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Idiopathic Inflammatory Myopathies: Laboratory Support for Diagnosis

This Clinical Focus provides an overview of the use of laboratory testing to diagnose myositis caused by the idiopathic inflammatory myopathies.

Clinical Focus

Idiopathic Inflammatory Myopathies

Laboratory Support for Diagnosis

Contents:

Clinical background

Table 1. Features of IIM Subtypes

Individuals suitable for testing

Test availability

Table 2. Laboratory Tests for Diagnosis of IIMs

Test selection and interpretation

Table 3. Clinical Significance of Autoantibodies in IIMs

References

Clinical background [return to contents]

The idiopathic inflammatory myopathies (IIMs) are a group of systemic autoimmune diseases characterized by muscle inflammation (myositis) and weakness. IIMs are rare, affecting 3 to 34 in 100,000 people,¹ and can affect both adults and children. In addition to muscle weakness, manifestations can include skin rashes, arthritis, dysphagia, and Raynaud phenomenon. Common complications include interstitial lung disease, cancer, and cardiac involvement, which are the leading causes of death in IIMs.^1,2

Antibodies considered to be myositis-specific autoantibodies (MSAs) define the major IIM subtypes, which differ in distribution, clinical presentation, and autoantibody profile (Table 1), though considerable heterogeneity exists.⁸ IIMs can also occur with other autoimmune rheumatic diseases, such as Sjögren syndrome, systemic sclerosis, and systemic lupus erythematosus, which is known as overlap myositis. Antibodies called myositis-associated autoantibodies (MAAs) may help identify these conditions.

Table 1. Features of IIM Subtypes [return to contents]

Subtype^a	Peak age(s) of onset, years^3,4	Sex distribution^1,3	Symptoms^1,3–5	Complications^3,4	Associated autoantibodies^1,6,7
ASyS	50	Female predominance	Symmetric proximal muscle weakness in upper and lower extremities Arthritis Raynaud phenomenon Mechanic’s hands Fever	ILD (70%-95%) Cardiac involvement	Jo-1 PL-7 PL-12 EJ OJ
DM	5-15 (juvenile DM), 40-50	Female predominance	Symmetric proximal muscle weakness in upper and lower extremities Possible absence of clinical myositis (amyopathic DM) Skin rash (heliotrope rash, Göttron sign, Göttron papules) Calcinosis Dysphagia	ILD (≤50%) Cancer (≤32%) Cardiac involvement	Mi-2 MDA-5 NXP-2 TIF1-γ
IBM	>50	Male predominance	Asymmetric muscle weakness in quadriceps and finger flexors Dysphagia		cN-1A
IMNM	30-70	Female predominance	Severe symmetric proximal muscle weakness in upper and lower extremities	ILD (5%-20%) Cancer Cardiac involvement	SRP HMGCR Absent (seronegative IMNM)
Overlap myositis	<50	Female predominance	Symmetric proximal muscle weakness in upper and lower extremities Variable, depending on overlapping disease	ILD (≤48%)	Fibrillarin (U3 RNP) Ku PM/Scl RNP SS-A

ASyS, antisynthetase syndrome; cN-1A, cytosolic 5′-nucleotidase 1A; DM, dermatomyositis; HMGCR, 3-hydroxy-3-methylglutaryl-coenzyme A reductase; IBM, inclusion body myositis; IIM, idiopathic inflammatory myopathy; ILD, interstitial lung disease; IMNM, immune-mediated necrotizing myopathy; MDA-5, melanoma differentiation-associated protein 5; MSA, myositis-specific autoantibody; NXP-2, nuclear matrix protein 2; RNP, ribonucleoprotein; SRP, signal recognition particle; SS-A, Sjögren syndrome antigen A; TIF1-γ, transcription intermediary factor 1 gamma.

