SERUM VITAMIN B12, FOLIC ACID, HOMOCYSTEINE, AND GLYCEMIC CONTROL MARKERS IN PATIENTS WITH TYPE 2 DIABETES BY METFORMIN AND OTHER ORAL ANTIDIABETIC MEDICATIONS.

BACKGROUND

Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorder associated with long-term complications. Metformin, the first-line therapy for T2DM, has been implicated in nutrient malabsorption, particularly vitamin B12, potentially leading to hyperhomocysteinemia and related metabolic dysfunction.

OBJECTIVES

This study examines how serum levels of vitamin B12, folic acid, homocysteine, and glycemic control markers are affected in patients with type 2 diabetes by metformin and other oral antidiabetic medications (OADs).

METHODS

A total of 330 participants were recruited and split into four groups: 30 healthy controls, 100 newly diagnosed T2DM patients not taking any medication, 100 T2DM patients taking other OADs, and 100 T2DM patients taking metformin. Vitamin B12, folic acid, homocysteine, fasting blood glucose (FBG), HbA1c, and creatinine were measured using CMIA and enzymatic techniques in fasting blood samples. Kruskal-Wallis, independent t-tests, and Pearson's correlation were all used in the statistical analysis.

RESULT: Compared to other groups, Group A (metformin users) had significantly higher homocysteine levels and significantly lower levels of folic acid and vitamin B12 (p<0.001). Age (r=-0.30), HbA1c (r=-0.54), homocysteine (r=-0.64), and FBG (r=-0.46) all showed a significant negative correlation with vitamin B12. Patients who took more than 1000 mg of metformin per day for more than five years had significantly lower vitamin B12 levels (p<0.001). Weight, creatinine, and BMI did not significantly differ between groups.

CONCLUSION

In patients with type 2 diabetes, prolonged high-dose metformin use is linked to worsened glycemic control, increased homocysteine, and vitamin B12 deficiency. For patients receiving long-term metformin therapy, routine vitamin B12 monitoring is advised to reduce the risk of complications from deficiencies.