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Year : 2012  |  Volume : 2  |  Issue : 1  |  Page : 61-69

Vitamin B12-homocysteine interaction and the efficacy of B12 therapy in relation to anemia and neurological disease in a North Indian population

1 Department of Medicine, Maulana Azad Medical College and Associated Hospitals, Bahadur Shah Zafar Marg, New Delhi, India
2 Department of Pathology, Maulana Azad Medical College and Associated Hospitals, Bahadur Shah Zafar Marg, New Delhi, India
3 Department of Ocular Pharmacology, Dr. Rajendra Prasad Eye Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India

Correspondence Address:
Madhumita Premkumar
Department of Medicine, Maulana Azad Medical College and Associated Hospitals, Bahadur Shah Zafar Marg, New Delhi 110 002
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Source of Support: Supported by a grant from the Indian Council of Medical Research, New Delhi, Conflict of Interest: None

DOI: 10.4103/2231-0738.93132

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Background: Vitamin B12 deficiency leads to myriad hematological and neurological changes leading to megaloblastic anemia and disorders of the nervous system like subacute combined degeneration of the spinal cord, cognitive impairment, peripheral neuropathy, etc. In this case series, an attempt was made to investigate the neurological manifestations of patients with diagnosed vitamin B12-deficient megaloblastic anemia, determine the cause of vitamin deficiency in these cases, and monitor their response to vitamin B12 therapy. Materials and Methods: The study was conducted in a tertiary care referral teaching hospital in New Delhi during a period of over 2 years from August 2007 to December 2009. Eighty-five consecutive patients with megaloblastic anemia (MA) due to vitamin B12 deficiency were screened and a total of 28 patients with neurological and psychiatric symptoms were selected for the study. In addition to bone marrow examination, blood counts, red cell indices, and biochemical tests, assays of serum vitamin B-12, folate, and homocysteine were done. Neuroimaging by magnetic resonance studies and nerve conduction studies (NCS) was done where clinically applicable. Follow-up was done at least twice at 3 months and 6 months to assess clinical, neurological, and hematological response to vitamin B12 therapy. Results: The primary study group of MA with B12 deficiency had 85 patients. Of these, only 28 (32.9%) patients had neurological and/or psychiatric features. There were 18 male and 10 female subjects (M: F ratio being 1.8:1). The mean age was 32.80 years with a range of 18-68 years. Though the majority of MA patients (77.6%) were vegetarian, a good 22% consumed a nonvegetarian diet. Neurological manifestations included peripheral neuropathy in 14 (50%), myelopathy in 2 (7.14%), myeloneuropathy in 2 (7.14%), acute confusional state in 4 (14.28%), and cognitive impairment in 20 (71.42%) patients. Mood disturbances, anxiety, and irritability were also seen. NCS was done in 18 cases and showed demyelinating peripheral neuropathy in 12 cases and both axonal and demyelinating changes in two cases. Magnetic resonance imaging (MRI) showed four cases with the classical demyelination on spinal MRI with white matter hyper intense lesions in the posterior tracts on T2 weighted images. At 6-month follow-up with B12 therapy, 10/14 patients with neuropathy recovered completely, 2/14 had partial recovery, and 2 had poor recovery. While the cases of myelopathy had only partial recovery at 6 months, all four cases with acute confusional state recovered completely in response to B12 therapy. Conclusion: The electrodiagnostic and neuroimaging changes in vitamin B12 deficiency are consistent with focal demyelination of white matter tracts in the brain, the spinal cord, and peripheral nerves. In this case series of B12 deficiency MA, we found demyelinating peripheral neuropathy to be the predominant presenting neurological disease. However, cognitive impairment with behavioral changes was found to be common on neurological and psychiatric examination. Many of these features were found to be reversible with B12 therapy.

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