4.4 Article

Arterial thrombosis triggered by methotrexate-induced hyperhomocysteinemia in a systemic lupus erythematosus patient with antiphospholipid antibodies

Journal

THROMBOSIS JOURNAL
Volume 21, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12959-023-00557-5

Keywords

Antiphospholipid antibodies; Methotrexate; Hyperhomocysteinemia; Systemic lupus erythematosus; Thrombosis

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Patients with systemic lupus erythematosus (SLE) are at increased risk of cardiovascular disease and thrombotic events, especially if they have antiphospholipid antibodies. In this case report, a SLE patient with triple positivity for antiphospholipid antibodies developed popliteal artery thrombosis due to severe hyperhomocysteinemia after starting methotrexate (MTX) treatment. It is known that MTX can induce hyperhomocysteinemia by interfering with folate metabolism, which further increases the risk of vascular complications. The findings suggest the need for monitoring homocysteine levels in high cardiovascular risk SLE patients receiving drugs that can induce hyperhomocysteinemia, such as MTX.
Systemic lupus erythematosus (SLE) patients have an increased risk of cardiovascular disease and thrombotic events, and the presence of antiphospholipid antibodies further raises the risk of these complications. Here we report a case of a patient with SLE and triple positivity for antiphospholipid antibodies who developed a popliteal artery thrombosis in the context of a severe hyperhomocysteinemia after the introduction of methotrexate (MTX) treatment. MTX is one of the most prescribed medications for a wide spectrum of autoimmune diseases, including SLE. On the other hand, by interfering with folate metabolism, it may induce hyperhomocysteinemia, which, in turn, may increase the risk of vascular complications. Current recommendations suggest screening and, when possible, treating classical and disease-related cardiovascular risk factors in all lupus patients. Based on what observed in our case, we suggest a follow-up of homocysteine levels after the introduction of drugs capable of inducing hyperhomocysteinemia, such as MTX, in SLE patients at high cardiovascular risk.

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