Adolescent Epstein–Barr virus–associated cholestatic jaundice with porta hepatis/pancreatic head lymphadenopathy and transient CA 19-9 elevation: a case report

TL;DR

A 15-year-old girl with Epstein-Barr virus (EBV) developed jaundice and elevated CA 19-9, mimicking biliary obstruction, but improved with conservative care and no invasive procedures.

Contribution

Highlights EBV-related cholestatic hepatitis in adolescents with transient CA 19-9 elevation and lymphadenopathy mimicking malignancy.

Findings

EBV-related cholestatic hepatitis in adolescents can present with transient CA 19-9 elevation and reactive lymphadenopathy.

Conservative management and serial assessments can avoid unnecessary invasive procedures in EBV-related cases.

MRCP is effective in excluding biliary obstruction in such cases.

Abstract

Cholestatic jaundice is uncommon in adolescents. Epstein–Barr virus (EBV)–related inflammatory lymphadenopathy can mimic malignant biliary obstruction and cause a transient rise in carbohydrate antigen 19-9 (CA 19-9), complicating diagnosis.

A previously healthy 15-year-old girl presented with 6 days of jaundice and dark urine without fever. Physical examination showed moderate generalized jaundice with mild scleral icterus; multiple mobile, non-tender lymph nodes in the bilateral cervical regions and right post-auricular area (largest ∼2 × 2 cm); palpable liver and spleen; and mild right upper-quadrant tenderness with equivocal Murphy's sign. Initial tests showed a cholestatic pattern (total/direct bilirubin 102.4/67.7 μmol/L at the referring hospital; and 133.2/126.3 μmol/L on admission) with elevated ALP/GGT and total bile acids. CT suggested a porta hepatis-to-pancreatic-head soft-tissue density with mild intrahepatic ductal prominence; CA 19-9 was 117.7 U/mL [ref <37 U/mL]. EBV POCT was positive; EBV DNA was detected at low level. MRI/MRCP (2025-09-29) showed no obvious biliary obstruction. After MRCP excluded fixed biliary obstruction, the patient improved with conservative management (diagnostic evaluation, close monitoring, and symptom-directed care) without invasive intervention; CA 19-9 declined. No causal inference regarding any medication effect should be drawn, and we do not recommend self-medication or routine off-label/unlicensed use of cholestasis-directed agents for EBV infection. In immunocompetent hosts, EBV-related lymphadenopathy is usually self-limited, and this case does not represent EBV-associated lymphoproliferative disease.

EBV-related cholestatic hepatitis in adolescents can present with transient CA 19-9 elevation and reactive porta hepatis/pancreatic head lymphadenopathy, mimicking malignant obstruction. Serial laboratory and imaging assessments—particularly MRCP—together with conservative management may obviate unnecessary invasive procedures.

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