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Article: Familiality and co-occurrence of clinical features of systemic lupus erythematosus

TitleFamiliality and co-occurrence of clinical features of systemic lupus erythematosus
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
Citation
Arthritis And Rheumatism, 2002, v. 46 n. 10, p. 2678-2685 How to Cite?
AbstractObjective. To evaluate familiality of 15 clinical and laboratory features in systemic lupus erythematosus (SLE)-affected sibpairs, and to estimate correlations with the age at SLE diagnosis in affected sibpairs and parent-offspring pairs. Methods. Concordance rates and sibling risk ratios were used as indicators of familiality for 15 manifestations of SLE. Pearson's correlations and paired t-tests were used to compare the age at SLE diagnosis in affected sibpairs and in parent-offspring pairs. Results. Increased sibling risk ratios (1.9-3.9) for thrombocytopenia, discoid rash, neurologic disorder (defined as seizure or psychosis), and hemolytic anemia were observed in 159 SLE-affected sibpairs. Among these clinical features, paired expression of hemolytic anemia plus thrombocytopenia and hemolytic anemia plus neurologic disorder appeared to be more frequent in 709 SLE patients than would be expected by chance (P < 0.00001 and P < 0.007, respectively). The ratio of the presence of both hemolytic anemia and neurologic disorder was ∼13 times higher in the younger affected sib than in the older affected sib (P < 0.02). Familiality of patient age at SLE diagnosis, as observed by relative correlations, was greater in 125 affected sibpairs (r = 0.67, P < 0.0001) than in 37 affected parent-offspring pairs (r = 0.47, P = 0.003). The median ± SD age at SLE diagnosis was significantly lower in offspring (21.5 ± 10.1 years) than in their parents (41.6 ± 15.8 years) (P < 0.0001) but was not different in sibpairs. The combined non-Caucasian sibpairs had a younger mean age at SLE diagnosis compared with Caucasian sibpairs (P = 0.014). Conclusion. Evidence for familiality of thrombocytopenia, discoid rash, neurologic disorder, hemolytic anemia, and co-occurring neurologic disorder plus hemolytic anemia in SLE was observed in 159 affected sibpairs. Familiality of the age at SLE diagnosis in relative pairs suggests that shared genes and/or shared environmental exposures impact disease susceptibility. Shared immediate environmental triggers appear less compelling, because the average time between dates of diagnosis was 11 years in parent-offspring pairs and 7.5 years in affected sibpairs. The significantly earlier age at disease diagnosis in offspring compared with their parents suggests that some forms of anticipation might play a role in susceptibility to SLE. Stratifying families by subphenotypes that are familial may reduce heterogeneity and facilitate identification of genetic risk factors for SLE.
Persistent Identifierhttp://hdl.handle.net/10722/162639
ISSN
2015 Impact Factor: 8.955
2015 SCImago Journal Rankings: 3.206
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsao, BPen_US
dc.contributor.authorGrossman, JMen_US
dc.contributor.authorRiemekasten, Gen_US
dc.contributor.authorStrong, Nen_US
dc.contributor.authorKalsi, Jen_US
dc.contributor.authorWallace, DJen_US
dc.contributor.authorChen, CJen_US
dc.contributor.authorLau, CSen_US
dc.contributor.authorGinzler, EMen_US
dc.contributor.authorGoldstein, Ren_US
dc.contributor.authorKalunian, KCen_US
dc.contributor.authorHarley, JBen_US
dc.contributor.authorArnett, FCen_US
dc.contributor.authorHahn, BHen_US
dc.contributor.authorCantor, RMen_US
dc.date.accessioned2012-09-05T05:21:57Z-
dc.date.available2012-09-05T05:21:57Z-
dc.date.issued2002en_US
dc.identifier.citationArthritis And Rheumatism, 2002, v. 46 n. 10, p. 2678-2685en_US
dc.identifier.issn0004-3591en_US
dc.identifier.urihttp://hdl.handle.net/10722/162639-
