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Systemic Lupus Erythematosus: HELP
Articles by Michael H. Weisman
Based on 58 articles published since 2009
(Why 58 articles?)
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Between 2009 and 2019, M. Weisman wrote the following 58 articles about Lupus Erythematosus, Systemic.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3
1 Editorial Editorial: The Effect of Ethnicity on Cardiovascular Outcomes in Systemic Lupus Erythematosus Is Perhaps Not a Paradox. 2017

Pope, Janet E / Weisman, Michael H / Sjöwall, Christopher. ·University of Western Ontario, St. Joseph's Health Care, London, Ontario, Canada. · Cedars-Sinai Medical Center, Los Angeles, California. · Linköping University, Linköping, Sweden. ·Arthritis Rheumatol · Pubmed #28598003.

ABSTRACT: -- No abstract --

2 Editorial Disparities in renal replacement in lupus nephritis: current practice and future implications. 2011

Ishimori, Mariko L / Gudsoorkar, Vineet / Venuturupalli, Swamy R / Weisman, Michael H. · ·Arthritis Care Res (Hoboken) · Pubmed #22127964.

ABSTRACT: -- No abstract --

3 Review New insights into mechanisms of therapeutic effects of antimalarial agents in SLE. 2012

Wallace, Daniel J / Gudsoorkar, Vineet S / Weisman, Michael H / Venuturupalli, Swamy R. ·Division of Rheumatology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Becker B-131, Los Angeles, CA 90048, USA. dwallace@ucla.edu ·Nat Rev Rheumatol · Pubmed #22801982.

ABSTRACT: Antimalarial agents have routinely been used for the treatment of systemic lupus erythematosus (SLE) for over 50 years. These agents continue to enjoy success as the initial pharmacotherapy for SLE even in the era of targeted therapies. Antimalarial agents have numerous biological effects that are responsible for their immunomodulatory actions in SLE. Their inhibitory effect on Toll-like receptor-mediated activation of the innate immune response is perhaps the most important discovery regarding their putative mechanism of action, but some other, previously known properties, such as antithrombotic and antilipidaemic effects, are now explained by new research. In the 1980s and 1990s, these antihyperlipidaemic and antithrombotic effects were demonstrated in retrospective clinical studies, and over the past few years prospective studies have confirmed those findings. Knowledge about the risk-benefit profile of antimalarial agents during pregnancy and lactation has evolved, as has the concept of retinal toxicity. Antimalarial agents have unique disease-modifying properties in SLE and newer iterations of this class of anti-inflammatory agents will have a profound effect upon the treatment of autoimmune disease.

4 Review Review: Male systemic lupus erythematosus: a review of sex disparities in this disease. 2010

Lu, L-J / Wallace, D J / Ishimori, M L / Scofield, R H / Weisman, M H. ·Cedars Sinai Medical Center, Los Angeles, California 90048, USA. ·Lupus · Pubmed #19946032.

ABSTRACT: Although males with systemic lupus erythematosus (SLE) represent 4-22% of all SLE patients, it may not be appropriate that these cases should be subordinated to females with SLE in terms of most health-related issues. Over the past few decades, some distinctive features of male lupus have been observed with regard to genetic and environmental aspects of sex differences, clinical features, and outcome. In addition, recent insights into sex disparities in this disease have brought forth a few plausible and novel pathogenetic hypotheses. This review discusses these findings and sex disparities in SLE that appear to be especially noteworthy and pertinent to our understanding of male SLE.

5 Clinical Trial Treatment of systemic lupus erythematosus patients with the BAFF antagonist "peptibody" blisibimod (AMG 623/A-623): results from randomized, double-blind phase 1a and phase 1b trials. 2015

Stohl, William / Merrill, Joan T / Looney, R John / Buyon, Jill / Wallace, Daniel J / Weisman, Michael H / Ginzler, Ellen M / Cooke, Blaire / Holloway, Donna / Kaliyaperumal, Arunan / Kuchimanchi, Kameswara Rao / Cheah, Tsui Chern / Rasmussen, Erik / Ferbas, John / Belouski, Shelley S / Tsuji, Wayne / Zack, Debra J. ·Los Angeles County and University of Southern California Medical Center and University of Southern California Keck School of Medicine, 1975 Zonal Ave., Los Angeles, CA, 90033, USA. stohl@usc.edu. · Division of Rheumatology, Los Angeles County + University of Southern California Medical Center and Keck School of Medicine of the University of Southern California, 2011 Zonal Ave., Los Angeles, CA, 90033, USA. stohl@usc.edu. · Oklahoma Medical Research Foundation, 825 NE 13th St., Oklahoma City, OK, 73104, USA. JTMmail@aol.com. · University of Rochester, 252 Elmwood Ave., Rochester, NY, 14627, USA. John_Looney@URMC.Rochester.edu. · Hospital for Joint Disease, 301 E 17th St., New York, NY, 10003, USA. Jbuyonic@aol.com. · Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA, 90048, USA. drdanielwallace@gmail.com. · Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA, 90048, USA. Michael.Weisman@cshs.org. · SUNY Downstate Medical Center, 450 Clarkson Ave., Brooklyn, NY, 11203, USA. ELLEN.GINZLER@downstate.edu. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. bcooke@amgen.com. · Formerly of Amgen, Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. donnalholloway@yahoo.com. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. arunank@amgen.com. · Formerly of Amgen, Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. Kamesh.Kuchimanchi@baxalta.com. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. tcheah@amgen.com. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. hansr@amgen.com. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. jferbas@amgen.com. · Formerly of Amgen, Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. sbelouski@yahoo.com. · Amgen Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. tsujiw@amgen.com. · Formerly of Amgen, Inc., 1 Amgen Center Dr., Thousand Oaks, CA, 91320, USA. djzk3tk@msn.com. ·Arthritis Res Ther · Pubmed #26290435.

ABSTRACT: INTRODUCTION: Blisibimod is a potent B cell-activating factor (BAFF) antagonist that binds to both cell membrane-expressed and soluble BAFF. The goal of these first-in-human studies was to characterize the safety, tolerability, and pharmacokinetic and pharmacodynamic profiles of blisibimod in subjects with systemic lupus erythematosus (SLE). METHODS: SLE subjects with mild disease that was stable/inactive at baseline received either a single dose of blisibimod (0.1, 0.3, 1, or 3 mg/kg subcutaneous [SC] or 1, 3, or 6 mg/kg intravenous [IV]) or placebo (phase 1a; N = 54), or four weekly doses of blisibimod (0.3, 1, or 3 mg/kg SC or 6 mg/kg IV) or placebo (phase 1b; N = 63). Safety and tolerability measures were collected, and B cell subset measurements and pharmacokinetic analyses were performed. RESULTS: All subjects (93 % female; mean age 43.7 years) carried the diagnosis of SLE for ≥ 1 year. Single- and multiple-dose treatment with blisibimod produced a decrease in the number of naïve B cells (24-76 %) and a transient relative increase in the memory B cell compartment, with the greatest effect on IgD(-)CD27+; there were no notable changes in T cells or natural killer cells. With time, memory B cells reverted to baseline, leading to a calculated 30 % reduction in total B cells by approximately 160 days after the first dose. In both the single- and multiple-dosing SC cohorts, the pharmacokinetic profile indicated slow absorption, dose-proportional exposure from 0.3 through 3.0 mg/kg SC and 1 through 6 mg/kg IV, linear pharmacokinetics across the dose range of 1.0-6.0 mg/kg, and accumulation ratios ranging from 2.21 to 2.76. The relative increase in memory B cells was not associated with safety signals, and the incidence of adverse events, anti-blisibimod antibodies, and clinical laboratory abnormalities were comparable between blisibimod- and placebo-treated subjects. CONCLUSIONS: Blisibimod changed the constituency of the B cell pool and single and multiple doses of blisibimod exhibited approximate dose-proportional pharmacokinetics across the dose range 1.0-6.0 mg/kg. The safety and tolerability profile of blisibimod in SLE was comparable with that of placebo. These findings support further studies of blisibimod in SLE and other B cell-mediated diseases. TRIAL REGISTRATION: Clinicaltrials.gov NCT02443506 . Registered 11 May 2015. NCT02411136 Registered 7 April 2015.

6 Article Serologic features of cohorts with variable genetic risk for systemic lupus erythematosus. 2018

Bhattacharya, Jyotsna / Pappas, Karalyn / Toz, Bahtiyar / Aranow, Cynthia / Mackay, Meggan / Gregersen, Peter K / Doumbo, Ogobara / Traore, Abdel Kader / Lesser, Martin L / McMahon, Maureen / Utset, Tammy / Silverman, Earl / Levy, Deborah / McCune, William J / Jolly, Meenakshi / Wallace, Daniel / Weisman, Michael / Romero-Diaz, Juanita / Diamond, Betty. ·The Feinstein Institute for Medical Research, Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, 350 Community Dr, Manhasset, NY, 11030, USA. · Department of Statistical Science, Cornell University, Ithaca, NY, USA. · Department of Internal Medicine, Istanbul University, Istanbul, Turkey. · The Feinstein Institute for Medical Research, Center for Genomics and Human Genetics, Manhasset, NY, USA. · Malaria Research and Training Center, Bamako, Mali. · Deputy of the Department of Internal Medicine, University Hospital, Bamako, Mali. · The Feinstein Institute for Medical Research, Center of Biostatistics Unit Manhasset, Manhasset, NY, USA. · UCLA David Geffen School of Medicine, Los Angeles, CA, 90095, USA. · University of Chicago Medical Center, Chicago, IL, USA. · Hospital for Sick Children, University of Toronto, Toronto, ON M5G, 1X8, Canada. · University of Michigan, Ann Arbor, MI, 48109, USA. · Rush University Medical Center, Chicago, IL, 60612, USA. · Cedars Sinai Medical Center, Los Angeles, CA, 90048, USA. · Instituto Nacional de Ciencias Medicas y Nutrician Salvador Zubiran, Mexico City, Mexico. · The Feinstein Institute for Medical Research, Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, 350 Community Dr, Manhasset, NY, 11030, USA. bdiamond@northwell.edu. ·Mol Med · Pubmed #30134810.

