On the Role of Mitochondrial Dysfunction in the Pathogenesis of Metformin-associated Lactic Acidosis
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 入组人数
- 10
- 试验地点
- 1
- 主要终点
- Platelet mitochondrial respiratory chain enzyme activity
研究概览
简要总结
Metformin is the first line drug of choice for the treatment of type II diabetes. Lactic acidosis can develop as a side effect, especially when renal failure leads to drug accumulation. Lactic acidosis is usually attributed to an abnormal inhibition of hepatic lactate clearance.
Growing evidence suggest that metformin can dose-dependently inhibit hepatocyte mitochondrial function. Whether a similar effect occurs in extra-hepatic human tissues remains unknown.
The investigators hypothesize that mitochondrial dysfunction occurs during metformin intoxication even in tissues other than the liver, thus contributing to the development of lactic acidosis. The aim of this study is to investigate mitochondrial integrity in circulating platelets of patients with lactic acidosis due to metformin intoxication.
研究设计
- 研究类型
- Observational
- 观察模型
- Case Only
- 时间视角
- Prospective
入排标准
- 年龄范围
- 18 Years 至 —（Adult, Older Adult）
- 性别
- All
- 接受健康志愿者
- 否
入选标准
- •Lactic acidosis (pH < 7.35 or base deficit > 5 mmol/L and lactate > 5 mmol/L)
- •Metformin intoxication (serum drug level > 4 mcg/mL)
- •Absence of evidence of any other condition that could primarily explain the lactic acidosis
排除标准
- •Less than 18 years of age
- •Hemoglobin < 8 g/dL (10 g/dL if ischemic cardiac disease)
结局指标
主要结局
Platelet mitochondrial respiratory chain enzyme activity
时间窗: Within 48 hours from admission to ICU
次要结局
未报告次要终点