Development of Pouchitis With Combination Therapy With Peg-Interferon α-2b and Ribavirin for Chronic Hepatitis C in a Patient With Ulcerative Colitis Who Underwent Pouch Surgery

Morimoto, Kenichi; Yamagami, Hirokazu; Hosomi, Shuhei; Ohira, Mizuki; Suekane, Takehisa; Kamata, Noriko; Sogawa, Mitsue; Watanabe, Kenji; Tominaga, Kazunari; Watanabe, Toshio; Fujiwara, Yasuhiro; Tamori, Akihiro; Oshitani, Nobuhide

doi:10.1038/ajg.2009.120

Cited by 9 publications

(9 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There have been many case reports associating the development of IBD with the initiation of type I IFN therapy 32–35. For example, a recent report from Morimoto and colleagues36 describes the development of endoscopically confirmed pouchitis in a patient who had previously been doing well following total colectomy for medication-resistant ulcerative colitis. However, the patient's symptoms worsened acutely following the initiation of IFN-α therapy for chronic hepatitis C. In contrast, certain studies have examined the potential therapeutic role of type I IFN for IBD 37–40.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis

Luther

Owyang

Takeuchi

et al. 2011

Gut

View full text Add to dashboard Cite

Background & Aims Recently there has been emerging epidemiological data to suggest Helicobacter pylori (H. pylori) may protect against certain chronic inflammatory diseases such as inflammatory bowel disease (IBD). However, the mechanism for the observed inverse association between H. pylori and IBD has not been described. Methods The frequency of immunoregulatory (IRS) to immunostimulatory (ISS) sequences within the genome of various bacteria was calculated using MacVector software. The induction of type I IFN and IL-12 responses by DNA-pulsed murine bone marrow–derived dendritic cells (BMDC) and human plasmacytoid dendritic cells (pDC) was analyzed by cytokine production. The effect of H. pylori DNA on E. coli DNA production of type I IFN and IL-12 was assessed. The in vivo significance of H. pylori DNA suppression was assessed in a DSS-model of colitis. The systemic levels of type I IFN were assessed in H. pylori-colonized and non-colonized patients. Results We showed that H. pylori DNA has a significantly elevated IRS:ISS ratio. In vitro experiments revealed the inability of H. pylori DNA to stimulate type I IFN or IL-12 production from mouse BMDCs or human pDCs. Additionally, H. pylori DNA was able to suppress E. coli-DNA production of type I IFN and IL-12. Administration of H. pylori DNA prior to the induction of DSS colitis significantly ameliorated the severity of colitis as compared to E. coli DNA or vehicle control in both an acute and chronic model. Finally, the systemic levels of type I IFN were found to be lower in H. pylori-colonized patients versus non-colonized controls. Conclusions Overall, our study indicates that H pylori DNA has the ability to down-regulate pro-inflammatory responses from DCs and this may in part explain the inverse association between H. pylori and IBD.

show abstract

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis

Luther

Owyang

Takeuchi

et al. 2011

Gut

View full text Add to dashboard Cite

show abstract

“…11,113,124,125 However, case reports have observed new-onset UC during interferon-a treatment or exacerbation of existing UC (or IBD with a predominance of UC). 116,[124][125][126][127][128][129][130][131][132][133] In one of these case reports, the administration of sulfasalazine allowed the patient to receive interferon-a again without a flare-up of UC. 126 This case suggests the possible efficacy of sulfasalazine therapy in patients with UC complicated by administration of interferon-a.…”

Section: What Is the Risk Of Exacerbation Of Ibd With Interferon?mentioning

confidence: 99%

Review article: prevention and management of hepatitis B and C infection in patients with inflammatory bowel disease

Gisbert

Chaparro

Esteve

2011

Alimentary Pharmacology &Amp; Therapeutics

105

View full text Add to dashboard Cite

“…Several case reports suggest a potential benefit of interferon in UC, [34][35][36] but other case reports have observed new-onset IBD during interferon treatment or exacerbation of existing IBD with a predominance of UC. [37][38][39][40][41][42][43] Tilg et al 44 performed a pilot study using low-dose peginterferon-a2b (0.5-1 lg/kg weekly for 12 weeks) in 60 UC patients with active disease showing no benefit on UC, but no statistically significant increase in adverse reactions. A Cochrane review including three other prospective studies of interferon-a and interferon-b in UC concluded that interferon was not an effective therapy for UC.…”

Section: Factors Unique To Ibdmentioning

confidence: 99%

Viral hepatitis and inflammatory bowel disease

Hou

Velayos

Terrault

et al. 2010

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

Viral hepatitis is common worldwide and in the United States. Inflammatory bowel disease (IBD) patients with chronic hepatitis B virus (HBV) with active disease (elevated alanine aminotransferase level and viral replication) should receive HBV treatment. HBV reactivation is associated with significant morbidity and mortality in patients receiving immunosuppression. IBD patients may require long-term immunosuppression, and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy. Tumor necrosis factor alpha antagonists and immunomodulators appear compatible with use in IBD patients with HCV, although prednisone may increase viral replication. HCV treatment with peg-interferon and ribavirin may exacerbate gastrointestinal symptoms, and therefore the decision to treat HCV needs to be individualized. Management of IBD patients with viral hepatitis is addressed in this review.

show abstract

Development of Pouchitis With Combination Therapy With Peg-Interferon α-2b and Ribavirin for Chronic Hepatitis C in a Patient With Ulcerative Colitis Who Underwent Pouch Surgery

Cited by 9 publications

References 4 publications

Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis

Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis

Review article: prevention and management of hepatitis B and C infection in patients with inflammatory bowel disease

Viral hepatitis and inflammatory bowel disease

Contact Info

Product

Resources

About