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.