scholarly journals Improvement in 5-year mortality in incident rheumatoid arthritis compared with the general population—closing the mortality gap

2016 ◽  
Vol 76 (6) ◽  
pp. 1057-1063 ◽  
Author(s):  
Diane Lacaille ◽  
J Antonio Avina-Zubieta ◽  
Eric C Sayre ◽  
Michal Abrahamowicz

ObjectiveExcess mortality in rheumatoid arthritis (RA) is expected to have improved over time, due to improved treatment. Our objective was to evaluate secular 5-year mortality trends in RA relative to general population controls in incident RA cohorts diagnosed in 1996–2000 vs 2001–2006.MethodsWe conducted a population-based cohort study, using administrative health data, of all incident RA cases in British Columbia who first met RA criteria between January 1996 and December 2006, with general population controls matched 1:1 on gender, birth and index years. Cohorts were divided into earlier (RA onset 1996–2000) and later (2001–2006) cohorts. Physician visits and vital statistics data were obtained until December 2010. Follow-up was censored at 5 years to ensure equal follow-up in both cohorts. Mortality rates, mortality rate ratios and HRs for mortality (RA vs controls) using proportional hazard models adjusting for age, were calculated. Differences in mortality in RA versus controls between earlier and later incident cohorts were tested via interaction between RA status (case/control) and cohort (earlier/later).Results24 914 RA cases and controls experienced 2747 and 2332 deaths, respectively. Mortality risk in RA versus controls differed across incident cohorts for all-cause, cardiovascular diseases (CVD) and cancer mortality (interactions p<0.01). A significant increase in mortality in RA versus controls was observed in earlier, but not later, cohorts (all-cause mortality adjusted HR (95% CI): 1.40 (1.30 to 1.51) and 0.97 (0.89 to 1.05), respectively).ConclusionsIn our population-based incident RA cohort, mortality compared with the general population improved over time. Increased mortality in the first 5 years was observed in people with RA onset before, but not after, 2000.

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 56.1-57
Author(s):  
E. Myasoedova ◽  
J. M. Davis ◽  
S. Achenbach ◽  
K. Wright ◽  
R. Kurmann ◽  
...  

Background:Heart failure (HF) is one of the most common cardiovascular conditions in patients with rheumatoid arthritis (RA). Previous studies showed a 2-fold excess risk of HF in RA versus the general population (1). Whether this has changed over time is not known. Longitudinal studies on trends in occurrence of HF in RA patients over time, and studies comparing trends in HF in RA versus the general population are lacking.Objectives:1) To assess trends in incidence of HF in patients with incident RA in 1980-2009; and 2) To compare incidence of HF in RA patients and population-based comparators without RA with RA incidence/ index date in 1980-2009.Methods:The study population comprised Olmsted County, Minnesota residents with incident RA (age ≥18 years, 1987 ACR criteria met in 1980-2009) and non-RA subjects from the same underlying population with similar age, sex and calendar year of index. All subjects were followed until death, migration, or 04/30/2019. Incident HF was defined using Framingham criteria. Patients with HF prior to RA incidence/index date were excluded. Cox proportional hazards models were used to compare incident HF events by decade, adjusting for age, sex and cardiovascular risk factors: smoking, obesity, diabetes mellitus, hypertension, dyslipidemia. Cumulative incidence of HF adjusted for death was also computed.Results:The study included 905 patients with RA (mean age 55.9 years; 69% female; median follow-up 13.4 years). The 10-year cumulative incidence of HF in RA cohort in the 1980s was 8.5% (95%CI 5.3-13.6%), 1990s was 10.8% (95%CI 7.7-15.1%), and 2000s was 7.1% (95%CI 4.9-10.3%). There was no difference in incidence of HF in 1990s (hazard ratio [HR] 0.91, 95% Confidence Interval [CI] 0.62-1.35) and 2000s (HR 0.73; 95%CI 0.46-1.18) compared to 1980s. Patients with incident RA were then compared to 903 individuals without RA (mean age 56.0 years; 69% female; median follow-up 13.8 years). The 10-year cumulative incidence of HF in these individuals in the 1980s was 7.4% (95%CI 4.5-12.3%), 1990s was 7.5% (95%CI 4.9-11.3%), and 2000s was 7.3% (95%CI 5.0-10.7%). Similar to RA, there was no statistically significant difference in incidence of HF in 1990s (HR 0.96, 95%CI 0.60-1.51) and 2000s (HR 0.75, 95%CI 0.44-1.30) compared to the 1980s. When comparing the risk of HF in RA and non-RA subjects, patients with RA in 2000s had no excess in HF risk as compared to the general population (HR 1.14, 95%CI 0.73-1.78, Figure 1). This is in contrast to the 2-fold excess risk of HF in patients with RA in 1980s (HR 2.20, 95%CI 1.44-3.34) and ~1.5-fold increase in risk of HF in 1990s (HR 1.54, 95%CI 1.04-2.29).Figure 1.Cumulative incidence of any HF event in RA and non-RA patients by decade of RA incidence/indexConclusion:We found a reduction in excess HF risk in patients with RA compared to individuals without RA in 2000s compared to 1980s. There were no statistically significant changes in incidence of HF in patients with RA and in individuals without RA over time. More studies are needed to understand the reasons and implications of these trends.References:[1]Nicola PJ, et al. The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years. Arthritis Rheum 2005;52:412–20.Acknowledgements:This work was supported by a grant from the National Institutes of Health, NIAMS (R01 AR46849) and NHLBI (HL120859). Research reported in this publication was supported by the National Institute of Aging of the National Institutes of Health under Award Number R01AG034676. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.Disclosure of Interests:Elena Myasoedova: None declared, John M Davis III Grant/research support from: Pfizer, Sara Achenbach: None declared, Kerry Wright: None declared, Reto Kurmann: None declared, Rekha Mankad: None declared, Veronique Roger: None declared, Cynthia S. Crowson: None declared


