Archives of neurology · 2005
Carbon 13-labeled magnetic resonance spectroscopy observation of cerebral glucose metabolism: metabolism in MELAS: case report.
Клинический случайСравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Otsuki Taisuke, Kanamatsu Tomoyuki, Tsukada Yasuzo, Goto Yuichi, Okamoto Kazuya, Watanabe Hidehiro
Аннотация
BACKGROUND: Carbon 13-labeled magnetic resonance spectroscopy ((13)C-MRS) with [(1-13)C]-glucose administration, the (13)C atom that behaves as a radio inactive tracer in the brain, can differentiate aerobic and anaerobic glucose metabolism by detecting [(4-13)C]-glutamate (Glu C4) and [(3-13)C]-lactate (Lac C3).
OBJECTIVE: To investigate the cerebral metabolic derangement resulting from mitochondrial dysfunction in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS).
DESIGN: Application of a new (13)C-MRS technique to a patient with MELAS compared with control subjects (n = 7).
PATIENT: A 19-year-old woman with an A3243G mitochondrial mutation who underwent (13)C-MRS for 30 minutes after oral administration of [(1-13)C]-glucose (0.75 g/kg).
RESULT: Decreased Glu C4-labeling (P<.001) and increased Lac C3 synthesis (>2 SDs) compared with controls were demonstrated in the patient with MELAS.
CONCLUSIONS: This first report on (13)C-MRS observation of cerebral glucose metabolism in a patient with MELAS demonstrated the presence of low glutamate production via the tricarboxylic acid cycle compared with high lactate synthesis by glycolysis. The present findings suggest that the clinical use of (13)C-MRS can be extended to diagnose mitochondrial dysfunction and monitor cerebral glucose metabolism in a variety of mitochondrial disorders.
OBJECTIVE: To investigate the cerebral metabolic derangement resulting from mitochondrial dysfunction in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS).
DESIGN: Application of a new (13)C-MRS technique to a patient with MELAS compared with control subjects (n = 7).
PATIENT: A 19-year-old woman with an A3243G mitochondrial mutation who underwent (13)C-MRS for 30 minutes after oral administration of [(1-13)C]-glucose (0.75 g/kg).
RESULT: Decreased Glu C4-labeling (P<.001) and increased Lac C3 synthesis (>2 SDs) compared with controls were demonstrated in the patient with MELAS.
CONCLUSIONS: This first report on (13)C-MRS observation of cerebral glucose metabolism in a patient with MELAS demonstrated the presence of low glutamate production via the tricarboxylic acid cycle compared with high lactate synthesis by glycolysis. The present findings suggest that the clinical use of (13)C-MRS can be extended to diagnose mitochondrial dysfunction and monitor cerebral glucose metabolism in a variety of mitochondrial disorders.