ABSTRACT: BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease with genetic, hormonal, and environmental influences. In Western Europe and North America, individuals of West African descent have a 3-4 fold greater incidence of SLE than Caucasians. Paradoxically, West Africans in sub-Saharan Africa appear to have a low incidence of SLE, and some studies suggest a milder disease with less nephritis. In this study, we analyzed sera from African American female SLE patients and four other cohorts, one with SLE and others with varying degrees of risk for SLE in order to identify serologic factors that might correlate with risk of or protection against SLE. METHODS: Our cohorts included West African women with previous malaria infection assumed to be protected from development of SLE, clinically unaffected sisters of SLE patients with high risk of developing SLE, healthy African American women with intermediate risk, healthy Caucasian women with low risk of developing SLE, and women with a diagnosis of SLE. We developed a lupus risk index (LRI) based on titers of IgM and IgG anti-double stranded DNA antibodies and levels of C1q. RESULTS: The risk index was highest in SLE patients; second highest in unaffected sisters of SLE patients; third highest in healthy African-American women and lowest in healthy Caucasian women and malaria-exposed West African women. CONCLUSION: This risk index may be useful in early interventions to prevent SLE. In addition, it suggests new therapeutic approaches for the treatment of SLE.

7 Article Psychometric validation of the Arthritis Helplessness Index in systemic lupus erythematosus. 2018

Gholizadeh, S / Azizoddin, D R / Mills, S D / Zamora-Racaza, G / Potemra, H M K / Wallace, D J / Weisman, M H / Nicassio, P M. ·1 SDSU/UC San Diego Joint Doctoral Program in Clinical Psychology, USA. · 2 School of Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University, USA. · 3 Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, USA. · 4 Department of Medicine, University of the Philippines - Philippine General Hospital, Philippines. · 5 Department of Psychology, University of California, Los Angeles, USA. · 6 Division of Rheumatology, Cedars-Sinai Medical Center, USA. · 7 Cousins Center for Psychoneuroimmunology, University of California, Los Angeles, USA. ·Lupus · Pubmed #30111237.

ABSTRACT: Objective Helplessness is a relevant construct in systemic lupus erythematosus (SLE), an unpredictable chronic illness with no known cure characterized by relapsing and remitting features. However, no measure of helplessness has been validated in this population. The present study examined the structural validity, reliability, and convergent validity of the Arthritis Helplessness Index, a measure initially developed for rheumatoid arthritis populations, in a sample of patients with SLE. Methods Patients with SLE ( N = 136) receiving medical care at a private hospital completed the Arthritis Helplessness Index and other self-report measures. The structural validity of the Arthritis Helplessness Index was examined using confirmatory factor analysis. Internal consistency reliability was evaluated with Cronbach's coefficient alpha. Pearson product-moment correlations were used to examine convergent validity with measures of depression, anxiety and mastery. Results The five-item Arthritis Helplessness Index-Helplessness measure demonstrated a tenable factor structure (comparative fit index 0.98, root mean square error of approximation 0.06, standardized root mean residual 0.04). Internal consistency reliability was fair (α = 0.69). Convergent validity was evidenced by significant correlations with measures of depression, anxiety and mastery. Conclusion The five-item Arthritis Helplessness Index-Helplessness scale can confidently be used as a measure of helplessness in SLE.

8 Article Genetic fine mapping of systemic lupus erythematosus MHC associations in Europeans and African Americans. 2018

Hanscombe, Ken B / Morris, David L / Noble, Janelle A / Dilthey, Alexander T / Tombleson, Philip / Kaufman, Kenneth M / Comeau, Mary / Langefeld, Carl D / Alarcon-Riquelme, Marta E / Gaffney, Patrick M / Jacob, Chaim O / Sivils, Kathy L / Tsao, Betty P / Alarcon, Graciela S / Brown, Elizabeth E / Croker, Jennifer / Edberg, Jeff / Gilkeson, Gary / James, Judith A / Kamen, Diane L / Kelly, Jennifer A / McCune, Joseph / Merrill, Joan T / Petri, Michelle / Ramsey-Goldman, Rosalind / Reveille, John D / Salmon, Jane E / Scofield, Hal / Utset, Tammy / Wallace, Daniel J / Weisman, Michael H / Kimberly, Robert P / Harley, John B / Lewis, Cathryn M / Criswell, Lindsey A / Vyse, Timothy J. ·Department of Medical and Molecular Genetics, King's College London, London, UK. · CHORI, Children's Hospital Oakland Research Institute, Oakland, California, USA. · Wellcome Trust Centre for Human Genetics, University of Oxford, UK. · Center for Autoimmune Genomics and Etiology (CAGE), Department of Pediatrics, Cincinnati Children's Medical Center & University of Cincinnati and the US Department of Veterans Affairs Medical Center, Cincinnati, OH, USA. · Center for Public Health Genomics, Wake Forest School of Medicine, Winston-Salem, NC, USA. · Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research (GENYO), Granada, Spain. · Unit of Chronic Inflammation, Institute of Environmental Medicine, Karolinska Institute, Sweden. · Arthritis & Clinical Immunology Research Program, Division of Genomics and Data Sciences, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. · Keck School of Medicine of USC, Los Angeles, CA, USA. · Department of Medicine, Medical University of South Carolina, Charleston, SC, USA. · Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, USA. · Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA. · Center for Clinical and Translational Science, University of Alabama at Birmingham, Birmingham, AL, USA. · Division of Rheumatology, Medical University of South Carolina, Charleston, SC, USA. · Division of Rheumatology, Cedars Sinai Medical Center, Los Angeles, CA, USA. · Michigan Medicine Rheumatology Clinic,Taubman Center Floor 3 Reception A, 1500 E Medical Center Dr SPC 5358, Ann Arbor, MI, USA. · Oklahoma Medical Research Foundation,825 N.E. 13th Street, Oklahoma City, OK, USA. · Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. · Feinberg School of Medicine,McGaw Pavilion Suite M-300, 240 E Huron, Chicago, IL, USA. · Department of Internal Medicine, The University of Texas, Fannin, MSB, Houston, TX, USA. · Division of Rheumatology, Hospital for Special Surgery-Weill Cornell Medicine, New York, NY, USA. · Oklahoma Clinical and Translational Science Institute,University of Oklahoma Health Sciences Center, 920 NE Stanton L. Young, Oklahoma City, OK, USA. · University of Chicago Pritzker School of Medicine, Chicago, IL, USA. · MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK. · Rosalind Russell / Ephraim P Engleman Rheumatology Research Center, Division of Rheumatology, UCSF School of Medicine, San Francisco, CA, USA. ·Hum Mol Genet · Pubmed #30085094.

ABSTRACT: Genetic variation within the major histocompatibility complex (MHC) contributes substantial risk for systemic lupus erythematosus, but high gene density, extreme polymorphism and extensive linkage disequilibrium (LD) have made fine mapping challenging. To address the problem, we compared two association techniques in two ancestrally diverse populations, African Americans (AAs) and Europeans (EURs). We observed a greater number of Human Leucocyte Antigen (HLA) alleles in AA consistent with the elevated level of recombination in this population. In EUR we observed 50 different A-C-B-DRB1-DQA-DQB multilocus haplotype sequences per hundred individuals; in the AA sample, these multilocus haplotypes were twice as common compared to Europeans. We also observed a strong narrow class II signal in AA as opposed to the long-range LD observed in EUR that includes class I alleles. We performed a Bayesian model choice of the classical HLA alleles and a frequentist analysis that combined both single nucleotide polymorphisms (SNPs) and classical HLA alleles. Both analyses converged on a similar subset of risk HLA alleles: in EUR HLA- B*08:01 + B*18:01 + (DRB1*15:01 frequentist only) + DQA*01:02 + DQB*02:01 + DRB3*02 and in AA HLA-C*17:01 + B*08:01 + DRB1*15:03 + (DQA*01:02 frequentist only) + DQA*02:01 + DQA*05:01+ DQA*05:05 + DQB*03:19 + DQB*02:02. We observed two additional independent SNP associations in both populations: EUR rs146903072 and rs501480; AA rs389883 and rs114118665. The DR2 serotype was best explained by DRB1*15:03 + DQA*01:02 in AA and by DRB1*15:01 + DQA*01:02 in EUR. The DR3 serotype was best explained by DQA*05:01 in AA and by DQB*02:01 in EUR. Despite some differences in underlying HLA allele risk models in EUR and AA, SNP signals across the extended MHC showed remarkable similarity and significant concordance in direction of effect for risk-associated variants.

9 Article Less than 7 hours of sleep per night is associated with transitioning to systemic lupus erythematosus. 2018

Young, K A / Munroe, M E / Harley, J B / Guthridge, J M / Kamen, D L / Gilkensen, G S / Weisman, M H / Karp, D R / Wallace, D J / James, J A / Norris, J M. ·1 Department of Epidemiology, University of Colorado Anschutz Medical Campus, Aurora, USA. · 2 Arthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, USA. · 3 Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, USA. · 4 US Department of Veterans Affairs Medical Center, Cincinnati, USA. · 5 Division of Rheumatology, Medical University of South Carolina, Charleston, USA. · 6 Division of Rheumatology, Cedars Sinai Medical Center, Los Angeles, USA. · 7 Division of Rheumatic Diseases, University of Texas Southwestern Dallas, USA. · 8 Departments of Medicine and Pathology, Oklahoma University Health Sciences Center, Oklahoma City, USA. ·Lupus · Pubmed #29804502.

