoms after carbon monoxide (CO) poisoning are caused by various biological processes in the damaged brain, with free radicals playing roles as mediators in establishing pathological processes leading to chronic neurological symptoms under CO poisoning. This study aimed to clarify the effects of a free radical scavenger, edaravone, in patients with CO poisoning. METHODS: We retrospectively compared two groups comprising patients treated with hyperbaric oxygenation alone (Group A, n=25) or edaravone in addition to hyperbaric oxygenation (Group B, n=25). Edaravone was administrated intravenously at 30 mg every 12h for 7 days. Patient characteristics, general conditions on admission, and frequency of chronic neurological symptoms were compared between groups. Among patients showing chronic neurological symptoms, cognitive function and daily activity were also compared between groups. RESULTS: No significant differences in characteristics or general conditions on admission were identified between groups. In Group B, no patients presented with marked complications caused by edaravone. Although chronic persisting symptoms were less frequent in Group B (n=1, 0.04%) than in Group A (n=5, 20%), this difference was not significant. In the 11 patients showing chronic symptoms, scores for cognitive function and daily activity in the chronic phase were better in Group B than in Group A, but no significant differences were apparent. CONCLUSIONS: The present results suggest that edaravone represents a tolerable and feasible treatment for CO-poisoned patients. Further studies are needed to clarify whether edaravone can favorably influence chronic neurological symptoms caused by CO poisoning.

[Detection of glimepiride and rosiglitazone from Chinese dietary supplements].

A 79-year-old man with diabetes mellitus developed prolonged hypoglycemia. The patient had ingested two Chinese dietary supplements in addition to his prescribed nateglinide (Fastic). Using liquid chromatography tandem mass spectrometry, glimepiride from sulfonylurea, as well as rosiglitazone from a thiazolidine derivative, were detected in the Chinese dietary supplements, which were then quantitatively analyzed using liquid chromatography with UV detector. Mean values (n=3) of glimepiride contents of the Chinese dietary supplements were 0.75 and 0.86 mg/capsule. Predicted intake of glimepiride in the patient was estimated to be 4.8-8.2 mg/day according to the glimepiride contents and directions of the Chinese dietary supplements. The daily intake of glimepiride in this patient was greater than daily maintenance doses (1-4 mg) of glimepiride for diabetic patients. Therefore, overdose of glimepiride by ingestion of the Chinese dietary supplements appears to be associated with the development of prolonged hypoglycemia.

1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning.

OBJECTIVE: The authors examined whether (1)H-magnetic resonance spectroscopy (MRS) can identify damage to the centrum semiovale in the subacute phase after CO exposure. METHODS: Subjects comprised 29 adult patients who were treated with hyperbaric oxygenation within a range of 4-95 h (mean 18.7 h) after CO exposure. Subjects were classified into three groups according to clinical behaviours: Group A, patients with transit acute symptoms only; Group P, patients with persistent neurological symptoms; and Group D, patients with 'delayed neuropsychiatric sequelae' occurring after a lucid interval. MRS of bilateral centrum semiovale was performed 2 weeks after CO inhalation for all patients and 13 healthy volunteers. The mean ratios of choline-containing compounds/creatine ((mean)Cho/Cr) and N-acetylaspartate/Cr ((mean)NAA/Cr) for bilateral centrum semiovale were calculated and compared between the three CO groups and controls. Myelin basic protein (MBP) concentration in cerebrospinal fluid was examined at 2 weeks to evaluate the degree of demyelination in patients. RESULTS: MBP concentration was abnormal for almost all patients in Groups P and D, but was not abnormal for any Group A patients. The (mean)Cho/Cr ratios were significantly higher in Groups P and D than in Group A. No significant difference in (mean)NAA/Cr ratio was seen between the three pathological groups and controls. A significant correlation was identified between MBP and (mean)Cho/Cr ratio. CONCLUSIONS: These results suggest that the Cho/Cr ratio in the subacute phase after CO intoxication represents early demyelination in the centrum semiovale, and can predict chronic neurological symptoms.

[Case of concrete hardener poisoning complicated with acute renal failure treated by hemodialysis].

A 54-year-old man took approximately 180 mL of rapid-hardening cement (75% sodium silicate) with suicidal intent and was transferred to our department after at least 2 hours had elapsed from the time he took the poison. Milk, sodium alginate, and a proton pump inhibitor were administered to the patient, and intravenous fluid infusion in a large dose with antibiotics was started. Upper gastrointestinal endoscopy revealed lesions in the oral cavity, pharynx, esophagus, and stomach. The most severe lesions observed were in the greater curvature of the stomach body. Hemodialysis was performed because of persistent oliguria and worsening of the renal function parameters. The patient underwent 8 sessions of hemodialysis over a period of 11 days, after which the dialysis was stopped. The serum level of silicon was 25.1 microg/mL on admission and 9.2 microg/mL at the time of withdrawal from hemodialysis. The gastrointestinal mucosal lesions resolved completely in response to the treatment. There were no residual lesions except for some scarring in the greater curvature of the stomach. Although the serum levels of silicon decreased transiently following each hemodialysis session, they increased again on the following day. Based on the observations in this case, it was proposed that a serum silicon level of less than 10 microg/mL is unlikely to cause renal dysfunction.