(TCP004) INCIDENCE OF VENOUS THROMBOEMBOLISM IN VITAMIN B12 DEFICIENCY

Background: This case presentation aims to highlight a pathophysiological relation between severe B12 deficiency and hyperhomocysteinemia leading to unprovoked pulmonary embolism. Venous thromboembolism is often secondarily due to malignancy, surgery, genetic factors, and immobility. An uncommon etiology of venous thrombosis which is often forgotten is hyperhomocysteinemia due to severe vitamin B12 deficiency

METHODS AND RESULTS: This case presents a 37-year-old male who presented with 3-day history of dyspnea without hemodynamic compromise. His past medical history was significant for a spermatocele, Graves disease, moderate alcohol use, and obesity. A CT PE revealed acute bilateral segment pulmonary emboli involving the distal left and right pulmonary arteries and extending to nearly all the lobar and segmental branches with evidence of right heart strain. He was thrombolysed with low dose tpa given his high-intermediate risk and was anticoagulated initially with enoxaparin, then transitioned to DOAC. A malignancy work-up was completed which includes tumor markers, and chest imaging which both yielded no identifiable sources of malignancy. Significant risk factors for this patient include a sedentary lifestyle and obesity. He was previously investigated for a spermatocele, however given the unprovoked pulmonary embolism, further investigations were pursued during this admission with a testicular ultrasound, blood work and Urology consultation which showed no evidence of malignancy. Megaloblastic anemia was noted on basic blood work and further investigation found a severe B12 deficiency at 41 picomoles per liters (pmol/L) (reference range of 140 – 700) with an MCV of 112 femtoliter (fL) (normal 80 – 96.0).

Conclusion: This paper aims to highlight a relationship between severe vitamin B 12 deficiency leading to a hypercoagulable state via excess homocysteine leading to a physiological disruption between anticoagulation and procoagulant factors leading to an increase incidence of venous thromboembolism. Vitamin B12 is one of the essential B vitamins that promotes the conversion of homocysteine to methionine in order to make cystine. Cystine is an essential amino acid used in protein synthesis. However, an accumulation of excess homocysteine in the absence of sufficient vitamin B12 leads to platelet activation via thromboxane A2 biosynthesis, endothelial damage and dysfunction, as well as activation of protein C via activation of factor Va leading to increase incidence of thrombosis.