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Rheumatoid Arthritis: HELP
Articles by Zhengqiang Luo
Based on 7 articles published since 2010
(Why 7 articles?)

Between 2010 and 2020, Zhen Luo wrote the following 7 articles about Arthritis, Rheumatoid.
+ Citations + Abstracts
1 Review Effects of tofacitinib and other DMARDs on lipid profiles in rheumatoid arthritis: implications for the rheumatologist. 2016

Charles-Schoeman, Christina / Gonzalez-Gay, Miguel A / Kaplan, Irina / Boy, Mary / Geier, Jamie / Luo, Zhen / Zuckerman, Andrea / Riese, Richard. ·University of California, Los Angeles, CA. Electronic address: CCharles@mednet.ucla.edu. · Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain. · Pfizer Inc., Groton, CT. · Pfizer Inc., New York, NY. · Pfizer Inc., Shanghai, China. ·Semin Arthritis Rheum · Pubmed #27079757.

ABSTRACT: Cardiovascular (CV) morbidity and mortality are increased in patients with active, untreated rheumatoid arthritis (RA), despite lower levels of total and low-density lipoprotein cholesterol reported in individuals with active RA compared with those without RA. Alterations in non-traditional lipid assessments, such as high-density lipoprotein (HDL) function and HDL-associated proteins, have been described in patients with active RA, including elevated HDL-associated serum amyloid A and decreased paraoxonase-1 activity. We review changes in both traditional lipoprotein concentrations and non-traditional lipoprotein assessments in multiple studies of treatment with disease-modifying antirheumatic drugs (DMARDs), including non-biologic and biologic DMARDs and tofacitinib. In addition, data from a recently published clinical trial with tofacitinib that describe a potential mechanism for suppression of cholesterol levels in active RA patients are reviewed. Finally, CV event data from various studies of DMARDs are presented, and the current management of RA patients with regard to the CV risk is reviewed.

2 Clinical Trial Efficacy and safety of tofacitinib monotherapy, tofacitinib with methotrexate, and adalimumab with methotrexate in patients with rheumatoid arthritis (ORAL Strategy): a phase 3b/4, double-blind, head-to-head, randomised controlled trial. 2017

Fleischmann, Roy / Mysler, Eduardo / Hall, Stephen / Kivitz, Alan J / Moots, Robert J / Luo, Zhen / DeMasi, Ryan / Soma, Koshika / Zhang, Richard / Takiya, Liza / Tatulych, Svitlana / Mojcik, Christopher / Krishnaswami, Sriram / Menon, Sujatha / Smolen, Josef S / Anonymous2630910. ·University of Texas Southwestern Medical Center and Metroplex Clinical Research Center, Dallas, TX, USA. Electronic address: rfleischmann@arthdocs.com. · Organización Médica de Investigación, Buenos Aires, Argentina. · Department of Medicine, Monash University, Cabrini Health, Malvern, VIC, Australia. · Altoona Center for Clinical Research, Duncansville, PA, USA. · Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK. · Pfizer Inc, Shanghai, China. · Pfizer Inc, Collegeville, PA, USA. · Pfizer Inc, Groton, CT, USA. · Pfizer Inc, New York, NY, USA. · Division of Rheumatology, Department of Medicine 3, Medical University of Vienna, Vienna, Austria. ·Lancet · Pubmed #28629665.

