Urinary Methylmalonic Acid in Patients with Acute Myocardial Infarction

Abstract

Objective: To investigate urinary methylmalonic acid (uMMA) levels and their relationship with markers of myocyte necrosis and inflammation in patients with acute myocardial infarction (AMI). Subjects and Methods: The study participants consisted of 80 consecutive patients with AMI and 72 age- and sex-matched consecutive controls. Of the patients, 38 had ST segment elevation myocardial infarction (STEMI) and 42 had non-ST segment elevation. All patients with STEMI underwent fibrinolytic therapy. Routine laboratory tests included troponin-I, creatinine phosphokinase MB (CK-MB), high-sensitivity C-reactive protein (hs-CRP), vitamin B₁₂, folate, homocysteine and methylmalonic acid analyses. uMMA measurements were made by a spectrophotometric method. Results: uMMA levels were significantly higher in patients with AMI than in controls (10.1 vs. 5.2 mmol/mol creatinine, p < 0.001) and higher in patients with anterior MI compared to those with non-anterior MI (18.9 vs. 8.7 mmol/mol creatinine, p < 0.001). In addition, uMMA levels were significantly higher in patients without successful reperfusion compared to those with successful reperfusion. In patients with STEMI, a strong positive association was found between urinary MMA and plasma hs-CRP levels (r = 0.81, p < 0.001), symptom duration (r = 0.91, p < 0.001) and wall motion score (r = 0.60, p = 0.006). More importantly, a strong positive association was observed between uMMA and the size of myocardial infarction in patients without successful reperfusion (for CK-MB r = 0.81, p = 0.013; for wall motion score r = 0.82, p = 0.012). Conclusion: uMMA levels were elevated in patients with AMI and, as such, may be a candidate biochemical indicator of larger infarct size and enhanced inflammation in patients with AMI.

Urinary Methylmalonic Acid as an Indicator of Early Vitamin B12 Deficiency and Its Role in Polyneuropathy in Type 2 Diabetes

“…The mechanism was unclear, and the probable mechanism was that methylmalonic acid affected energy metabolism and the citric acid cycle and then led to neurotoxicity and the occurrence of DPN. In addition, uMMA was reported related to the enhanced inflammation in acute myocardial infarction [20]. The uMMA measurements are a noninvasive method that requires only a 1 mL urine specimen, and for months if frozen, it may offer a new method of analysis for identifying true tissue cobalamin deficiency [21].…”

Functional cobalamin (vitamin B12) deficiency: role of advanced age and disorders associated with increased oxidative stress

“…14 It is noteworthy then that Cbl is an active superoxide scavenger; 15,16 reduced forms of Cbl are required for its coenzyme activity; 2 cellular uptake of Cbl may be impaired by oxidative byproducts; 17 and functional Cbl deficiency occurs after exercise and in many other pro-oxidant disorders. [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] Significantly, diabetes and folate excess, both of which are associated with increased oxidative stress, have been linked to functional Cbl deficiency in the elderly but not in younger individuals. 10,18,21 These observations suggest that functional Cbl deficiency may be associated with oxidative stress and that this relationship may be particularly prevalent in the elderly.…”