Owing to the discovery of MSAs and the identification of other subtypes, polymyositis is now considered a diagnosis of exclusion. Many patients who were previously diagnosed with polymyositis are now classified as having another subtype based on autoantibody profile.^1,4

Diagnosis of IIM involves (1) excluding conditions with similar presentation (eg, muscular dystrophy and myopathies of known cause) and (2) identifying the IIM subtype.^1,9 Evaluation may include electromyography, imaging, biopsy, and laboratory tests for muscle enzymes and autoantibodies.^1,5

This Clinical Focus provides information about laboratory tests that are useful in diagnosing IIMs. This 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]

Individuals with symptoms of IIM (Table 1)

Test availability [return to contents]

Quest Diagnostics offers several tests and panels that may be useful for diagnosing IIMs (Table 2).

Table 2. Laboratory Tests for Diagnosis of IIMs [return to contents]

Test code	Test name	Clinical use
Muscle enzyme tests
823	Alanine Aminotransferase (ALT)	Diagnose IIM
227	Aldolase	Diagnose IIM
822	Aspartate Aminotransferase (AST)	Diagnose IIM
374	Creatine Kinase (CK), Total	Diagnose IIM
593	Lactate Dehydrogenase (LD)	Diagnose IIM
Autoantibody panels
10257	Extended Myositis Specific Antibody (MSA) Panel^a,b Includes cytosolic 5′-nucleotidase 1A (cN-1A, IgG, test code 10266), EJ, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR, IgG, test code 39044), Jo-1, MDA-5, Mi-2α, Mi-2β, NXP-2, OJ, PL-7, PL-12, SRP, and TIF1-γ antibodies.	Diagnose ASyS, DM, IBM, and IMNM
39149	Interstitial Lung Disease Panel^a,b Includes centromere A and B, cyclic citrullinated peptide (CCP, IgG, test code 11173), EJ, fibrillarin, Jo-1, Ku, MDA-5, mutated citrullinated vimentin (MCV, test code 13828), OJ, PL-7, PL-12, PM/Scl-75, PM/Scl-100, rheumatoid factor (test code 4418), RNA polymerase III (test code 19899), RNP (test code 19887), SS-A, Scl-70, and Th/To antibodies.	Diagnose overlap of IIM and MCTD, RA, SLE, SS, or SSc Identify connective tissue disease as a possible cause of interstitial lung disease
94777	Myositis Specific 11 Antibody Panel^a Includes EJ, Jo-1, MDA-5, Mi-2α, Mi-2β, NXP-2, OJ, PL-7, PL-12, SRP, and TIF1-γ antibodies.	Diagnose ASyS, DM, and IMNM
Individual autoantibody tests
94646	Anti-PM/Scl-100 Ab^c	Diagnose overlap of IIM and SSc
10266	Cytosolic 5′-Nucleotidase 1A (cN-1A) Antibody (IgG)^b	Diagnose IBM
34262	Fibrillarin (U3 RNP) Antibody, IgG^d	Diagnose overlap of IIM and SSc
39044	3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase (HMGCR) Antibody (IgG)	Diagnose IMNM
5810	Jo-1 Antibody	Diagnose ASyS
19887	RNP Antibody	Diagnose overlap of IIM and MCTD, SLE, or SSc
38568	Sjögren's Antibody (SS-A)	Diagnose overlap of IIM and SLE, SS, or SSc
38567	Sm/RNP Antibody	Diagnose overlap of IIM and MCTD, SLE, or SSc

ASyS, antisynthetase syndrome; CLIA, Clinical Laboratory Improvement Amendments; DM, dermatomyositis; IBM, inclusion body myositis; IIM, idiopathic inflammatory myopathy; IMNM, immune-mediated necrotizing myopathy; MCTD, mixed connective tissue disease; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; SS, Sjögren syndrome; SSc, systemic sclerosis.
a	This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by the US Food and Drug Administration. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.
b	Panel components may be ordered separately.
c	This test was developed and its performance characteristics have been determined by Labcorp. It has not been cleared or approved by the US Food and Drug Administration. This test is performed in a CLIA-certified laboratory and is intended for clinical purposes.
c	This test was developed and its performance characteristics have been determined by ARUP Laboratories. It has not been cleared or approved by the US Food and Drug Administration. This test is performed in a CLIA-certified laboratory and is intended for clinical purposes.

