Lactic Acidosis, Metformin
Conditions
Brief summary
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.
Interventions
None listed
Sponsors
Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico
Study design
Observational model
CASE_ONLY
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
1. Lactic acidosis (pH \< 7.35 or base deficit \> 5 mmol/L and lactate \> 5 mmol/L) 2. Metformin intoxication (serum drug level \> 4 mcg/mL) 3. Absence of evidence of any other condition that could primarily explain the lactic acidosis
Exclusion criteria
1. Less than 18 years of age 2. Hemoglobin \< 8 g/dL (10 g/dL if ischemic cardiac disease)
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Platelet mitochondrial respiratory chain enzyme activity | Within 48 hours from admission to ICU |
Countries
Italy
Outcome results
None listed