Ulcerative colitis associated with interferon treatment for chronic hepatitis C

Mavrogiannis, Christos; Papanikolaou, Ioannis S.; Elefsiniotis, Ioannis; Psilopoulos, Dimitrios; Karameris, Andreas; Karvountzis, G.

doi:10.1016/s0168-8278(01)00022-8

Cited by 41 publications

(30 citation statements)

References 5 publications

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“…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

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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

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“…Alpha interferon therapy has been linked to both the exacerbation, as well as new onset of many other autoimmune conditions, including psoriasis, 53 ulcerative colitis, 54,55 type 1 diabetes, 56,57 celiac disease, 58,59 lupus erythematosus, 60 thrombocytopenic purpura, 61,62 hemolytic anemia, 63 rheumatoid arthritis, [64][65][66] and autoimmune hepatitis. 67,68 For these reasons, a pre-existing autoimmune disease or diathesis is considered a relative contraindication to interferon therapy.…”

Section: Treatment Of Hepatitis C In Understudied Populationsmentioning

confidence: 99%

Understudied populations with hepatitis C

Strader

2002

Hepatology

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Managing patients with hepatitis C virus (HCV) infection consists primarily of antiviral treatment, currently with peginterferon and ribavirin. Unfortunately, treatment recommendations derive largely from trials that have focused on highly selected patient populations. As a consequence of the strict inclusion and exclusion criteria in these studies, more than half of all HCV-infected patients would be ineligible for enrollment. Even among the selected patients enrolled into studies, only 50% achieve a sustained virological response (SVR).Patients not eligible for current therapies include those with mild disease and normal alanine aminotransferase (ALT) levels, patients with advanced and decompensated liver disease, children, the elderly, patients with ongoing or recent alcohol and substance abuse, renal disease, human immunodeficiency virus ( H epatitis C is an important cause of acute and chronic liver disease worldwide and the most common indication for liver transplantation in adults in the United States. Since the discovery of the hepatitis C virus (HCV) in 1989 and its linkage to non-A, non-B hepatitis, there have been major advances in knowledge of the incidence and prevalence of this infection, its clinical manifestations, natural history, molecular virology, histopathology, and treatment. At present, the management of patients with hepatitis C focuses largely on combination antiviral treatment using a 24-or 48-week course of peginterferon and ribavirin. Two large trials evaluating the safety and efficacy of this combination therapy have demonstrated sustained virological responses (SVR) in slightly more than 50% of patients. 1,2 It is important to stress, however, that response rates of 50% in randomized, controlled trials of therapy do not guarantee that 50% of all patients with chronic hepatitis C can be or will be successfully treated. Patients enrolled in the registration trials of combination therapy were highly selected and not fully representative of the broader population of patients with chronic HCV infection. The strict inclusion and exclusion criteria used in registration trials often exclude populations that have high rates of hepatitis C. Furthermore, chronic hepatitis C is common in populations that are not reached by clinical trials of new and investigational therapies. Because patients enrolled in registration trials of new antiviral treatments are a selected group, the applicability of results of these trials to the general population is problematic.

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“…One of the more established therapeutic indications for IFN-␣ has taken advantage of its antiviral properties in the long-term treatment of viral hepatitides (10). However, case reports indicate that an unwelcome side effect of this therapy is the spontaneous development of an intestinal inflammatory condition which is similar to ulcerative colitis (11)(12)(13), but reversible on discontinuation of IFN therapy.…”

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confidence: 99%

Control of IFN-αA by CD73: Implications for Mucosal Inflammation

Louis

Robinson

MacManus

et al. 2008

The Journal of Immunology

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Inflammatory diseases influence tissue metabolism, altering regulation of extracellular adenine nucleotides, with a resultant protective influence of adenosine. Ecto-5′-nucleotidase (CD73) is a central surface enzyme generating extracellular adenosine. Thus, we hypothesized that CD73 is protective in mucosal inflammation as modeled by trinitrobenzene sulfonate (TNBS) colitis. Initial studies revealed a >3-fold induction of CD73 mRNA levels after TNBS colitis. Additionally, the severity of colitis was increased, as determined by weight loss and colonic shortening, in cd73−/− mice relative to cd73+/+ controls. Likewise, enteral administration of the selective CD73 inhibitor α,β-methylene ADP to cd73+/+ mice resulted in a similar increase in severity of TNBS colitis. Gene array profiling of cytokine mRNA expression, verified by real-time PCR, revealed a >90% down-regulation of IFN-αA in cd73−/− mice and α,β-methylene ADP-treated cd73+/+ mice, compared with cd73+/+ mice. Exogenous administration of recombinant IFN-αA partially protected TNBS-treated cd73−/− mice. Cytokine profiling revealed similar increases in both IFN-γ and TNF-α mRNA in colitic animals, independent of genotype. However, IL-10 mRNA increased in wild-type mice on day 3 after TNBS administration, whereas cd73−/− mice mounted no IL-10 response. This IL-10 response was restored in the cd73−/− mice by exogenous IFN-αA. Further cytokine profiling revealed that this IL-10 induction is preceded by a transient IFN-αA induction on day 2 after TNBS exposure. Together, these studies indicate a critical regulatory role for CD73-modulated IFNαA in the acute inflammatory phase of TNBS colitis, thereby implicating IFN-αA as a protective element of adenosine signaling during mucosal inflammation.

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Ulcerative colitis associated with interferon treatment for chronic hepatitis C

Cited by 41 publications

References 5 publications

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

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

Understudied populations with hepatitis C

Control of IFN-αA by CD73: Implications for Mucosal Inflammation

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