Clinical heterogeneity and prognostic features of South Australian patients with anti‐synthetase autoantibodies
Identifieur interne : 001573 ( Main/Exploration ); précédent : 001572; suivant : 001574Clinical heterogeneity and prognostic features of South Australian patients with anti‐synthetase autoantibodies
Auteurs : M. Dugar [Australie] ; S. Cox ; V. Limaye ; P. Blumbergs ; P. J. Roberts-Thomson [Australie]Source :
- Internal Medicine Journal [ 1444-0903 ] ; 2011-09.
English descriptors
- Teeft :
- Aerobic capacity, Antisynthetase syndrome, Arthritis, Arthritis rheum, Assay, Australian patients, Autoantibody, Autoimmune conditions, Capillary dilatation, Clinical characteristics, Clinical features, Clinical heterogeneity, Clinical manifestations, Commercial assay, Commonest antigenic target, Creatine kinase, Deforming arthropathy, Eipah, Euroline myositis antigen, Further studies, Hazard ratios, Idiopathic myopathy, Immunosorbent assay, Interstitial, Interstitial lung disease, Japanese patients, Laboratory databases, Line immunoassay, Lung disease program, Medical records, Medicine journal, Milder muscle disease, Muscle biopsy, Muscle weakness, Myopathy, Myositis, Myositis registry, Nailfold capillaroscopy, Normal laboratory values, Overlap syndrome, Perth, Polymyositis, Poor prognosis, Poor prognostic indicators, Prognostic, Prognostic features, Qualitative nailfold capillaroscopy, Retrospective review, Rheum, Rheumatoid arthritis, Rheumatoid factor, Royal adelaide hospital, Royal australasian college, Royal perth hospital, Screening test, Serological, Serological features, Squamous cell lung cancer, Syndrome, Synthetase, Targoff, Western australia.
Abstract
Aim: To determine the clinical, serological and prognostic features of patients with autoantibodies against three aminoacyl‐transfer RNA synthetases (ARS), namely Jo‐1 (histidyl‐tRNA synthetase), PL‐7 (threonyl‐tRNA synthetase) and PL‐12 (alanyl‐tRNA synthetase) in South Australia. Methods: Patients with autoantibodies against ARS detected by line immunoassay (anti‐Jo1, anti‐PL7, anti‐PL12) or enzyme‐linked immunosorbent assay (anti‐Jo1) were identified from existing laboratory databases for the period 1994–2009. Demographic, clinical and serological data were obtained by retrospective review of patients' medical records and laboratory databases. Results: Forty‐two patients with autoantibodies were identified (anti‐Jo1 = 37, anti‐PL7 = 4, anti‐PL12 = 1). Females were more commonly affected than males (M : F = 12:30). Twenty‐one patients had polymyositis (anti‐Jo1 = 17, anti‐PL7 = 4), seven dermatomyositis (anti‐Jo1 = 6, anti‐PL12 = 1), 10 overlap syndrome (anti‐Jo1 = 10; lupus = 4, scleroderma = 3, Sjögren's syndrome = 2 and rheumatoid arthritis = 2) and four had interstitial lung disease (ILD) only (anti‐Jo1 = 4). ILD was present in 69%, polyarthritis in 59% and positive anti‐nuclear antibody (ANA) in 43% of patients. Concurrence of autoantibodies against Ro‐52 with Jo‐1 was seen in 12 patients. The mean follow‐up period was 8.3 years (95% CI 5.8–10.8) with 12 deaths. Poor prognostic indicators were age of onset >60 years (P= 0.001), cancer (P= 0.002), negative ANA (P= 0.006) and negative autoantibodies to extractable nuclear antigens (P= 0.02). Conclusion: Patients with autoantibodies against ARS present with varied clinical features and occasionally with isolated lung involvement (amyopathic ILD). Older age of onset, malignancy and negative immunologic tests are predictors of poor prognosis. Concurrence of autoantibodies against Jo‐1 and Ro‐52 may reflect a coupling effect during generation of autoimmunity.