2013 ◽  
Vol 55 (4) ◽  
pp. 267-275 ◽  
Author(s):  
Tjard R. Schermer ◽  
Winifred Malbon ◽  
Robert Adams ◽  
Michael Morgan ◽  
Michael Smith ◽  
...  

Rheumatology ◽  
2020 ◽  
Author(s):  
Liselotte Tidblad ◽  
Helga Westerlind ◽  
Bénédicte Delcoigne ◽  
Johan Askling ◽  
Saedis Saevarsdottir

Abstract Objectives Comorbidities contribute to the morbidity and mortality in rheumatoid arthritis (RA), and are thus important to capture and treat early. In contrast to the well-studied comorbidity risks in established RA, less is known about the comorbidity pattern up until diagnosis of RA. We therefore compared if the occurrence of defined conditions, and the overall comorbidity burden at RA diagnosis, is different from that in the general population, and if it differs between seropositive and seronegative RA. Methods Using Swedish national clinical and demographic registers, we identified new-onset RA patients (n = 11 086), and matched (1:5) to general population controls (n = 54 813). Comorbidities prior to RA diagnosis were identified in the Patient and Prescribed Drug Registers, and compared using logistic regression. Results At diagnosis of RA, respiratory (OR = 1.58, 95% CI = 1.44–1.74), endocrine (OR = 1.39, 95% CI = 1.31–1.47), and certain neurological diseases (OR = 1.73, 95% CI = 1.59–1.89) were more common in RA vs controls, with a similar pattern in seropositive and seronegative RA. In contrast, psychiatric disorders (OR = 0.87, 95% CI = 0.82–0.92) and malignancies (OR = 0.88, 95% CI = 0.79–0.97) were less commonly diagnosed in RA vs controls. The comorbidity burden was slightly higher in RA patients compared with controls (p&lt; 0.0001). Conclusion We found several differences in comorbidity prevalence between patients with new-onset seropositive and seronegative RA compared with matched controls from the general population. These findings are important both for our understanding of the evolvement of comorbidities in established RA and for early detection of these conditions.


2014 ◽  
Vol 74 (6) ◽  
pp. 1212-1217 ◽  
Author(s):  
Elizabeth V Arkema ◽  
Jerker Jonsson ◽  
Eva Baecklund ◽  
Judith Bruchfeld ◽  
Nils Feltelius ◽  
...  