Test selection and interpretation [return to contents]

Laboratory workup for suspected IIM includes testing muscle enzyme levels in serum and testing for the presence of MSAs and MAAs.

Muscle enzymes

Patients with IIM often have elevated levels of muscle enzymes in serum, indicating active muscle disease.^1,4,5 An elevated level of any of the following enzymes is consistent with IIM: creatine kinase (test code 374), lactate dehydrogenase (test code 593), aspartate aminotransferase (test code 822), alanine aminotransferase (test code 823), and aldolase (test code 227).^1,9 Creatine kinase is the most sensitive muscle enzyme^1,5; patients with IIM often have creatine kinase levels up to 50 times the upper limit of normal (ULN), with the highest levels seen in immune-mediated necrotizing myopathy (IMNM, up to 100 times the ULN) and the lowest seen in inclusion body myositis (IBM, up to 10 times the ULN).⁵ However, not all patients with IIM have elevated muscle enzyme levels, especially those with IBM and amyopathic dermatomyositis.¹

Autoantibodies

Consensus guidelines from the European Neuromuscular Centre (ENMC) include testing for MSAs and MAAs (Table 3) as part of an optimal testing strategy for suspected IIM.⁸ MSAs and MAAs are found in up to 80% of patients with IIM⁵ and are strongly associated with homogenous patient subgroups. MSAs are virtually 100% specific for IIM,^6,7 and individual MSAs, which are usually mutually exclusive, are highly specific for certain IIM subtypes. MAAs are often found in IIM but are not specific for it^6,7; they can also be found in other autoimmune rheumatic diseases and thus are associated with overlap myositis.^1,6

Quest offers testing in accordance with the ENMC’s optimal testing strategy, which includes testing most MSAs.⁸ Quest’s MSA panels include the Extended Myositis Panel (test code 10257) and the Myositis Specific 11 Antibody Panel (test code 94777), which does not include cN-1A (test code 10266) or HMGCR (test code 39044) antibodies (available individually). Jo-1 antibody is also available individually (test code 5810).

If any autoantibody result is positive, further autoantibody testing may not be necessary, as patients rarely have more than 1 type of MSA (estimated prevalence, 0.11%).^7,13 However, if all MSAs are negative, testing for MAAs may be appropriate. Quest offers individual tests for fibrillarin (U3 RNP, test code 34262), PM/Scl-100 (test code 94646), RNP (test code 19887), SS-A (test code 38568), and Sm/RNP (test code 38567). These and additional MAAs (Ku and PM/Scl-75) are available in the Interstitial Lung Disease panel (test code 39149), which includes 20 autoantibodies found in connective tissue diseases associated with interstitial lung disease.

The presence of an MSA or MAA is highly suggestive of IIM. Individual autoantibodies are highly specific for IIM subtypes and may be associated with certain clinical features, complications, and outcomes (Table 3).^1,6,7 The absence of MSAs and MAAs does not rule out IIM, as up to 30% of patients with IIM do not have these autoantibodies.¹ Some of these patients may have seronegative IMNM, which has no known autoantibody associations.^1,4

Table 3. Clinical Significance of Autoantibodies in IIMs [return to contents]

