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85 results on '"Greenberg, J.D."'

3. The National Psoriasis Foundation psoriasis treatment targets in real‐world patients: prevalence and association with patient‐reported outcomes in the Corrona Psoriasis Registry

Author

Merola, J.F., primary, Perez Chada, L.M., additional, Siegel, M., additional, Bagel, J., additional, Evans, C., additional, Lockshin, B., additional, Mason, M., additional, Guo, N., additional, McLean, R.R., additional, Greenberg, J.D., additional, and Van Voorhees, A.S., additional

Published
2020
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4. Association of methotrexate and tumour necrosis factor antagonists with risk of infectious outcomes including opportunistic infections in the CORRONA registry

Author

Greenberg, J.D., Reed, G., Kremer, J.M., Tindall, E., Kavanaugh, A., Zheng, C., Bishai, W., and Hochberg, M.C.

Subjects
Opportunistic infections -- Drug therapy, Opportunistic infections -- Research, Opportunistic infections -- Patient outcomes, Methotrexate -- Dosage and administration, Methotrexate -- Research, Tumor necrosis factor -- Research, Rheumatoid arthritis -- Drug therapy, Rheumatoid arthritis -- Patient outcomes, Rheumatoid arthritis -- Research, Health
Published
2010

5. Elevated liver enzyme tests among patients with rheumatoid arthritis or psoriatic arthritis treated with methotrexate and/or leflunomide

Author

Curtis, J.R., Beukelman, T., Onofrei, A., Cassell, S., Greenberg, J.D., Kavanaugh, A., Reed, G., Strand, V., and Kremer, J.M.

Subjects
Rheumatoid arthritis -- Drug therapy, Rheumatoid arthritis -- Research, Psoriatic arthritis -- Drug therapy, Psoriatic arthritis -- Research, Methotrexate -- Complications and side effects, Methotrexate -- Research, Leflunomide -- Complications and side effects, Leflunomide -- Research, Alanine aminotransferase -- Measurement, Alanine aminotransferase -- Physiological aspects, Alanine aminotransferase -- Research, Aspartate aminotransferase -- Measurement, Aspartate aminotransferase -- Physiological aspects, Aspartate aminotransferase -- Research, Patient monitoring -- Research, Health
Published
2010

6. Methotrexate combined with isoniazid treatment for latent tuberculosis is well tolerated in patients with rheumatoid arthritis: experience from an urban arthritis clinic

Author

Mor, A., C.O. Bingham, III, Kishimoto, M., Izmirly, P.M., Greenberg, J.D., Reddy, S., and Rosenthal, P.B.

Subjects
Methotrexate -- Usage, Methotrexate -- Health aspects, Isoniazid -- Usage, Isoniazid -- Health aspects, Tuberculosis -- Drug therapy, Tuberculosis -- Patient outcomes, Rheumatoid arthritis -- Drug therapy, Rheumatoid arthritis -- Patient outcomes, Drug therapy, Combination -- Usage, Drug therapy, Combination -- Patient outcomes, Health
Published
2008

7. Cardiovascular outcomes in high risk patients with osteoarthritis treated with ibuprofen, naproxen and lumiracoxib

Author

Farkouh, M.E., Greenberg, J.D., Jeger, R.V., Ramanathan, K., Verheugt, F.W.A., Chesebro, J.H., Kirshner, H., Hochman, J.S., Lay, C.L., Ruland, S., Mellein, B., Matchaba, P.T., Fuster, V., and Abramson, S.B.

Subjects
Osteoarthritis -- Care and treatment, Osteoarthritis -- Complications and side effects, Ibuprofen -- Complications and side effects, Naproxen -- Complications and side effects, Lumiracoxib -- Complications and side effects, Cardiovascular diseases -- Risk factors, Cardiovascular diseases -- Patient outcomes, Cardiovascular diseases -- Research, Health
Published
2007

8. Utilization of the validated Psoriasis Epidemiology Screening Tool to identify signs and symptoms of psoriatic arthritis among those with psoriasis: a cross‐sectional analysis from the US ‐based Corrona Psoriasis Registry

