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Drugs for Treatment of Ulcerative Colitis in IBD

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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
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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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T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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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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Colitis induced by IL-17A-inhibitors.

Lea Grümme1, Sophia Dombret1, Thomas Knösel2

  • 1Division of Rheumatology and Clinical Immunology, Department of Medicine IV, LMU Clinic Munich, Pettenkoferstraße 8a, 80336, Munich, Germany.

Clinical Journal of Gastroenterology
|December 7, 2023
PubMed
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Interleukin (IL)-17A inhibitors may increase the risk of developing colitis in patients without inflammatory bowel disease (IBD). Careful screening and patient notification are crucial for those on IL-17A inhibitor therapy.

Keywords:
ColitisIL-17A-inhibitorsIxekizumabRheumatologySecukinumab

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Area of Science:

  • Immunology
  • Gastroenterology
  • Dermatology

Background:

  • Interleukin (IL)-17A is vital for maintaining intestinal mucosal integrity and preventing conditions like infectious colitis and inflammatory bowel disease (IBD).
  • Neutralizing IL-17A is generally avoided in IBD due to potential disease exacerbation.
  • The risk of IL-17A inhibitors inducing colitis in non-IBD patients remains a subject of debate.

Observation:

  • Two cases of colitis developed in patients treated with IL-17A inhibitors: one with SAPHO syndrome on secukinumab, and another with psoriatic arthritis who switched from secukinumab to ixekizumab.
  • Both patients experienced severe gastrointestinal symptoms including bloody diarrhea, abdominal pain, fever, and weight loss.
  • Treatment cessation of IL-17A inhibitors and initiation of tumor necrosis factor inhibitors led to recovery in both individuals.

Findings:

  • The study presents two distinct cases of colitis occurring during IL-17A inhibitor therapy (secukinumab and ixekizumab).
  • Both patients recovered after discontinuing IL-17A inhibitors and commencing tumor necrosis factor inhibitors.
  • These cases highlight a potential adverse effect of IL-17A inhibitors.

Implications:

  • The precise role of IL-17A inhibitors in the development of infectious colitis and new-onset IBD requires further investigation.
  • Healthcare providers must carefully screen patients initiating IL-17A inhibitor therapy and inform them about potential side effects.
  • This research underscores the importance of vigilant monitoring for gastrointestinal adverse events in patients receiving IL-17A inhibitors.