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Related Concept Videos

Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

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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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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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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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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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Inflammatory Bowel Disease IV: Pharmacological Management01:29

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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.
Pharmacologic...
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Inflammatory Bowel Disease II: Crohn's Disease01:30

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Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
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Linear IgA bullous dermatosis associated with immunotherapy.

Bahar Momin1, Tue F Nguyen, Daniel Glade

  • 1Long School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.

Dermatology Online Journal
|March 13, 2024
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Summary

Linear IgA bullous dermatosis (LABD), a rare autoimmune blistering disease, can be triggered by cancer immunotherapy. Early diagnosis with biopsy and prompt dapsone treatment are crucial for managing this condition.

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Area of Science:

  • Dermatology
  • Immunology
  • Oncology

Background:

  • Linear IgA bullous dermatosis (LABD) is a rare autoimmune blistering disease.
  • Its clinical presentation can mimic bullous pemphigoid (BP).
  • Immunotherapy-induced BP is documented, but LABD is rarely associated with immunotherapy.

Observation:

  • A 67-year-old woman with metastatic ovarian cancer developed pruritic tense bullae after receiving anti-PD1 and anti-CTLA4 immunotherapy.
  • Histopathology revealed subepidermal blisters with neutrophils (H&E) and linear IgA deposition (direct immunofluorescence).
  • The patient's condition was diagnosed as LABD.

Findings:

  • LABD developed secondary to immunotherapy in this patient.
  • Initial prednisone treatment was ineffective.
  • Dapsone therapy led to rapid resolution of blisters.

Implications:

  • This case underscores the importance of considering LABD in patients on immunotherapy presenting with blistering disorders.
  • Accurate diagnosis using H&E histology and direct immunofluorescence is critical.
  • Prompt initiation of appropriate treatment, such as dapsone, can effectively manage immunotherapy-induced LABD, potentially avoiding treatment discontinuation.