Severe lithium intoxication: management without dialysis and report of a possible teratogenic effect of lithium.
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Abnormalities, Drug-Induced↗
Biomedical subjects
F Y Aoki
Publications and source records attributed to F Y Aoki.
Slow release theophylline disposition and effect in elderly patients with chronic obstructive lung disease: influence of dose formulation and institutionalization.
We studied the steady-state disposition of slow release theophylline tablets and granules in 12 institutionalized (I) and 12 community-dwelling (C) elderly patients with fixed chronic obstructive lung disease. Design was open label with random order crossover; each formulation was given 5 min before food every 12 h for 7 days. Age (median 70 y, range 55-88), sex, smoking status, and baseline lung function off drug were similar. Though plasma concentration (Cp) was higher with the tablets as was the area under the Cp vs time curve: 134 (74-252) vs 121 (75-197) mg h l-1; p = 0.028. The standard deviation of Cp over one dose interval was lower with the granules. FEV 1.0 was slightly improved over baseline. Dose required to reach target Cp was higher in the institutionalized group (12.6 vs 8.6 mg kg-1 day-1; p = 0.003) as was apparent clearance; I:94 (43-148) ml hr-1 kg-1 vs C:68 (34-163); p = 0.003. Although bioavailability was slightly reduced for the granules, fluctuations of Cp was less, and we failed to find a food effect that was clinically important in geriatric subjects.
Aged↗
Prospective, randomized, comparative trials in the therapy for intraabdominal and female genital tract infections.
The results of four prospective, randomized comparative trials, in which the authors' two university teaching hospitals participated, that compared selected antimicrobial regimens with the combination of clindamycin and an aminoglycoside in the therapy for intraabdominal and female genital tract infections are reviewed. In the first trial, the rates of cure for patients with intraabdominal infections were 33 (79%) of 42 treated with clindamycin and gentamicin, 43 (81%) of 53 treated with chloramphenicol and gentamicin, and 35 (90%) of 39 treated with ticarcillin and gentamicin. The rates of cure for females with genital tract infections were 16 (94%) of 17, 11 (100%) of 11, and 12 (92%) of 13 treated with the three respective combinations. The rates of cure in the second study were 22 (88%) of 25 treated with metronidazole and gentamicin and 23 (88%) of 26 treated with clindamycin and gentamicin. In the third study, the rates of cure were 23 (82%) of 28 treated with cefoxitin and tobramycin as compared with 24 (89%) of 27 treated with clindamycin and tobramycin. In the fourth study, 21 (87%) of 24 patients treated with ceftizoxime alone are cured as compared with 13 (87%) of 15 treated with clindamycin and tobramycin. These prospective, randomized trials suggest that chloramphenicol and gentamicin, ticarcillin and gentamicin, metronidazole and gentamicin, cefoxitin and tobramycin, or ceftizoxime alone are as effective as clindamycin and gentamicin or tobramycin in therapy for mixed aerobic/anaerobic infections.
Abscess↗
Amantadine acetylation may be effected by acetyltransferases other than NAT1 or NAT2.
Amantadine is a drug with a primary amino group, and consequently a likely candidate for metabolism by acetylation. This study assessed the possibility that a person's polymorphic (NAT2) acetylator phenotype could be used to predict the extent of amantadine acetylation. Thirty-eight normal, healthy volunteers were NAT2 acetylator phenotyped with sulfapyridine. Of the six fastest (75-86%) and six slowest (34-40%) sulfapyridine acetylators, two and three, respectively, had acetylamantadine present (18-338 microg) in the 8-h urine collection. There was no correlation between NAT2 acetylator phenotype and amantadine acetylation (p<0.5), and no difference in the total urine amantadine excreted over 8 h between acetylators and nonacetylators (28.3+/-9.7 vs. 30.4+/-9.6 mg, respectively, mean +/- SD). Acetylamantadine represented 0.1-1.5% (median 0.5%) of urinary drug content over 8 h. Our data confirm that amantadine is acetylated in humans and demonstrate for the first time that the extent is not correlated with NAT2 acetylator phenotype. Parallel in vitro enzyme studies indicate the possibility that neither NATI nor NAT2 is responsible for acetylation of amantadine.
Acetylation↗