A 25-year-old male with no significant past medical history presented to his primary care physician with one day of severe headache, sore throat, fatigue, and myalgias. Physical examination was notable for pharyngeal erythema and left posterior cervical lymphadenopathy. Point-of-care testing was negative for Group A Streptococcus, influenza A/B, and respiratory syncytial virus. SARS-CoV-2 was detected via nucleic acid testing of a nasopharyngeal swab, and the patient was managed conservatively at home.
Over the next five days, the patient developed progressive symptoms including worsening cough, congestion, persistent fever, chills, night sweats, and right upper quadrant abdominal pain. Dark urine and scleral icterus followed, prompting re-evaluation. Laboratory studies revealed markedly elevated transaminases (ALT 1,414 U/L; AST 891 U/L), hyperbilirubinemia (total bilirubin 9.7 mg/dL), a mild leukocytosis, thrombocytopenia, and a slight elevation in alkaline phosphatase. The complete comprehensive metabolic panel is shown in Table 1. The initial urinalysis was bright orange in color and uninterpretable microscopically due to pigment interference.
Blood chemistry on admission
He was referred to the Emergency Department for further evaluation. He denied alcohol use, recent travel, gastrointestinal symptoms, or relevant family history. His vital signs were within normal limits. Physical examination revealed jaundice, pharyngeal erythema, mild tonsillar enlargement, and palpable left posterior cervical lymphadenopathy.
Laboratory investigations revealed normal creatine kinase, lipase, and coagulation studies (protime and international normalized ratio). Acetaminophen and ethanol levels were undetectable. Viral hepatitis panel was nonreactive for hepatitis A, B, and C. An EBV anti-viral capsid antigen immunoglobulin M (anti-VCA IgM) and anti-viral capsid antigen immunoglobulin G (anti-VCA IgG) were drawn. Repeat urinalysis showed elevated specific gravity, 3 + bilirubin, and trace protein. Direct bilirubin was 7.6 mg/dL. Abdominal ultrasound demonstrated hepatomegaly and a contracted gallbladder without visible cholelithiasis; however, small stones could not be excluded “due to recent oral intake,” per the ultrasound read. Computed tomography of the abdomen and pelvis revealed nonspecific gallbladder wall edema, hepatosplenomegaly, and trace ascites. The liver measured up to 22.9 cm craniocaudally, and the spleen measured up to 18.2 cm. Magnetic resonance imaging with and without contrast confirmed hepatomegaly without steatosis, mild periportal edema, a contracted gallbladder with wall thickening, and splenomegaly. Magnetic resonance cholangiopancreatography was non-diagnostic due to motion artifacts. A chest radiograph was unremarkable.
The constellation of findings, including significant transaminitis, hepatosplenomegaly, and systemic symptoms, was deemed atypical for COVID-19. The degree of transaminitis was out of proportion for isolated COVALI. The patient was admitted for further workup and Hepatology consultation. Supportive care, including IV fluids, tramadol for pain, and benzocaine-menthol lozenges for pharyngitis, was initiated. The patient experienced progressive symptomatic improvement. Liver function tests, including bilirubin levels, improved during admission.
The patient was discharged in stable condition with a presumptive diagnosis of acute viral hepatitis due to COVID-19. EBV serologies, HIV screening, blood cultures, and autoimmune hepatitis panels were pending at the time of hospital discharge. The final viral and autoimmune hepatitis panel results are shown in Table 2. Later, anti-VCA IgM returned strongly positive at > 160.00 U/mL, with negative anti-VCA IgG. The patient was advised to avoid contact sports and strenuous activity for 3–4 weeks. At one-week follow-up, liver function tests and bilirubin levels had further decreased to 289 U/L ALT, 126 U/L AST, and 3.3 mg/dL total bilirubin. At ten months, the patient had fully recovered with complete normalization of laboratory values and no evidence of long-term sequelae (Fig. 1).
Viral and autoimmune hepatitis testing
This graph shows the trend in laboratory findings starting on the day of admission