MedElevator
Войти в исследования Journal of the neurological sciences · 2025
Exposure to sertraline and ranolazine is common among adult patients with genetically uncharacterized lipid storage myopathy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Jones Felipe J S, Mirman Igal, Milone Margherita, Liewluck Teerin
Аннотация
BACKGROUND: To investigate sertraline and ranolazine exposure in adult patients with lipid storage myopathy (LSM), given recent reports of their potential association with the condition.
METHODS: We reviewed electronic health records to identify adult patients with a pathological and/or genetic diagnosis of LSM, who were evaluated at the Mayo Clinic (January 2000-December 2021). Patients without genetic testing were excluded.
RESULTS: We identified 10 patients with LSM, including 8 with multiple acyl-CoA dehydrogenase deficiency (MADD) and 2 with subacute LSM after ranolazine initiation. Genetic testing revealed an underlying molecular defect in only 3 MADD patients. Sertraline exposure was noted in 4 MADD patients, none of whom had an identified genetic defect. Muscle biopsy findings were similar across patients with hereditary MADD, sertraline-associated MADD, and ranolazine-associated LSM, all demonstrating excessive lipid accumulation and attenuation of succinate dehydrogenase reactivity. MADD patients showed a favorable response to riboflavin and coenzyme Q10 supplementation, regardless of genetic test results. Patients with ranolazine-associated LSM improved following discontinuation of the drug.
CONCLUSIONS: LSM is rare in adults but important to recognize due to its treatability and potential drug-induced cases in a significant proportion of patients. Weakness in individuals taking sertraline or ranolazine should prompt consideration of LSM.
METHODS: We reviewed electronic health records to identify adult patients with a pathological and/or genetic diagnosis of LSM, who were evaluated at the Mayo Clinic (January 2000-December 2021). Patients without genetic testing were excluded.
RESULTS: We identified 10 patients with LSM, including 8 with multiple acyl-CoA dehydrogenase deficiency (MADD) and 2 with subacute LSM after ranolazine initiation. Genetic testing revealed an underlying molecular defect in only 3 MADD patients. Sertraline exposure was noted in 4 MADD patients, none of whom had an identified genetic defect. Muscle biopsy findings were similar across patients with hereditary MADD, sertraline-associated MADD, and ranolazine-associated LSM, all demonstrating excessive lipid accumulation and attenuation of succinate dehydrogenase reactivity. MADD patients showed a favorable response to riboflavin and coenzyme Q10 supplementation, regardless of genetic test results. Patients with ranolazine-associated LSM improved following discontinuation of the drug.
CONCLUSIONS: LSM is rare in adults but important to recognize due to its treatability and potential drug-induced cases in a significant proportion of patients. Weakness in individuals taking sertraline or ranolazine should prompt consideration of LSM.