Author

Mease, P.J., primary, Palmer, J.B., additional, Hur, P., additional, Strober, B.E., additional, Lebwohl, M., additional, Karki, C., additional, Reed, G.W., additional, Etzel, C.J., additional, Greenberg, J.D., additional, and Helliwell, P. S., additional

Published
2019
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12. The Role of Rare Protein-Coding Variants in Anti-Tumor Necrosis Factor Treatment Response in Rheumatoid Arthritis

Author

Cui, J., Diogo, D., Stahl, E.A., Canhao, H., Mariette, X., Greenberg, J.D., Okada, Y., Pappas, D.A., Fulton, R.S., Tak, P.P., Nurmohamed, M.T., Lee, A., Larson, D.E., Kurreeman, F., Deluca, T.L., O'Laughlin, M., Fronick, C.C., Fulton, L.L., Mardis, E.R., Horst-Bruinsma, I.E. van der, Wolbink, G.J., Gregersen, P.K., Kremer, J.M., Crusius, J.B.A., Vries, N. de, Huizinga, T.W.J., Fonseca, J.E., Miceli-Richard, C., Karlson, E.W., Coenen, M.J.H., Barton, A., Plenge, R.M., and Raychaudhuri, S.

Published
2017

16. Brief Report: The Role of Rare Protein-Coding Variants in Anti-Tumor Necrosis Factor Treatment Response in Rheumatoid Arthritis

Author

Cui, J., Diogo, D., Stahl, E.A., Canhao, H., Mariette, X., Greenberg, J.D., Okada, Y., Pappas, D.A., Fulton, R.S., Tak, P.P., Nurmohamed, M.T., Lee, A., Larson, D.E., Kurreeman, F., Deluca, T.L., O'Laughlin, M., Fronick, C.C., Fulton, L.L., Mardis, E.R., Horst-Bruinsma, I.E., Wolbink, G.J., Gregersen, P.K., Kremer, J.M, Crusius, J.B.A., Vries, N. de, Huizinga, T.W.J., Fonseca, J.E., Miceli-Richard, C., Karlson, E.W., Coenen, M.J.H., Barton, A., Plenge, R.M., Raychaudhuri, S., Cui, J., Diogo, D., Stahl, E.A., Canhao, H., Mariette, X., Greenberg, J.D., Okada, Y., Pappas, D.A., Fulton, R.S., Tak, P.P., Nurmohamed, M.T., Lee, A., Larson, D.E., Kurreeman, F., Deluca, T.L., O'Laughlin, M., Fronick, C.C., Fulton, L.L., Mardis, E.R., Horst-Bruinsma, I.E., Wolbink, G.J., Gregersen, P.K., Kremer, J.M, Crusius, J.B.A., Vries, N. de, Huizinga, T.W.J., Fonseca, J.E., Miceli-Richard, C., Karlson, E.W., Coenen, M.J.H., Barton, A., Plenge, R.M., and Raychaudhuri, S.

Abstract

Item does not contain fulltext, OBJECTIVE: In many rheumatoid arthritis (RA) patients, disease is controlled with anti-tumor necrosis factor (anti-TNF) biologic therapies. However, in a significant number of patients, the disease fails to respond to anti-TNF therapy. We undertook the present study to examine the hypothesis that rare and low-frequency genetic variants might influence response to anti-TNF treatment. METHODS: We sequenced the coding region of 750 genes in 1,094 RA patients of European ancestry who were treated with anti-TNF. After quality control, 690 genes were included in the analysis. We applied single-variant association and gene-based association tests to identify variants associated with anti-TNF treatment response. In addition, given the key mechanistic role of TNF, we performed gene set analyses of 27 TNF pathway genes. RESULTS: We identified 14,420 functional variants, of which 6,934 were predicted as nonsynonymous 2,136 of which were further predicted to be "damaging." Despite the fact that the study was well powered, no single variant or gene showed study-wide significant association with change in the outcome measures disease activity or European League Against Rheumatism response. Intriguingly, we observed 3 genes, of 27 with nominal signals of association (P < 0.05), that were involved in the TNF signaling pathway. However, when we performed a rigorous gene set enrichment analysis based on association P value ranking, we observed no evidence of enrichment of association at genes involved in the TNF pathway (Penrichment = 0.15, based on phenotype permutations). CONCLUSION: Our findings suggest that rare and low-frequency protein-coding variants in TNF signaling pathway genes or other genes do not contribute substantially to anti-TNF treatment response in patients with RA.

