Test Guide - Quest Test Directory

Myasthenia Gravis and Autoantibodies

This Clinical Focus provides information relating to the appropriate use and interpretation of antibody tests for myasthenia gravis diagnosis and management.

Clinical Focus

Myasthenia Gravis Autoantibodies

Contents:

Clinical background

Table 1. Myasthenia Gravis Subgroups

Individuals suitable for testing

Test availability

Table 2. Tests Available for Diagnosis and Management of Myasthenia Gravis

Test selection and interpretation

Table 3. Sensitivity and Specificity of MG-Related Antibodies for Thymoma in Individuals with MG
Figure 1. Selection of Antibody Tests in the Confirmation and Assessment of Suspected Ocular Myasthenia Gravis
Figure 2. Selection of Antibody Tests in the Confirmation and Assessment of Suspected Generalized Myasthenia Gravis
Figure 3. Reflex Testing in the Confirmation Suspected Generalized Myasthenia Gravis

References

Clinical background [return to contents]

Myasthenia gravis (MG) is an autoimmune neuromuscular disease caused by autoantibodies against proteins found in the neuromuscular junction of skeletal muscle; these antibodies impede nerve transmission.¹ Skeletal muscle weakness is the sole disease manifestation. MG almost always affects eye muscles, often asymmetrically, leading to diplopia (double vision) and ptosis (eye-lid droop). Otherwise, muscle weakness is usually symmetric, can be generalized or localized, and is more proximal than distal. Weakness increases over the course of any given day, with fatigue caused by repetitive motion and exercise.¹

In 2021, the prevalence of MG was 37 cases per 100,000 individuals in the United States.² Among adults, early-onset MG (<50 years) has a nearly 3-fold higher prevalence in women, whereas late-onset MG (≥50 years) is more common in men.¹ Juvenile-onset MG (<19 years) is rare.³

Reported mortality rates for MG range from 5% to 9% and are slightly higher in men than women.¹ Advanced age and respiratory failure are predictors of in-hospital mortality.⁴ Nearly full remission of MG signs and symptoms is possible with therapy, and prognosis is generally good.¹

Clinical history, signs and symptoms can vary by MG subgroup (Table 1)^4-6 and play key roles in diagnosis. Diagnostic methods can include CT scans of the chest, which are used to diagnose thymomas associated with MG, or ice pack tests⁷; however, confirmation with “gold standard” tests is required for the final diagnosis.⁸ These include electrophysiological tests (repetitive nerve stimulation or single-fiber electromyography), which can be uncomfortable for the patient,⁹ or serologic tests for MG-associated autoantibodies.

Table 1. Myasthenia Gravis Subgroups [return to contents]

Subgroup^4-6	Estimated MG cases,⁶ %	Primary autoantibody targets^4,6	Distinguishing clinical features^4-6
Early-onset	67^a	AChR	Thymic hyperplasia, onset <50 years
Late-onset	67^a	AChR, RyR, titin	Thymic atrophy, onset ≥50 years
Thymoma	10	AChR, RyR, titin	Cancer-associated
Ocular	15	AChR and LRP4	Does not progress to generalized MG
MuSK	1-10	MuSK	Cranial and bulbar muscular weakness^b
LRP4	<1-40	LRP4	Possibly milder disease severity (in absence of agrin autoantibody)
Seronegative	10-15	Unknown	Milder disease severity

AChR, acetylcholine receptor; LRP4, low-density lipoprotein receptor-related protein 4; MG, myasthenia gravis; MuSK, muscle-specific receptor tyrosine kinase; RyR, ryanodine receptor.
a	Percentage represents combined early- and late-onset MG.
b	Associated with neck and respiratory involvement.⁴ Compared with AChR-autoantibody seropositive patients, individuals with MuSK MG, have less ocular and limb weakness and fewer fluctuations in muscle strength.¹ When present, limb weakness tends to be severe and associated with atrophy.⁴ Distinctive ocular manifestations in MuSK MG are observed in the early stages of disease progression, including symmetrical ophthalmoparesis of horizontal or (rarely) vertical gaze with rapid remittance of diplopia; fluctuation of symptoms may be less evident, and nonocular symptoms typically appear 2 to 3 weeks after ocular onset.¹⁰ Purely ocular MuSK has been reported but is rare.⁹ Patients with autoantibodies to MuSK tend to be predominantly female (up to 85%).⁴ Geographic variations in prevalence in European, East Asian, and African regions suggest a genetic predisposition.^1,4 MuSK-associated MG has been associated with DQB105* and HLA-DRB114/DRB116 alleles.⁴

Approximately 15% of individuals with MG may have coexisting disorders, including thyroiditis, systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). These comorbidities should be considered when evaluating patients with MG, especially early-onset MG.¹

MG treatment options include anticholinesterase drugs, immunosuppressive therapy, corticosteroids, neonatal Fc receptor blockers, complement inhibitors, and thymectomy.^11-15 Laboratory testing may help inform and guide treatment by confirming the type(s) of autoantibody present in a patient being evaluated for MG-like muscle weakness as well as providing a means of monitoring treatment response.