Url:
DOI: 10.1111/j.1445-5994.2010.02164.x
Affiliations:
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Roberts-Thomson</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Immunology, SA Pathology, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Internal Medicine Journal</title><title level="j" type="alt">INTERNAL MEDICINE JOURNAL</title><idno type="ISSN">1444-0903</idno><idno type="eISSN">1445-5994</idno><imprint><biblScope unit="vol">41</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="674">674</biblScope><biblScope unit="page" to="679">679</biblScope><biblScope unit="page-count">6</biblScope><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2011-09">2011-09</date></imprint><idno type="ISSN">1444-0903</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1444-0903</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Aerobic capacity</term><term>Antisynthetase syndrome</term><term>Arthritis</term><term>Arthritis rheum</term><term>Assay</term><term>Australian patients</term><term>Autoantibody</term><term>Autoimmune conditions</term><term>Capillary dilatation</term><term>Clinical characteristics</term><term>Clinical features</term><term>Clinical heterogeneity</term><term>Clinical manifestations</term><term>Commercial assay</term><term>Commonest antigenic target</term><term>Creatine kinase</term><term>Deforming arthropathy</term><term>Eipah</term><term>Euroline myositis antigen</term><term>Further studies</term><term>Hazard ratios</term><term>Idiopathic myopathy</term><term>Immunosorbent assay</term><term>Interstitial</term><term>Interstitial lung disease</term><term>Japanese patients</term><term>Laboratory databases</term><term>Line immunoassay</term><term>Lung disease program</term><term>Medical records</term><term>Medicine journal</term><term>Milder muscle disease</term><term>Muscle biopsy</term><term>Muscle weakness</term><term>Myopathy</term><term>Myositis</term><term>Myositis registry</term><term>Nailfold capillaroscopy</term><term>Normal laboratory values</term><term>Overlap syndrome</term><term>Perth</term><term>Polymyositis</term><term>Poor prognosis</term><term>Poor prognostic indicators</term><term>Prognostic</term><term>Prognostic features</term><term>Qualitative nailfold capillaroscopy</term><term>Retrospective review</term><term>Rheum</term><term>Rheumatoid arthritis</term><term>Rheumatoid factor</term><term>Royal adelaide hospital</term><term>Royal australasian college</term><term>Royal perth hospital</term><term>Screening test</term><term>Serological</term><term>Serological features</term><term>Squamous cell lung cancer</term><term>Syndrome</term><term>Synthetase</term><term>Targoff</term><term>Western australia</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aim: To determine the clinical, serological and prognostic features of patients with autoantibodies against three aminoacyl‐transfer RNA synthetases (ARS), namely Jo‐1 (histidyl‐tRNA synthetase), PL‐7 (threonyl‐tRNA synthetase) and PL‐12 (alanyl‐tRNA synthetase) in South Australia. Methods: Patients with autoantibodies against ARS detected by line immunoassay (anti‐Jo1, anti‐PL7, anti‐PL12) or enzyme‐linked immunosorbent assay (anti‐Jo1) were identified from existing laboratory databases for the period 1994–2009. Demographic, clinical and serological data were obtained by retrospective review of patients' medical records and laboratory databases. Results: Forty‐two patients with autoantibodies were identified (anti‐Jo1 = 37, anti‐PL7 = 4, anti‐PL12 = 1). Females were more commonly affected than males (M : F = 12:30). Twenty‐one patients had polymyositis (anti‐Jo1 = 17, anti‐PL7 = 4), seven dermatomyositis (anti‐Jo1 = 6, anti‐PL12 = 1), 10 overlap syndrome (anti‐Jo1 = 10; lupus = 4, scleroderma = 3, Sjögren's syndrome = 2 and rheumatoid arthritis = 2) and four had interstitial lung disease (ILD) only (anti‐Jo1 = 4). ILD was present in 69%, polyarthritis in 59% and positive anti‐nuclear antibody (ANA) in 43% of patients. Concurrence of autoantibodies against Ro‐52 with Jo‐1 was seen in 12 patients. The mean follow‐up period was 8.3 years (95% CI 5.8–10.8) with 12 deaths. Poor prognostic indicators were age of onset >60 years (P= 0.001), cancer (P= 0.002), negative ANA (P= 0.006) and negative autoantibodies to extractable nuclear antigens (P= 0.02). Conclusion: Patients with autoantibodies against ARS present with varied clinical features and occasionally with isolated lung involvement (amyopathic ILD). Older age of onset, malignancy and negative immunologic tests are predictors of poor prognosis. Concurrence of autoantibodies against Jo‐1 and Ro‐52 may reflect a coupling effect during generation of autoimmunity.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><noCountry><name sortKey="Blumbergs, P" sort="Blumbergs, P" uniqKey="Blumbergs P" first="P." last="Blumbergs">P. Blumbergs</name><name sortKey="Cox, S" sort="Cox, S" uniqKey="Cox S" first="S." last="Cox">S. Cox</name><name sortKey="Limaye, V" sort="Limaye, V" uniqKey="Limaye V" first="V." last="Limaye">V. Limaye</name></noCountry><country name="Australie"><noRegion><name sortKey="Dugar, M" sort="Dugar, M" uniqKey="Dugar M" first="M." last="Dugar">M. Dugar</name></noRegion><name sortKey="Roberts Homson, P J" sort="Roberts Homson, P J" uniqKey="Roberts Homson P" first="P. J." last="Roberts-Thomson">P. J. Roberts-Thomson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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