S5929 First Fatal Case Report of Post-COVID-19 Cholangiopathy in a Liver Transplant Recipient

Introduction: Post-COVID cholangiopathy (PCC) is a rare variant of secondary sclerosing cholangitis, typically arising after severe COVID-19, particularly in ICU patients or those requiring prolonged ventilation. It is marked by rapid biliary injury, dramatic elevations in alkaline phosphatase and bilirubin, and can progress to liver failure. PCC affects <0.1% of hospitalized COVID-19 patients and carries a 30%–50% mortality. In liver transplant recipients, it can lead to significant graft dysfunction or loss. Case Description/Methods: We report a case of a 67-year-old woman with type 2 diabetes, COPD, emphysema, and alpha-1 antitrypsin deficiency-related cirrhosis who underwent liver transplantation. She was maintained on cyclosporin due to tacrolimus-induced neurotoxicity and experienced post-transplant biliary strictures managed with ERCPs and stents, for which she received Augmentin for prophylaxis at least 3 times. Her bilirubin remained ≤1.9 mg/dL until post-op month 10. At month 11, she contracted COVID-19, for which she was previously vaccinated. Symptoms were mild, and she recovered at home without treatment. Meanwhile, she also completed a 2-week course of augmentin for otitis media. By month 12, on routine lab check, bilirubin sharply rose to 8.4 mg/dL, with gamma-glutamyl transferase persistently ranging at 200–300 U/L. Repeat ERCPs showed no new strictures. Bilirubin continued to rise. Ursodiol was initiated, and immunosuppression was switched back to tacrolimus, though levels remained therapeutic and there was no clinical improvement. At post-op month 13, she was admitted with acute liver failure and shock. Liver biopsy revealed mild rejection, severe cholestasis, and focal lymphocytic cholangitis, without signs of drug-induced liver injury (DILI). Due to frailty, she was not re-listed for transplant. She died 4 days after being transferred for a second opinion. Final labs: bilirubin 55.3 mg/dL, alkaline phosphatase 293 U/L, aspartate aminotransferase 69 U/L, alanine aminotransferase 43 U/L, international normalized ratio 1.6. Discussion: This is the first reported case of PCC in a liver transplant recipient. Uniquely, the patient developed PCC after a mild COVID-19 illness. Chronic immunosuppression may have contributed to the severity and fatality. SARS-CoV-2 directly injures cholangiocytes via ACE2 receptors. Although DILI was not evident on biopsy, repeated Augmentin use may have played a role. Given its high mortality, early recognition of PCC in transplant patients is critical to consider re-listing before irreversible graft loss.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001151176.64748.fc
Primary Topic
Liver Diseases and Immunity
Type
article
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article

S5929 First Fatal Case Report of Post-COVID-19 Cholangiopathy in a Liver Transplant Recipient

Nathalie Sela, John L. Klein, Giovannie Isaac-Coss, Aryanna Sousa et al.
The American Journal of Gastroenterology
Liver Diseases and Immunity
article

S5929 First Fatal Case Report of Post-COVID-19 Cholangiopathy in a Liver Transplant Recipient

Nathalie Sela, John L. Klein, Giovannie Isaac-Coss, Aryanna Sousa, Nancy S. Reau, Justin Mitchell, Edie Y. Chan, Lloyd Brown
article en

Abstract

Introduction: Post-COVID cholangiopathy (PCC) is a rare variant of secondary sclerosing cholangitis, typically arising after severe COVID-19, particularly in ICU patients or those requiring prolonged ventilation. It is marked by rapid biliary injury, dramatic elevations in alkaline phosphatase and bilirubin, and can progress to liver failure. PCC affects <0.1% of hospitalized COVID-19 patients and carries a 30%–50% mortality. In liver transplant recipients, it can lead to significant graft dysfunction or loss. Case Description/Methods: We report a case of a 67-year-old woman with type 2 diabetes, COPD, emphysema, and alpha-1 antitrypsin deficiency-related cirrhosis who underwent liver transplantation. She was maintained on cyclosporin due to tacrolimus-induced neurotoxicity and experienced post-transplant biliary strictures managed with ERCPs and stents, for which she received Augmentin for prophylaxis at least 3 times. Her bilirubin remained ≤1.9 mg/dL until post-op month 10. At month 11, she contracted COVID-19, for which she was previously vaccinated. Symptoms were mild, and she recovered at home without treatment. Meanwhile, she also completed a 2-week course of augmentin for otitis media. By month 12, on routine lab check, bilirubin sharply rose to 8.4 mg/dL, with gamma-glutamyl transferase persistently ranging at 200–300 U/L. Repeat ERCPs showed no new strictures. Bilirubin continued to rise. Ursodiol was initiated, and immunosuppression was switched back to tacrolimus, though levels remained therapeutic and there was no clinical improvement. At post-op month 13, she was admitted with acute liver failure and shock. Liver biopsy revealed mild rejection, severe cholestasis, and focal lymphocytic cholangitis, without signs of drug-induced liver injury (DILI). Due to frailty, she was not re-listed for transplant. She died 4 days after being transferred for a second opinion. Final labs: bilirubin 55.3 mg/dL, alkaline phosphatase 293 U/L, aspartate aminotransferase 69 U/L, alanine aminotransferase 43 U/L, international normalized ratio 1.6. Discussion: This is the first reported case of PCC in a liver transplant recipient. Uniquely, the patient developed PCC after a mild COVID-19 illness. Chronic immunosuppression may have contributed to the severity and fatality. SARS-CoV-2 directly injures cholangiocytes via ACE2 receptors. Although DILI was not evident on biopsy, repeated Augmentin use may have played a role. Given its high mortality, early recognition of PCC in transplant patients is critical to consider re-listing before irreversible graft loss.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 48%
Liver Diseases and Immunity
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