This Clinical Focus discusses the role of laboratory testing in MG, from diagnosis to disease management. The information is provided for informational purposes only and is not intended as medical advice. Test selection and interpretation, diagnosis, and patient management decisions should be based on the physician’s education, clinical expertise, and assessment of the patient.

Individuals suitable for testing [return to contents]

Patients being evaluated for differential diagnosis of MG-like muscle weakness
Patients being monitored for treatment response

Test availability [return to contents]

Quest Diagnostics offers many laboratory testing options related to the diagnosis and monitoring of MG (Table 2).

Table 2. Tests Available for Diagnosis and Management of Myasthenia Gravis [return to contents]

Test code	Assay^a	Method	Clinical use
206	Acetylcholine Receptor Binding Antibody	RIA	Diagnose AChR Ab MG (early or late onset, ocular, thymoma MG)
94222	Acetylcholine Receptor Binding Antibody With Reflex to MuSK Antibody^b	RIA	Differentially diagnose AChR Ab MG vs MuSK MG
38359	Acetylcholine Receptor Binding Antibody With Reflex to MuSK/LRP4 Antibodies^b	IFA, RIA	Differentially diagnose AChR Ab MG vs MuSK MG vs LRP4 MG
34459	Acetylcholine Receptor Blocking Antibody	RBA	Diagnose AChR Ab MG (early or late onset, ocular, thymoma MG)
26474	Acetylcholine Receptor Modulating Antibody^c	RBA
11306	Lambert-Eaton Antibody Panel	IA, IFA, RBA	Differentially diagnose LEMS vs MG
94744	LRP4 Autoantibody Test	Cell-based IFA	Diagnose LRP4 MG in patients who are both AChR Ab- and MuSK Ab-negative, or ocular MG in AChR Ab-negative patients
1490	MuSK and LRP4 Antibodies Panel Includes LRP4 and MuSK antibody tests.	Cell-based IFA, RIA	Diagnose MuSK or LRP4 MG in AChR Ab-negative patients
18842	MuSK Antibody Test	RIA	Diagnose MuSK MG in AChR Ab-negative patients and (rarely) ocular MG in patients who are both AChR Ab- and LRP4 Ab-negative; assess disease severity and treatment response
7550(X)	Myasthenia Gravis Panel 1^c Includes acetylcholine receptor binding antibody and striated muscle antibody screen with reflex to titer.	IFA	Diagnose AChR Ab MG and assess disease severity
10104	Myasthenia Gravis Panel 2^c Includes acetylcholine receptor binding, blocking, and modulating antibodies.	IFA	Diagnose AChR Ab MG
93859	Myasthenia Gravis Panel 2 With Reflex to MuSK Antibody^b,c Includes acetylcholine receptor binding, blocking, and modulating antibodies with reflex to MuSK antibody.	IFA, RIA	Differentially diagnose AChR Ab MG vs MuSK MG in patients with generalized MG
10211(X)	Myasthenia Gravis Panel 3^b,c Includes acetylcholine receptor binding, blocking, and modulating antibodies and striated muscle antibody screen with reflex to titer.	IFA, RIA	Diagnose AChR Ab MG and assess disease severity
94743	RyR Autoantibody Test^d	Western blot	Help diagnose late-onset MG and thymoma MG; assess disease severity and treatment response
266	Striated Muscle Antibody With Reflex to Titer^c	IFA
92792	Titin Autoantibody Test^d	ELISA
93882	Voltage-Gated Calcium Channel (VGCC) Type N Antibody	RIA	Differentially diagnose LEMS vs MG

AChR, acetylcholine receptor; ELISA, enzyme-linked immunoassay; IFA, immunofluorescence assay; LEMS, Lambert-Eaton myasthenic syndrome; LRP4, low-density lipoprotein receptor-related protein 4; MG, myasthenia gravis; MuSK, muscle-specific receptor tyrosine kinase; RBA, radiobinding assay; RIA, radioimmunoassay; RyR, ryanodine receptor.
a	Panel components may be ordered separately.
b	Reflex tests are performed at an additional charge and are associated with additional CPT^® codes.
c	This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by FDA. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.
d	This test was developed and its analytical performance characteristics have been determined by Athena Diagnostics. It has not been cleared or approved by FDA. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.