Autoantibody	Clinical associations^{1,2,4,6,7,10–12}	IIM subtype^a
MSAs
Jo-1	Higher survival rate than other ASyS autoantibodies More frequent mechanic’s hands, arthritis, and myositis than other ASyS autoantibodies	ASyS highly likely
PL-7	Higher risk of ILD than Jo-1
PL-12	Higher risk of ILD than Jo-1
EJ	Unknown^b
OJ	Unknown^b
Mi-2α	Classical DM phenotype Good prognosis and response to treatment	DM highly likely
Mi-2β
MDA-5	Amyopathic DM Risk of ILD
NXP-2	Risk of cancer (except for juvenile DM) Muscle involvement more prominent than skin involvement
TIF1-γ	Risk of cancer (except for juvenile DM) Skin involvement more prominent than muscle involvement
cN-1A	Also found in SLE and SSc	IBM likely
SRP	More severe muscle disease and poorer prognosis than HMGCR Risk of cardiac involvement	IMNM highly likely
HMGCR	Less severe muscle disease and better prognosis than SRP Possible association with statin exposure	IMNM highly likely
MAAs
Fibrillarin (U3 RNP)	Overlap with SSc	Overlap myositis likely
Ku	Risk of ILD Overlap with SLE or SSc
PM/Scl-75	Risk of ILD Overlap with SSc
PM/Scl-100	Risk of ILD Overlap with SSc
U1 RNP	Raynaud phenomenon Risk of ILD Overlap with MCTD, SLE, or SSc
SS-A	Risk of ILD Overlap with SLE, SS, or SSc

ASyS, antisynthetase syndrome; cN-1A, cytosolic 5′-nucleotidase 1A; DM, dermatomyositis; HMGCR, 3-hydroxy-3-methylglutaryl-coenzyme A reductase; IBM, inclusion body myositis; IIM, idiopathic inflammatory myopathy; ILD, interstitial lung disease; IMNM, immune-mediated necrotizing myopathy; MAA, myositis-associated autoantibody; MCTD, mixed connective tissue disease; MDA-5, melanoma differentiation-associated protein 5; MSA, myositis-specific autoantibody; NXP-2, nuclear matrix protein 2; RNP, ribonucleoprotein; SLE, systemic lupus erythematosus; SRP, signal recognition particle; SS, Sjögren syndrome; SSc, systemic sclerosis; SS-A, Sjögren syndrome antigen A; TIF1-γ, transcription intermediary factor 1 gamma.
a	When clinical features are consistent.
b	Because of the rarity of these autoantibodies, clinical associations have not yet been established.
c	cN-1A is commonly considered an MSA but is not 100% specific for IIM.^6,7

References [return to contents]

Lundberg IE, Fujimoto M, Vencovsky J, et al. Idiopathic inflammatory myopathies. Nat Rev Dis Prim. 2021;7(1):86. doi:10.1038/s41572-021-00321-x
Oldroyd AGS, Callen JP, Chinoy H, et al. International guideline for idiopathic inflammatory myopathy-associated cancer screening: an International Myositis Assessment and Clinical Studies Group (IMACS) initiative. Nat Rev Rheumatol. 2023;19(12):805-817. doi:10.1038/s41584-023-01045-w
van Rilland EDZ, Yao L, Stevens KJ, et al. Myositis and its mimics: guideline updates, MRI characteristics, and new horizons. Am J Roentgenol. 2024;223(2):e2431359. doi:10.2214/ajr.24.31359
Tsamis KI, Boutsoras C, Kaltsonoudis E, et al. Clinical features and diagnostic tools in idiopathic inflammatory myopathies. Crit Rev Clin Lab Sci. 2022;59(4):219-240. doi:10.1080/10408363.2021.2000584
Dalakas MC. Chapter 18: Autoimmune inflammatory myopathies. In: Younger DS, ed. Motor System Disorders, Part I: Normal Physiology and Function and Neuromuscular Disorders. Vol 195. Handbook of Clinical Neurology. Elsevier; 2023:425-460. doi:10.1016/b978-0-323-98818-6.00023-6
Ogawa-Momohara M, Muro Y. Myositis-specific and myositis-associated autoantibodies: their clinical characteristics and potential pathogenic roles. Immunol Med. 2024. doi:10.1080/25785826.2024.2413604
Halilu F, Christopher-Stine L. Myositis-specific antibodies: overview and clinical utilization. Rheumatol Immunol Res. 2022;3(1):1-10. doi:10.2478/rir-2022-0001
Damoiseaux J, Mammen AL, Piette Y, et al. 256th ENMC International Workshop: myositis specific and associated autoantibodies (MSA-ab), Amsterdam, The Netherlands, 8-10 October 2021. Neuromuscul Disord. 2022;32(7):594-608. doi:10.1016/j.nmd.2022.05.011
Lundberg IE, Tjärnlund A, Bottai M, et al. 2017 European League Against Rheumatism/American College of Rheumatology classification criteria for adult and juvenile idiopathic inflammatory myopathies and their major subgroups. Ann Rheum Dis. 2017;76(12):1955. doi:10.1136/annrheumdis-2017-211468
Kwiatkowska D, Reich A. The significance of autoantibodies in juvenile dermatomyositis. BioMed Res Int. 2021;2021(1):551354. doi:10.1155/2021/5513544
Salam S, Dimachkie MM, Hanna MG, et al. Diagnostic and prognostic value of anti-cN1A antibodies in inclusion body myositis. Clin Exp Rheumatol. 2022;40(2):384-393. doi:10.55563/clinexprheumatol/r625rm
Satoh M, Ceribelli A, Hasegawa T, et al. Clinical Significance of Antinucleolar Antibodies: Biomarkers for Autoimmune Diseases, Malignancies, and others. Clin Rev Allergy Immunol. 2022;63(2):210-239. doi:10.1007/s12016-022-08931-3
Lega JC, Fabien N, Reynaud Q, et al. The clinical phenotype associated with myositis-specific and associated autoantibodies: A meta-analysis revisiting the so-called antisynthetase syndrome. Autoimmun Rev. 2014;13(9):883-891. doi:10.1016/j.autrev.2014.03.004