ABSTRACT: BACKGROUND: Tofacitinib is an oral Janus kinase inhibitor for the treatment of rheumatoid arthritis. The Oral Rheumatoid Arthritis triaL (ORAL) Strategy aimed to assess the comparative efficacy of tofacitinib monotherapy, tofacitinib plus methotrexate, and adalimumab plus methotrexate for the treatment of rheumatoid arthritis in patients with a previous inadequate response to methotrexate. METHODS: ORAL Strategy was a 1 year, double-blind, phase 3b/4, head-to-head, non-inferiority, randomised controlled trial in patients aged 18 years or older with active rheumatoid arthritis despite methotrexate therapy. Patients were randomly assigned (1:1:1) to receive oral tofacitinib (5 mg twice daily) monotherapy, oral tofacitinib (5 mg twice daily) plus methotrexate, or subcutaneous adalimumab (40 mg every other week) plus methotrexate at 194 centres in 25 countries. Eligible patients received live zoster vaccine at investigators' discretion. The primary endpoint was the proportion of patients who attained an American College of Rheumatology response of at least 50% (ACR50) at month 6 in the full analysis set (patients who were randomly assigned to a group and received at least one dose of the study treatment). Non-inferiority between groups was shown if the lower bound of the 98·34% CI of the difference between comparators was larger than -13·0%. This trial is registered with ClinicalTrials.gov, number NCT02187055. FINDINGS: 1146 patients received treatment (384 had tofacitinib monotherapy; 376 had tofacitinib and methotrexate; and 386 had adalimumab and methotrexate). At 6 months, ACR50 response was attained in 147 (38%) of 384 patients with tofacitinib monotherapy, 173 (46%) of 376 patients with tofacitinib and methotrexate, and 169 (44%) of 386 patients with adalimumab and methotrexate. Non-inferiority was declared for tofacitinib and methotrexate versus adalimumab and methotrexate (difference 2% [98·34% CI -6 to 11]) but not for tofacitinib monotherapy versus either adalimumab and methotrexate (-6 [-14 to 3]) or tofacitinib and methotrexate (-8 [-16 to 1]). In total, 23 (6%) of 384 patients receiving tofacitinib monotherapy, 26 (7%) of 376 patients receiving tofacitinib plus methotrexate, and 36 (9%) of 386 patients receiving adalimumab plus methotrexate discontinued due to adverse events. Two (1%) of the 384 patients receiving tofacitinib monotherapy died. No new or unexpected safety issues were reported for either treatment in this study for up to 1 year. INTERPRETATION: Tofacitinib and methotrexate combination therapy was non-inferior to adalimumab and methotrexate combination therapy in the treatment of rheumatoid arthritis in patients with an inadequate response to methotrexate in this trial. Tofacitinib monotherapy was not shown to be non-inferior to either combination. FUNDING: Pfizer Inc.

3 Clinical Trial Potential mechanisms leading to the abnormal lipid profile in patients with rheumatoid arthritis versus healthy volunteers and reversal by tofacitinib. 2015

Charles-Schoeman, Christina / Fleischmann, Roy / Davignon, Jean / Schwartz, Howard / Turner, Scott M / Beysen, Carine / Milad, Mark / Hellerstein, Marc K / Luo, Zhen / Kaplan, Irina V / Riese, Richard / Zuckerman, Andrea / McInnes, Iain B. ·University of California, Los Angeles. ·Arthritis Rheumatol · Pubmed #25470338.

ABSTRACT: OBJECTIVE: Tofacitinib is an oral JAK inhibitor for the treatment of rheumatoid arthritis (RA). Systemic inflammation is proposed to play a fundamental role in the altered lipid metabolism associated with RA; however, the underlying mechanisms are unknown. We undertook this study to compare cholesterol and lipoprotein kinetics in patients with active RA with those in matched healthy volunteers. METHODS: This was a phase I open-label mechanism-of-action study. Cholesterol and lipoprotein kinetics were assessed with (13) C-cholesterol and (13) C-leucine infusions. RA patients were reevaluated after receiving oral tofacitinib 10 mg twice daily for 6 weeks. RESULTS: Levels of high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, total cholesterol, and apolipoprotein A-I (Apo A-I) as well as HDL cholesterol particle number were lower in RA patients (n = 36) than in healthy volunteers (n = 33). In contrast, the cholesterol ester fractional catabolic rate was higher in RA patients, but no differences were observed in cholesterol ester transfer protein, cholesterol ester production rate, HDL-associated Apo A-I fractional catabolic rate, or LDL-associated Apo B fractional catabolic rate. Following tofacitinib treatment in RA patients, the cholesterol ester fractional catabolic rate decreased and cholesterol levels increased. The decrease in cholesterol ester fractional catabolic rate correlated significantly with the increase in HDL cholesterol. Additionally, HDL cholesterol particle number increased and markers of HDL cholesterol function improved. CONCLUSION: This is the first study to assess cholesterol and lipoprotein kinetics in patients with active RA and matched healthy volunteers. The data suggest that low cholesterol levels in patients with active RA may be driven by increases in cholesterol ester catabolism. Tofacitinib treatment reduced cholesterol ester catabolism, thereby increasing cholesterol levels toward those in healthy volunteers, and markers of antiatherogenic HDL function improved.