ABSTRACT: Background The role of sleep in the etiology of systemic lupus erythematosus (SLE) has not been well studied. We examined whether sleep duration was associated with subsequent transitioning to SLE in individuals at risk for SLE. Methods Four hundred and thirty-six relatives of SLE patients who did not have SLE themselves at baseline were evaluated again an average of 6.3 (± 3.9) years later. Fifty-six individuals transitioned to SLE (≥ 4 cumulative American College of Rheumatology (ACR) criteria). Sleep duration, medication use and medical history were assessed by questionnaire; ACR criteria were confirmed by medical record review. Vitamin D was measured by ELISA. Generalized estimating equations, accounting for correlation within families, assessed associations between baseline sleep and the outcome of transitioning to SLE. Results Reporting sleeping less than 7 hours per night at baseline was more common in those who subsequently transitioned than those who did not transition to SLE (55% versus 32%, p = 0.0005; OR: 2.8, 95% CI 1.6-4.9). Those who transitioned to SLE were more likely to sleep less than 7 hours per night than those who did not transition to SLE adjusting for age, sex and race (OR: 2.8, 95% CI 1.6-5.1). This association remained after individual adjustment for conditions and early symptoms that could affect sleep, including prednisone use, vitamin D deficiency and number of ACR criteria (OR: 2.0, 95% CI 1.1-4.2). Conclusion Lack of sleep may be associated with transitioning to SLE, independent of early clinical manifestations of SLE that may influence sleep duration. Further evaluation of sleeping patterns and biomarkers in at-risk individuals is warranted.

10 Article Disease-specific quality of life in patients with lupus nephritis. 2018

Jolly, M / Toloza, S / Goker, B / Clarke, A E / Navarra, S V / Wallace, D / Weisman, M / Mok, C C. ·1 Department of Medicine, Rush University Medical Center, Rush University, Chicago, IL, USA. · 2 Ministry of Health, San Fernando del Valle de Catamarca, Argentina. · 3 Gazi University, Ankara, Turkey. · 4 University of Calgary, Canada. · 5 Santo Tomas University, Manila, Philippines. · 6 Cedars Sinai Medical Center, Los Angeles, CA, USA. · 7 Tuen Mun HospitaL, Hong Kong SAR, China. ·Lupus · Pubmed #28728507.

ABSTRACT: Background Patient-reported outcomes in lupus nephritis (LN) are not well studied. Studies with disease-targeted PRO tool in LN do not exist. Herein, we describe quality of life (QOL: HRQOL & non-HRQOL) among LN patients using LupusPRO. Methods International, cross-sectional data from 1259 patients with systemic lupus erythematosus (SLE) and LupusPRO were compared, stratified by (a) presence of LN (ACR classification criteria (ACR-LN)) at any time and, (b) active LN (on SLEDAI) at study visit. Damage was assessed by SLICC/ACR-SDI. Multivariate regression analyses for QOL against ACR-LN (active LN) after adjusting for age, gender, ethnicity and country of recruitment were performed. Results Mean (SD) age was 41.7 (13.5) yrs, 93% were women. Five hundred and thirty-nine of 1259 SLE patients had ACR-LN. ACR-LN group was younger, were more often on immunosuppressive medications, had worse QOL on lupus medications and procreation than non-ACR-LN patients. HRQOL and non-HRQOL scores were similar in both groups. One hundred and twenty-nine of 539 ACR-LN patients had active LN. Active LN group was younger, had greater disease activity and had worse HRQOL and non-HRQOL compared to patients without active LN. Specific domains adversely affected were lupus symptoms, lupus medications, procreation, emotional health, body image and desires-goals domains. Patients with ACR-LN and active LN fared significantly worse in lupus medications and procreation HRQOL domains, even after adjusting for age, ethnicity, gender and country of recruitment. Conclusions Lupus nephritis patients have poor QOL. Patients with active LN have worse HRQOL and non-HRQOL. Most domains affected are not included in the generic QOL tools used in SLE. LN patients must receive discussion on lupus medications and procreation issues. Patients with active LN need comprehensive assessments and addressal of QOL, along with treatment for active LN.

11 Article Role of psychosocial reserve capacity in anxiety and depression in patients with systemic lupus erythematosus. 2018

Zamora-Racaza, Geraldine / Azizoddin, Desiree R / Ishimori, Mariko L / Ormseth, Sarah R / Wallace, Daniel J / Penserga, Ester G / Sumner, Lekeisha / Ayeroff, Julia / Draper, Taylor / Nicassio, Perry M / Weisman, Michael H. ·Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA. · Department of Medicine, University of the Philippines - Philippine General Hospital, Manila, Philippines. · Department of Psychology, Loma Linda University, Loma Linda, California, USA. · Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine UCLA, Los Angeles, California, USA. · Department of Psychology, Alliant University, Alhambra, California, USA. · Post-baccalaureate Premedical Program, University of Southern California, Los Angeles, California, USA. · Cousins Center for Psychoneuroimmunology, University of California Los Angeles, Los Angeles, California, USA. ·Int J Rheum Dis · Pubmed #28261991.

ABSTRACT: AIM: To examine the relationship between reserve capacity measures and anxiety/depression among patients with systemic lupus erythematosus (SLE) from Southern California (SoCal), United States and Manila, Philippines. METHODS: A total of 235 participants with SLE completed self-reported scales to assess anxiety/depression and psychosocial reserve capacity measures (self-esteem, optimism, personal mastery/coping skills, social support), socioeconomic status (SES) data, and Mexican SLE Disease Activity Index. Statistical analyses included independent sample t-tests, Chi-square, and point-biserial and Pearson correlations. RESULTS: Overall, participants from Manila reported lower SES than SoCal participants. Over half of Manila and SoCal participants (69% and 59.1%, respectively) reported high anxiety scores. SoCal participants had higher depression scores than Filipinos (66%, 27%, respectively, P < 0.001) despite appearing to be more resilient by exhibiting higher scores for all reserve capacity measures (P < 0.001). Participants with low self-esteem scores from both groups had higher anxiety and depression scores. SoCal participants who reported lower optimism, lower personal mastery and lower social support were more anxious and depressed, while Filipinos low on these three variables reported less depressive symptoms. CONCLUSION: Reduced psychosocial reserve capacity in individuals leads to vulnerabilities that may ultimately result in greater disease burden and psychological distress. Low self-esteem, optimism, coping and social support were associated with depression and low self-esteem was associated with anxiety for both groups. Despite the Filipino cohort's lower reserve capacity and SES, Filipino patients exhibited less depression than their SoCal counterparts, suggesting that other factors may protect them from experiencing depression.

12 Article Psychological Factors that Link Socioeconomic Status to Depression/Anxiety in Patients with Systemic Lupus Erythematosus. 2017

Azizoddin, Desiree R / Zamora-Racaza, Geraldine / Ormseth, Sarah R / Sumner, Lekeisha A / Cost, Chelsie / Ayeroff, Julia R / Weisman, Michael H / Nicassio, Perry M. ·Department of Psychology, Loma Linda University, Loma Linda, CA, 92350, USA. Dazizodd@gmail.com. · Department of Anesthesiology, Stanford University Medical Center, Palo Alto, CA, USA. Dazizodd@gmail.com. · Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Department of Medicine, University of the Philippines - Philippine General Hospital, Manila, Philippines. · Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. · Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Pepperdine University, Malibu, CA, USA. · Postbaccalaureate Premedical Program, University of Southern California, Los Angeles, CA, USA. · Cousins Center for Psychoneuroimmunology, University of California Los Angeles, Los Angeles, CA, USA. ·J Clin Psychol Med Settings · Pubmed #28776205.

ABSTRACT: Our analyses examined whether reserve capacity factors would explain the relationship between socioeconomic status (SES) and symptoms of depression/anxiety in patients with systemic lupus erythematosus (SLE). We assessed disease activity, depression/anxiety symptoms, and intrapersonal and interpersonal reserve capacity measures in 128 patients with SLE. Multiple meditational analyses revealed that intrapersonal and interpersonal psychosocial aspects of reserve capacity fully mediated the relationship between SES and depression/anxiety. Lower SES was indirectly associated with higher symptoms of depression and anxiety through the effects of psychosocial resilience. Interventions aimed at improving modifiable reserve capacity variables, such as self-esteem and optimism, may improve anxious/depressive symptomatology in patients with SLE.