ObjectiveTo estimate the risk of tuberculosis (TB) in patients with rheumatoid arthritis (RA) both with and without exposure to biological therapy and to directly compare the risks between therapies.MethodsData from the Swedish National Population Registers, Tuberculosis Register and the Swedish Biologics Register were used to conduct a prospective population-based national cohort study (2002–2011). We estimated the rate of incident TB in the general population and in a cohort of biological-naïve and biological-exposed patients diagnosed with RA. Cox models were used to estimate HRs with particular attention to risks by calendar and follow-up time and individual biologics.ResultsCompared to the general population, RA patients not exposed to biologicals had a fourfold increased risk of TB (HR 4.2; 95% CI 2.7 to 6.7), which did not decline over calendar time. In contrast, the risk of TB in the biological-exposed RA population decreased since 2002 compared with biological-naïve; from HR=7.9 (95% CI 3.3 to 18.9) in 2002–2006 to HR=2.4 (95% CI 0.9 to 6.1) in 2007–2011. The HRs for most recent exposure to adalimumab and infliximab compared with etanercept were 3.1 (95% CI 0.8 to 12.5) and 2.7 (95% CI 0.7 to 10.9), respectively, and the HR for etanercept compared with biological-naïve RA was 1.7 (95% CI 0.6 to 4.6).ConclusionsIn the past decade, the risk of TB has decreased among biological-exposed RA patients but remains higher than in biological-naïve RA patients. Most cases of TB in RA occur in biological-naïve RA patients, underscoring the elevated risk also in these patients.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 15-17
Author(s):  
Renata Abrahao ◽  
Ann M Brunson ◽  
Justine M. Kahn ◽  
Qian Li ◽  
Aaron S Rosenberg ◽  
...  

Introduction Second primary malignancy (SPM) is one of the most devastating late complications following Hodgkin lymphoma (HL) treatment. Historically, the most common SPMs in patients treated for HL are solid tumors, which are largely related to radiation exposure during initial therapy. For the last three decades, efforts to address the risk of SPM after HL therapy have focused on reducing exposure to radiation, as well as refining the approach for patients where radiation is indicated. To date, few population-based studies in the United States have quantified the burden of SPMs and evaluated the potential effect of changes in therapeutic management over time. Additionally, to our knowledge, no study has compared SPM risk between human immunodeficiency virus (HIV)-infected and HIV-uninfected HL survivors. Methods We used data from the California Cancer Registry on 21,043 patients diagnosed with primary HL between 1988 and 2015 with follow-up through 2017. We calculated standardized incidence ratios (SIRs) with corresponding 95% confidence intervals (CIs) and absolute excess risks (AERs) to compare SPM incidence in our HL cohort with the expected number of first primary cancer incidence in the general California population, based on patient's age at diagnosis (5-year categories), sex, calendar year (3-year intervals), cancer site, and race/ethnicity. SIRs are presented by HIV status, SPM latency, treatment era, and cancer type. P-values for trends were used to examine whether SPM risk changed over time. Findings Among 20,303 HIV-uninfected patients (median follow-up of 14.1 years), overall SPM risk was increased 1.95-fold compared with the general population (SIR=1.95, 95% CI 1.86-2.04). In 740 HIV-infected patients (median follow-up of 11.7 years), overall risk was increased 2.68-fold compared with the general population (SIR=2.68, 95% CI 2.0-3.40), translating to an 37% higher incidence of SPM in HIV-infected vs. HIV-uninfected patients. The AER (per 10,000 person-years) of SPM was 43.1 in HIV-uninfected and 76.5 in HIV-infected patients, resulting in a 33.4 excess SPM per 10,000 person-years in HL survivors with HIV. Malignancies that contributed the most to overall AER were non-Hodgkin lymphoma (NHL), female breast and lung cancers in HIV-uninfected patients; and Kaposi sarcoma, NHL, anorectal and head & neck (HNC) cancers in HIV-infected patients. Notably, among HIV-uninfected patients, the highest overall risk of SPM occurred ≥20 years after diagnosis (SIR= 2.27, 95% CI 1.99-2.58) (Figure). In contrast, the highest overall risk in HIV-infected patients was observed &lt;2 years after diagnosis (SIR=4.42, 95% CI 2.53-7.19). Radiation used decreased from 46.9% in 1988-1996 to 29.5% in 2007-2015. Among HIV-uninfected patients, there was a trend towards decreased risk over time of overall and selected solid SPMs (lung, female breast, and gastrointestinal cancers) (Table). In an analysis restricted to HIV-uninfected patients who received radiation irrespective of chemotherapy, findings also suggested a declined risk of overall and selected solid SPMs over time: any solid (SIR=2.15 in 1988-1996 and SIR=1.30 in 2007-2015, p&lt;0.0001), lung (SIR=3.69 in 1988-1996 and SIR=1.81 in 2007-2015, p=0.0031), and female breast (SIR=2.95 in 1988-1996 and SIR=0.63 in 2007-2015, p&lt;0.0001). Conclusion Compared with the general population, the risk of developing a SPM following HL treatment was significantly higher among both HIV-uninfected and HIV-infected patients, with the absolute excess risk greater for those with HIV infection. There were different temporal patterns and types of SPM between HIV-uninfected and HIV-infected patients. These findings prompt the question on whether earlier and/or more intensive cancer screening should be pursued for HIV-infected survivors. The trend towards decreased risk for selected solid SPMs among HIV-uninfected patients, especially lung and female breast cancers, suggest that strategies to reduce radiation in HL survivors may be working. Despite promising trends in this group, the observation that SPM risk was highest ≥20 years after initial therapy further highlights the need for long-term surveillance and survivorship care in this at-risk population. Disclosures Rosenberg: Takeda: Speakers Bureau; Janssen: Speakers Bureau; Amgen: Membership on an entity's Board of Directors or advisory committees; Seattle Genetics: Membership on an entity's Board of Directors or advisory committees. Wun:Glycomimetics, Inc.: Consultancy.


