Portal Vein Thrombosis Due to Concomitant Cytomegalovirus and Epstein-Barr Virus Infection: An Underestimated Complication.

A young immunocompetent male developed acute portal vein thrombosis in the setting of concomitant acute CMV and EBV infection.

• The patient presented with fever, fatigue, and vague abdominal pain.
• Initial investigation showed mild elevation in liver enzymes and mild hepatosplenomegaly on abdominal ultrasound.
• Serological testing revealed high titers of IgM for both CMV and EBV, with negative IgG titers for both viruses, suggesting recent acute infection.
• CT scan of the abdomen demonstrated acute portal vein thrombosis.

A thorough workup to exclude primary and secondary causes of portal vein thrombosis yielded entirely negative results.

• The workup was performed to rule out thrombophilia and other primary and secondary causes of PVT.
• All tests were negative, supporting the diagnosis of acute PVT secondary to CMV and EBV infection.
• Non-cirrhotic non-malignant PVT is considered a rare disorder in patients without a risk of thrombophilia.

The patient was managed with anticoagulation therapy initiated in the ICU and was successfully discharged on oral anticoagulation.

• Anticoagulation was initiated immediately with unfractionated heparin via intravenous bolus of 80 u/kg followed by 18 u/kg/hr.
• Target aPTT was set at 1.5–2.3 times control.
• The patient's symptoms gradually improved and he was discharged home on oral anticoagulation.

Acute viral infection, including CMV and EBV, has been reported to be associated with an increased risk of venous thromboembolism, more often in immunocompromised patients.

• The association between acute viral infection and venous thromboembolism is noted as occurring more often in immunocompromised patients.
• This case demonstrates that thromboembolism can occur even in immunocompetent patients with acute CMV and/or EBV infection.
• The authors characterize this complication as 'underestimated.'

The authors conclude that treating acute CMV and/or EBV infection as a provoked risk factor for thromboembolism can guide early detection and avoid unnecessary lifelong anticoagulation.

• Classifying the infection as a triggered/provoked risk factor supports time-limited rather than indefinite anticoagulation therapy.
• Early recognition of this association is emphasized as important for management.
• The authors state: 'by treating it as a triggered risk, unnecessary lifelong anticoagulation can be avoided.'