Test selection and interpretation [return to contents]

Selection of laboratory tests in patients with suspected MG, when indicated, depends on clinical presentation and results of previous laboratory tests. Panel and/or reflex testing may help expedite a diagnosis.

The sections below provide a brief overview of relevant autoantibody tests and interpretation of their results and follow-up.

AChR (acetylcholine receptor)-autoantibodies testing

Elevated serum levels of acetylcholine receptor (AChR) autoantibodies are found in most individuals with MG, including 80% to 85% of those with generalized MG, 50% to 75% of those with ocular MG, and nearly 100% of those with thymoma.¹⁶ Specificity of these autoantibodies for MG is close to 100%.¹⁶ However, AChR autoantibody-positivity has been infrequently reported in patients with other diseases such as Lambert-Eaton myasthenic syndrome (LEMS).^17,18

AChR autoantibodies include binding (test code 206), blocking (test code 34459), and modulating (test code 26474) autoantibodies, which are differentiated by the sites that they target on the surface of the AChRs or their effect. Tests are also available as panels with/without reflex testing to identify other MG autoantibodies or to assess disease severity (Table 2).

Binding and modulating AChR autoantibodies are the most prevalent. In a study involving 349 patients with MG, 86% had binding AChR autoantibodies.¹⁸ Combining binding and modulating autoantibody assay results improved diagnostic sensitivity to 90%.¹⁸ Fewer than 1% of patients had blocking autoantibodies without binding autoantibodies, and blocking autoantibodies are rare in non-MG disease.¹⁸

Tests for binding, blocking and modulating antibodies to the AChR are performed using radioimmunoassay (RIA). They are done differently but all depend on the the ability of a snake toxin called alpha-bungarotoxin to bind to AChR in vitro, similarly to the way they block neuromuscular transmission in vivo. The toxin is labeled with radioactivity.

Binding antibodies are detected by adding patient serum to AChR-labeled toxin complexes and measuring the amount of binding. Binding is required for any pathogenicity of anti-AChR antibodies. Binding alone may activate the complement system, causing inflammatory destruction of the post-synaptic membrane. But binding of AChR may also cause neuromuscular disease by other mechanisms.
Blocking antibodies are measured by detecting competition of antibody in the patient’s sample with the labeled toxin. If antibodies are able to prevent the toxin from binding, it indicates that they may be able to block acetylcholine binding and receptor activation in the patient. Blocking antibodies are seldom detected in the absence of binding antibodies.
Modulating antibodies are measured by allowing antibodies in the patient’s sample to interact with live cells expressing the AChR. After incubation, the cells are allowed to interact with labeled toxin and examined to see if the labeled toxin was able to bind to their surface. If not, it means that the anti-AChR antibodies cross-linked the AChR molecules and caused them to be internalized. In the patient, this results in a decrease in the number of functional receptors in the post-synaptic membrane. Modulating antibodies may be present in a small percentage of patients who are negative using the test for binding antibodies.

Whether higher levels of AChR antibody are associated with more severe disease, and lower levels are associated with treatment response, is unclear.^17,19

According to the Myasthenia Gravis Foundation of America Task Force (MGFA TF) 2020 recommendations, AChR-antibody positivity prompts¹¹

Consideration of thymectomy in
Individuals with nonthymomatous generalized MG ages 18 to 50 years
Any individuals with MG who do not respond to immunosuppressive therapy or cannot tolerate its side effects
Individuals with ocular MG who

Do not respond adequately to anticholinesterase drugs and prefer not to take immunosuppressive therapy and/or
Have contraindications, or do not respond, to immunosuppressive therapy

Consideration of rituximab for patients who do not respond to, or tolerate, other immunosuppressive therapies (although the efficacy of rituximab in refractory AChR-antibody positive MG is uncertain)
Consideration of eculizumab in patients with severe, refractory, generalized MG

For the treatment of generalized MG in adult patients who are anti-AChR positive, the FDA has also approved the following neonatal Fc receptor blockers and complement inhibitors^14,20-24 :

