Oxidative Stress Markers in Vitamin B12 Deficiency.

In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r = 0.54; P < 0.01), TAC with female gender (r = 0.43; P = 0.002) and joint position impairment (r = -0.34; P = 0.01), and MDA with LDH (r = 0.41; P = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.