Study On the Role of Mitochondrial Dysfunction in the Pathogenesis of Metformin-associated Lactic Acidosis
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.
|Study Design:||Observational Model: Case-Only
Time Perspective: Prospective
|Official Title:||On the Role of Mitochondrial Dysfunction in the Pathogenesis of Metformin-associated Lactic Acidosis|
- Platelet mitochondrial respiratory chain enzyme activity [ Time Frame: Within 48 hours from admission to ICU ]
|Study Start Date:||January 2009|
|Study Completion Date:||October 2011|
|Primary Completion Date:||December 2010 (Final data collection date for primary outcome measure)|
Please refer to this study by its ClinicalTrials.gov identifier: NCT00942123
|Ospedale Maggiore Policlinico|
|Milano, MI, Italy, 20122|