Neonatal Fc receptor blockers: efgartigimod alfa-fcab, efgartigimod alfa and hyaluronidase-qvfc, nipocalimab-aahu, and rozanolixizumab-noli
Complement inhibitors: eculizumab, ravulizumab-cwvz, and zilucoplan

Striated (striational) muscle, titin, and ryanodine receptor antibody testing

The striated muscle antibody test (test code 266) has a reported sensitivity of 75% to 77% and specificity of 58% to 73% for detecting thymoma in individuals with MG. A large-scale study involving 1,141 individuals with MG found that the positive predictive value (AChR plus striated muscle autoantibodies) of this test was poor for thymoma in late-onset patients (<9%) but higher in early-onset patients (50%).²⁵

Striated muscle autoantibodies in patient sera are detected using an immunofluorescence assay (IFA), which involves binding of the autoantibodies to muscle antigens. Results are reported as negative or positive, with positive results reflexing to titer defined as the highest dilution that produces a 1+ fluorescence intensity.

Ryanodine receptor (RyR, test code 94743) and titin (test code 92792) antibodies are component striated muscle antibodies. Side-by-side comparisons of MG autoantibodies indicated that RyR and titin had improved specificity for thymoma over the striated muscle antibody IFA^26,27 (1 study also demonstrated improved sensitivity using titin autoantibodies).²⁶ Both RyR and titin autoantibodies are also more specific than AChR autoantibodies, which are generally more sensitive for thymoma in individuals with MG (Table 3).^26-28 The presence of RyR and/or titin autoantibodies is associated with more severe disease.²⁹

Table 3. Sensitivity and Specificity of MG-Related Autoantibodies for Thymoma in Individuals with MG^a [return to contents]

Antibody	Sensitivity,^26,28 %	Specificity,^26,28 %
AChR²⁷	99-100	17-25
RyR	47-70	86-95
Titin	51-95	76-97

MG, myasthenia gravis.
a	One study included 146 individuals with MG, of whom 20 had thymoma²⁶; the second study included 44 patients, of whom 13 had thymoma²⁷; the third study included 437 patients, of whom 128 had thymoma.²⁸

An enzyme-linked immunosorbent assay (ELISA) detects titin antibody in patient sera. Results are reported as negative, borderline, or positive. Presence of RyR is detected by Western blot. The presence of 1 or both autoantibodies raises clinical suspicion of thymoma MG or late-onset MG, or early-onset MG with thymoma.

RyR autoantibodies are rare in early-onset MG but are present in up to 40% of patients with late-onset MG.²⁹ Sensitivity and specificity estimates (Table 3) indicate that presence of RyR is suggestive of the presence of thymoma. Titin autoantibodies present in only 6% of early-onset MG but of those 50% to 95% have thymoma; thus, presence of titin is strongly suggestive of thymoma in early-onset patients. Titin autoantibodies are also present in 50% to 80% patients with late-onset MG.²⁹ High titin antibody titer indicates severe MG in all age groups.²⁹

The MGFA TF does not include any specific recommendations regarding testing or monitoring striated muscle autoantibodies, including RyR nor titin.^11,12

Muscle-specific receptor tyrosine kinase (MuSK)-antibody testing

Muscle-specific receptor tyrosine kinase (MuSK) antibody testing (test code 18844) is useful for MG diagnosis in patients who test negative for AChR autoantibodies, including up to 40% of AChR-antibody seronegative patients with generalized disease.⁴ For patients with ocular MG, testing should be reserved for those who have negative results for both AChR and LRP4 autoantibodies.³⁰

MuSK autoantibodies are detected using an RIA; a titer of 1:10 or greater is considered positive for antibody presence and provides a definitive diagnosis of MG.⁶ In contrast to AChR-autoantibodies, changes in MuSK antibody levels over time more clearly reflect disease activity.^4,6

Patients with MuSK-positive MG are much less likely to have thymoma or belong to the ocular MG subgroup and tend to have poor response to anticholinesterase therapy and thymectomy.¹² However, they generally respond well to corticosteroids and to many steroid-sparing immunosuppressant agents.¹² These patients also usually respond well to plasma exchange, which is more effective than IV immunoglobin for this MG subgroup.¹²