13 Article Transancestral mapping and genetic load in systemic lupus erythematosus. 2017

Langefeld, Carl D / Ainsworth, Hannah C / Cunninghame Graham, Deborah S / Kelly, Jennifer A / Comeau, Mary E / Marion, Miranda C / Howard, Timothy D / Ramos, Paula S / Croker, Jennifer A / Morris, David L / Sandling, Johanna K / Almlöf, Jonas Carlsson / Acevedo-Vásquez, Eduardo M / Alarcón, Graciela S / Babini, Alejandra M / Baca, Vicente / Bengtsson, Anders A / Berbotto, Guillermo A / Bijl, Marc / Brown, Elizabeth E / Brunner, Hermine I / Cardiel, Mario H / Catoggio, Luis / Cervera, Ricard / Cucho-Venegas, Jorge M / Dahlqvist, Solbritt Rantapää / D'Alfonso, Sandra / Da Silva, Berta Martins / de la Rúa Figueroa, Iñigo / Doria, Andrea / Edberg, Jeffrey C / Endreffy, Emőke / Esquivel-Valerio, Jorge A / Fortin, Paul R / Freedman, Barry I / Frostegård, Johan / García, Mercedes A / de la Torre, Ignacio García / Gilkeson, Gary S / Gladman, Dafna D / Gunnarsson, Iva / Guthridge, Joel M / Huggins, Jennifer L / James, Judith A / Kallenberg, Cees G M / Kamen, Diane L / Karp, David R / Kaufman, Kenneth M / Kottyan, Leah C / Kovács, László / Laustrup, Helle / Lauwerys, Bernard R / Li, Quan-Zhen / Maradiaga-Ceceña, Marco A / Martín, Javier / McCune, Joseph M / McWilliams, David R / Merrill, Joan T / Miranda, Pedro / Moctezuma, José F / Nath, Swapan K / Niewold, Timothy B / Orozco, Lorena / Ortego-Centeno, Norberto / Petri, Michelle / Pineau, Christian A / Pons-Estel, Bernardo A / Pope, Janet / Raj, Prithvi / Ramsey-Goldman, Rosalind / Reveille, John D / Russell, Laurie P / Sabio, José M / Aguilar-Salinas, Carlos A / Scherbarth, Hugo R / Scorza, Raffaella / Seldin, Michael F / Sjöwall, Christopher / Svenungsson, Elisabet / Thompson, Susan D / Toloza, Sergio M A / Truedsson, Lennart / Tusié-Luna, Teresa / Vasconcelos, Carlos / Vilá, Luis M / Wallace, Daniel J / Weisman, Michael H / Wither, Joan E / Bhangale, Tushar / Oksenberg, Jorge R / Rioux, John D / Gregersen, Peter K / Syvänen, Ann-Christine / Rönnblom, Lars / Criswell, Lindsey A / Jacob, Chaim O / Sivils, Kathy L / Tsao, Betty P / Schanberg, Laura E / Behrens, Timothy W / Silverman, Earl D / Alarcón-Riquelme, Marta E / Kimberly, Robert P / Harley, John B / Wakeland, Edward K / Graham, Robert R / Gaffney, Patrick M / Vyse, Timothy J. ·Center for Public Health Genomics, Wake Forest School of Medicine, Winston-Salem, North Carolina 27101, USA. · Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina 27101, USA. · Divisions of Genetics and Molecular Medicine and Immunology, Infection and Inflammatory Diseases, King's College London, Guy's Hospital, London SE1 9RT, UK. · Arthritis &Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA. · Center for Human Genomics and Personalized Medicine Research, Wake Forest School of Medicine, Winston-Salem, North Carolina 27101, USA. · Department of Public Health Sciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA. · Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA. · Division of Clinical Immunology and Rheumatology, UAB School of Medicine, Birmingham, Alabama 35294, USA. · Department of Medical Sciences, Molecular Medicine and Science for Life Laboratory, Uppsala University, Uppsala 752 36, Sweden. · Departamento de Reumatología, Hospital G. Almenara y Facultad de Medicina, Universidad Nacional Mayor de San Marcos, Lima 15081, Perú. · Hospital Italiano de Córdoba, Córdoba X5004BAL, Argentina. · Hospital de Pediatría, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico. · Department of Clinical Sciences, Rheumatology, Lund University, Lund 22362, Sweden. · Hospital Eva Perón, Granadero Baigorria S2152EDD, Argentina. · Department of Internal Medicine and Rheumatology, Martini Hospital, Van Swietenplein 1, 9728, NT, Groningen, The Netherlands. · Division of Rheumatology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center and the University of Cincinnati, Cincinnati, Ohio 45229, USA. · Centro de Investigación Clínica de Morelia, Morelia, Michoacán 58070, Mexico. · Hospital Italiano de Buenos Aires, 1181, Buenos Aires C1181ACH, Argentina. · Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Barcelona, Catalonia 08007, Spain. · Department of Public Health and Clinical Medicine, Division of Rheumatology, Umeå University, Umeå 901 87, Sweden. · Department of Health Sciences and Institute of Research in Autoimmune Diseases (IRCAD), University of Eastern Piedmont, Novara 28100, Italy. · Unidade Multidisciplinar em Investigação Biomédica/Instituto de Ciências Biomédicas de Abel Salazar-Universidade do Porto, Porto 4099-003, Portugal. · Department of Rheumatology, Hospital Universitario de Gran Canaria Dr Negrín, Las Palmas de Gran Canaria 35010, Spain. · Division of Rheumatology, Department of Medicine (DIMED), University of Padua, Padua 35122, Italy. · Department of Pediatrics and Child Health Center, Albert Szent-Györgyi Medical Center, Faculty of Medicine, University of Szeged, Szeged H-6720, Hungary. · Hospital Universitario 'Dr José Eleuterio González' Universidad Autonoma de Nuevo León, Monterrey 64020, México. · CHU de Québec Université Laval, Québec, Canada G1R 2JG. · Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, North Carolina 27101, USA. · Institute of Environmental Medicine, Unit of Immunology and Chronic diseases, Karolinska Institutet, Stockholm 171 77, Sweden. · Division of Rheumatology, Hospital Interzonal General de Agudos General San Martín, La Plata 1900, Argentina. · University of Guadalajara, Departamento de Fisiología, Guadalajara, Jalisco 44100, Mexico. · Centre for Prognosis Studies in The Rheumatic Diseases, Krembil Research Institute, Toronto Western Hospital, Toronto, Ontario M5T 2S8, Canada. · Unit of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm SE-171 76, Sweden. · Departments of Medicine and Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA. · Department of Rheumatology and Clinical Immunology,University Medical Center Groningen,University of Groningen, Groningen 9713 GZ, The Netherlands. · Department of Immunology, University of Texas SouthWestern Medical Center, Dallas, Texas 75235, USA. · Department of Pediatrics, Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. · Department of Rheumatology, Albert Szent-Györgyi Medical Centre, University of Szeged, Szeged H-6720, Hungary. · Department of Rheumatology, Odense University Hospital, Odense 5000, Denmark. · Rheumatology, Cliniques Universitaires Saint-Luc &Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Louvain-la-Neuve 1348, Belgium. · Hospital General de Culiacán, Sinaloa 80220, Mexico. · Instituto de Parasitología y Biomedicina López Neyra, CSIC, Granada 18100, Spain. · University of Michigan Medical Center, Ann Arbor, Michigan 48103, USA. · Centro de Estudios Reumatológicos, Santiago de Chile, Santiago 7500000, Chile. · Departamento de Reumatología, Hospital General de México, Mexico D.F., Mexico. · Department of Rheumatology, Mayo Clinic, Rochester, Minnesota 94158, USA. · Instituto Nacional de Medicina Genómica (INMEGEN), México City 14610, México. · Unidad de Enfermedades Autoimmunes Sistémicas, UGC Medicina Interna, Hospital Universitario San Cecilio, Granada 18007, Spain. · Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21218, USA. · Rheumatology Division, McGill University, Montreal, Quebec H3A 0G4, Canada. · Department of Rheumatology, Sanatorio Parque, Rosario S2000, Argentina. · University of Western Ontario, London, Ontario, Canada M5T 2S8. · Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA. · The University of Texas Health Science Center at Houston (UTHealth) Medical School, Houston, Texas 77030, USA. · Hospital Universitario Virgen de las Nieves, Granada 18014, Spain. · Instituto Nacional de Ciencias Médicas y Nutrición, Department of Endocrinology and Metabolism, Vasco de Quiroga 15, Mexico City 14080, Mexico. · Unidad Reumatología y Enfermedades Autoinmunes H.I.G.A. Dr Alende Mar del Plata, Buenos Aires B7600, Argentina. · Referral Center for Systemic Autoimmune Diseases, Fondazione IRCCS Ca'Granda Ospedale Ma Repiore Policlinico and University of Milan, Milan 20122, Italy. · Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, Sacramento, California 95616, USA. · Rheumatology Division of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping 581 83, Sweden. · Ministry of Health, San Fernando del Valle de Catamarca, Catamarca K4700, Argentina. · Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University, Lund 221 00, Sweden. · Unidad de Biología Molecular y Medicina Genómica Instituto de Investigaciones Biomédicas/UNAM Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City 14080, Mexico. · Hospital Santo Antonio, Universidade do Porto, Porto 4099-003, Portugal. · University of Puerto Rico School of Medicine, San Juan 00936, Puerto Rico. · Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California 90048, USA. · Human Genetics, Genentech Inc, South San Francisco, California 94080, USA. · Department of Neurology and Institute of Human Genetics, University of California at San Francisco, San Francisco, California 94158, USA. · Université de Montréal and the Montreal Heart Institute, Montreal, Quebec, Canada H1T 1C8. · Center for Genomics &Human Genetics, The Feinstein Institute for Medical Research, Manhasset, New York 11030, USA. · Department of Medical Sciences, Rheumatology, Uppsala University, 752 36, Sweden. · Rosalind Russell/Ephraim P Engleman Rheumatology Research Center, Division of Rheumatology, UCSF School of Medicine, San Francisco, California 94158, USA. · Keck School of Medicine of USC, Los Angeles, California 90033, USA. · Department of Pediatrics, Duke University, Durham, North Carolina 27708, USA. · Department of Pediatrics and the Institute of Medical Sciences, The Hospital for Sick Children, Hospital for Sick Children Research Institute and University of Toronto, Ontario, Canada M5G 1X8. · Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research (GENYO), Granada 18007, Spain. · Unit of Institute of Environmental Medicine, Karolinska Institute, Solnavägen 171 77, Sweden. ·Nat Commun · Pubmed #28714469.

ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and ethnic disparities. We report a large transancestral association study of SLE using Immunochip genotype data from 27,574 individuals of European (EA), African (AA) and Hispanic Amerindian (HA) ancestry. We identify 58 distinct non-HLA regions in EA, 9 in AA and 16 in HA (∼50% of these regions have multiple independent associations); these include 24 novel SLE regions (P<5 × 10

14 Article Rare X Chromosome Abnormalities in Systemic Lupus Erythematosus and Sjögren's Syndrome. 2017

Sharma, Rohan / Harris, Valerie M / Cavett, Joshua / Kurien, Biji T / Liu, Ke / Koelsch, Kristi A / Fayaaz, Anum / Chaudhari, Kaustubh S / Radfar, Lida / Lewis, David / Stone, Donald U / Kaufman, C Erick / Li, Shibo / Segal, Barbara / Wallace, Daniel J / Weisman, Michael H / Venuturupalli, Swamy / Kelly, Jennifer A / Pons-Estel, Bernardo / Jonsson, Roland / Lu, Xianglan / Gottenberg, Jacques-Eric / Anaya, Juan-Manuel / Cunninghame-Graham, Deborah S / Huang, Andrew J W / Brennan, Michael T / Hughes, Pamela / Alevizos, Ilias / Miceli-Richard, Corinne / Keystone, Edward C / Bykerk, Vivian P / Hirschfield, Gideon / Nordmark, Gunnel / Bucher, Sara Magnusson / Eriksson, Per / Omdal, Roald / Rhodus, Nelson L / Rischmueller, Maureen / Rohrer, Michael / Wahren-Herlenius, Marie / Witte, Torsten / Alarcón-Riquelme, Marta / Mariette, Xavier / Lessard, Christopher J / Harley, John B / Ng, Wan-Fai / Rasmussen, Astrid / Sivils, Kathy L / Scofield, R Hal. ·Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center, and Department of Veterans Affairs Medical Center, Oklahoma City. · Oklahoma Medical Research Foundation and University of Oklahoma Health Sciences Center, Oklahoma City. · Cincinnati Children's Hospital Medical Center and University of Cincinnati, Cincinnati, Ohio. · Department of Veterans Affairs Medical Center, Oklahoma City, Oklahoma. · University of Oklahoma Health Sciences Center, Oklahoma City. · Johns Hopkins University, Baltimore, Maryland, and King Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia. · University of Minnesota Medical School, Minneapolis. · Cedars-Sinai Medical Center, Los Angeles, California. · Oklahoma Medical Research Foundation, Oklahoma City. · Sanatorio Parque, Rosario, Argentina. · University of Bergen and Haukeland University Hospital, Bergen, Norway. · Strasbourg University, Strasbourg, France. · Universidad del Rosario, Bogota, Colombia. · King's College London, London, UK. · University of Minnesota, Minneapolis. · Carolinas Medical Center, Charlotte, North Carolina. · National Institute of Dental and Craniofacial Research, NIH, Bethesda, MD. · Department of Rheumatology, Université Paris-Sud, AP-HP, INSERM U1012, Le Kremlin-Bicêtre, France. · Mount Sinai Hospital and University of Toronto, Toronto, Ontario, Canada. · Hospital for Special Surgery, New York, New York. · University of Birmingham, Birmingham, UK. · Uppsala University, Uppsala, Sweden. · Örebro University Hospital, Örebro, Sweden. · Linköping University, Linköping, Sweden. · Stavanger University Hospital, Stavanger, Norway. · The Queen Elizabeth Hospital, Woodville South, and University of Adelaide, Adelaide, South Australia, Australia. · Karolinska Institutet, Stockholm, Sweden. · Hannover Medical School, Hannover, Germany. · Pfizer-University of Granada-Andalusian Regional Government, Granada, Spain, and Karolinska Institutet, Stockholm, Sweden. · Cincinnati Children's Hospital Medical Center, University of Cincinnati, and Ohio Department of Veterans Affairs Medical Center, Cincinnati. · Newcastle University, Newcastle upon Tyne, UK. ·Arthritis Rheumatol · Pubmed #28692793.

ABSTRACT: OBJECTIVE: Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) are related by clinical and serologic manifestations as well as genetic risks. Both diseases are more commonly found in women than in men, at a ratio of ~10 to 1. Common X chromosome aneuploidies, 47,XXY and 47,XXX, are enriched among men and women, respectively, in either disease, suggesting a dose effect on the X chromosome. METHODS: We examined cohorts of SS and SLE patients by constructing intensity plots of X chromosome single-nucleotide polymorphism alleles, along with determining the karyotype of selected patients. RESULTS: Among ~2,500 women with SLE, we found 3 patients with a triple mosaic, consisting of 45,X/46,XX/47,XXX. Among ~2,100 women with SS, 1 patient had 45,X/46,XX/47,XXX, with a triplication of the distal p arm of the X chromosome in the 47,XXX cells. Neither the triple mosaic nor the partial triplication was found among the controls. In another SS cohort, we found a mother/daughter pair with partial triplication of this same region of the X chromosome. The triple mosaic occurs in ~1 in 25,000-50,000 live female births, while partial triplications are even rarer. CONCLUSION: Very rare X chromosome abnormalities are present among patients with either SS or SLE and may inform the location of a gene(s) that mediates an X dose effect, as well as critical cell types in which such an effect is operative.

15 Article The psychometric properties of the Perceived Stress Scale-10 among patients with systemic lupus erythematosus. 2017

Mills, S D / Azizoddin, D / Racaza, G Z / Wallace, D J / Weisman, M H / Nicassio, P M. ·1 San Diego State University/University of California, San Diego Joint Doctoral Program in Clinical Psychology, USA. · 2 Department of Psychology, Loma Linda University, Loma Linda, USA. · 3 Section of Rheumatology, Department of Medicine, University of the Philippines-Philippine General Hospital, Manila, Philippines. · 4 Division of Rheumatology, Cedars Sinai Medical Center, Los Angeles, USA. · 5 Cousins Center for Psychoneuroimmunology, University of California, Los Angeles, USA. ·Lupus · Pubmed #28406052.

ABSTRACT: Objective Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease characterized by periods of remission and recurrent flares, which have been associated with stress. Despite the significance of stress in this disease, the Perceived Stress Scale-10 has yet to be psychometrically evaluated in patients with SLE. Methods Exploratory factor analysis was used to examine the structural validity of the Perceived Stress Scale-10 among patients with SLE ( N = 138) receiving medical care at Cedars Sinai Medical Center. Cronbach's coefficient alpha was used to examine internal consistency reliability, and Pearson product-moment correlations were used to examine convergent validity with measures of anxiety, depression, helplessness, and disease activity. Results Exploratory factor analysis provided support for a two-factor structure (comparative fit index = .95; standardized root mean residual = .04; root mean square error of approximation = .08). Internal consistency reliability was good for both factors (α = .84 and .86). Convergent validity was evidenced via significant correlations with measures of anxiety, depression, and helplessness. There were no significant correlations with the measure of disease activity. Conclusion The Perceived Stress Scale-10 can be used to examine perceived stress among patients with SLE.

16 Article MicroRNA-302d targets IRF9 to regulate the IFN-induced gene expression in SLE. 2017

Smith, Siobhán / Fernando, Thilini / Wu, Pei Wen / Seo, Jane / Ní Gabhann, Joan / Piskareva, Olga / McCarthy, Eoghan / Howard, Donough / O'Connell, Paul / Conway, Richard / Gallagher, Phil / Molloy, Eamonn / Stallings, Raymond L / Kearns, Grainne / Forbess, Lindsy / Ishimori, Mariko / Venuturupalli, Swamy / Wallace, Daniel / Weisman, Michael / Jefferies, Caroline A. ·Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin 2, Ireland. · Division of Rheumatology, Department of Medicine, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA; Department of Biomedical Sciences, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA. · Department of Rheumatology, Beaumont Hospital, Dublin 9, Ireland. · Department of Rheumatology, St. Vincent's University Hospital, Dublin 4, Ireland. · Department of Biomedical Sciences, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA. · Division of Rheumatology, Department of Medicine, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA. · Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin 2, Ireland; Division of Rheumatology, Department of Medicine, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA; Department of Biomedical Sciences, Cedars-Sinai Medical Centre, 8700 Beverly Blvd, Los Angeles, CA 90048, USA. Electronic address: Caroline.Jefferies@cshs.org. ·J Autoimmun · Pubmed #28318807.

ABSTRACT: Systemic lupus erythematosus (SLE) is a complex disease targeting multiple organs as a result of overactivation of the type I interferon (IFN) system, a feature currently being targeted by multiple biologic therapies against IFN-α. We have identified an estrogen-regulated microRNA, miR-302d, whose expression is decreased in SLE patient monocytes and identify its target as interferon regulatory factor (IRF)-9, a critical component of the transcriptional complex that regulates expression of interferon-stimulated genes (ISGs). In keeping with the reduced expression of miR-302d in SLE patient monocytes, IRF9 levels were increased, as was expression of a number of ISGs including MX1 and OAS1. In vivo evaluation revealed that miR-302d protects against pristane-induced inflammation in mice by targeting IRF9 and hence ISG expression. Importantly, patients with enhanced disease activity have markedly reduced expression of miR-302d and enhanced IRF9 and ISG expression, with miR-302d negatively correlating with IFN score. Together these findings identify miR-302d as a key regulator of type I IFN driven gene expression via its ability to target IRF9 and regulate ISG expression, underscoring the importance of non-coding RNA in regulating the IFN pathway in SLE.

17 Article Prevalence of resting-ECG abnormalities in systemic lupus erythematosus: a single-center experience. 2017

Myung, Gihyun / Forbess, Lindsy J / Ishimori, Mariko L / Chugh, Sumeet / Wallace, Daniel / Weisman, Michael H. ·Division of Rheumatology/Department of Internal Medicine, University of California-Los Angeles, 1000 Veteran Ave, Los Angeles, CA, 90024, USA. gmyung@mednet.ucla.edu. · Division of Rheumatology/Department of Internal Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. ·Clin Rheumatol · Pubmed #28238088.