2019 ◽  
Vol 71 (11) ◽  
pp. 2825-2832 ◽  
Author(s):  
Jacob Bodilsen ◽  
Michael Dalager-Pedersen ◽  
Diederik van de Beek ◽  
Matthijs C Brouwer ◽  
Henrik Nielsen

Abstract Background We aimed to determine the long-term risks of mortality and new-onset epilepsy after brain abscess. Methods Using nationwide population-based medical registries, we examined all patients with first-time brain abscess in Denmark, 1982–2016. Comparison cohorts individually matched on age, sex, and residence were identified, as were siblings of all study participants. Next, we computed cumulative incidences and hazard rate ratios (HRRs) with 95% confidence intervals of mortality and new-onset epilepsy among study populations. Results We identified 1384 brain abscess patients (37% females) with a median follow-up time of 5.9 years (interquartile range [IQR] 1.1–14.2). The 1-year, 2–5 year, and 6–30 year mortality of patients after brain abscess was 21%, 16%, and 27% as compared to 1%, 6%, and 20% for population controls. Cox regression analyses adjusted for Charlson comorbidity index score showed 1-year, 2–5 year, and 6–30 year HRRs of 17.5 (13.9–22.0), 2.61 (2.16–3.16), and 1.94 (1.62–2.31). The mortality in brain abscess patients was significantly increased regardless of sex or age group except among subjects 80 years or older, and in both previously healthy individuals and immunocompromised persons. Among the 30-day survivors of brain abscess (median follow-up 7.6 years [IQR 2.2–15.5]), new-onset epilepsy occurred in 32% compared to 2% in matched population controls. Cause-specific Cox regression analysis adjusted for stroke, head trauma, alcohol abuse, and cancer showed 1-year, 2–5 year, and 6–30 year HRRs for new-onset epilepsy of 155 (78.8–304), 37.7 (23.0–59.9), and 8.93 (5.62–14.2). Conclusions Brain abscess is associated with an increased long-term risk of mortality and new-onset epilepsy for several years after infection.


