S2905 Prolonged Cholestasis After COVID-19

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Introduction: The coronavirus SARS-CoV-2 (COVID-19) is known to cause both pulmonary and hepatic injury. Cholangiocytes have an abundance of angiotensin-converting enzyme 2 receptors, which are the main mode of entry for the virus. Whether the liver injury is caused directly by the virus or as a result of the cytokine storm remains unknown. We present a case of prolonged cholestatic liver injury secondary to COVID-19. Case Description/Methods: A 55-year-old woman presented to our institution with sudden onset of right leg pain and swelling. She had hypertension, diabetes, obesity, and hypothyroidism. She denied any history of liver disease, toxic habits and was not taking any hepatotoxic medications or supplements. Two months prior to presentation, she was admitted to another hospital with severe COVID-19 pneumonia requiring mechanical ventilation. She had received Remdesivir, Convalescent Plasma, Extra Corporeal Membrane Oxygenation (ECMO), and hemodialysis for acute renal failure, before being discharged. During this admission, she was found to have a right lower extremity thrombus and was started on Enoxaparin. Her liver function tests were significant for a markedly elevated alkaline phosphatase level. An ultrasound abdomen was significant only for a fatty liver. CT scan of the abdomen with contrast and an MRCP did not reveal any hepatobiliary abnormalities. Viral hepatitis serology and autoimmune workup were negative. She underwent a liver biopsy which demonstrated cholestasis, mild lobular necroinflammation, and macrovesicular steatosis. There was no PCR evidence of SARS-CoV-2. Her hospital course was complicated by MRSA and pseudomonas pneumonia. She suffered a cardiac arrest and ultimately succumbed to her infection 2 months later. Her Alkaline phosphatase remained elevated throughout her hospital stay. Discussion: Although our patient’s liver biopsy did not demonstrate PCR evidence of SARS-COV-2, it was consistent with histological features of COVID-19 related hepatic injury. Macrovesicular steatosis is the most common histological finding, followed by lobular necroinflammation, according to a case series of 40 patients who died of COVID-19. PCR for SARS-COV-2 in liver biopsy was positive in only 55% of patients. Recent reports have identified ECMO as a cause of secondary sclerosing cholangitis in critically ill patients, which remains a possibility in our case. However, a normal bilirubin level and MRCP did not support this diagnosis in our patient.Figure 1.: (A) 4 x magnification, (B) 10 x magnification, and (C) 40 x magnification of a liver biopsy specimen demonstrating hepatocellular cholestasis with feathery degeneration of hepatocytes, mild lobular neuroinflammation, and mild macrovesicular steatosis. There is sinusoidal dilatation and glycogenated nuclei. Portal tracts show mild to moderate mixed cellular infiltration, including eosinophils, endothelilitis, ductular reaction, and focal mild bile duct damage. There is no pericellular fibrosis to indicate non-alcoholic chronic steatohepatitis, although rare perivenular ballooned hepatocytes are noted on the H&E slide. CK7 immunostain shows moderate to marked ductular reaction, rare cholestatic hepatocytes, and damaged bile ducts. Findings are those of subacute cholestatic hepatitis.Table 1.: Laboratory values from the previous hospitalization, on admission day of this hospitalization, at 1-month of hospitalization, and prior to death.