Content reviewed 3/2025

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Related tests (17)

5810 - Jo-1 Antibody

Jo-1 Antibody occurs most frequently (31%) in patients with polymyositis, but has also been found in patients with dermatomyositis, and the polymyositis/scleroderma "overlap syndrome" (PM/SCL) or polymyositis/systemic lupus erythematosis "overlap syndrome" (PM/SLE).

38567 - Sm/RNP Antibody

Smith (Sm)/U1-RNP Antibody is detected in patients with mixed connective tissue disease (having features of systemic lupus erythematosus (SLE), scleroderma, and polymyositis).

10266 - Cytosolic 5'-Nucleotidase 1A (cN-1A) Antibody (IgG)

The cN-1A Ab assay is a useful aid for the diagnosis of inclusion body myositis (IBM). The analytical sensitivity of this assay is 35-70%, based on published reports [1, 2]. In our validation study with 120 healthy adult subjects, 1.7% had a positive cN-1A Ab result and 6.7% had an equivocal result. However, published reports and our own internal studies suggest that patients with Sjogren’s syndrome, systemic lupus erythematosus, dermatomyositis (DM), or polymyositis (PM), are significantly more likely to have a positive cN-1A Ab result [1, 2, 3]. In contrast, patients presenting clinically with IBM rarely produce autoantibodies associated with a diagnosis of DM or PM [3]. Therefore, cN-1A Ab results must be interpreted in context with other details of the patient’s clinical evaluation.

References
1. Larman HB, et al. Cytosolic 5'-nucleotidase 1A autoimmunity in sporadic inclusion body myositis. Ann Neurol. 2013 Mar;73(3):408-18.
2. Felice KJ, et al. Neuromuscul Disord. 2018 Aug;28(8):660-664
3. Kramp SL, et al. Auto Immun Highlights. 2016 Dec;7(1):16. doi: 10.1007/s13317-016-0088-8

19899 - RNA Polymerase III Antibody

Autoantibodies to RNA Polymerase III antigen are found in 11% to 23% of patients with systemic sclerosis. Patients who are positive for RNA Polymerase III antibodies do not have any of the other antibodies typically found in systemic sclerosis patients such as anti-centromere, anti-Scl-70, or anti-Pm/Scl antibodies. Thus, they are a separate serologic group. Numerous studies have shown that these patients have an increased risk of the diffuse cutaneous form of scleroderma, with high likelihood of skin involvement and hypertensive renal disease.

