Background & aims: Recent non-malignant non-cirrhotic portal venous system thrombosis (PVT) is a rare condition. Among risk factors for PVT, cytomegalovirus (CMV) disease is usually listed based on a small number of reported cases. The aim of this study was to determine the characteristics and outcomes of PVT associated with CMV disease.

Methods: We conducted a French multicenter retrospective study comparing patients with recent PVT and CMV disease (« CMV positive »; n = 23) to patients with recent PVT for whom CMV testing was negative (« CMV negative »; n = 53) or unavailable (« CMV unknown »; n = 297).

Results: Compared to patients from the « CMV negative » and « CMV unknown » groups, patients from the « CMV positive » group were younger, more frequently had fever, and had higher heart rate, lymphocyte count and serum ALT levels (p ≤0.01 for all). The prevalence of immunosuppression did not differ between the 3 groups (4%, 4% and 6%, respectively). Extension of PVT was similar between the 3 groups. Thirteen out of 23 « CMV positive » patients had another risk factor for thrombosis. Besides CMV disease, the number of risk factors for thrombosis was similar between the 3 groups. Heterozygosity for the prothrombin G20210A gene variant was more frequent in « CMV positive » patients (22%) than in the « CMV negative » (4%, p = 0.01) and « CMV unknown » (8%, p = 0.03) groups. Recanalization rate was not influenced by CMV status.

Conclusions: In patients with recent PVT, features of mononucleosis syndrome should raise suspicion of CMV disease. CMV disease does not influence thrombosis extension nor recanalization. More than half of « CMV positive » patients have another risk factor for thrombosis, with a particular link to the prothrombin G20210A gene variant.

Lay summary: Patients with cytomegalovirus (CMV)-associated portal venous system thrombosis have similar thrombosis extension and evolution as patients without CMV disease. However, patients with CMV-associated portal venous system thrombosis more frequently have the prothrombin G20210A gene variant, suggesting that these entities act synergistically to promote thrombosis.