ABSTRACT: Cardiovascular complications are a major cause of morbidity and even mortality among systemic lupus erythematosus (SLE) patients. Whether cardiac arrhythmias contribute to this burden among SLE patients, however, is not currently known. The goal of this study was to determine the prevalence of cardiac conduction abnormalities among SLE patients from a single center. We retrospectively reviewed the medical records of SLE patients who had 12-lead electrocardiograms (ECGs) available from various settings at a single academic center over the period of 10 years. In addition, ICD-9 codes for arrhythmias were obtained for the SLE patients whose ECGs were reviewed. The hospital setting (in-patient, out-patient, emergency department) and the indication for obtaining the ECG were evaluated. Two hundred thirty-five SLE patients had available ECGs. Sinus tachycardia was most common (18%). With direct ECG review, tachyarrhythmias were found in 6% of SLE patients, with the most common being atrial fibrillation (3%). Atrial fibrillation was seen even more frequently (9%) when ICD-9 codes were reviewed. No patients had brady-arrhythmias. QT prolongation was present in 17% of patients upon direct ECG review. More ECGs with tachyarrhythmias and QT prolongation were found among inpatients, with preoperative evaluation and gastrointestinal symptoms being the most common indications. Sinus tachycardia was the most common finding seen among our SLE patients with ECGs. Further study into the possible mechanisms behind this is warranted, including the possibility of autonomic nervous system involvement in SLE.

18 Article Failure of a systemic lupus erythematosus response index developed from clinical trial data: lessons examined and learned. 2017

Forbess, L J / Bresee, C / Wallace, D J / Weisman, M H. ·1 Cedars-Sinai Medical Center, Division of Rheumatology, USA. · 2 Cedars-Sinai Medical Center, Department of Biostatistics and Bioinformatics, USA. ·Lupus · Pubmed #28173737.

ABSTRACT: Background Our primary goal was to create an outcome change score index similar to a standard rheumatoid arthritis (RA) model utilizing real-world data in systemic lupus erythematosus (SLE) patients that occurred during their phase 3 trials with a Food and Drug Administration-approved drug. Methods We utilized raw data from trials of belimumab for the treatment of SLE. Data were split 80/20 into training/validation sets. Index variables present in a majority of patients and with face validity were selected. Variables were scored for each patient as percentage improvement from baseline after one year. The percentage of placebo- and drug-treated patients considered improved after the application of various criteria was ascertained. Logistic regression was employed to determine the ability of the new index to predict treatment assignment. Results A total of 1693 subjects had data for analyses. Eight variables were chosen: arthritis, rash, physician global assessment, fatigue, anti-double stranded DNA antibodies, C3, C4 and C-reactive protein. In the training dataset, ≥20% improvement in ≥4 of eight variables produced the largest difference between placebo- and drug-treated patients (22.1%) with an acceptable rate of improved placebo-treated patients (25%). This resulted in an odds ratio for belimumab (10 mg/kg) vs placebo of 2.7 (95% CI: 2.0-3.6; p < 0.001). However, in the validate dataset the odds ratio was not significant at 1.3 (95% CI: 0.8-2.2; p = 0.863). Conclusions The index created from training data did not achieve statistical significance when tested in the validation set. We have speculated why this happened. Is the lack of success of therapeutics for SLE caused by ineffective medications, study design and outcome instruments that fail to inform us, or is the heterogeneity of the disease too daunting? The lessons learned here can help direct future endeavors intended to improve SLE outcome instruments.

19 Article A multi-group confirmatory factor analyses of the LupusPRO between southern California and Filipino samples of patients with systemic lupus erythematosus. 2017

Azizoddin, D R / Olmstead, R / Cost, C / Jolly, M / Ayeroff, J / Racaza, G / Sumner, L A / Ormseth, S / Weisman, M / Nicassio, P M. ·1 Department of Psychology, Loma Linda University, USA. · 2 Cousin's Center for Psychoneuroimmunology, University of California Los Angeles, USA. · 3 Department of Psychology, Pepperdine University, USA. · 4 Department of Medicine and Behavioral Science, Rush University, USA. · 5 Postbaccalaureate Premedical Program, University of Southern California, USA. · 6 Department of Medicine, University of the Philippines - Philippine General Hospital, Philippines. · 7 Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, USA. · 8 Division of Rheumatology, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute. · 9 Division of Rheumatology, Cedars-Sinai Medical Center, USA. ·Lupus · Pubmed #28059025.

ABSTRACT: Introduction Systemic lupus erythematosus (SLE) leads to a range of biopsychosocial health outcomes through an unpredictable and complex disease path. The LupusPRO is a comprehensive, self-report measure developed specifically for populations with SLE, which assesses both health-related quality of life and non-health related quality of life. Given its increasingly widespread use, additional research is needed to evaluate the psychometric integrity of the LupusPRO across diverse populations. The objectives of this study were to evaluate the performance of the LupusPRO in two divergent patient samples and the model fit between both samples. Methods Two diverse samples with SLE included 136 patients from an ethnically-diverse, urban region in southern California and 100 from an ethnically-homogenous, rural region in Manila, Philippines. All patients met the ACR classification criteria for SLE. Confirmatory factor analysis (CFAs) were conducted in each sample separately and combined to provide evidence of the factorial integrity of the 12 subscales in the LupusPRO. Results Demographic analyses indicated significant differences in age, disease activity and duration, education, income, insurance, and medication use between groups. Results of the separate CFAs indicated moderate fit to the data for the hypothesized 12-factor model for both the Manila and southern California groups, respectively [χ

20 Article Discerning Risk of Disease Transition in Relatives of Systemic Lupus Erythematosus Patients Utilizing Soluble Mediators and Clinical Features. 2017

Munroe, Melissa E / Young, Kendra A / Kamen, Diane L / Guthridge, Joel M / Niewold, Timothy B / Costenbader, Karen H / Weisman, Michael H / Ishimori, Mariko L / Wallace, Daniel J / Gilkeson, Gary S / Karp, David R / Harley, John B / Norris, Jill M / James, Judith A. ·Oklahoma Medical Research Foundation, Oklahoma City. · Colorado School of Public Health, Aurora. · Medical University of South Carolina, Charleston. · Mayo Clinic, Rochester, Minnesota. · Brigham and Women's Hospital, Boston, Massachusetts. · Cedars-Sinai Medical Center, Los Angeles, California. · University of Texas Southwestern Medical Center, Dallas. · Cincinnati Children's Hospital Medical Center and US Department of Veterans Affairs Medical Center, Cincinnati, Ohio. · Oklahoma Medical Research Foundation and University of Oklahoma Health Sciences Center, Oklahoma City. ·Arthritis Rheumatol · Pubmed #27863174.

ABSTRACT: OBJECTIVE: Systemic lupus erythematosus (SLE) and other autoimmune diseases cause significant morbidity. Identifying populations at risk of developing SLE is essential for curtailing irreversible inflammatory damage. The aim of this study was to identify factors associated with transition to classified disease that would inform our understanding of the risk of SLE. METHODS: Previously identified blood relatives of patients with SLE, who had <4 American College of Rheumatology (ACR) classification criteria for SLE at baseline, were enrolled in this follow-up study (n = 409 unaffected relatives). Participants provided detailed family, demographic, and clinical information, including the SLE-specific portion of the Connective Tissue Disease Screening Questionnaire (SLE-CSQ). Serum and plasma samples were tested for the presence of lupus-associated autoantibodies and 52 soluble mediators. Generalized estimating equations (GEEs) were applied to identify factors predictive of disease transition. RESULTS: Of the 409 unaffected relatives of SLE patients, 45 (11%) had transitioned to classified SLE at follow-up (mean time to follow-up 6.4 years). Relatives who transitioned to SLE displayed more lupus-associated autoantibody specificities and higher SLE-CSQ scores (P < 0.0001) at baseline than did relatives who did not transition. Importantly, those who had developed SLE during the follow-up period also had elevated baseline plasma levels of inflammatory mediators, including B lymphocyte stimulator, stem cell factor (SCF), and interferon-associated chemokines (P ≤ 0.02), with concurrent decreases in the levels of regulatory mediators, transforming growth factor β (TGFβ), and interleukin-10 (P ≤ 0.03). GEE analyses revealed that baseline SLE-CSQ scores or ACR scores (number of ACR criteria satisfied) and plasma levels of SCF and TGFβ, but not autoantibodies, were significant and independent predictors of SLE transition (P ≤ 0.03). CONCLUSION: Preclinical alterations in levels of soluble mediators may predict transition to classified disease in relatives of SLE patients. Thus, immune perturbations precede SLE classification and can help identify high-risk relatives for rheumatology referral and potential enrollment in prevention trials.

21 Article Combined role of vitamin D status and CYP24A1 in the transition to systemic lupus erythematosus. 2017

Young, Kendra A / Munroe, Melissa E / Guthridge, Joel M / Kamen, Diane L / Niewold, Timothy B / Gilkeson, Gary S / Weisman, Michael H / Ishimori, Mariko L / Kelly, Jennifer / Gaffney, Patrick M / Sivils, Kathy H / Lu, Rufei / Wallace, Daniel J / Karp, David R / Harley, John B / James, Judith A / Norris, Jill M. ·Colorado School of Public Health, Aurora, Colorado, USA. · Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA. · Medical University of South Carolina, Charleston, South Carolina, USA. · Mayo Clinic, Rochester, Minnesota, USA. · Cedars-Sinai Medical Center, Los Angeles, California, USA. · Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA. · University of Texas Southwestern Medical Center, Dallas, Texas, USA. · Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA. · US Department of Veterans Affairs Medical Center, Cincinnati, Ohio, USA. ·Ann Rheum Dis · Pubmed #27283331.