According to MGFA TF 2020 recommendations, MuSK-antibody positivity suggests that patients are not good candidates for thymectomy and prompts consideration of rituximab as an early therapeutic option in patients who do not respond adequately to initial immunosuppressive therapy.¹¹ Importantly, since the 2020 guidelines were published, rozanolixizumab-noli is now available as an FDA-approved treatment of adults with generalized MG and MuSK-antibody positivity in addition to those who are AChR-antibody positive.¹⁴

Low-density lipoprotein receptor-related protein 4 testing

LRP4 testing is useful for MG diagnosis in patients who test negative for AChR autoantibodies. However, reported prevalence rates vary widely in individuals with MG (Table 1) and in patients who are negative for both AChR and MuSK autoantibodies (<1% to 50%).⁵ The variance has been ascribed to differences in detection methods and geographical regions in the different studies.¹⁶ In a multicenter study of 181 individuals with MG who were negative for both AChR and MuSK autoantibodies, 13% were positive for LRP4 autoantibodies.⁵ Most LRP4-positive patients in that study also tested positive for agrin autoantibodies and presented with generalized and more severe disease than antibody-negative patients.

LRP4 autoantibodies in patient sera are detected in a cell-based IFA. Results are reported as positive or negative. Positive results in AChR-, MuSK-negative individuals with MG are indicative of LRP4 MG; however, LRP4 autoantibodies have been reported in 10% to 25% of ALS patients.¹⁶ Consequently, detection of LRP4 autoantibodies alone does not establish a diagnosis of MG.

The MGFA TF does not include any specific recommendations regarding testing or monitoring LRP4 autoantibodies. However, it does suggest that patients with LRP4 autoantibodies are not good candidates for thymectomy.^11,12

Panels and reflex testing

A generalized overview of test selection for individuals with symptoms suggestive of ocular (Figure 1)^1,6,30 or generalized (Figure 2)^1,6,30 MG is provided. The testing sequence in these figures is largely based on the prevalence of each antibody in individuals with ocular and generalized MG beginning with AChR autoantibody testing using Myasthenia Gravis Panel 2 without reflex testing for ocular MG (test code 10104) and with reflex testing for generalized MS (test code 93859):

Individuals with MG with localized ocular involvement (Figure 1)^1,6,30 rarely have striated muscle autoantibodies, such as titin and ryanodine receptor (RyR) autoantibodies. MuSK MG autoantibodies are also rare in individuals with localized ocular involvement and should only be considered in those negative for both AChR and LRP4 autoantibodies.³⁰
Individuals with MG with generalized muscle weakness may benefit by testing for MuSK and LRP4 autoantibodies early in the diagnostic work up if AChR-antibody test results are negative. In addition, early detection of titin and/or RyR autoantibodies may help differentiate among MG subgroups and assess disease severity for patients with generalized disease (Figure 2).^1,6,16

Figure 1.Selection of Antibody Tests in the Confirmation and Assessment of Suspected Ocular Myasthenia Gravis.^1,6,30
[return to contents]

Figure 2. Selection of Antibody Tests in the Confirmation and Assessment of Suspected Generalized Myasthenia Gravis.^1,6,16
[return to contents]

Given the overlap between binding and both blocking and modulating AChR autoantibodies, testing starting with AChR binding autoantibodies (test code 38359) but reflexing to MuSK and LRP4 antibody testing if the AChR binding assay is negative may provide a more efficient option for the confirmation of generalized MG (Figure 3).^1,6,16

Figure 3. Reflex Testing in the Confirmation Suspected Generalized Myasthenia Gravis.^1,6,16
[return to contents]

Seronegative MG

Negativity for the autoantibodies discussed above does not rule out a diagnosis of MG. Reevaluation by repeating the antibody tests after 6 to 12 months may be considered.¹

Decreased response to repetitive nerve stimulation or increased jitter on single-fiber electromyography can also confirm a diagnosis of MG.⁶ If LEMS is being considered in the differential diagnosis, presence of voltage-gated calcium channel (VGCC) type N antibody (test code 93882) is associated with LEMS and can rule out a diagnosis of MG.⁶ For seronegative children, the MGFA TF recommends considering the possibility of congenital myasthenic syndromes or other neuromuscular diseases.¹²

The MGFA TF has no specific recommendations for management of seronegative MG, but noted that seronegativity is more common in MG that is associated with immune checkpoint inhibitor treatment during cancer immunotherapy.¹¹

References [return to contents]

