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Related Concept Videos

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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
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Baricitinib and primary biliary cholangitis.

Stuart C Gordon1,2, Sheri Trudeau3, Arie Regev4

  • 1Division of Gastroenterology and Hepatology, Henry Ford Health System, Detroit, MI, USA.

Journal of Translational Autoimmunity
|July 1, 2021
PubMed
Summary
This summary is machine-generated.

Baricitinib shows promise for primary biliary cholangitis (PBC) patients unresponsive to ursodeoxycholic acid (UDCA). A single patient experienced significant improvements in liver enzymes and itching, suggesting potential efficacy for this JAK inhibitor in PBC treatment.

Keywords:
12-WeekItchJak1/2 inhibitorsLiver disease

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Area of Science:

  • Hepatology
  • Immunology
  • Pharmacology

Background:

  • Primary biliary cholangitis (PBC) is a chronic liver disease with limited treatment options for non-responders to ursodeoxycholic acid (UDCA).
  • Janus kinase (JAK) inhibitors represent a potential therapeutic avenue for autoimmune liver conditions.
  • Baricitinib, an orally administered JAK 1 and 2 inhibitor, was investigated for its efficacy in PBC patients.

Purpose of the Study:

  • To evaluate the proof-of-concept for baricitinib in treating primary biliary cholangitis (PBC) patients.
  • To assess the impact of baricitinib on liver biochemistry, pruritus, and fatigue in UDCA-refractory PBC.
  • To explore baricitinib's effect on inflammatory and fibrotic markers in PBC.

Main Methods:

  • A randomized, double-blinded, placebo-controlled trial was conducted.
  • Eligible patients with PBC and inadequate response or intolerance to UDCA were enrolled.
  • Participants received either baricitinib (2 mg/day) or placebo for 12 weeks, with endpoints including alkaline phosphatase (ALP), itch, and fatigue scores.

Main Results:

  • The study was terminated early due to low enrollment, with only two patients completing the trial (one on baricitinib, one on placebo).
  • The baricitinib-treated patient showed a 30% decrease in ALP, a 7-point improvement in itch NRS, and reductions in hs-CRP and ELF score.
  • The placebo-treated patient exhibited no significant changes in primary or secondary endpoints. A single non-serious adverse event (sinusitis) was reported.

Conclusions:

  • A single patient with primary biliary cholangitis (PBC) demonstrated a significant clinical response to baricitinib over a 12-week treatment period.
  • Baricitinib may offer a potential new treatment strategy for patients with PBC who do not respond adequately to ursodeoxycholic acid (UDCA).
  • Further investigation with larger sample sizes is warranted to confirm these preliminary findings.