Acute Pancreatitis Associated with Pegylated Interferon and Ribavirin Treatment of Chronic Hepatitis C, Genotype 1b with High Viral Load

• Published in: Case reports in gastroenterology Vol. 3; no. 3; pp. 372 - 376
• Main Authors: Ando, Kenji, Kim, Soo Ryang, Imoto, Susumu, Nakajima, Taisuke, Mita, Keiji, Fukuda, Katsumi, Taniguchi, Miyuki, Sasase, Noriko, Muramatsu, Akira, Matsuoka, Toshiyuki, Kudo, Masatoshi, Hayashi, Yoshitake
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 21.11.2009; Karger Publishers
• Subjects: Acute pancreatitis; Chronic hepatitis C, high serum hepatitis C viral RNA; Drug-induced pancreatitis; Genotype 1b; Interleukin-6; Pegylated interferon; Published: November 2009; Ribavirin; Tumor necrosis factor-α; Chronic hepatitis C, high serum hepatitis C viral RNA; Drug-induced pancreatitis; Acute pancreatitis; Pegylated interferon; Tumor necrosis factor-α; Ribavirin; Genotype 1b; Interleukin-6
• ISSN: 1662-0631; 1662-0631
• DOI: 10.1159/000256557

Acute pancreatitis, an uncommon side effect of pegylated interferon α (PEG-IFN α) and ribavirin (RBV) combination therapy, has rarely been reported in the English language literature. Here, acute pancreatitis associated with PEG-IFN plus RBV treatment is described in three patients with chronic hepatitis C, genotype 1b with high serum hepatitis C virus RNA levels. The patients had been started on weekly subcutaneous injections of PEG-IFN α (60, 80, and 90 μg) plus a daily oral dose of RBV (600 mg). The therapy was discontinued, however, because of the onset of acute pancreatitis (after 15 weeks, 48 weeks, and 3 weeks respectively). The drug-induced pancreatitis was diagnosed on the basis of elevated levels of amylase and lipase and the absence of other identifiable causes. High tumor necrosis factor-α was found in one patient and high interleukin-6 in the other two. The immune system stimulated by PEG-IFN and RBV combination therapy might have caused the acute pancreatitis. Further study is needed to clarify the mechanism of the onset of drug-induced pancreatitis by PEG-IFN and RBV combination therapy.