Gilhus NE. Myasthenia gravis. N Engl J Med. 2016;375(26):2570-2581. doi:10.1056/NEJMra1602678
Rodrigues E, Umeh E, Aishwarya, et al. Incidence and prevalence of myasthenia gravis in the United States: A claims-based analysis. Muscle Nerve. 2024;69(2):166-171. doi:10.1002/mus.28006
Finnis MF, Jayawant S. Juvenile myasthenia gravis: a paediatric perspective. Autoimmune Dis. 2011;2011:404101. doi:10.4061/2011/404101
Dresser L, Wlodarski R, Rezania K, et al. Myasthenia gravis: epidemiology, pathophysiology and clinical manifestations. J Clin Med. 2021;10(11)doi:10.3390/jcm10112235
Rivner MH, Quarles BM, Pan JX, et al. Clinical features of LRP4/agrin-antibody-positive myasthenia gravis: a multicenter study. Muscle Nerve. 2020;62(3):333-343. doi:10.1002/mus.26985
Gilhus NE, Tzartos S, Evoli A, et al. Myasthenia gravis. Nat Rev Dis Primers. 2019;5(1):30. doi:10.1038/s41572-019-0079-y
Beloor SA, Asuncion RMD. Myasthenia Gravis. StatPearls [internet]. Updated August 8, 2023. Accessed May 30, 2025. https://www.ncbi.nlm.nih.gov/books/NBK559331/
Fakiri MO, Tavy DL, Hama-Amin AD, et al. Accuracy of the ice test in the diagnosis of myasthenia gravis in patients with ptosis. Muscle Nerve. 2013;48(6):902-904. doi:10.1002/mus.23857
Caress JB, Hunt CH, Batish SD. Anti-MuSK myasthenia gravis presenting with purely ocular findings. Arch Neurol. 2005;62(6):1002-1003. doi:10.1001/archneur.62.6.1002
Rodolico C, Bonanno C, Toscano A, et al. MuSK-associated myasthenia gravis: clinical features and management. Front Neurol. 2020;11:660. doi:10.3389/fneur.2020.00660
Narayanaswami P, Sanders DB, Wolfe G, et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology. 2021;96(3):114-122. doi:10.1212/WNL.0000000000011124
Sanders DB, Wolfe GI, Benatar M, et al. International consensus guidance for management of myasthenia gravis: executive summary. Neurology. 2016;87(4):419-425. doi:10.1212/WNL.0000000000002790
DeHart-McCoyle M, Patel S, Du X. New and emerging treatments for myasthenia gravis. BMJ Med. 2023;2(1):e000241. doi:10.1136/bmjmed-2022-000241
Rystiggo^® (rozanolixizumab-noli) injection. Prescribing information. UCB. Accessed April 14, 2025. https://www.ucb-usa.com/RYSTIGGO-prescribing-information.pdf
Howard JF, Jr. Myasthenia gravis: the role of complement at the neuromuscular junction. Ann N Y Acad Sci. 2018;1412(1):113-128. doi:10.1111/nyas.13522
Frykman H, Kumar P, Oger J. Immunopathology of autoimmune myasthenia gravis: implications for improved testing algorithms and treatment strategies. Front Neurol. 2020;11:596621. doi:10.3389/fneur.2020.596621
Meriggioli MN, Sanders DB. Muscle autoantibodies in myasthenia gravis: beyond diagnosis? Expert Rev Clin Immunol. 2012;8(5):427-438. doi:10.1586/eci.12.34
Howard FM, Jr., Lennon VA, Finley J, et al. Clinical correlations of antibodies that bind, block, or modulate human acetylcholine receptors in myasthenia gravis. Ann N Y Acad Sci. 1987;505:526-538. doi:10.1111/j.1749-6632.1987.tb51321.x
Husain AM, Massey JM, Howard JF, et al. Acetylcholine receptor antibody measurements in acquired myasthenia gravis. Diagnostic sensitivity and predictive value for thymoma. Ann N Y Acad Sci. 1998;841:471-474. doi:10.1111/j.1749-6632.1998.tb10965.x
Vyvgart Hytrulo^® (efgartigimod alfa and hyaluronidase-qvfc) injection, for subcutaneous use Prescribing information. Halozyme. Updated April 2025. Accessed June 5, 2025. https://argenx.com/content/dam/argenx-corp/products/vyvgart-hytrulo-prescribing-information.pdf
Soliris^® (eculizumab) injection, for intravenous use Prescribing information. Alexion Pharmaceuticals. Accessed June 5, 2025. https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/125166s431lbl.pdf
Ultomiris^® (ravulizumab-cwvz) injection, for intravenous use Prescribing information. Alexion Pharmaceuticals. Updated April 2022. Accessed June 5, 2025. https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/761108s023lbl.pdf
Zilbrysq (zilucoplan) injection, for subcutaneous use Prescribing information. UCB. Updated October 2023. Accessed June 5, 2025. https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/216834s000lbl.pdf
Imaavy (nipocalimab-aahu) injection, for intravenous use. Prescribing information. Janssen Pharmaceutical Companies. Accessed June 23, 2025. https://www.janssenlabels.com/package-insert/product-monograph/prescribing-information/IMAAVY-pi.pdf
Choi Decroos E, Hobson-Webb LD, Juel VC, et al. Do acetylcholine receptor and striated muscle antibodies predict the presence of thymoma in patients with myasthenia gravis? Muscle Nerve. 2014;49(1):30-34. doi:10.1002/mus.23882
Romi F, Skeie GO, Aarli JA, et al. Muscle autoantibodies in subgroups of myasthenia gravis patients. J Neurol. 2000;247(5):369-375. doi:10.1007/s004150050604
Voltz RD, Albrich WC, Nägele A, et al. Paraneoplastic myasthenia gravis: detection of anti-MGT30 (titin) antibodies predicts thymic epithelial tumor. Neurology. 1997;49(5):1454-1457. doi:10.1212/wnl.49.5.1454
Hong Y, Li HF, Skeie GO, et al. Autoantibody profile and clinical characteristics in a cohort of Chinese adult myasthenia gravis patients. J Neuroimmunol. 2016;298:51-57. doi:10.1016/j.jneuroim.2016.07.001
Lazaridis K, Tzartos SJ. Myasthenia gravis: autoantibody specificities and their role in MG management. Front Neurol. 2020;11:596981. doi:10.3389/fneur.2020.596981
Fortin E, Cestari DM, Weinberg DH. Ocular myasthenia gravis: an update on diagnosis and treatment. Curr Opin Ophthalmol. 2018;29(6):477-484. doi:10.1097/ICU.0000000000000526

