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Related Concept Videos

Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

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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.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which...
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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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Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
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Disorders of the Skeletal Muscle01:28

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
Musculoskeletal disorders involve injuries and conditions affecting the skeletal muscles and associated connective tissues. These disorders can arise from acute biomechanical stresses or chronic overuse and can occur across different age groups. Common injuries include sprains, fractures, and muscular strains, often resulting from...
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Skeletal Muscle Relaxants: Adverse Effects01:21

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Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
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Profiling Ubiquitin and Ubiquitin-like Dependent Post-translational Modifications and Identification of Significant Alterations
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Gemcitabine-induced myopathy.

Lionel Spielmann1, Laurent Messer2, Paul Moreau2

  • 1Service de Rhumatologie, Centre de Référence des Maladies Auto-immunes Rares, Hôpitaux Universitaires, CHRU de Strasbourg, Cedex, France.

Seminars in Arthritis and Rheumatism
|January 7, 2014
PubMed
Summary
This summary is machine-generated.

Gemcitabine monotherapy can cause muscle damage (myopathy) by affecting blood vessels. Stopping the drug led to full recovery, suggesting a direct link between gemcitabine and this rare side effect.

Keywords:
GemcitabineMyopathyVasculopathy

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Area of Science:

  • Oncology
  • Neurology
  • Pathology

Background:

  • Limited research exists on cytotoxic agent-induced muscle injury in cancer patients.
  • Few cases of muscle issues linked to gemcitabine chemotherapy have been documented, with gemcitabine suspected in only one instance.

Observation:

  • A patient with pancreatic cancer developed leg weakness and muscle breakdown (myolysis) after two months of gemcitabine monotherapy.
  • Symptoms included proximal motor deficiency, elevated creatinine kinase, and thigh erythema.

Findings:

  • Muscle MRI showed quadriceps edema; biopsy revealed regenerative changes and vascular proliferation.
  • Inflammatory infiltrates were minimal, and MHC class I expression was normal.
  • Discontinuation of gemcitabine resolved symptoms without cancer recurrence or positive anti-TIF-1γ antibodies.

Implications:

  • Gemcitabine monotherapy may induce myopathy via vascular damage, a mechanism relevant to other known side effects.
  • This finding has significant therapeutic implications for managing gemcitabine-related toxicity.