Metformin Does Not Induce Hyperlactatemia in Patients Admitted to Internal Medicine Ward
Concerns about metformin-associated lactic acidosis (MALA) prohibit the use of metformin in a large subset of diabetic patients, mostly in patients with chronic kidney disease. Increasing evidence suggests that the current safety regulations may be overly restrictive. To examine the association betw...
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Published in | The Israel Medical Association journal Vol. 19; no. 5; pp. 300 - 303 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Israel
01.05.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Concerns about metformin-associated lactic acidosis (MALA) prohibit the use of metformin in a large subset of diabetic patients, mostly in patients with chronic kidney disease. Increasing evidence suggests that the current safety regulations may be overly restrictive.
To examine the association between chronic metformin treatment and lactate level in acute illness on the first day of admission to an internal medicine ward.
We compared diabetic and non-diabetic hospitalized patients treated or not treated with metformin in different sets of kidney function.
A total of 140 patients participated in the study, 54 diabetic patients on chronic metformin treatment, 33 diabetic patients without metformin and 53 patients with no diabetes. Most participants were admitted for conditions that prohibit metformin use, such as heart failure, hypoxia and sepsis. Average lactate level was significantly higher in the diabetes + metformin group compared to the diabetes non-metformin group. Metformin treatment was not associated with higher than normal lactate level (hyperlactatemia) or low pH. No patient was hospitalized for lactic acidosis as the main diagnosis.
Chronic metformin treatment mildly increases lactate level, but does not induce hyperlactatemia or lactic acidosis in acute illness on the first day of admission to an internal medicine ward. These data support the expansion of metformin use. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1565-1088 |