Achr-acetyl Choline Receptor Antibodies, Serum

What is ACHR, Acetyl choline receptor antibody test?

 

A blood test that detects autoantibodies against acetylcholine receptors at the neuromuscular junction; these antibodies interfere with nerve-to-muscle signaling and are strongly associated with myasthenia gravis (MG).

 

Why consider ACHR, Acetyl choline receptor antibody test?

• To support the diagnosis of MG in patients with compatible symptoms and to distinguish MG from other causes of fatigable weakness.
• To establish a serologic baseline and, in some cases, track antibody levels over time alongside clinical response.
• To evaluate for autoimmune risk when a thymoma is present, or when MG is suspected but clinical tests are inconclusive.

Who should get this ACHR, Acetyl choline receptor antibody test?

• Individuals with suggestive MG features: fluctuating muscle weakness that worsens with activity and improves with rest, ptosis, diplopia, dysphagia, dysarthria, neck flexor weakness, or exertional fatigue.
• Patients with generalized or ocular MG suspicion, or with imaging evidence of thymic pathology (thymic hyperplasia/thymoma).
• Seronegative patients for whom alternative antibodies (e.g., MuSK, LRP4) and electrophysiologic testing are being considered as part of a comprehensive workup.

 

More Information

OTHER NAMES: AChR Antibodies; Acetylcholine Receptor Antibody,  Binding/Blocking/Modulating , Myasthenia Gravis Antibodies, Anti-AChR (Serum)

 

Autoantibodies against acetylcholine receptors (AChRs) at the neuromuscular junction are immune proteins that mistakenly target the nicotinic AChRs on the muscle endplate, disrupting nerve-to-muscle signaling and causing fatigable weakness typical of myasthenia gravis. These antibodies can:

• Bind and directly block ACh from activating the receptor, reducing ion channel opening and endplate depolarization.
• Cross-link receptors, accelerating their internalization and degradation (antigenic modulation), which lowers receptor density.
• Activate complement on the postsynaptic membrane, damaging the junctional folds and further impairing neuromuscular transmission.