Published
2017

32. TYK2 protein-coding variants protect against rheumatoid arthritis and autoimmunity, with no evidence of major pleiotropic effects on non-autoimmune complex traits

Author

Diogo, D., Bastarache, L., Liao, K.P., Graham, R.R., Fulton, R.S., Greenberg, J.D., Eyre, S., Bowes, J., Cui, J., Lee, A., Pappas, D.A., Kremer, H., Barton, A., Coenen, M.J.H., Franke, B., Kiemeney, L.A.L.M., Mariette, X., Richard-Miceli, C., Canhao, H., Fonseca, J.E., Vries, N. de, Tak, P.P., Crusius, J.B.A., Nurmohamed, M.T., Kurreeman, F., Mikuls, T.R., Okada, Y., Stahl, E.A., Larson, D.E., Deluca, T.L., O'Laughlin, M., Fronick, C.C., Fulton, L.L., Kosoy, R., Ransom, M., Bhangale, T.R., Ortmann, W., Cagan, A., Gainer, V., Karlson, E.W., Kohane, I., Murphy, S.N., Martin, J., Zhernakova, A., Klareskog, L., Padyukov, L., Worthington, J., Mardis, E.R., Seldin, M.F., Gregersen, P.K., Behrens, T., Raychaudhuri, S., Denny, J.C., Plenge, R.M., Diogo, D., Bastarache, L., Liao, K.P., Graham, R.R., Fulton, R.S., Greenberg, J.D., Eyre, S., Bowes, J., Cui, J., Lee, A., Pappas, D.A., Kremer, H., Barton, A., Coenen, M.J.H., Franke, B., Kiemeney, L.A.L.M., Mariette, X., Richard-Miceli, C., Canhao, H., Fonseca, J.E., Vries, N. de, Tak, P.P., Crusius, J.B.A., Nurmohamed, M.T., Kurreeman, F., Mikuls, T.R., Okada, Y., Stahl, E.A., Larson, D.E., Deluca, T.L., O'Laughlin, M., Fronick, C.C., Fulton, L.L., Kosoy, R., Ransom, M., Bhangale, T.R., Ortmann, W., Cagan, A., Gainer, V., Karlson, E.W., Kohane, I., Murphy, S.N., Martin, J., Zhernakova, A., Klareskog, L., Padyukov, L., Worthington, J., Mardis, E.R., Seldin, M.F., Gregersen, P.K., Behrens, T., Raychaudhuri, S., Denny, J.C., and Plenge, R.M.

Abstract

Contains fulltext : 154077.pdf (publisher's version ) (Open Access), Despite the success of genome-wide association studies (GWAS) in detecting a large number of loci for complex phenotypes such as rheumatoid arthritis (RA) susceptibility, the lack of information on the causal genes leaves important challenges to interpret GWAS results in the context of the disease biology. Here, we genetically fine-map the RA risk locus at 19p13 to define causal variants, and explore the pleiotropic effects of these same variants in other complex traits. First, we combined Immunochip dense genotyping (n = 23,092 case/control samples), Exomechip genotyping (n = 18,409 case/control samples) and targeted exon-sequencing (n = 2,236 case/controls samples) to demonstrate that three protein-coding variants in TYK2 (tyrosine kinase 2) independently protect against RA: P1104A (rs34536443, OR = 0.66, P = 2.3 x 10(-21)), A928V (rs35018800, OR = 0.53, P = 1.2 x 10(-9)), and I684S (rs12720356, OR = 0.86, P = 4.6 x 10(-7)). Second, we show that the same three TYK2 variants protect against systemic lupus erythematosus (SLE, Pomnibus = 6 x 10(-18)), and provide suggestive evidence that two of the TYK2 variants (P1104A and A928V) may also protect against inflammatory bowel disease (IBD; P(omnibus) = 0.005). Finally, in a phenome-wide association study (PheWAS) assessing >500 phenotypes using electronic medical records (EMR) in >29,000 subjects, we found no convincing evidence for association of P1104A and A928V with complex phenotypes other than autoimmune diseases such as RA, SLE and IBD. Together, our results demonstrate the role of TYK2 in the pathogenesis of RA, SLE and IBD, and provide supporting evidence for TYK2 as a promising drug target for the treatment of autoimmune diseases.