2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Khalid Almutairi ◽  
Johannes Nossent ◽  
David Preen ◽  
Helen Keen ◽  
Charles Inderjeeth

Abstract Background To describe temporal changes in mortality rates for patients with Rheumatoid arthritis (RA) in relation to comorbidity accrual from 1980-2015 in Western Australia (WA). Methods Using population-level linked data from WA health administrative datasets (hospital morbidity, emergency department and death data) we followed 17,125 RA patients (ICD-10-AM M05.00–M06.99, ICD-9-CM 714) from 1980- 2015. Comorbidity was ascertained using the Charlson Comorbidity Index (CCI). Mortality rate ratios (MRR) were calculated per decade between the RA cohort and the WA general population by direct age standardisation method, Results During 356,069 patient-years, a total of 8955 (52%) deaths occurred in the RA cohort. The highest prevalence of comorbidity (688.6 per 1000 separations) was in the period 1991-2000 following a 1.3% average annual increase since 1980. In-hospital mortality rate was highest (26.7 deaths per 1000 separations) in the same period. After 2001, both RA comorbidity and mortality rates decreased annually by -0.5% and -4.8%, respectively, with annual changes of -4.4% to -2% and from 2011-2015, respectively. The overall mortality rate in RA patients after age adjustment was 2.5-times (95%CI: 2.52-2.65) higher than the general population between 1980-2015 and 1.5-times (95%CI: 1.39-1.81) for 2011-2015. Conclusions The annual comorbidity prevalence and mortality rates in WA have decreased significantly since 2001 reflecting improvements in the management of RA and comorbidity. Key messages The mortality rate in Rheumatoid Arthritis patients in Western Australia remains 1.5-times higher than their community.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Christina Bergqvist ◽  
François Hemery ◽  
Arnaud Jannic ◽  
Salah Ferkal ◽  
Pierre Wolkenstein

AbstractNeurofibromatosis 1 (NF1) is an inherited, autosomal-dominant, tumor predisposition syndrome with a birth incidence as high as 1:2000. A patient with NF1 is four to five times more likely to develop a malignancy as compared to the general population. The number of epidemiologic studies on lymphoproliferative malignancies in patients with NF1 is limited. The aim of this study was to determine the incidence rate of lymphoproliferative malignancies (lymphoma and leukemia) in NF1 patients followed in our referral center for neurofibromatoses. We used the Informatics for Integrated Biology and the Bedside (i2b2) platform to extract information from the hospital’s electronic health records. We performed a keyword search on clinical notes generated between Jan/01/2014 and May/11/2020 for patients aged 18 years or older. A total of 1507 patients with confirmed NF1 patients aged 18 years and above were identified (mean age 39.2 years; 57% women). The total number of person-years in follow-up was 57,736 (men, 24,327 years; women, 33,409 years). Mean length of follow-up was 38.3 years (median, 36 years). A total of 13 patients had a medical history of either lymphoma or leukemia, yielding an overall incidence rate of 22.5 per 100,000 (0.000225, 95% confidence interval (CI) 0.000223–0.000227). This incidence is similar to that of the general population in France (standardized incidence ratio 1.07, 95% CI 0.60–1.79). Four patients had a medical history leukemia and 9 patients had a medical history of lymphoma of which 7 had non-Hodgkin lymphoma, and 2 had Hodgkin lymphoma. Our results show that adults with NF1 do not have an increased tendency to develop lymphoproliferative malignancies, in contrast to the general increased risk of malignancy. While our results are consistent with the recent population-based study in Finland, they are in contrast with the larger population-based study in England whereby NF1 individuals were found to be 3 times more likely to develop both non-Hodgkin lymphoma and lymphocytic leukemia. Large-scale epidemiological studies based on nationwide data sets are thus needed to confirm our findings.


BMJ Open ◽  
2017 ◽  
Vol 7 (11) ◽  
pp. e016667 ◽  
Author(s):  
Herng-Ching Lin ◽  
Sudha Xirasagar ◽  
Cha-Ze Lee ◽  
Chung-Chien Huang ◽  
Chao-Hung Chen