dc.description.abstractObjective. To evaluate familiality of 15 clinical and laboratory features in systemic lupus erythematosus (SLE)-affected sibpairs, and to estimate correlations with the age at SLE diagnosis in affected sibpairs and parent-offspring pairs. Methods. Concordance rates and sibling risk ratios were used as indicators of familiality for 15 manifestations of SLE. Pearson's correlations and paired t-tests were used to compare the age at SLE diagnosis in affected sibpairs and in parent-offspring pairs. Results. Increased sibling risk ratios (1.9-3.9) for thrombocytopenia, discoid rash, neurologic disorder (defined as seizure or psychosis), and hemolytic anemia were observed in 159 SLE-affected sibpairs. Among these clinical features, paired expression of hemolytic anemia plus thrombocytopenia and hemolytic anemia plus neurologic disorder appeared to be more frequent in 709 SLE patients than would be expected by chance (P < 0.00001 and P < 0.007, respectively). The ratio of the presence of both hemolytic anemia and neurologic disorder was ∼13 times higher in the younger affected sib than in the older affected sib (P < 0.02). Familiality of patient age at SLE diagnosis, as observed by relative correlations, was greater in 125 affected sibpairs (r = 0.67, P < 0.0001) than in 37 affected parent-offspring pairs (r = 0.47, P = 0.003). The median ± SD age at SLE diagnosis was significantly lower in offspring (21.5 ± 10.1 years) than in their parents (41.6 ± 15.8 years) (P < 0.0001) but was not different in sibpairs. The combined non-Caucasian sibpairs had a younger mean age at SLE diagnosis compared with Caucasian sibpairs (P = 0.014). Conclusion. Evidence for familiality of thrombocytopenia, discoid rash, neurologic disorder, hemolytic anemia, and co-occurring neurologic disorder plus hemolytic anemia in SLE was observed in 159 affected sibpairs. Familiality of the age at SLE diagnosis in relative pairs suggests that shared genes and/or shared environmental exposures impact disease susceptibility. Shared immediate environmental triggers appear less compelling, because the average time between dates of diagnosis was 11 years in parent-offspring pairs and 7.5 years in affected sibpairs. The significantly earlier age at disease diagnosis in offspring compared with their parents suggests that some forms of anticipation might play a role in susceptibility to SLE. Stratifying families by subphenotypes that are familial may reduce heterogeneity and facilitate identification of genetic risk factors for SLE.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/en_US
dc.relation.ispartofArthritis and Rheumatismen_US
dc.subject.meshAge Of Onseten_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnemia, Hemolytic - Epidemiology - Immunologyen_US
dc.subject.meshAutoantibodies - Blooden_US
dc.subject.meshAutoantigensen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshFamily Healthen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin G - Blooden_US
dc.subject.meshLupus Erythematosus, Systemic - Epidemiology - Genetics - Immunologyen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshParentsen_US
dc.subject.meshRibonucleoproteins, Small Nuclear - Chemistry - Immunologyen_US
dc.subject.meshRisk Factorsen_US
dc.subject.meshSiblingsen_US
dc.subject.meshThrombocytopenia - Epidemiology - Immunologyen_US
dc.subject.meshSnrnp Core Proteinsen_US
dc.titleFamiliality and co-occurrence of clinical features of systemic lupus erythematosusen_US
dc.typeArticleen_US
dc.identifier.emailLau, CS:cslau@hku.hken_US
dc.identifier.authorityLau, CS=rp01348en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/art.10519en_US
dc.identifier.pmid12384927-
dc.identifier.scopuseid_2-s2.0-0036822311en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036822311&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume46en_US
dc.identifier.issue10en_US
dc.identifier.spage2678en_US
dc.identifier.epage2685en_US
dc.identifier.isiWOS:000178633500019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTsao, BP=7005956550en_US
dc.identifier.scopusauthoridGrossman, JM=7202411114en_US
dc.identifier.scopusauthoridRiemekasten, G=6603671625en_US
dc.identifier.scopusauthoridStrong, N=7003697363en_US
dc.identifier.scopusauthoridKalsi, J=7003994115en_US
dc.identifier.scopusauthoridWallace, DJ=7402643779en_US
dc.identifier.scopusauthoridChen, CJ=13612509100en_US
dc.identifier.scopusauthoridLau, CS=14035682100en_US
dc.identifier.scopusauthoridGinzler, EM=7003727930en_US
dc.identifier.scopusauthoridGoldstein, R=7403010472en_US
dc.identifier.scopusauthoridKalunian, KC=7003667407en_US
dc.identifier.scopusauthoridHarley, JB=7201902945en_US
dc.identifier.scopusauthoridArnett, FC=7004819793en_US
dc.identifier.scopusauthoridHahn, BH=7201798489en_US
dc.identifier.scopusauthoridCantor, RM=35375307600en_US

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