ABSTRACT: OBJECTIVE: We examined whether measures of vitamin D were associated with transitioning to systemic lupus erythematosus (SLE) in individuals at risk for SLE. METHODS: 436 individuals who reported having a relative with SLE but who did not have SLE themselves were evaluated at baseline and again an average of 6.3 (±3.9) years later. Fifty-six individuals transitioned to SLE (≥4 cumulative American College of Rheumatology criteria). 25-Hydroxyvitamin D (25[OH]D) levels were measured by ELISA. Six single-nucleotide polymorphisms in four vitamin D genes were genotyped. Generalised estimating equations, adjusting for correlation within families, were used to test associations between the vitamin D variables and the outcome of transitioning to SLE. RESULTS: Mean baseline 25[OH]D levels (p=0.42) and vitamin D supplementation (p=0.65) were not different between those who did and did not transition to SLE. Vitamin D deficiency (25[OH]D <20 ng/mL) was greater in those who transitioned compared with those who did not transition to SLE (46% vs 33%, p=0.05). The association between 25[OH]D and SLE was modified by CYP24A1 rs4809959, where for each additional minor allele increased 25[OH]D was associated with decreased SLE risk: zero minor alleles (adjusted OR: 1.03, CI 0.98 to 1.09), one minor allele (adjusted OR: 1.01, CI 0.97 to 1.05) and two minor alleles (adjusted OR: 0.91, CI 0.84 to 0.98). Similarly, vitamin D deficiency significantly increased the risk of transitioning to SLE in those with two minor alleles at rs4809959 (adjusted OR: 4.90, CI 1.33 to 18.04). CONCLUSIONS: Vitamin D status and CYP24A1 may have a combined role in the transition to SLE in individuals at increased genetic risk for SLE.

22 Article Klinefelter's syndrome (47,XXY) is in excess among men with Sjögren's syndrome. 2016

Harris, Valerie M / Sharma, Rohan / Cavett, Joshua / Kurien, Biji T / Liu, Ke / Koelsch, Kristi A / Rasmussen, Astrid / Radfar, Lida / Lewis, David / Stone, Donald U / Kaufman, C Erick / Li, Shibo / Segal, Barbara / Wallace, Daniel J / Weisman, Michael H / Venuturupalli, Swamy / Kelly, Jennifer A / Alarcon-Riquelme, Marta E / Pons-Estel, Bernardo / Jonsson, Roland / Lu, Xianglan / Gottenberg, Jacques-Eric / Anaya, Juan-Manuel / Cunninghame-Graham, Deborah S / Huang, Andrew J W / Brennan, Michael T / Hughes, Pamela / Alevizos, Ilias / Miceli-Richard, Corinne / Keystone, Edward C / Bykerk, Vivian P / Hirschfield, Gideon / Xie, Gang / Siminovitch, Katherine A / Ng, Wan-Fai / Nordmark, Gunnel / Bucher, Sara Magnusson / Eriksson, Per / Omdal, Roald / Rhodus, Nelson L / Rischmueller, Maureen / Rohrer, Michael / Wahren-Herlenius, Marie / Witte, Torsten / Mariette, Xavier / Lessard, Christopher J / Harley, John B / Sivils, Kathy L / Scofield, R Hal. ·Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Pathology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. · Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Medical Service, Department of Veterans Affairs Medical Center, Oklahoma City, OK, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Medical Service, Department of Veterans Affairs Medical Center, Oklahoma City, OK, USA. · Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; College of Medicine, University of Cincinnati, Cincinnati, OH, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. · Department of Oral Diagnosis and Radiology, College of Dentistry, University of Oklahoma Health Sciences Center, Oklahoma City, USA. · Dean McGee Eye Institute and Department of Ophthalmology, University of Oklahoma College of Medicine, Oklahoma City, OK, USA. · Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. · Department of Pediatrics, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. · Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA. · Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Center Pfizer, University of Granada, Andalusian Government for Genomics and Oncological Research, PTS Granada, 18016, Spain. · Sanatorio Parque, Rosario, Argentina. · Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen 5021, Norway; Department of Rheumatology, Haukeland University Hospital, Bergen 5021, Norway. · Strasbourg University, Strasbourg, France. · Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia. · Division of Genetics and Molecular Medicine and Division of Immunology, Infection and Inflammatory Disease, King's College London, London, UK. · Department of Developmental and Surgical Sciences, University of Minnesota, Minneapolis, MN, USA. · Department of Oral Medicine, Carolinas Medical Center, Charlotte, NC 28232, USA. · Molecular Physiology & Therapeutic Branch, National Institute of Dental and Craniofacial Research, Bethesda, MD, USA. · Department of Rheumatology, Université Paris-Sud, AP-HP, INSERM U1012, Le Kremlin-Bicêtre, France. · Department of Medicine, Mount Sinai Hospital and University of Toronto, Toronto, Ontario, Canada. · Hospital for Special Surgery, New York, USA. · NIHR Biomedical Research Unit, University of Birmingham, Birmingham, UK. · Samuel Lunenfeld and Toronto General Research Institutes, Departments of Medicine, Immunology and Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. · Musculoskeletal Research Group, Institute of Cellular Medicine & NIHR Newcastle Biomedical Research Centre, Newcastle University, Newcastle upon Tyne, UK. · Section of Rheumatology, Department of Medical Sciences and Science for Life Laboratory, Uppsala University, Uppsala, Sweden. · Department of Rheumatology, Örebro University Hospital, Örebro, Sweden. · Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway. · Rheumatology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. · Department of Diagnostic and Biological Sciences, School of Dentistry, University of Minnesota, Minneapolis, USA. · Rheumatology Department, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia; Discipline of Medicine, University of Adelaide, Adelaide, SA 5000, Australia. · Rheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Clinic for Immunology and Rheumatology, Hannover Medical School, 30625 Hannover, Germany. · Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; College of Medicine, University of Cincinnati, Cincinnati, OH, USA; Medical Service, Department of Veterans Affairs Medical Center, Cincinnati, OH, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Pathology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Department of Medicine, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Medical Service, Department of Veterans Affairs Medical Center, Oklahoma City, OK, USA. Electronic address: hal-scofield@omrf.ouhsc.edu. ·Clin Immunol · Pubmed #27109640.

ABSTRACT: Primary Sjögren's syndrome (pSS) has a strong female bias. We evaluated an X chromosome dose effect by analyzing 47,XXY (Klinefelter's syndrome, 1 in 500 live male births) among subjects with pSS. 47,XXY was determined by examination of fluorescence intensity of single nucleotide polymorphisms from the X and Y chromosomes. Among 136 pSS men there were 4 with 47,XXY. This was significantly different from healthy controls (1 of 1254 had 47,XXY, p=0.0012 by Fisher's exact test) as well men with rheumatoid arthritis (0 of 363 with 47,XXY), but not different compared to men with systemic lupus erythematosus (SLE) (4 of 136 versus 8 of 306, Fisher's exact test p=NS). These results are consistent with the hypothesis that the number of X chromosomes is critical for the female bias of pSS, a property that may be shared with SLE but not RA.

23 Article Previous diagnosis of Sjögren's Syndrome as rheumatoid arthritis or systemic lupus erythematosus. 2016

Rasmussen, Astrid / Radfar, Lida / Lewis, David / Grundahl, Kiely / Stone, Donald U / Kaufman, C Erick / Rhodus, Nelson L / Segal, Barbara / Wallace, Daniel J / Weisman, Michael H / Venuturupalli, Swamy / Kurien, Biji T / Lessard, Christopher J / Sivils, Kathy L / Scofield, R Hal. ·Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation. · Department of Oral Diagnosis and Radiology, University of Oklahoma College of Dentistry. · Department of Oral Pathology, University of Oklahoma College of Dentistry, Oklahoma City, OK. · Department of Ophthalmology, Johns Hopkins University, Baltimore, MD, USA King Khaled Eye Specialist Hospital, Riyadh, Kingdom of Saudi Arabia. · College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK. · Department of Oral Surgery, University of Minnesota School of Dentistry. · Department of Medicine, Hennepin County Medical Center, Minneapolis, MN. · Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA. · Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation College of Medicine, Department of Medicine, Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center and. · Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation College of Medicine, Department of Medicine, Section of Endocrinology and Diabetes, University of Oklahoma Health Sciences Center and Department of Medicine, The Department of Veterans Affairs Medical Center, Oklahoma City, OK, USA Hal-Scofield@omrf.org. ·Rheumatology (Oxford) · Pubmed #26998859.

ABSTRACT: OBJECTIVE: The diagnosis of SS is often difficult and many patients are symptomatic for years with other diagnoses before confirmation of SS. Our aim was to determine whether overlapping clinical and serologic features with RA and SLE may in part drive the misdiagnoses. METHODS: A total of 1175 sicca patients were evaluated in a multidisciplinary clinic and classified as having SS based on the American-European Consensus Group Criteria. They were interrogated for a past history of suspicion or diagnosis of RA, SLE or SSc. These diseases were confirmed or ruled out by applying the corresponding classification criteria if the patients responded affirmatively. RESULTS: Of these, 524 (44.6%) subjects reported previous diagnosis or suspicion of RA, SLE or SSc, which was confirmed in 130 (24.8%) but excluded in 394 (75.2%) subjects. Of those previously diagnosed with another illness, 183 (34.9%) met the criteria for primary SS. RF was present in 70/191 patients with previous diagnosis of RA compared with 445/845 without a prior RA diagnosis (P = 3.38E-05), while 128/146 with a diagnosis of SLE had positive ANA compared with 622/881 without the diagnosis (P = 8.77E-06). Age also influenced former diagnoses: people with suspected RA were older than those without the diagnosis (P = 5.89E-06), while patients with SLE suspicion were younger (P = 0.0003). Interestingly, the previous diagnoses did not significantly delay a final classification of SS. CONCLUSION: Among subjects classified as SS, the presence of a positive ANA or RF was associated with a previous, apparently erroneous diagnosis of SLE or RA, respectively.

