P1835 - Index Case: Acute Portal Venous Thromboses in the Setting of Acute Hepatitis A

Ahmad Abulawi, MBBS¹, Omar Tageldin, MD², Asra Batool, MD^2
1Albany Medical College, Albany, NY; ²Albany Medical Center, Albany, NY

Introduction: Acute portal vein thrombosis (PVT) is a life-threatening condition. Among the many infective causes, viral hepatitis has been reported as a rare associated condition. To the best of our knowledge, we report the first case of acute PVT as a manifestation of acute hepatitis A virus (HAV) infection.

Case Description/Methods: A 34-year-old-male presented with a two-week history of nausea, vomiting, right upper quadrant abdominal pain, jaundice, and abdominal fullness. Few days before his symptoms’ onset, he reported eating crab legs at a local restaurant. Physical exam was remarkable for jaundice, abdominal distention, and tenderness on the RUQ. Laboratory investigation was remarkable for mildly elevated liver enzymes with a total bilirubin of 7.1, direct bilirubin of 6.1, and WBCs 20.0. Further investigation revealed a negative hepatitis panel except for HAV IgM antibodies. CT scan of the abdomen and pelvis showed a nonocclusive, eccentric portal vein thrombus measuring 3.5 cm in length extending into portosplenic confluence and an occlusive thrombus within the anterior branch of the right portal vein. All autoimmune antibodies were negative. Serum complement values were within the normal range and cryoglobulins were not detected in the serum. Antithrombin III, factor V Leiden, and protein C and S levels were also within normal limits. The patient was treated with anticoagulation. On follow-up, he continued to show symptom resolution.

Discussion: Predisposing factors of acute PVT include hepatitis B and C virus infections. Although HAV is considered one of the risk factors for venous thromboembolism, the only reported case in the literature was for a patient with cerebral vein thrombosis. The pathogenesis is likely related to induction of inflammatory changes in the surrounding tissues, in particular the endothelium of the portal vein system, leading to activation of the coagulation cascade and increasing the risk of PVT. Also, antiphospholipid antibodies may have a role in the pathogenesis. Our patient suffered from acute PVT few days after the onset of HAV infection. The characteristic clinical picture of the patient, abnormal liver enzymes, absence of hypergammaglobulinaemia, and presence of serum IgM antibodies to HAV are strongly supportive of recent infection and an initial acute phase of the disease. In our report, HAV was the only risk factor predisposing to acute PVT. Hence, we suggest that HAV serologic markers should be included in the investigation of acute PVT of unknown etiology.



Disclosures:


Ahmad Abulawi, MBBS¹, Omar Tageldin, MD², Asra Batool, MD². P1835 - Index Case: Acute Portal Venous Thromboses in the Setting of Acute Hepatitis A, ACG 2021 Annual Scientific Meeting Abstracts. Las Vegas, Nevada: American College of Gastroenterology.