4 Clinical Trial Open-label tofacitinib and double-blind atorvastatin in rheumatoid arthritis patients: a randomised study. 2014

McInnes, Iain B / Kim, Ho-Youn / Lee, Sang-Heon / Mandel, David / Song, Yeong-Wook / Connell, Carol A / Luo, Zhen / Brosnan, M Julia / Zuckerman, Andrea / Zwillich, Samuel H / Bradley, John D. ·Glasgow Biomedical Research Centre, University of Glasgow, , Glasgow, UK. ·Ann Rheum Dis · Pubmed #23482473.

ABSTRACT: OBJECTIVES: To evaluate the efficacy and safety of atorvastatin versus placebo in modifying lipids in patients with rheumatoid arthritis (RA) receiving the oral Janus kinase inhibitor, tofacitinib. METHODS: A randomised, placebo controlled, multicentre phase 2 study, open-label for tofacitinib and blinded for atorvastatin. Patients received tofacitinib 10 mg twice daily for 12 weeks; at week 6, patients were randomly assigned 1:1 to receive oral atorvastatin 10 mg once daily or placebo for 6 weeks. Main outcome measures were lipid moieties, American College of Rheumatology (ACR) response rates, disease activity score in 28 joint counts and safety. RESULTS: 111 patients meeting ACR 1987 RA criteria with active disease were enrolled. Tofacitinib-induced elevation of mean total, low-density lipoprotein (LDL) and high-density lipoprotein-cholesterol, triglycerides and apolipoprotein A-1 concentrations were sustained in placebo recipients to week 12; atorvastatin added at week 6 significantly reduced tofacitinib-associated increases in total and LDL-cholesterol, triglycerides and apolipoprotein B to below week 0 levels. Co-administration of atorvastatin resulted in a significant reduction of LDL-cholesterol versus placebo (primary endpoint; p<0.0001); from week 6 to week 12 the least squares mean reduction was 35.3% with atorvastatin, versus 5.8% increase with placebo. ACR responses were observed with tofacitinib; numerically greater rates were seen with atorvastatin versus placebo. Adverse events were consistent with phase 3 studies. CONCLUSIONS: Tofacitinib-associated elevated total and LDL-cholesterol and triglycerides were rapidly and significantly reduced by atorvastatin. Further investigation is required to explore the significance of reductions in RA disease activity in patients receiving tofacitinib and atorvastatin. (Pfizer protocol A3921109).

5 Article Live Zoster Vaccine in Patients with Rheumatoid Arthritis Treated with Tofacitinib with or without Methotrexate, or Adalimumab with Methotrexate. 2019

Calabrese, Leonard H / Abud-Mendoza, Carlos / Lindsey, Stephen M / Lee, Sang-Heon / Tatulych, Svitlana / Takiya, Liza / Iikuni, Noriko / Soma, Koshika / Luo, Zhen / Fleischmann, Roy. ·Cleveland Clinic Foundation, Cleveland, OH, USA. · Hospital Central, San Luis Potosí, Mexico. · LSU School of Medicine, Baton Rouge, LA, USA. · Konkuk University School of Medicine, Seoul. · Pfizer Inc, Groton, CT, USA. · Pfizer Inc, Collegeville, PA, USA. · Pfizer Inc, New York, NY, USA. · Pfizer Inc, Shanghai, China. · Metroplex Clinical Research Center and University of Texas Southwestern Medical Center, Dallas, TX, USA. ·Arthritis Care Res (Hoboken) · Pubmed #31207152.

