Familial vs sporadic rheumatoid arthritis (RA). A prospective study in an early RA inception cohort

Radstake, T.R.D.J.; Barrera, Pilar; Albers, Joachim; Swinkels, H.L.; Putte, L. B. A. Van De; Riel, P.L.C.M. van

doi:10.1093/rheumatology/39.3.267

Cited by 25 publications

(22 citation statements)

References 29 publications

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“…For the prospective analysis of demographic and disease characteristics, data from 148 patients and 108 patients at 3 years and 6 years of followup, respectively, were available. For the whole patient group, the distribution of women (67%), IgM-RF positivity (82%), presence of HLA-DR4 (59%), and presence of the SE (65%) was comparable with that in previous studies (30,31). As shown in Table 2, no statistically significant differences in demographic or clinical features were observed, although the level of IgG-CCP antibodies tended to be increased in RA patients carrying the MIF Ϫ173C and/or the MIF CATT 7 allele (P ϭ 0.09 in both cases).…”

Section: Resultssupporting

confidence: 85%

“…To this aim, a staged approach to model building was used, first by entering the known prognostic factors one by one, and then by adding the MIF Ϫ173GϾC and MIF CATT [5][6][7][8] functional variants. On the basis of observations in earlier studies, the following prognostic factors (independent variables) were included in the analysis: presence/absence of RF and IgG-CCP antibodies, HLA-DR4, the SE, and radiologic damage at baseline (30).…”

Section: Methodsmentioning

confidence: 99%

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Correlation of rheumatoid arthritis severity with the genetic functional variants and circulating levels of macrophage migration inhibitory factor

Radstake

Sweep

Welsing

et al. 2005

Arthritis & Rheumatism

190

184

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Objective. To study whether genetic variants of macrophage migration inhibitory factor (MIF), the MIF ؊173G>C and CATT 5-8 alleles, are associated with disease severity and levels of circulating MIF in patients with rheumatoid arthritis (RA).Methods. Genotyping was performed in patients with early RA and in healthy controls. Demographic data, disease activity, and outcome measurements were compared between patients with and without the MIF variants. MIF ؊173G>C and CATT 5-8 polymorphisms were genotyped, and a newly developed enzyme-linked immunosorbent assay for human MIF was used. Allele and genotype distributions of the MIF ؊173G>C and CATT 5-8 polymorphisms were compared between patients and controls by chi-square test. Multiple regression analysis was performed to assess the independence of the MIF functional genetic variants as risk factors for radiologic joint damage.Results. Genotyping of the ؊173G>C and CATT 5-8 polymorphisms of MIF in RA patients and healthy individuals (n ‫؍‬ 277 each) revealed similar frequencies of genotypes and haplotypes in both groups. No significant differences in demographic or clinical features were observed between RA patients carrying the MIF ؊173C allele or the MIF CATT 7 allele or both and noncarrier RA patients. Radiologic joint damage was significantly higher in patients carrying risk alleles of the MIF ؊173G>C or the MIF CATT 5-8 functional variants. No synergistic effects between both genetic variants were observed. Multivariate regression analysis revealed that presence of the MIF ؊173C/C and MIF CATT 7/7 genotypes and having 1 MIF ؊173C allele were independent prognostic variables. Carriership of the MIF ؊173C allele (P ‫؍‬ 0.002) or MIF CATT 7 allele (P ‫؍‬ 0.004) was associated with significantly higher circulating MIF levels compared with those in subjects having none of the risk-conferring alleles, and greater circulating MIF levels correlated with more severe radiologic joint damage (r ‫؍‬ 0.64, P ‫؍‬ 0.001).Conclusion. The MIF polymorphisms are not associated with RA susceptibility but are associated with high levels of radiologic joint damage. High circulating MIF levels were shown to correlate strongly with radiologic joint damage, suggesting that MIF expression is genetically determined and can be used as a novel prognostic tool in RA.

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Section: Resultssupporting

confidence: 85%

Section: Methodsmentioning

confidence: 99%

Correlation of rheumatoid arthritis severity with the genetic functional variants and circulating levels of macrophage migration inhibitory factor

Radstake

Sweep

Welsing

et al. 2005

Arthritis & Rheumatism

190

184

View full text Add to dashboard Cite

show abstract

“…There is a wide range of results on the association between familial RA and radiographic progression. Some studies report a lack of association [17][18][19][20][21][22][23] and others a considerable influence of familial RA on damage progression [24][25][26][27][28][29]. These apparently contradictory results may be explained by differences in the definitions of familial RA and radiographic progression across studies, and in the study designs and statistical methods used ( Table 3).…”

Section: Discussionmentioning

confidence: 99%

Familial disease, the HLA-DRB1 shared epitope and anti-CCP antibodies influence time at appearance of substantial joint damage in rheumatoid arthritis

Rojas-Villarraga

Díaz

Calvo-Páramo

et al. 2009

Journal of Autoimmunity

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“…For the current study we examined the familial clustering of RA disease features utilizing a unique national resource of multicase families. Because some researchers have suggested that the clustering of RA cases within families is an artifact of large sibships (4–6), we also examined the distribution of siblings affected by RA and those without RA within this large sample of multicase families.…”

mentioning

confidence: 99%

Clustering of disease features within 512 multicase rheumatoid arthritis families

Jawaheer¹,

Lum²,

Amos³

et al. 2004

Arthritis & Rheumatism

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Objective. To determine whether specific rheumatoid arthritis (RA) disease features demonstrate the presence of significant familial clustering.Methods. We studied 1,097 individuals with RA from 512 multicase families enrolled in the North American Rheumatoid Arthritis Consortium. All patients were interviewed and examined to collect standardized information about demographic and clinical characteristics. Affected individuals also underwent radiography of the hands and wrists and were genotyped for the HLA-DRB1 shared epitope. Familial clustering of disease features was assessed using contingency table analysis and Pearson correlation coefficients. Multivariate logistic and linear regression analyses were used to account for other characteristics that might influence familial clustering, such as disease duration, sex, and age at diagnosis.Results. Several disease characteristics exhibited significant familial clustering, including seropositivity (multivariate odds ratio [OR] 4.3, P < 0.0001), nodules (OR 2.3, P < 0.0001), and age at RA diagnosis (multivariate regression coefficient [␤] 0.44, P < 0.0001).

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Familial vs sporadic rheumatoid arthritis (RA). A prospective study in an early RA inception cohort

Cited by 25 publications

References 29 publications

Correlation of rheumatoid arthritis severity with the genetic functional variants and circulating levels of macrophage migration inhibitory factor

Correlation of rheumatoid arthritis severity with the genetic functional variants and circulating levels of macrophage migration inhibitory factor

Familial disease, the HLA-DRB1 shared epitope and anti-CCP antibodies influence time at appearance of substantial joint damage in rheumatoid arthritis

Clustering of disease features within 512 multicase rheumatoid arthritis families

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