Published
2015

36. AB1157 Characteristics of a US Psoriatic Arthritis/Spondyloarthritis Cohort: Baseline Data from the Corrona PSA/SPA Registry

Author

Mease, P.J., primary, Etzel, C.J., additional, Kremer, J.M., additional, Deveikis, S., additional, Li, Y., additional, O'Connor, J., additional, Kavanaugh, A., additional, Ruderman, E., additional, Curtis, J.R., additional, Ritchlin, C.T., additional, van der Heijde, D., additional, Solomon, D., additional, and Greenberg, J.D., additional

Published
2015
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40. Genetics of rheumatoid arthritis contributes to biology and drug discovery

Author

Okada, Y., Wu, D., Trynka, G., Raj, T., Terao, C., Ikari, K., Kochi, Y., Ohmura, K., Suzuki, A., Yoshida, S., Graham, R.R., Manoharan, A., Ortmann, W., Bhangale, T., Denny, J.C., Carroll, R.J., Eyler, A.E., Greenberg, J.D., Kremer, J.M, Pappas, D.A., Jiang, L., Yin, J., Ye, L, Su, D.F., Yang, J., Xie, G., Keystone, E., Westra, H.J., Esko, T., Metspalu, A., Zhou, X., Gupta, N., Mirel, D., Stahl, E.A., Diogo, D., Cui, J., Liao, K., Guo, M.H., Myouzen, K., Kawaguchi, T., Coenen, M.J.H., Riel, P.L.C.M. van, Laar, M.A. van der, Guchelaar (LUMC), H.J., Huizinga, T.W.J., Dieude, P., Mariette, X., Bridges, S.L., Jr., Zhernakova, A., Toes, R.E., Tak, P.P., Miceli-Richard, C., Bang, S.Y., Lee, H.S., Martin, J., Gonzalez-Gay, M.A., Rodriguez-Rodriguez, L., Rantapaa-Dahlqvist, S., Arlestig, L., Choi, H.K., Kamatani, Y., Galan, P., Lathrop, M., Eyre, S., Bowes, J., Barton, A., Vries, N. de, Moreland, L.W., Criswell, L.A., Karlson, E.W., Taniguchi, A., Yamada, R., Kubo, M., Liu, J.S., Bae, S.C., Worthington, J., Padyukov, L., Klareskog, L., Gregersen, P.K., Raychaudhuri, S., Stranger, B.E., Jager, P.L. De, Franke, L., Visscher, P.M., Brown, M.A., Yamanaka, H., Mimori, T., Takahashi, A., Xu, H., Behrens, T.W., Siminovitch, K.A., Momohara, S., Matsuda, F., Yamamoto, K., Plenge, R.M., et al., Okada, Y., Wu, D., Trynka, G., Raj, T., Terao, C., Ikari, K., Kochi, Y., Ohmura, K., Suzuki, A., Yoshida, S., Graham, R.R., Manoharan, A., Ortmann, W., Bhangale, T., Denny, J.C., Carroll, R.J., Eyler, A.E., Greenberg, J.D., Kremer, J.M, Pappas, D.A., Jiang, L., Yin, J., Ye, L, Su, D.F., Yang, J., Xie, G., Keystone, E., Westra, H.J., Esko, T., Metspalu, A., Zhou, X., Gupta, N., Mirel, D., Stahl, E.A., Diogo, D., Cui, J., Liao, K., Guo, M.H., Myouzen, K., Kawaguchi, T., Coenen, M.J.H., Riel, P.L.C.M. van, Laar, M.A. van der, Guchelaar (LUMC), H.J., Huizinga, T.W.J., Dieude, P., Mariette, X., Bridges, S.L., Jr., Zhernakova, A., Toes, R.E., Tak, P.P., Miceli-Richard, C., Bang, S.Y., Lee, H.S., Martin, J., Gonzalez-Gay, M.A., Rodriguez-Rodriguez, L., Rantapaa-Dahlqvist, S., Arlestig, L., Choi, H.K., Kamatani, Y., Galan, P., Lathrop, M., Eyre, S., Bowes, J., Barton, A., Vries, N. de, Moreland, L.W., Criswell, L.A., Karlson, E.W., Taniguchi, A., Yamada, R., Kubo, M., Liu, J.S., Bae, S.C., Worthington, J., Padyukov, L., Klareskog, L., Gregersen, P.K., Raychaudhuri, S., Stranger, B.E., Jager, P.L. De, Franke, L., Visscher, P.M., Brown, M.A., Yamanaka, H., Mimori, T., Takahashi, A., Xu, H., Behrens, T.W., Siminovitch, K.A., Momohara, S., Matsuda, F., Yamamoto, K., Plenge, R.M., and et al.

