Elizabeth V. Arkema

Dr. Elizabeth V. Arkema

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Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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28 July 2016 in European Respiratory Journal
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Journal Article
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EAElizabeth V. Arkema
Elizabeth V. Arkema
JGJohan Grunewald
Johan Grunewald
SKSusanna Kullberg
Susanna Kullberg
AEAnders Eklund
Anders Eklund
JAJohan Askling
Johan Askling
Our objective was to estimate the contemporary incidence and prevalence of sarcoidosis using Swedish population-based register data.Adults with any sarcoidosis-coded visit were identified from the National Patient Register (hospitalisations 1964–2013 and outpatient care 2001–2013). Demographic and medication dispensing data were retrieved from national registers. We estimated the prevalence of sarcoidosis in 2013 overall and by county of residence. The incidence of sarcoidosis during 2003–2012 was estimated by sex, age, education level and year of diagnosis. Case definitions were varied to test their robustness.More than 16 000 individuals had a history of sarcoidosis in 2013. When defined as two or more sarcoidosis-coded visits, the prevalence was 160 per 100 000. Using different definitions, the prevalence ranged from 152 (requiring a specialist visit) to 215 per 100 000 (only one visit required). The highest prevalence was observed in northern less densely populated counties. The incidence was 11.5 per 100 000 per year and varied by −10% to +30% depending on case definition. The incidence peaked in males aged 30–50 years and in females aged 50–60 years, but did not differ by education level and was stable over time.This study represents the largest epidemiological investigation of sarcoidosis using population-based individual-level data. Age at diagnosis in men was 10 years younger than in women and geographical variation was observed.

24 August 2018 in Therapeutic Advances in Chronic Disease
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EAElizabeth V. Arkema
Elizabeth V. Arkema
YCYvette C. Cozier
Yvette C. Cozier
Sarcoidosis is a granulomatous inflammatory disease with unknown etiology. Epidemiological studies have contributed greatly to our knowledge about sarcoidosis, providing critical information on the determinants and distribution of the disease. In this review, we summarize recently published findings from epidemiological studies on sarcoidosis. We review the epidemiological tools used, the incidence and prevalence of disease, mortality and cancer risk after sarcoidosis and nongenetic risk factors for sarcoidosis. Genetics studies have not been included as they deserve a separate review. Leveraging existing epidemiological data to conduct etiological studies aimed towards understanding and preventing disease is critical for future sarcoidosis research.

1 September 2020 in Current Opinion in Pulmonary Medicine
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EAElizabeth V. Arkema
Elizabeth V. Arkema
YCYvette Cozier
Yvette Cozier
Purpose of review The aim of this review is to describe the latest studies on sarcoidosis incidence, prevalence and risk factors with a special focus on reports in the last 2 years. The potential biases affecting these studies are discussed. Recent findings The prevalence and incidence of sarcoidosis vary greatly depending on region of the world. Variations in data sources and settings can affect estimates of the burden of sarcoidosis, sometimes making them difficult to compare across countries. It is not well understood how the distribution of sarcoidosis phenotypes differs across populations. Age, sex and race are the most important sources of variation in incidence and prevalence. Recent epidemiological studies provide new insights on the role of genetic and nongenetic risk factors for sarcoidosis. Summary High-quality and systematically collected data, with depth (detailed information per individual) and breadth (many individuals), is needed to further understand the complexity and heterogeneity of sarcoidosis.

1 November 2014 in Annals of the Rheumatic Diseases
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BLBing Lu
Bing Lu
LHLinda T Hiraki
Linda T Hiraki
JSJeffrey A. Sparks
Jeffrey A. Sparks
SMSusan Malspeis
Susan Malspeis
CCChia-Yen Chen
Chia-Yen Chen
EKElizabeth W Karlson
Elizabeth W Karlson
Objectives To examine the relationship between being overweight or obese and developing rheumatoid arthritis (RA) in two large prospective cohorts, the Nurses’ Health Study (NHS) and Nurses’ Health Study II (NHSII). Methods We followed 109 896 women enrolled in NHS and 108 727 in NHSII who provided lifestyle, environmental exposure and anthropometric information through biennial questionnaires. We assessed the association between time-varying and cumulative Body Mass Index (BMI) in WHO categories of normal, overweight and obese (18.5–<25, 25.0–<30, ≥30.0 kg/m2) and incident RA meeting the 1987 American College of Rheumatology (ACR) criteria. We estimated HRs for overall RA and serologic subtypes with Cox regression models adjusted for potential confounders. We repeated analyses restricted to RA diagnosed at age 55 years or younger. Results During 2 765 195 person-years of follow-up (1976–2008) in NHS and 1 934 518 person-years (1989–2009) in NHSII, we validated 1181 incident cases of RA (826 in NHS, 355 in NHSII). There was a trend toward increased risk of all RA among overweight and obese women (HR (95% CI) 1.37 (0.95 to 1.98) and 1.37 (0.91, 2.09), p for trend=0.068). Among RA cases diagnosed at age 55 years or younger, this association appeared stronger (HR 1.45 (1.03 to 2.03) for overweight and 1.65 (1.34 to 2.05) for obese women (p trend <0.001)). Ten cumulative years of being obese, conferred a 37% increased risk of RA at younger ages (HR 1.37 (1.11 to 1.69)). Conclusions Risks of seropositive and seronegative RA were elevated among overweight and obese women, particularly among women diagnosed with RA at earlier ages.

