Search Medication
| Level | Qualifying studies |
|---|---|
| A | Systematic review or meta-analysis of human trials |
| B | Human RDBPC trials. ≥ 2 studies and/or 1 study with ≥ 50 subjects |
| C | Human RDBPC trials or RCTs. 1 study < 50 subjects |
| D | Human trials or in-vivo animal trials |
| N/A | Insufficient evidence to suggest that any significant nutrient depletions exist |
Results for Metformin: 2
Evidence Rating ScaleFolic Acid
Summary: Pharmacological doses of folate supplementation lowered plasma homocysteine and serum malondialdehyde levels and improved serum total antioxidant capacity and folate and B12 levels in patients with type 2 diabetes.
Pharmacological doses of folate supplementation lowered plasma homocysteine and serum malondialdehyde levels and improved serum total antioxidant capacity and folate and B12 levels in patients with type 2 diabetes.
Even short-term treatment with metformin causes a decrease in serum Cbl folic acid and increase in Hcy, which leads to peripheral neuropathy in Type 2 diabetes patients. A multicenter study with heterogeneous population would have increased the power of the study. We suggest prophylactic Vitamin B12 and folic acid supplementation or periodical assay in metformin user.
In patients with type 2 diabetes, metformin reduces levels of folate and vitamin B(12) and increases Hcy. Conversely, rosiglitazone decreases Hcy levels in this time period. The clinical significance of these findings remains to be investigated.
Vitamin B12
Summary: Even short-term treatment with metformin causes a decrease in serum Cbl folic acid and increase in Hcy, which leads to peripheral neuropathy in Type 2 diabetes patients. A multicenter study with heterogeneous population would have increased the power of the study. We suggest prophylactic Vitamin B12 and folic acid supplementation or periodical assay in metformin user.
Even short-term treatment with metformin causes a decrease in serum Cbl folic acid and increase in Hcy, which leads to peripheral neuropathy in Type 2 diabetes patients. A multicenter study with heterogeneous population would have increased the power of the study. We suggest prophylactic Vitamin B12 and folic acid supplementation or periodical assay in metformin user.
Pharmacological doses of folate supplementation lowered plasma homocysteine and serum malondialdehyde levels and improved serum total antioxidant capacity and folate and B12 levels in patients with type 2 diabetes.
Long term treatment with metformin increases the risk of vitamin B-12 deficiency, which results in raised homocysteine concentrations. Vitamin B-12 deficiency is preventable; therefore, our findings suggest that regular measurement of vitamin B-12 concentrations during long term metformin treatment should be strongly considered.
Even though the direct effect of metformin treatment on the plasma Hcy could not be concluded from the present study, it was found that there was a significant depletion of level of serum vitamin B12 among patients who had been on long-term metformin treatment. Therefore, vitamin B12 supplement is suggested for diabetic patients who are receiving metformin medication.
In patients with type 2 diabetes, metformin reduces levels of folate and vitamin B(12) and increases Hcy. Conversely, rosiglitazone decreases Hcy levels in this time period. The clinical significance of these findings remains to be investigated.
Vitamin-B(12) malabsorption has been found in 21 (30%) of 71 diabetic patients taking long-term metformin therapy in addition to dietary management. The causes and implications of these findings are discussed and it is concluded that all patients on long-term metformin therapy should have annual serum B(12) estimations.
Here we report a case of 60 year old diabetic male presenting with clinical features of Vitamin B-12 deficiency on long term metformin therapy, which was confirmed on investigations. Patient showed symptomatic improvement with change in treatment.
Among patients with type 2 diabetes using metformin, the prevalence of vitamin B12 deficiency is higher than compared with patients not using metformin. However, metformin use did not predict the chance of having anaemia or neuropathy.
Metformin-induced B12 lowering in diabetes was associated with elevation of homocysteine, and hyperhomocysteinemia was independently related to retinopathy. Metformin-induced B12 deficiency was correctable with B12 supplementation.
The present findings suggest a high prevalence of vitamin B12 deficiency in metformin-treated diabetic patients. Older patients, patients in long term treatment with metformin and low vitamin B12 intake are probably more prone to this deficiency.
In type 2 diabetic patients, treatment with metformin is associated to lower vitamin B12 plasma levels. Vitamin B12 deficiency associated with metformin is relatively common in our area.
This study confirms the higher prevalence of vitamin B₁₂ deficiency in metformin-treated patients with type 2 diabetes than in those not treated with metformin. This study also suggests that vitamin D deficiency is not a clinical concern among metformin-treated patients with type 2 diabetes and that metformin does not negatively affect treatment of vitamin D deficiency in these patients.
Metformin therapy is associated with a higher prevalence of biochemical B(12) deficiency. The amount of B(12) recommended by the Institute of Medicine (IOM) (2.4 μg/day) and the amount available in general multivitamins (6 μg) may not be enough to correct this deficiency among those with diabetes.
Metformin use was associated with impaired cognitive performance. Vitamin B12 and calcium supplements may alleviate metformin-induced vitamin B12 deficiency and were associated with better cognitive outcomes. Prospective trials are warranted to assess the beneficial effects of vitamin B12 and calcium use on cognition in older people with diabetes who are taking metformin.