Antibodies to several different types of RNA Polymerases are found in patients with systemic sclerosis. The immunodominant epitope or RNA Pol III was identified and cloned. The recombinant immunodominant epitope of RNA Pol III can be used in ELISA with high specificity to detect anti-RNA Pol III antibodies in patients with the diffuse cutaneous form of systemic sclerosis, with a high incidence of skin involvement.

19887 - RNP Antibody

RNP Antibodies have been associated with Mixed Connective Tissue disease.

374 - Creatine Kinase (CK), Total

This test measures creatine kinase (CK), an enzyme found primarily in striated muscle and heart tissue, and may be useful in assessing muscle damage.

CK is a dimeric enzyme composed of either 2 B subunits (CK-BB), 2 M subunits (CK-MM), or an M and a B subunit (CK-MB). CK-MM is the primary isoenzyme found in the skeletal muscle and heart tissue. CK-BB is mainly found in the brain and smooth muscle of gastrointestinal tract and urinary bladder. CK-MB is mainly found in the heart with a small amount in skeletal muscle [1]. An elevated level of any isoenzyme results in an elevated total CK level.

An increase in the CK level is often observed in inflammatory myopathy (eg, viral myositis, polymyositis, and immune-mediated myopathies), muscular dystrophy (eg, Duchenne sex-linked muscular dystrophy), rhabdomyolysis, or malignant hyperthermia [1]. In patients with neuromuscular disorders, an increased CK level may be the only initial manifestation [1]. Increased CK activity may also be caused by hypothyroidism, acute myocardial infarction, chronic renal failure, direct muscle trauma (eg, surgery and intramuscular injection), excessive exercise, certain medications (eg, statins, fibrates, antiretrovirals, and angiotensin II receptor antagonists), or brain damage or very low birth weight in newborns [1].

The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.

Reference
1. Panteghini M, et al. Serum enzymes. In: Rifai N, et al. eds. Tietz Textbook of Laboratory Medicine. 7th ed. Elservier Inc; 2022:4149-4299.

39149 - Interstitial Lung Disease Panel

A subset of interstitial lung disease (ILD) patients have underlying connective tissue diseases (CTDs). This panel serves as an aid for the diagnosis of CTDs, including rheumatoid arthritis, inflammatory myositis, systemic sclerosis, and Sjogren’s syndrome, that are associated with the development of ILD. If left untreated, these CTD patients may develop lung fibrosis and inflammation. ILD is a direct consequence of these pathological changes. When severe, ILD leads to restrictive lung disease, pulmonary arterial hypertension, and cardiac disease (cor pulmonale).

822 - Aspartate Aminotransferase (AST)

AST is widely distributed throughout the tissues with significant amounts being in the heart and liver. Lesser amounts are found in skeletal muscles, kidneys, pancreas, spleen, lungs, and brain. Injury to these tissues results in the release of the AST enzyme to general circulation. In myocardial infarction, serum AST may begin to rise within 6-8 hours after onset, peak within two days and return to normal by the fourth or fifth day post infarction. An increase in serum AST is also found with hepatitis, liver necrosis, cirrhosis, and liver metastasis.

823 - Alanine Aminotransferase (ALT)

Alanine Aminotransferase (ALT) measurements are particularly useful in the diagnosis and management of certain liver diseases, e.g., viral hepatitis and cirrhosis. ALT activity in tissue is generally much lower than aspartate aminotransferase (AST) activity and is found in highest concentrations in the liver. Significant elevations of ALT occur only in diseases of the liver. ALT is often measured in conjunction with AST to determine whether the source of the AST is the liver or the heart. ALT is normally not elevated in cases of myocardial infarction, i.e., a normal ALT, in conjunction with an elevated AST, tends to suggest cardiac disease. However, slight elevations of ALT may occur if an infarct destroys a very large volume of heart muscle.

39044 - 3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase (HMGCR) Antibody (IgG)

3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase (HMGCR) antibody is associated with necrotizing myopathy and is often associated with the use of statin medications.