Content reviewed 06/2025

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Related tests (15)

93882 - Voltage-Gated Calcium Channel (VGCC) Type N Antibody

N-type calcium channel antibodies are more highly associated with primary lung cancer than P/Q-type. One or all of the autoantibodies in the myasthenia gravis (MG)/LEMS evaluation can occur with neoplasia without evidence of neurological impairment. One or both calcium channel antibodies (P/Q and N) can occur with paraneoplastic and idiopathic cerebellar ataxia, encephalomyeloneuropathies, and autonomic neuropathy. Classical symptoms of LEMS include proximal muscle weakness, fatigability, dry mouth and impotence. When presentation is further complicated with oculobulbar weakness, these symptoms can easily be misinterpreted as MG. However, because VGCC antibodies are positive in only approximately 5% of MG patients, the measurement of these antibodies is very useful in distinguishing LEMS from MG.

26474 - Acetylcholine Receptor Modulating Antibody

Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder characterized by muscle weakness, most commonly due to autoantibody-mediated loss of functional acetylcholine receptors (AChR) in the neuromuscular junction. AChR binding autoantibodies are diagnostic of MG, and are found in 85-90% of MG patients. AChR modulating antibodies cross-link AChR molecules on cell surface, promoting internalization, and decreasing AChR surface density. The AChR binding and modulating antibody assays have similar sensitivities, but performing them together increases sensitivity of antibody detection by approximately 5%.

94744 - LRP4 Autoantibody Test

Detects anti-LRP4 (low density lipoprotein receptor-related protein 4) in the sera of patients with Myasthenia Gravis (MG). The LRP4 protein activates MuSK kinase activity and promotes the clustering of AChR and their stabilization at the NMJ. Anti-LRP4 antibodies are found in approximately 9.2% (range 2% to 50%) of MG patients who are negative for both anti-AChR and anti-MuSK.

206 - Acetylcholine Receptor Binding Antibody

Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder characterized by muscle weakness, most commonly due to autoantibody-mediated loss of functional acetylcholine receptors (AChR) in the neuromuscular junction. AChR binding autoantibodies are diagnostic of MG, and are found in 85-90% of MG patients. This assay aids in the differential diagnosis of conditions with MG-like muscle weakness and in monitoring therapeutic response. If binding antibodies are negative, assays for modulating and blocking antibodies should be considered.