Abstract

Item does not contain fulltext, A major challenge in human genetics is to devise a systematic strategy to integrate disease-associated variants with diverse genomic and biological data sets to provide insight into disease pathogenesis and guide drug discovery for complex traits such as rheumatoid arthritis (RA). Here we performed a genome-wide association study meta-analysis in a total of >100,000 subjects of European and Asian ancestries (29,880 RA cases and 73,758 controls), by evaluating approximately 10 million single-nucleotide polymorphisms. We discovered 42 novel RA risk loci at a genome-wide level of significance, bringing the total to 101 (refs 2 - 4). We devised an in silico pipeline using established bioinformatics methods based on functional annotation, cis-acting expression quantitative trait loci and pathway analyses--as well as novel methods based on genetic overlap with human primary immunodeficiency, haematological cancer somatic mutations and knockout mouse phenotypes--to identify 98 biological candidate genes at these 101 risk loci. We demonstrate that these genes are the targets of approved therapies for RA, and further suggest that drugs approved for other indications may be repurposed for the treatment of RA. Together, this comprehensive genetic study sheds light on fundamental genes, pathways and cell types that contribute to RA pathogenesis, and provides empirical evidence that the genetics of RA can provide important information for drug discovery.

Published
2014

47. SAT0134 Prevalence of Cardiovascular Risk Factors and Cardiovascular Disease in Rheumatoid Arthritis Patients across International Regions: A Comparison of the Corrona International and Corrona US Registries

Author

Pappas, D.A., primary, Lampl, K., additional, Kremer, J.M., additional, Radominski, S.C., additional, Gal, J., additional, Nyberg, F., additional, Malaviya, A., additional, Whitworth, A., additional, Rillo, O.L., additional, Gibofsky, A., additional, Popkova, T.V., additional, Ho, M., additional, Laurindo, I., additional, Reed, G.W., additional, Kerzberg, E.M., additional, Horne, L., additional, Zahora, R., additional, Saunders, K.C., additional, Pons-Estel, B.A., additional, Onofrei, A.U., additional, and Greenberg, J.D., additional

Published
2014
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48. THU0179 Cross-National Comparison of Biological Disease-Modifying Antirheumatic Drug Discontinuation Practice among Rheumatoid Arthritis Patients in Remission: Corrona and Ninja Collaboration

Author

Yoshida, K., primary, Radner, H., additional, Mjaavatten, M.D., additional, Greenberg, J.D., additional, Kavanaugh, A., additional, Kishimoto, M., additional, Matsui, K., additional, Okada, M., additional, Reed, G., additional, Saeki, Y., additional, Tohma, S., additional, Kremer, J., additional, and Solomon, D.H., additional

Published
2014
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50. FRI0052 Variations in Disease Activity and Therapeutic Management of Rheumatoid Arthritis in Different International Regions: A Comparison of Data from the Corrona International and Corrona US Registries

Author

Pappas, D.A., primary, Lampl, K., additional, Kremer, J.M., additional, Radominski, S.C., additional, Gal, J., additional, Nyberg, F., additional, Malaviya, A., additional, Whitworth, A., additional, Rillo, O., additional, Gibofsky, A., additional, Popkova, T., additional, Ho, M., additional, Laurindo, I., additional, Reed, G.W., additional, Kerzberg, E.M., additional, Horne, L., additional, Zahora, R., additional, Saunders, K.C., additional, Pons-Estel, B.A., additional, Onofrei, A.U., additional, and Greenberg, J.D., additional

Published
2014
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