11173 - Cyclic Citrullinated Peptide (CCP) Antibody (IgG)

A synthetic circular peptide containing citrulline called CCP IgG (cyclic citrullinated peptide) has been found to be better at discriminating Rheumatoid Arthritis patients from patients with other diseases such as hepatitis C infection. Rheumatoid Arthritis Classification Criteria include CCP IgG Antibody, rheumatoid factor, C-reactive protein and erythrocyte sedimentation rate (ESR). Approximately 70% of patients with Rheumatoid Arthritis are positive for Anti-CCP IgG, while only about 2% of random blood donors and disease controls subjects are positive.

227 - Aldolase

Aids in the diagnosis of primary disease of skeletal muscle myocardial infarction and viral hepatitis.

38568 - Sjogren's Antibody (SS-A)

Sjögren's Antibodies (SS-B) is detected in approximately 15% of patients with Sjögren's Syndrome. Sjögren's Antibody (SS-B) is present only if Sjögren's Antibody (SS-A) is also detected. The presence of both antibodies (SS-A and SS-B) strengthen the diagnosis of Sjögren's Syndrome and conveys prognostic information.

94777 - Myositis Specific 11 Antibody Panel

Myositis-specific autoantibodies (MSAs) are highly selective, usually exclusive and are associated with particular clinical phenotypes within the myositis spectrum. Myositis-specific autoantibodies to cytoplasmic enzymes that catalyze the binding of specific amino acids to their cognate tRNA define the anti-synthetase syndrome characterized by myositis and lung inflammation, and include autoantibodies to Jo-1 (antihistidyl-tRNA synthetase), PL-7 (threonyl), PL-12 (alanyl), EJ (glycyl), and OJ (isoleucyl). A further subset of myositis patients is characterized by the presence of autoantibodies directed against the signal recognition particle (SRP). Autoantibodies to Mi-2 (Mi-2/nucleosome remodeling and deacetylase (NuRD) complex) are detected in patients with hallmark dermatomyositis features. Autoantibody to a cytoplasmic 140-kDa protein, melanoma-differentiation associated gene 5 (MDA5), also known as anti-CADM140, identified patients with clinically amyopathic dermatomyositis (CADM) and rapidly progressive lung disease. Autoantibodies to transcriptional intermediary factor 1-gamma (TIF-1 y), a p155/140 nuclear protein involved in cellular differentiation, have been reported in adult and juvenile dermatomyositis; in adults, it is associated with malignancy. Autoantibodies to nuclear matrix protein NXP-2, another 140-kDa protein, is found in juvenile dermatomyositis (JDM). Anti-TIF-1 y and anti-NXP-2, two novel serological subsets in JDM, occur collectively in >40% of children and appear to identify those with more severe disease.

4418 - Rheumatoid Factor

Elevated RF is found in collagen vascular diseases such as SLE, rheumatoid arthritis, scleroderma, Sjogren's syndrome, and in other conditions such as leprosy, tuberculosis, syphilis, malignancy, thyroid disease and in a significant percentage of otherwise normal elderly patients.

593 - Lactate Dehydrogenase (LD)

Elevations in serum lactate dehydrogenase occur from myocardial infarction, liver disease, pernicious and megaloblastic anemia, pulmonary emboli, malignancies, and muscular dystrophy. Since lactic dehydrogenase is present in many body tissues, it's diagnosis usefulness is limited. Tissue specificity may be enhanced by isoenzyme analysis.

10257 - Extended Myositis Specific Antibody (MSA) Panel

The Extended Myositis Specific Antibody (MSA) panel is designed as an aid for the diagnosis of myopathies associated with autoantibody production. These include inflammatory myopathies (polymyositis, anti-synthetase syndrome, dermatomyositis), necrotizing myopathies, including statin associated myopathy, and inclusion body myositis.

Related guides (1)

Interstitial Lung Disease (ILD) Panel

This test is used to identify connective tissue disease (CTD) as a possible cause of interstitial lung disease (ILD).

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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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