2021 年 47 巻 5 号 p. 264-271
We experienced two cases with mild to moderate renal dysfunction in which amantadine hydrochloride (amantadine) intoxication was followed by increases in its blood levels. Case 1 was a patient with mild to moderate renal dysfunction [estimated glomerular filtration rate (eGFRcreat): 48.9 mL/min/1.73m2; glomerular filtration rate (GFR) category: G3a] taking amantadine 300 mg daily. In Case 1, the blood level of amantadine at 13 hours and 30 mins after administration was 2,368 ng/mL, pyrexia, myoclonus, and psychological symptoms were observed. After discontinuing amantadine, the patient’s myoclonus improved, but he died of acute respiratory distress syndrome. Case 2 was a patient with mild to moderate renal dysfunction [eGFRcreat: 55.6 mL/min/1.73m2; GFR category: G3a] taking amantadine 100 mg daily. In the patient, pyrexia, myoclonus, and consciousness disorder were observed. The blood level of amantadine 88 hours after the last dose was 265 ng/mL, and the blood level that was collected 24 hours after the end of administration was estimated to be about 2,600 to 4,200 ng/mL. In all cases, the clinical features were consistent with the common symptoms of amantadine intoxication, and improved by discontinuing amantadine. Taken together, these findings suggest that the patients were intoxicated with amantadine. These results indicate that amantadine intoxication due to elevated blood levels also occurs in patients with mild to moderate renal dysfunction during the administration of the usual dose of amantadine. In addition, the measurement of amantadine blood levels may be useful in avoiding amantadine intoxication.