94743 - RyR Autoantibody Test

Detects anti-RyR (ryanodine receptor) in the sera of patients with Myasthenia Gravis (MG). Other striational antibodies, such as titin, are rarely found in acetylcholine receptor (AChR) antibody-negative MG. Anti-titin is detected in 20% to 40% of all MG patients and anti-RyR in 13% to 38%. Anti-titin (49% to 95%) and anti-RyR (70% to 80%) are frequently found in thymoma associated-MG cases.

1490 - MuSK and LRP4 Antibodies Panel

Detects anti-MuSK (muscle specific receptor tyrosine kinase) and anti-LRP4 (low density lipoprotein receptor-related protein 4) in the sera of patients with Myasthenia Gravis (MG). MuSK is a transmembrane endplate polypeptide involved in a signaling pathway that maintains the normal functional integrity of the neuromuscular junction (NMJ). The LRP4 protein activates MuSK kinase activity and promotes the clustering of the acetylcholine receptor (AChR) and its stabilization at the NMJ. Approximately 8% to 10% of all MG cases and 20% to 50% of the generalized MG cases who lack anti-AChR have anti-MuSK. Anti-LRP4 antibodies are detected in the serum of approximately 9.2% (range 2% to 50%) of MG patients who are negative for both anti-AChR and anti-MuSK.

10104 - Myasthenia Gravis Panel 2

Myasthenia Gravis is a neurological disorder characterized by a decrease in acetylcholine receptors. Patients exhibit skeletal muscle weakness and fatigability. Approximately 80% of patients with Myasthenia Gravis, excluding ocular involvement only, have detectable acetylcholine receptor antibody.

10211 - Myasthenia Gravis Panel 3

11306 - Lambert-Eaton Syndrome Antibody Panel

Lambert-Eaton myasthenic syndrome is a paraneoplastic phenomena associated with small cell lung cancer. There is a decrease of voltage-gated calcium channels on presynaptic nerve terminals due to an auto-antibody reactive with the channels. There is an associated proximal muscle weakness and often coexisting thyroid autoimmune disease and vitiligo.

18842 - MuSK Antibody Test

Detection of antibodies to muscle-specific receptor tyrosine kinase (MuSK) (titer test).

93859 - Myasthenia Gravis Panel 2 with Reflex to MuSK Antibody

Myasthenia gravis (MG) is an autoimmune disorder affecting the neuromuscular junction. 80% of patients with generalized MG have serum antibodies to AChR - Blocking, Binding, or Modulating. Antibodies to MuSK make up a variable proportion of the remaining 20%.

34459 - Acetylcholine Receptor Blocking Antibody

Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder characterized by muscle weakness, most commonly due to autoantibody-mediated loss of functional acetylcholine receptors (AChR) in the neuromuscular junction. AChR binding autoantibodies are diagnostic of MG, and are found in 85-90% of MG patients. AChR blocking autoantibodies prevent inter-action of binding antibodies with the AChR. Fewer than 1% of patients have blocking antibodies without binding antibodies. Blocking antibodies are present in about 50% of patients with MG, but rare in other conditions. Therefore, blocking antibodies have utility in ruling out a possible false positive binding assay and detecting the rare patient without AChR binding antibodies.

92792 - Titin Autoantibody Test

Anti-titin antibody is a striational antibody that is associated with myasthenia gravis with an older age of onset (approximately >60 years). Anti-titin antibodies are detected in patients with thymoma associated-MG.

38359 - Acetylcholine Receptor Binding Antibody with Reflex to MuSK/LRP4 Antibodies

Detects binding antibodies to the acetylcholine receptor (anti-AChR) by a quantitative radioimmunoassay in the sera of patients with Myasthenia Gravis (MG). About 80% to 85% of patients with generalized MG and 50% to 75% of patients with ocular MG have anti-AChR. Negative anti-AChR results are reflexed to testing for anti-MuSK (muscle specific receptor tyrosine kinase) and anti-LRP4 (low density lipoprotein receptor-related protein 4). Approximately 8% to 10% of all MG cases and 20% to 50% of the generalized MG cases who lack binding anti-AChR have anti-MuSK. Anti-LRP4 antibodies are detected in the serum of approximately 9.2% (range 2% to 50%) of MG patients who are negative for both binding anti-AChR and anti-MuSK.

7550 - Myasthenia Gravis Panel 1

Useful in the diagnosis of Myasthenia Gravis

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Reference ranges are provided as general guidance only. To interpret test results use the reference range in the laboratory report.

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