ABSTRACT: OBJECTIVE: To explore herpes zoster (HZ) rates, and live zoster vaccine (LZV) safety, in a subset of patients with rheumatoid arthritis (RA) who received LZV before tofacitinib ± methotrexate (MTX), or adalimumab (ADA) + MTX, in ORAL Strategy. METHODS: ORAL Strategy (NCT02187055) was a 1-year, Phase 3b/4, randomized triple-dummy, active-comparator-controlled study. MTX-inadequate responder patients received tofacitinib 5 mg BID, tofacitinib 5 mg BID + MTX, or ADA 40 mg every other week + MTX (1:1:1 randomization). Eligible patients aged ≥50 years could opt to receive LZV 28 days before initiating study treatment. HZ incidence rates (IR; patients with events per 100 patient-years) were calculated. Opportunistic HZ infections (multidermatomal/disseminated), serious HZ events, and LZV-related adverse events, were monitored. RESULTS: In ORAL Strategy, 216/1146 patients (18.8%) received LZV. Overall, 18 patients (1.6%) developed HZ (vaccinated: n=3; non-vaccinated: n=15). HZ IRs (95% CI) were 1.1 (0.3, 2.9), 2.3 (1.0, 4.6), and 1.7 (0.6, 3.7) for tofacitinib monotherapy, tofacitinib + MTX, and ADA + MTX, respectively, and were generally similar between vaccinated and non-vaccinated patients. Three multidermatomal, one disseminated, and two serious HZ events occurred. No vaccinated patients had zoster-like lesions within 42 days of vaccination; one patient had vaccination-site erythema. CONCLUSION: LZV was well tolerated, and HZ IRs were generally similar between treatment groups and vaccinated versus non-vaccinated patients. However, ORAL Strategy was not powered for comparisons between vaccinated and non-vaccinated patients as <20% of all patients were vaccinated. Furthermore, LZV has been shown to be effective only in around 50% of individuals. This article is protected by copyright. All rights reserved.

6 Article NLRP6 facilitates the interaction between TAB2/3 and TRIM38 in rheumatoid arthritis fibroblast-like synoviocytes. 2017

Lin, Yang / Luo, Zhengqiang. ·Department of Orthopedics, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. ·FEBS Lett · Pubmed #28295271.

ABSTRACT: In the present study, we investigated the role of nucleotide oligomerization domain-like receptor family pyrin domain containing 6 (NLRP6) in rheumatoid arthritis (RA) and explored the underlying mechanism. We found that both mRNA and protein levels of NLRP6 are attenuated in synovial tissues and fibroblast-like synoviocytes (FLS) of RA patients compared to patients with osteoarthritis. We also observed that pro-inflammatory cytokine production is decreased and nuclear factor-kappa B activation is inhibited in NLRP6-overexpressing RA-FLS. Furthermore, we found that NLRP6 overexpression promotes transforming growth factor-b-activated kinase 1-binding protein 2/3 lysosome-dependent degradation, and we provide evidence showing that NLRP6 plays the role of providing the docking site to facilitate the interaction between transforming growth factor-b-activated kinase 1-binding protein 2/3 and tripartite motif 38 in RA-FLS.

7 Article Aberrant methylation patterns affect the molecular pathogenesis of rheumatoid arthritis. 2017

Lin, Yang / Luo, Zhengqiang. ·Department of Orthopedics, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, 1095#, Jiefang Ave, Wuhan 430030, PR China. · Department of Orthopedics, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, 1095#, Jiefang Ave, Wuhan 430030, PR China. Electronic address: zhengqiangLuolzhq@126.com. ·Int Immunopharmacol · Pubmed #28282578.

ABSTRACT: This study aims to investigate DNA methylation signatures in fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA), and to explore the relationship with transcription factors (TFs) that help to distinguish RA from osteoarthritis (OA). Microarray dataset of GSE46346, including six FLS samples from patients with RA and five FLS samples from patients with OA, was downloaded from the Gene Expression Omnibus database. RA and OA samples were screened for differentially methylated loci (DMLs). The corresponding differentially methylated genes (DMGs) were identified, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) enrichment analysis. A transcriptional regulatory network was built with TFs and their corresponding DMGs. Overall, 280 hypomethylated loci and 561 hypermethylated loci were screened. Genes containing hypermethylated loci were enriched in pathways in cancer, ECM-receptor interaction, focal adhesion and neurotrophin signaling pathways. Genes containing hypomethylated loci were enriched in the neurotrophin signaling pathway. Moreover, we found that CCCTC-binding factor (CTCF), Yin Yang 1 (YY1), v-myc avian myelocytomatosis viral oncogene homolog (c-MYC), and early growth response 1 (EGR1) were important TFs in the transcriptional regulatory network. Therefore, DMGs might participate in the neurotrophin signaling pathway, pathways in cancer, ECM-receptor interaction and focal adhesion pathways in RA. Furthermore, CTCF, c-MYC, YY1, and EGR1 may play important roles in RA through regulating DMGs.