1 February 2015 in Annals of the Rheumatic Diseases
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Journal Article
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MNM Neovius
M Neovius
EAElizabeth V. Arkema
Elizabeth V. Arkema
HOH Olsson
H Olsson
JEJ K Eriksson
J K Eriksson
LKL E Kristensen
L E Kristensen
RVR van Vollenhoven
R van Vollenhoven
Objective To compare drug survival on adalimumab, etanercept and infliximab in patients with rheumatoid arthritis (RA). Methods Patients with RA (n=9139; 76% women; mean age 56 years) starting their first tumour necrosis factor (TNF) inhibitor between 2003 and 2011 were identified in the Swedish Biologics Register (ARTIS). Data were collected through 31 December 2011. Drug survival over up to 5 years of follow-up was compared overall and by period of treatment start (2003–2005/2006–2009; n=3168/4184) with adjustment for age, sex, education, period, health assessment questionnaire (HAQ), disease duration, concomitant disease modifying antirheumatic drug (DMARD) treatment and general frailty (using hospitalisation history as proxy). Results During 20 198 person-years (mean/median 2.2/1.7 years) of follow-up, 3782 patients discontinued their first biological (19/100 person-years; 51% due to inefficacy, 36% due to adverse events). Compared with etanercept, infliximab (adjusted HR 1.63, 95% CI 1.51 to 1.77) and adalimumab initiators had higher discontinuation rates (1.26, 95% CI 1.16 to 1.37), and infliximab had a higher discontinuation rate than adalimumab (1.28, 95% CI 1.18 to 1.40). These findings were consistent across periods, but were modified by time for adalimumab versus etanercept (p<0.001; between-drug difference highest the 1st year in both periods). The discontinuation rate was higher for starters in 2006–2009 than 2003–2005 (adjusted HR 1.12, 95% CI 1.04 to 1.20). The composition of 1-year discontinuations also changed from 2003–2005 vs 2006–2009: adverse events decreased from 45% to 35%, while inefficacy increased from 43% to 53% (p<0.001). Conclusions Discontinuation rates were higher for infliximab compared with adalimumab and etanercept initiators, and for adalimumab versus etanercept during the 1st year. Discontinuation rates increased with calendar period, as did the percentage discontinuations due to inefficacy.

1 January 2017 in Annals of the Rheumatic Diseases
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KHKarin Hellgren
Karin Hellgren
LDLene Dreyer
Lene Dreyer
EAElizabeth V. Arkema
Elizabeth V. Arkema
BGBente Glintborg
Bente Glintborg
LJLennart T H Jacobsson
Lennart T H Jacobsson
JAJohan Askling
Johan Askling
Background Safety data on cancer risks following tumour necrosis factor α inhibitors (TNFi) in patients with spondyloarthritis (SpA) (here defined as ankylosing spondylitis (AS), undifferentiated spondarthropaties (SpA UNS), psoriatic arthritis (PsA)) are scarce. Our objective was to assess risks for cancer overall and for common subtypes in patients with SpA treated with TNFi compared with TNFi-naïve patients with SpA and to the general population. Methods From the Swedish (Anti-Rheumatic Therapy in Sweden (ARTIS)) and Danish (DANBIO) biologics registers, we assembled 8703 (ARTIS=5448, DANBIO=3255) patients with SpA initiating a first TNFi 2001–2011. From the Swedish National Patient and Population Registers we assembled a TNFi-naïve SpA cohort (n=28,164) and a Swedish age-matched and sex-matched general population comparator cohort (n=131 687). We identified incident cancers by linkage with the nationwide Swedish and Danish Cancer Registers 2001–2011, and calculated age-standardised and sex-standardised incidence ratios as measures of relative risk (RR). Results Based on 1188 cancers among the TNFi-naïve patients with SpA, RR of cancer overall was 1.1 (95% CI 1.0 to 1.2). Based on 147 cancers among TNFi initiators with SpA, RR versus TNFi-naïve was 0.8 (95% CI 0.7 to 1.0) and results were similar for AS and PsA when analysed separately. Site-specific cancer RRs: prostate 0.5 (95% CI 0.3 to 0.8), lung 0.6 (95% CI 0.3 to 1.3), colorectal 1.0 (95% CI 0.5 to 2.0), breast 1.3 (95% CI 0.9 to 2.0), lymphoma 0.8 (95% CI 0.4 to 1.8) and melanoma 1.4 (95% CI 0.7 to 2.6). Conclusions In patients with SpA, treatment with TNFi was not associated with increased risks of cancer, neither overall nor for the six most common cancer types.