Lab Test

Acetylcholine Receptor Binding Antibody

Acetylcholine Receptor (Muscle AChR) Binding Antibody, Muscle AChR, Myasthenia Gravis (MG)

Test Codes

EPIC: LAB592, Beaker: XARBI, ARUP #80009


Send Outs

Specimen Collection Criteria

Collect (preferred specimen): One Gold-top SST tube.
Also acceptable: One plain Red-top tube. 

Physician Office/Draw Specimen Preparation

Let specimen clot 30-60 minutes then centrifuge to separate serum from cells within two hours of collection. Transfer serum to a plastic transport tube and refrigerate (2-8°C or 36-46°F).

Preparation for Courier Transport

Transport: 0.5 mL serum, refrigerated (2-8°C or 36-46°F). (Minimum: 0.3 mL)

Rejection Criteria

  • Plasma
  • Hemolyzed specimens.
  • Severly lipemic specimens.
  • Specimens not collected and processed as indicated.

In-Lab Processing

Let specimen clot 30-60 minutes then centrifuge to separate serum from cells within two hours of collection. Transfer serum to a plastic transport tube and refrigerate (2-8°C or 36-46°F).

Transport: 0.5 mL serum, refrigerated (2-8°C or 36-46°F). (Minimum: 0.3 mL)


Specimen Stability for Testing:

Room Temperature (20-26°C or 68-78.8°F): 2 hours, after centrifugation 48 hours
Refrigerated (2-8°C or 36-46°F): 14 days
Frozen (-20°C/-4°F or below): 1 year

Specimen Storage in Department Prior to Disposal:

Specimen retention time is determined by the policy of the reference laboratory. Contact the Send Outs Laboratory with any questions.


Sent to ARUP Laboratories, Salt Lake City, UT.


Sunday – Saturday.
Results available in 3-4 days.

Reference Range

Negative: 0.0 - 0.4 nmol/L.
Positive: 0.5 nmol/L or greater. 

Test Methodology

Quantitative Radioimmunoassay.


Approximately 90% of patients with myasthenia gravis (MG) express antibodies to the acetylcholine receptor (AChR), which can be divided into binding, blocking, and modulating antibody. Binding antibody can activate complement and lead to loss of AChR. Blocking antibody may impair AChR binding to the receptor leading to poor muscle contraction. Modulating antibody causes receptor endocytosis resulting in loss of AChR expression, which correlates most closely with clinical severity of disease.

Approximately 10% of persons with confirmed myasthenia gravis have no measurable binding, blocking, or modulating antibody.

Clinical Utility

This assay aids in the diagnosis of myasthenia gravis (MS).

MG is an autoimmune disease in which an acetylcholine receptor (AChR) is the antibody target. The AChR in the endplate of skeletal muscle is an integral membrane protein consisting of five subunits. The alpha chain carries both the binding site for cholinergic ligands (acetylcholine and bungarotoxin) and the main immunogenic region. The majority of the autoantibodies of MG patients are directed to the alpha subunit. In MG, acetylchoine-dependent neuromuscular transmission is impaired by a loss of signal transduction. The final result is that the threshold potential in the cell is never reached and the muscle cannot contract. The patient experiences voluntary muscle weakness and fatigue characteristic of the disease, as well as difficulty in swallowing, doplopia, ptosis (in ocular MG) and, in severe cases, death.

Patients who have AChR antibodies generally do not express a single, monoclonal antibody population. These antibodies are divided into three classes: binding, blocking, and modulating. Binding antibodies are those that are directed to the large hydrophilic domain of the receptor. This class of antibodies can activate the complement cascade, resulting in tissue damage and receptor loss. The AChR binding assay detects a wide population of autoantibodies. The binding assay utilizes a soluble antigen and measures the extracellular and intracellular determinants of the receptor. This assay cannot differentiate general binding antibodies from the more specific modulating population. Moreover, the binding assay does not easily measure a blocking population.

Blocking autoantibodies prevent the binding of acetylcholine to the receptor. They may act by direct steric interference or by an allosteric mechanism. The pathology associated with this type of antibody will result in the most rapid loss of receptor function.

Modulating antibodies can accelerate endocytosis, resulting in loss of receptors. As a class, modulating autoantibodies have been most closely associated with clinical severity. However, Drachman, et al. have shown that the blocking population has a disease severity correlation nearly as high as that of modulating antibodies (88% vs. 91%). (1)

In approximately 10% of confirmed MG cases, there is no measurable antibody by any method. The reason for this observation is unclear because the disease pathology is a direct consequence of the autoimmune reaction.


  1. Drachman DB, et al. Functional activities of autoantibodies to acetylcholine receptors and the clinical severity of myasthenia gravis. N Engl J Med. 1982;307;769-775.

CPT Codes



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