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Abstrak :
Background. Metformin is the first-line oral antidiabetic agent used in the treatment of diabetes mellitus. One of the adverse reactions of the long term use of metformin is cobalamin malabsorption. Clinical and laboratory findings are important in the diagnosis of cobalamin deficiency. Objective. This study aimed to evaluate the risk of cobalamin deficiency symptoms related to long-term use of metformin in type 2 diabetes mellitus patients at Pasar Rebo General Hospital in Jakarta. Setting. This quantitative, observational study with retrospective cohort design was conducted in outpatient department Pasar Rebo General Hospital November 2015 until January 2016. Methods. 200 subjects were recruited and divided into two groups, patients who had been taking metformin for 1-3 years and patients who had been taking metformin for more than 3 years. Each patient was assessed for the presence of cobalamin deficiency symptoms. Main outcome measure. Cobalamin deficiency symptoms evaluated were symptoms of neuropathy (measured by DN4 questionnaire) and hematologic abnormalities associated to cobalamin deficiency, i.e. macrocytic erythrocyte, hypersegmented neutrophils, and giant bands. Results. There are significant differences in the proportions of neuropathy symptoms (RR 2.36, 95%, p=0.000) and hematologic abnormalities (RR 1.5, 95%, p=0.007) between the two groups. Conclusions. Long-term use of metformin (≥3 years) may increase the risk of cobalamin deficiency symptoms in type 2 diabetes mellitus patients.

Abstrak :
Defisiensi kobalamin dapat menyebabkan berkurangnya donor metil yang berpotensi menggangu metabolisme jantung. Defisiensi kobalamin dapat terjadi pada pasien dengan malnutrisi, ulkus peptikum, diabetes melitus, dan alkoholisme. Berbagai studi pada defisiensi vitamin B12 masih berfokus pada aterogenesis dan stress oksidatif. Penelitian ini bertujuan mengetahui korelasi defisiensi vitamin B12 dengan penurunan fungsi jantung melalui gambaran EKG, ekspresi protein PGC-1α dan protein BNP. Empat belas tikus Sprague-Dawley jantan usia 24-28 minggu dibagi dalam 2 kelompok (kontrol dan perlakuan). Kelompok kontrol diberikan pakan standar dengan nutrisi lengkap, sementara kelompok perlakuan diberikan pakan AIN-93M termodifikasi defisien vitamin B12. Kedua kelompok diberikan pakan dalam periode yang sama yakni selama 16 minggu. Pada akhir minggu ke-16 dilakukan pemeriksaan EKG, pemeriksaan ELISA vitamin B12 plasma, Hcy plasma, ekspresi PGC-1α dan kadar BNP-45 plasma. Hasil penelitian pada kelompok perlakuan menunjukkan terdapat penurunan kadar vitamin B12 plasma, peningkatan kadar Hcy plasma disertai dengan penurunan ekspresi protein PGC-1α dan peningkatan kadar BNP-45 plasma. Pada kelompok perlakuan didapatkan hasil tebal miokardium lebih besar dari kelompok kontrol. Pada kelompok perlakuan juga didapatkan aritmia pada rekam EKG 2 dari 7 tikus. Terdapat korelasi negatif dengan kekuatan sedang antara penurunan ekspresi PGC-1α dengan peningkatan BNP-45 plasma. Defisiensi kobalamin terbukti menyebabkan gangguan metabolisme energi kardiomiosit yang ditandai dengan penurunan ekspresi protein PGC-1α dan berujung pada aritmia serta hipertrofi/pembesaran ventrikel kiri yang ditandai dengan peningkatan tebal miokardium dan peningkatan kadar BNP-45 plasma. ......Cobalamin deficiency may cause lack of dietary methyl donors which alter heart metabolism. Cobalamin deficiency are common in patients with malnutrition, gastrics ulcers, diabetes mellitus, and alcoholism. Most studies on cobalamin deficiencies are focused on its relationship with oxidative stress and atherogenesis. Therefore, this study aims to find the corelation between cobalamin deficiency and heart function deterioration through analysis of ECG pattern, expression of PGC-1α protein, and plasma BNP-45 level. Fourteen male Sprague-Dawley rats (age 24-28 weeks) were divided into 2 groups: control group and treatment group. The control group was given standard diet while the treatment group received a modified diet type AIN-93M. Both groups are fed with the same 16-weeks period. ECG and ELISA was performed to evaluate plasma vitamin B12, Hcy levels, expression of PGC-1α protein and plasma BNP-45 levels in each group at the end of the treatment period. At the end of study period, higher Hcy level was observed in the treatment group with lower plasma cobalamin followed by two rats has developed arrythmias and decreased expression of PGC-1α protein and also increased in plasma BNP-45 levels. There is a relatively strong correlation between deterioration of PGC-1α protein with the increased in plasma BNP-45 levels. Cobalamin deficiency has proven to alter cardiomyocites energy metabolism which resulted in arrythmia and tendency to developed left ventricular hypertrophy.