Venous thromboembolism due to hyperhomocysteinaemia and TB
Tuberculosis and hyperhomocysteinaemia are both pro-coagulant states. Acquired and genetic factors predispose to hypercoagulability, endothelial injury and stasis that cause thrombosis. It has also been reported as a rare systemic complication of tuberculosis due to systemic inflammatory changes causing hypercoagulability.

The occurrence of an acquired and inherited factor in the same patient causing thrombosis is a rare coincidence. Published in The National Medical Journal of India, the authors describe such a patient.

An 18-year-old male presented with complaints of episodic abdominal pain, dry cough and right pleuritic chest pain. He was diagnosed as a case of right tuberculous pleural effusion on the basis of the pleural fluid Genexpert report of Mycobacterium tuberculosis detected sensitive to rifampicin and was started on antituberculous therapy.

Forty-five days later, he presented with acute onset breathlessness, swelling of the right leg, streaky haemoptysis and a fresh left-sided pleural effusion. Evaluation revealed venous thromboembolism (right lower lobar segment pulmonary embolism with right leg deep vein thrombosis).

Workup for malignancy was negative. However, he had vitamin B12 deficiency with increased homocysteine levels and heterozygous mutation of the MTHFR gene at A1298C.

He was treated with optimal anticoagulation, vitamin B12 supplementation and antitubercular treatment. This is a rare combination of events perhaps related to the MTHFR gene mutation.

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