5 DISCUSSION
Vitamin B12 deficiency is a significant public health issue worldwide, with various adverse effects [6]. Vitamin B12 is required as an enzyme co-factor to convert methylmalonyl coenzyme A to succinyl coenzyme A and homocysteine to methionine. Its deficiency results in accumulation of methylmalonyl Co-A causing defective myelin sheath synthesis that leads to various central and peripheral dysfunctions. SCD is one such neurological manifestation [1]. HHcy, on the other hand, is a modifiable risk factor for atherothrombotic diseases such as myocardial infarction, stroke, and DVT [2, 4]. The underlying mechanism of these events is not very well understood, however, some studies suggest it may cause endothelial dysfunction by decreasing the availability of nitric oxide (which maintains vascular homeostasis), while other studies propose HHcy induced alteration in the function of plasma proteins such as fibrinogen [2, 7]. The daily requirement of vitamin B12 is 2 mcg(micrograms) and the common causes of vitamin B12 deficiency include nutritional deficiency, malabsorption syndromes such as pernicious anemia and gastritis [8], with a high prevalence of this deficiency seen in the elderly [9]. In our case study, spinal MRI of the patient showed the typical lesions seen in patients with SCD. Moreover, EMG/NCS and hematological findings were also consistent with the condition [1,10]. Although our study has limitations in testing for genetic mutations involved in the metabolism of homocysteine, however, in the absence of other major risk factors and a negative family history for thrombosis, it can be assumed that HHcy secondary to vitamin B12 deficiency was the most probable cause of DVT in this patient. Nevertheless, comprehensive cohort studies with fewer limitations are required to fully understand the association.
To our knowledge, this is the first case of SCD concomitant with DVT, which demonstrates that vitamin B12 deficiency may cause SCD and can also predispose a patient to an increased risk of thrombosis. Early detection through screening of vitamin B12 levels, especially in high risk patients, can help prevent life threatening complications of thrombosis.