What are the autoantibodies associated with Inclusion Body Myositis (IBM), and is this type of Idiopathic Inflammatory Myopathy (IIM) associated with nerve affection, such as thickened nerves and Acute Inflammatory Demyelinating Polyneuropathy (AIDP), skin manifestations like ulceration, and respiratory symptoms like shortness of breath?

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From the Research

Inclusion body myositis (IBM) is associated with several autoantibodies, most notably anti-cN1A (cytosolic 5'-nucleotidase 1A) antibodies, which are found in approximately 30-40% of IBM patients, as well as anti-NDUFA11 autoantibodies, which have been recently identified as a potential biomarker for IBM 1.

Autoantibodies in IBM

The autoantibodies associated with IBM include:

  • Anti-cN1A (cytosolic 5'-nucleotidase 1A) antibodies, which are found in approximately 30-40% of IBM patients 2, 3
  • Anti-NDUFA11 autoantibodies, which have been recently identified as a potential biomarker for IBM 1

Neurological Involvement

IBM does have neurological involvement, with both myopathic and neuropathic features, including:

  • Nerve involvement, which can include thickened nerves and neuropathic changes
  • Neuropathic changes, though acute inflammatory demyelinating polyneuropathy is not typically considered a classic feature of IBM

Skin and Respiratory Manifestations

Regarding skin manifestations, IBM generally does not cause skin ulcerations or significant cutaneous involvement, which distinguishes it from dermatomyositis. If a patient with IBM presents with shortness of breath, this is less likely to be directly related to the IBM itself, as IBM typically does not cause significant interstitial lung disease or respiratory muscle weakness to the extent seen in other inflammatory myopathies like polymyositis or dermatomyositis. However, dysphagia (swallowing difficulty) is common in IBM and can lead to aspiration pneumonia, which might present as shortness of breath.

Management and Pathophysiology

IBM is generally resistant to conventional immunosuppressive therapies, and management focuses on physical therapy, occupational therapy, and supportive care to maintain function and quality of life. The pathophysiology of IBM is complex, involving both inflammatory and degenerative processes, with accumulation of abnormal proteins in muscle fibers, which explains why it responds poorly to immunosuppression compared to other inflammatory myopathies. The most recent and highest quality study on this topic is 1, which highlights the importance of anti-NDUFA11 autoantibodies as a potential biomarker for IBM.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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