Jawad Ahmad1, K Rajender Reddy2, Hans L Tillmann3, Paul H Hayashi4, Naga Chalasani5, Robert J Fontana6, Victor J Navarro7, Andrew Stolz8, Huiman Barnhart9, Gavin A Cloherty10, Jay H Hoofnagle11. 1. Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. jawad.ahmad@mountsinai.org. 2. Division of Gastroenterology and Hepatology, University of Pennsylvania, Philadelphia, USA. 3. Division of Gastroenterology, Hepatology and Nutrition, East Carolina University, Greenville, USA. 4. Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, USA. 5. Division of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, USA. 6. Division of Gastroenterology and Hepatology, University of Michigan Medical School, Ann Arbor, USA. 7. Einstein Medical Center, Philadelphia, USA. 8. Division of Gastrointestinal and Liver Diseases, Keck School of Medicine of University of Southern California, Los Angeles, USA. 9. Duke Clinical Research Institute, Duke University, Durham, USA. 10. Volwiler Society, Head Infectious Disease Research, Abbott Laboratories, Lake Bluff, USA. 11. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, USA.
Abstract
BACKGROUND AND AIMS: The aims were to review the diagnosis, testing and presentation of acute hepatitis C (HCV) in patients initially diagnosed to have drug-induced liver injury (DILI) enrolled in the US DILI Network. METHODS: All patients with suspected DILI underwent testing for competing causes of liver injury and returned for 6-month follow-up. Causality was adjudicated by consensus expert opinion. RESULTS: Between 2004 and 2016, 1518 patients were enrolled and adjudicated and underwent 6 months of follow-up. Initial locally acquired anti-HCV results were available in 1457 (96%), but HCV RNA in only 795 (52%). Stored sera were available for repeat testing, so that results were available on all 1518 patients (1457 for anti-HCV and 1482 for HCV RNA). A total of 104 subjects (6.9%) had evidence of HCV infection-10 positive for HCV RNA alone, 16 for anti-HCV alone and 78 for both. All 104 HCV-positive cases were reviewed, and 23 cases were adjudicated as acute HCV. All presented with acute hepatocellular injury with median ALT 1448 U/L, alkaline phosphatase 232 U/L and total bilirubin 10.8 mg/dL. Twenty-two (96%) patients were jaundiced. While all 23 cases initially had been suspected of having DILI, 19 were adjudicated as acute HCV and not DILI at the 6-month follow-up; while 4 were still considered DILI. CONCLUSIONS: Twenty-three of 1518 (1.5%) cases of suspected DILI were due to acute HCV infection. We recommend that initial and follow-up HCV RNA testing should be performed to exclude HCV in patients with acute hepatocellular injury and suspected DILI.
BACKGROUND AND AIMS: The aims were to review the diagnosis, testing and presentation of acute hepatitis C (HCV) in patients initially diagnosed to have drug-induced liver injury (DILI) enrolled in the US DILI Network. METHODS: All patients with suspected DILI underwent testing for competing causes of liver injury and returned for 6-month follow-up. Causality was adjudicated by consensus expert opinion. RESULTS: Between 2004 and 2016, 1518 patients were enrolled and adjudicated and underwent 6 months of follow-up. Initial locally acquired anti-HCV results were available in 1457 (96%), but HCV RNA in only 795 (52%). Stored sera were available for repeat testing, so that results were available on all 1518 patients (1457 for anti-HCV and 1482 for HCV RNA). A total of 104 subjects (6.9%) had evidence of HCV infection-10 positive for HCV RNA alone, 16 for anti-HCV alone and 78 for both. All 104 HCV-positive cases were reviewed, and 23 cases were adjudicated as acute HCV. All presented with acute hepatocellular injury with median ALT 1448 U/L, alkaline phosphatase 232 U/L and total bilirubin 10.8 mg/dL. Twenty-two (96%) patients were jaundiced. While all 23 cases initially had been suspected of having DILI, 19 were adjudicated as acute HCV and not DILI at the 6-month follow-up; while 4 were still considered DILI. CONCLUSIONS: Twenty-three of 1518 (1.5%) cases of suspected DILI were due to acute HCV infection. We recommend that initial and follow-up HCV RNA testing should be performed to exclude HCV in patients with acute hepatocellular injury and suspected DILI.
Entities:
Keywords:
Acute hepatitis C; Drug-induced liver injury; Hepatitis C RNA
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