ObjectiveGastro-oesophageal reflux disease (GORD) is a common comorbidity among patients with rheumatoid arthritis (RA). While GORD has been attributed to the antirheumatic medications, no studies of human cohorts have investigated a link between GORD and RA. This study investigates whether GORD is associated with a subsequent RA diagnosis over a 5-year follow-up using a population-based dataset.SettingTaiwanParticipantsWe used data from the Taiwan Longitudinal Health Insurance Database. The study group consisted of 13 645 patients with an ambulatory claim showing a GORD diagnosis. We used propensity score matching to select 13 645 comparison patients (one per study patient with GORD).InterventionWe tracked each patient’s claims over a 5-year period to identify those who subsequently received a diagnosis of RA. Cox proportional hazard (PH) regression modelling was used for analysis.ResultsOver 5-year follow-up, RA incidence rate per 1000 person-years was 2.81 among patients with GORD and 0.84 among the comparison group. Cox PH modelling showed that GORD was independently associated with a 2.84-fold increased risk of RA (95% CI 2.09 to 3.85) over 5-year follow-up, after adjusting for the number of ambulatory care visits within the year following the index date (to mitigate surveillance bias).ConclusionsWe observed that GORD might associate with subsequent RA occurrence. Because current treatment guidelines for RA emphasise early diagnosis and prompt treatment, the observed association between GORD and RA may help acquaint clinicians to patients with GORD with higher RA risk and facilitate early diagnosis and treatment.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 156.1-156
Author(s):  
E. Yen ◽  
D. Singh ◽  
M. Wu ◽  
R. Singh

Background:Premature mortality is an important way to quantify disease burden. Patients with systemic sclerosis (SSc) can die prematurely of disease, however, the premature mortality burden of SSc is unknown. The years of potential life lost (YPLL), in addition to age-standardized mortality rate (ASMR) in younger ages, can be used as measures of premature death.Objectives:To evaluate the premature mortality burden of SSc by calculating: 1) the proportions of SSc deaths as compared to deaths from all other causes (non-SSc) by age groups over time, 2) ASMR for SSc relative to non-SSc-ASMR by age groups over time, and 3) the YPLL for SSc relative to other autoimmune diseases.Methods:This is a population-based study using a national mortality database of all United States residents from 1968 through 2015, with SSc recorded as the underlying cause of death in 46,798 deaths. First, we calculated the proportions of deaths for SSc and non-SSc by age groups for each of 48 years and performed joinpoint regression trend analysis1to estimate annual percent change (APC) and average APC (AAPC) in the proportion of deaths by age. Second, we calculated ASMR for SSc and non-SSc causes and ratio of SSc-ASMR to non-SSc-ASMR by age groups for each of 48 years, and performed joinpoint analysis to estimate APC and AAPC for these measures (SSc-ASMR, non-SSc-ASMR, and SSc-ASMR/non-SSc-ASMR ratio) by age. Third, to calculate YPLL, each decedent’s age at death from a specific disease was subtracted from an arbitrary age limit of 75 years for years 2000 to 2015. The years of life lost were then added together to yield the total YPLL for each of 13 preselected autoimmune diseases.Results:23.4% of all SSc deaths as compared to 13.5% of non-SSc deaths occurred at <45 years age in 1968 (p<0.001, Chi-square test). In this age group, the proportion of annual deaths decreased more for SSc than for non-SSc causes: from 23.4% in 1968 to 5.7% in 2015 at an AAPC of -2.2% (95% CI, -2.4% to -2.0%) for SSc, and from 13.5% to 6.9% at an AAPC of -1.5% (95% CI, -1.9% to -1.1%) for non-SSc. Thus, in 2015, the proportion of SSc and non-SSc deaths at <45 year age was no longer significantly different. Consistently, SSc-ASMR decreased from 1.0 (95% CI, 0.8 to 1.2) in 1968 to 0.4 (95% CI, 0.3 to 0.5) per million persons in 2015, a cumulative decrease of 60% at an AAPC of -1.9% (95% CI, -2.5% to -1.2%) in <45 years old. The ratio of SSc-ASMR to non-SSc-ASMR also decreased in this age group (cumulative -20%, AAPC -0.3%). In <45 years old, the YPLL for SSc was 65.2 thousand years as compared to 43.2 thousand years for rheumatoid arthritis, 18.1 thousand years for dermatomyositis,146.8 thousand years for myocarditis, and 241 thousand years for type 1 diabetes.Conclusion:Mortality at younger ages (<45 years) has decreased at a higher pace for SSc than from all other causes in the United States over a 48-year period. However, SSc accounted for more years of potential life lost than rheumatoid arthritis and dermatomyositis combined. These data warrant further studies on SSc disease burden, which can be used to develop and prioritize public health programs, assess performance of changes in treatment, identify high-risk populations, and set research priorities and funding.References:[1]Yen EY….Singh RR. Ann Int Med 2017;167:777-785.Disclosure of Interests:None declared


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