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Related Concept Videos

Myasthenia Gravis: Overview and Treatment01:20

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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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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Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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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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Myasthenia Gravis: Diagnostic Tests01:15

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Myasthenia gravis is an autoimmune condition affecting neuromuscular transmission, causing generalized weakness in skeletal muscles. Initial diagnoses rely on patients' signs, symptoms, and medical history. The challenge lies in distinguishing myasthenia from other muscular dystrophies. An important diagnostic feature is the significant improvement of symptoms after administering anticholinesterase inhibitors.
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Related Experiment Video

Updated: Sep 7, 2025

Assessment of Human Natural Killer Cell Events Driven by FcγRIIIa Engagement in the Presence of Therapeutic Antibodies
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Rituximab in Refractory Myositis and Acute Neuropathy Secondary to Checkpoint Inhibitor Therapy.

Varun Jain1, William Remley2, Cyra Bunag1

  • 1Department of Neurology, University of Florida College of Medicine, Gainesville, USA.

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|June 23, 2022
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Summary

Checkpoint inhibitor immunotherapies can cause rare, severe autoimmune neurological complications. Rituximab offers a promising treatment option for patients unresponsive to steroids, IVIG, and plasmapheresis.

Keywords:
check point therapy complicationmyositis from checkpoint inhibitor therapyneuropathy from checkpoint inhibitor therapyrefractory neurological complication from check point therapyrituximab in myasthenia from ipilimumab

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Area of Science:

  • Oncology
  • Immunology
  • Neurology

Background:

  • Immune checkpoint inhibitors (ICIs) represent a significant advancement in cancer therapy.
  • Increasing ICI use has revealed a spectrum of immune-related adverse events affecting multiple organ systems, including the nervous system.
  • Management of ICI-induced neurological complications can be challenging, especially in steroid-refractory cases.

Observation:

  • An 85-year-old male treated with nivolumab and ipilimumab developed severe neurological symptoms including diplopia, ptosis, dysphagia, and generalized weakness.
  • Diagnostic workup revealed refractory myositis, acute neuropathy, and autoimmune thyroiditis, with negative acetylcholine receptor and MuSK antibodies.
  • The patient's condition did not improve with standard treatments such as steroids, intravenous immunoglobulins (IVIG), and plasmapheresis (PLEX).

Findings:

  • This case highlights refractory autoimmune myositis and neuropathy secondary to ICI therapy.
  • The patient experienced significant symptom improvement after initiating rituximab treatment.
  • Neurological complications from ICIs can be diverse and may require alternative immunosuppressive strategies beyond first-line therapies.

Implications:

  • Awareness of ICI-induced neurological complications is crucial for timely diagnosis and management.
  • Rituximab demonstrates potential efficacy in managing severe, refractory ICI-associated autoimmune neurological disorders.
  • Further research is needed to establish formal guidelines for managing ICI-induced neurological toxicities.