The Canadian journal of clinical pharmacology = Journal canadien de pharmacologie clinique · 2003
Thiamine deficiency in congestive heart failure patients receiving long term furosemide therapy.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zenuk Cecli, Healey Jeff, Donnelly James, Vaillancourt Régis, Almalki Yussuff, Smith Stuart
Аннотация
OBJECTIVE: To assess the presence of thiamine deficiency in congestive heart failure patients receiving furosemide therapy.
DESIGN: Prospective, biochemical analysis of thiamine status was performed in outpatients and inpatients of the University of Ottawa Heart Institute.
SUBJECTS: Thirty-two patients with congestive heart failure who received at least 40 mg/day of furosemide were included. Patients were then separated into two groups depending on whether the dose of furosemide was greater than or equal to 80 mg/day.
METHODS: The primary measure was actual thiamine status as assessed by the erythrocyte transketolase enzyme activity and the degree of thiamine pyrophosphate effect.
RESULTS: Biochemical evidence of severe thiamine deficiency was found in 98% (24 of 25) patients receiving at least 80 mg/day of furosemide and in 57% (four of seven) of patients taking 40 mg furosemide daily, odds ratio (OR) 19.0 (1.13<OR<601.29). Thiamine status was not associated with any other clinical variables.
CONCLUSIONS: These findings suggest that thiamine deficiency occurs in a substantial proportion of congestive heart failure patients being treated with furosemide.
DESIGN: Prospective, biochemical analysis of thiamine status was performed in outpatients and inpatients of the University of Ottawa Heart Institute.
SUBJECTS: Thirty-two patients with congestive heart failure who received at least 40 mg/day of furosemide were included. Patients were then separated into two groups depending on whether the dose of furosemide was greater than or equal to 80 mg/day.
METHODS: The primary measure was actual thiamine status as assessed by the erythrocyte transketolase enzyme activity and the degree of thiamine pyrophosphate effect.
RESULTS: Biochemical evidence of severe thiamine deficiency was found in 98% (24 of 25) patients receiving at least 80 mg/day of furosemide and in 57% (four of seven) of patients taking 40 mg furosemide daily, odds ratio (OR) 19.0 (1.13<OR<601.29). Thiamine status was not associated with any other clinical variables.
CONCLUSIONS: These findings suggest that thiamine deficiency occurs in a substantial proportion of congestive heart failure patients being treated with furosemide.