BACKGROUND: Portal vein thrombosis (PVT) generally results from a local cause (hepatocellular and pancreatic carcinoma). Spontaneous PVT related to a general cause is less common. We report here a case of spontaneous PVT associated with acute cytomegalovirus (CMV) infection in an immunocompetent patient. CASE REPORT: A 31-year-old white female was admitted with fever and lymph node enlargement. The patient was a heavy smoker and was taking oral contraception. Blood tests revealed an inflammatory syndrome. Liver enzymes were elevated (2N) and platelet count was 118 G/l. Abdominal ultrasonography disclosed partial portal thrombosis. Computed tomography did not show any evidence of a hepatic or pancreatic mass. Protein S, protein C, and anti-thrombin III levels were normal. No antiphospholipid antibodies, no mutation for factors II and V and no abnormality suggestive of paroxysmal nocturnal hemoglobinuria at flow cytometry could be demonstrated. Acute CMV infection was diagnosis with positive viremia (PCR). The patient was given anticoagulation treatment and has done well with no relapse. CONCLUSION: Cytomegalovirus, by damaging endothelial cells, is thought to trigger a cascade of events leading to deep vein thrombosis. CMV infection does not appear to act alone on endothelial cells but rather behaves as an associated factor.
BACKGROUND: Portal vein thrombosis (PVT) generally results from a local cause (hepatocellular and pancreatic carcinoma). Spontaneous PVT related to a general cause is less common. We report here a case of spontaneous PVT associated with acute cytomegalovirus (CMV) infection in an immunocompetent patient. CASE REPORT: A 31-year-old white female was admitted with fever and lymph node enlargement. The patient was a heavy smoker and was taking oral contraception. Blood tests revealed an inflammatory syndrome. Liver enzymes were elevated (2N) and platelet count was 118 G/l. Abdominal ultrasonography disclosed partial portal thrombosis. Computed tomography did not show any evidence of a hepatic or pancreatic mass. Protein S, protein C, and anti-thrombin III levels were normal. No antiphospholipid antibodies, no mutation for factors II and V and no abnormality suggestive of paroxysmal nocturnal hemoglobinuria at flow cytometry could be demonstrated. Acute CMV infection was diagnosis with positive viremia (PCR). The patient was given anticoagulation treatment and has done well with no relapse. CONCLUSION: Cytomegalovirus, by damaging endothelial cells, is thought to trigger a cascade of events leading to deep vein thrombosis. CMV infection does not appear to act alone on endothelial cells but rather behaves as an associated factor.