24 Article X Chromosome Dose and Sex Bias in Autoimmune Diseases: Increased Prevalence of 47,XXX in Systemic Lupus Erythematosus and Sjögren's Syndrome. 2016

Liu, Ke / Kurien, Biji T / Zimmerman, Sarah L / Kaufman, Kenneth M / Taft, Diana H / Kottyan, Leah C / Lazaro, Sara / Weaver, Carrie A / Ice, John A / Adler, Adam J / Chodosh, James / Radfar, Lida / Rasmussen, Astrid / Stone, Donald U / Lewis, David M / Li, Shibo / Koelsch, Kristi A / Igoe, Ann / Talsania, Mitali / Kumar, Jay / Maier-Moore, Jacen S / Harris, Valerie M / Gopalakrishnan, Rajaram / Jonsson, Roland / Lessard, James A / Lu, Xianglan / Gottenberg, Jacques-Eric / Anaya, Juan-Manuel / Cunninghame-Graham, Deborah S / Huang, Andrew J W / Brennan, Michael T / Hughes, Pamela / Illei, Gabor G / Miceli-Richard, Corinne / Keystone, Edward C / Bykerk, Vivian P / Hirschfield, Gideon / Xie, Gang / Ng, Wan-Fai / Nordmark, Gunnel / Eriksson, Per / Omdal, Roald / Rhodus, Nelson L / Rischmueller, Maureen / Rohrer, Michael / Segal, Barbara M / Vyse, Timothy J / Wahren-Herlenius, Marie / Witte, Torsten / Pons-Estel, Bernardo / Alarcon-Riquelme, Marta E / Guthridge, Joel M / James, Judith A / Lessard, Christopher J / Kelly, Jennifer A / Thompson, Susan D / Gaffney, Patrick M / Montgomery, Courtney G / Edberg, Jeffrey C / Kimberly, Robert P / Alarcón, Graciela S / Langefeld, Carl L / Gilkeson, Gary S / Kamen, Diane L / Tsao, Betty P / McCune, W Joseph / Salmon, Jane E / Merrill, Joan T / Weisman, Michael H / Wallace, Daniel J / Utset, Tammy O / Bottinger, Erwin P / Amos, Christopher I / Siminovitch, Katherine A / Mariette, Xavier / Sivils, Kathy L / Harley, John B / Scofield, R Hal. ·Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA. · College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA. · College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. · Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. · U.S. Department of Veterans Affairs Medical Center, Oklahoma City, OK 73104, USA. · Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. · U.S. Department of Veterans Affairs Medical Center, Cincinnati, Ohio, USA. · Department of Ophthalmology, Howe Laboratory, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA. · Department of Oral Diagnosis and Radiology, College of Dentistry, University of Oklahoma Health Sciences Center, Oklahoma City, USA. · Dean McGee Eye Institute and Department of Ophthalmology, University of Oklahoma College of Medicine, Oklahoma City, OK, USA. · Department of Clinical Laboratory Sciences, University of Texas at El Paso, El Paso, TX 79968. · Department of Developmental and Surgical Sciences, University of Minnesota, Minneapolis, MN, USA. · Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen 5021, Norway. · Department of Rheumatology, Haukeland University Hospital, Bergen 5021, Norway. · Valley Bone & Joint Clinic, 3035 DeMers Avenue, Grand Forks, ND 58201, USA. · Strasbourg University, Strasbourg, France. · Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia. · Division of Genetics and Molecular Medicine and Division of Immunology, Infection and Inflammatory Disease, King's College London, London. · Department of Oral Medicine, Carolinas Medical Center, Charlotte, NC 28232, USA. · Sjögren's Syndrome Clinic, National Institute of Dental and Craniofacial Research, Molecular Physiology and Therapeutics Branch, National Institutes of Health, Bethesda, MD 20892, USA. · Department of Rheumatology, Université Paris-Sud, AP-HP, INSERM U1012, Le Kremlin-Bicêtre, France. · Department of Medicine, Mount Sinai Hospital and University of Toronto, Toronto, Ontario. · Hospital for Special Surgery, New York, USA. · NIHR Biomedical Research Unit, University of Birmingham, Birmingham, UK. · Lunenfeld Tanenbaum and Toronto General Research Institutes, Departments of Medicine, Immunology and Molecular Genetics, University of Toronto, Toronto Ontario. · Musculoskeletal Research Group, Institute of Cellular Medicine & NIHR Newcastle Biomedical Research Centre, Newcastle University, Newcastle upon Tyne, United Kingdom. · Section of Rheumatology, Department of Medical Sciences and Science for Life Laboratory, Uppsala University, Uppsala, Sweden. · Rheumatology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. · Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway. · Department of Diagnostic and Biological Sciences, School of Dentistry, University of Minnesota, Minneapolis, USA. · Rheumatology Department, The Queen Elizabeth Hospital, Woodville South, SA 5011, Australia. · Discipline of Medicine, University of Adelaide, Adelaide, SA 5000, Australia. · Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA. · Rheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Clinic for Immunology and Rheumatology, Hannover Medical School, 30625 Hannover, Germany. · Sanatorio Parque, Rosario, Argentina. · Center Pfizer, University of Granada, Andalusian Government for Genomics and Oncological Research, PTS Granada, 18016, Spain. · Division of Clinical Immunology and Rheumatology, University of Alabama, Birmingham, AL. · Center for Public Health Genomics and Department of Biostatistical Sciences, Division of Public Health Sciences, Wake Forest University, Winston-Salem, NC. · Division of Rheumatology & Immunology, Medical University of South Carolina, Charleston, SC. · Ralph H. Johnson VA Medical Center, Charleston, SC. · Division of Rheumatology, Department of Medicine, UCLA School of Medicine. · Division of Rheumatology, Department of Medicine, University of Michigan College of Medicine, Ann Arbor, Michigan. · Division of Rheumatology, Hospital for Special Surgery and Weill Cornell Medical College, New York, NY. · Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA. · University of Chicago Pritzker School of Medicine, Chicago, IL. · Charles R. Bronfman Institute for personalized medicine, Mount Sinai Hospital, 1468 Madison Avenue, New York, NY 10029. · Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Hanover, NH, USA. · Rhumatologie, Responsable de l'Unité de Recherche Clinique Hôpitaux Universitaire Paris-Sud Université Paris-Sud, INSERM U1184 Head of Autoimmunity team, IMVA : Immunology of viral Infections and Autoimmune Diseases. ·Arthritis Rheumatol · Pubmed #26713507.

ABSTRACT: OBJECTIVE: More than 80% of autoimmune disease predominantly affects females, but the mechanism for this female bias is poorly understood. We suspected that an X chromosome dose effect accounts for this, and we undertook this study to test our hypothesis that trisomy X (47,XXX; occurring in ∼1 in 1,000 live female births) would be increased in patients with female-predominant diseases (systemic lupus erythematosus [SLE], primary Sjögren's syndrome [SS], primary biliary cirrhosis, and rheumatoid arthritis [RA]) compared to patients with diseases without female predominance (sarcoidosis) and compared to controls. METHODS: All subjects in this study were female. We identified subjects with 47,XXX using aggregate data from single-nucleotide polymorphism arrays, and, when possible, we confirmed the presence of 47,XXX using fluorescence in situ hybridization or quantitative polymerase chain reaction. RESULTS: We found 47,XXX in 7 of 2,826 SLE patients and in 3 of 1,033 SS patients, but in only 2 of 7,074 controls (odds ratio in the SLE and primary SS groups 8.78 [95% confidence interval 1.67-86.79], P = 0.003 and odds ratio 10.29 [95% confidence interval 1.18-123.47], P = 0.02, respectively). One in 404 women with SLE and 1 in 344 women with SS had 47,XXX. There was an excess of 47,XXX among SLE and SS patients. CONCLUSION: The estimated prevalence of SLE and SS in women with 47,XXX was ∼2.5 and ∼2.9 times higher, respectively, than that in women with 46,XX and ∼25 and ∼41 times higher, respectively, than that in men with 46,XY. No statistically significant increase of 47,XXX was observed in other female-biased diseases (primary biliary cirrhosis or RA), supporting the idea of multiple pathways to sex bias in autoimmunity.

25 Article Chest pain in lupus patients: the emergency department experience. 2015

Modi, Masoom / Ishimori, Mariko L / Sandhu, Vaneet K / Wallace, Daniel J / Weisman, Michael H. ·Division of Rheumatology, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Suite B131, Los Angeles, CA, 90048, USA. · Division of Rheumatology, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Suite B131, Los Angeles, CA, 90048, USA. weisman@cshs.org. ·Clin Rheumatol · Pubmed #25912215.

ABSTRACT: Heart disease, a major cause of morbidity and mortality in SLE patients, often manifests as chest pain (CP). Our goal was to understand the prevalence and outcome of CP presentations for SLE patients in the emergency department (ED). Billing records of patients who presented to Cedars-Sinai Medical Center ED with ICD-9 codes for SLE and secondary ICD-9 codes for CP (786.50-786.59) between March 2009 and October 2013 were reviewed. Two study groups were formed: discharge from ED versus hospital admission. Visits were evaluated for basic cardiac work-up with an electrocardiogram (EKG) and cardiac enzymes; hospital admissions were evaluated for CP etiology and discharge diagnoses. Of 2675 ED visits with ICD-9 codes for SLE, 397 visits had secondary codes for CP (15%); 173 were discharged and 224 became hospital admissions. While 92% of admissions had basic cardiac work-up, over 50% had chest pain attributed to non-cardiac causes. Only 7.2% had a discharge diagnosis related to cardiovascular disease. Fifteen percent of all SLE coded patients had complaints of CP, a figure higher than the national average for non-SLE CP (10%). There is a majority of non-cardiac diagnoses given to SLE patients at discharge. CP is likely to be a window of opportunity to address the known cardiac morbidity and mortality in SLE patients perhaps at an early stage of development of this complication. Our study strengthens the need for more investigations to assess the etiology of CP in this population.

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