Evidence map›Paper›PMID 20302639›Full record

ArticleArthritis research & therapy2010

Anticentromere antibody positive Sjögren's Syndrome: a retrospective descriptive analysis.

Vasiliki-Kalliopi K Bournia, Konstantina D Diamanti, Panayiotis G Vlachoyiannopoulos, Haralampos M Moutsopoulos

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Article in Arthritis research & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

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25citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

25 citing papers in PubMed.

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  12. Prognostic value of Sjögren's syndrome autoantibodies.Journal of laboratory and precision medicine · 2018
    Article
  13. Article
  14. Review
  15. Article
  16. Autoantibodies in Sjögren's Syndrome.Rheumatic diseases clinics of North America · 2016
    Review
  17. Article
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  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Vasiliki-Kalliopi K BourniaDepartment of Pathophysiology, Medical School, National and Kapodistrian University, 75 Mikras Asias Street, 11527, Athens, Greece.
Konstantina D Diamanti
Panayiotis G Vlachoyiannopoulos
Haralampos M Moutsopoulos

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionA subgroup of patients with primary Sjögren's Syndrome (SS) and positive anticentromere antibodies (ACA) were recognized as having features intermediate between SS and systemic sclerosis (SSc). Our goal was to describe this group clinically and serologically and define its tendency to evolve to full blown SSc.

methodsAmong 535 patients with primary SS we identified 20 ACA positive (ACA+/SS). We compared them to 61 randomly selected ACA negative SS patients (ACA-/SS), 31 ACA positive SSc patients with sicca manifestations [SSc/(+) sicca] and 20 ACA positive SSc patients without sicca manifestations [SSc/(-) sicca].

resultsPrevalence of ACA among SS patients was 3.7%. Cases and controls did not differ in sex ratio and age at disease onset. ACA+/SS patients had a lower prevalence of dry eyes, hypergammaglobulinaemia, anti-Ro and anti-La antibodies and a higher prevalence of Raynaud's phenomenon and dysphagia compared to ACA-/SS patients. They also had lower prevalence of telangiectasias, puffy fingers, sclerodactyly, Raynaud's phenomenon, digital ulcers and gastroesophageal reflux in comparison to both of the SSc subgroups and a lower prevalence of dyspnoea and lung fibrosis compared to the SSc/(+) sicca subgroup. Two patients originally having ACA+/SS evolved to full blown SSc. Four deaths occurred, all among SSc patients. Kaplan Meier analysis showed a significant difference between cases and controls in time from disease onset to development of gastroesophageal reflux, telangiectasias, digital ulcers, arthritis, puffy fingers, xerostomia, hypergammaglobulinaemia and dysphagia.

conclusionsACA+/SS has a clinical phenotype intermediate between ACA-/SS and SSc and shows little tendency to evolve to SSc.

Indexed as

AdultAutoantibodiesCentromereDeglutition DisordersFemaleHumansKeratoconjunctivitis SiccaMaleMiddle AgedRaynaud DiseaseRetrospective StudiesScleroderma, SystemicSjogren's SyndromeAutoantibodies

Identifiers

PMID20302639
PMCPMC2888196

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