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Seminars in Arthritis and Rheumatism 50 (2020) 571 575

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Seminars in Arthritis and Rheumatism


journal homepage: www.elsevier.com/locate/semarthrit

Mortality in psoriatic arthritis: Risk, causes of death, predictors for death


Ofir Elaloufa,b, Anastasiya Muntyanua, Ari Polachekb, Daniel Pereiraa, Justine Y. Yea,
Ker-Ai Leec, Vinod Chandrana,d,e, Richard J. Cookc, Dafna D. Gladmana,e,*
a
Centre for Prognostic Studies in the Rheumatic Diseases, Toronto Western Hospital, University of Toronto, Toronto, ON Canada
b
Department of Rheumatology, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
c
Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, ON Canada
d
Departments of Medicine, Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON Canada
e
Institute of Medical Science, University of Toronto, Toronto, ON Canada

A R T I C L E I N F O A B S T R A C T

Keywords: Background/Objectives: Mortality studies in psoriatic arthritis (PsA) have provided inconsistent results. This
Psoriatic arthritis study aimed to: 1) Estimate trends in mortality rates among PsA patients over calendar time; 2) Evaluate
Mortality cause-specific mortality rates in patients with PsA compared to the general population; 3) Identify predictors
Standardized mortality ratios for mortality in PsA.
Cause specific mortality
Methods: The study was carried out at the University of Toronto Psoriatic Arthritis Clinic where patients are
followed prospectively according to a standard protocol at 6- to 12- month intervals. Standardized mortality
ratios (SMRs) were calculated overall, by age, and by sex with reference to the Ontario population. Causes of
death were recorded by ICD9 and ICD10 codes and cause-specific SMRs were computed. Cox regression mod-
els were used to identify predictors for mortality among PsA patients.
Results: Among 1490 patients followed over 15062.8 patient-years, 225 (15%) confirmed deaths were
recorded (111 females, 114 males). The overall SMR was 0.92 (95% CI: 0.81-1.05), the sex-specific SMRs were
1.08 (95% CI: 0.89-1.30) for females and 0.81 (95% CI: 0.66-0.97) for males. The age-specific SMRs were 3.36
(95% CI: 1.61-6.18), 0.97 (95% CI: 0.68-1.34), 0.88 (95% CI: 0.73-1.06) and 0.86 (95% CI: 0.66-1.11) for 20-39,
40-59, 60-79 and above 80 years of age, respectively. Major causes of death included malignant neoplasms
(n=61; SMR=0.97, 95% CI: 0.72-1.28), acute myocardial infarction (n=32; SMR=1.11, 95% CI: 0.74-1.58), and
pneumonia (n=14; SMR=2.46, 95% CI: 1.27-4.31). Factors found to be associated with increased mortality
include elevated acute phase reactants, presence of comorbidities such as heart disease and cancer, and
lower education level.
Conclusion: Young patients with PsA are at increased mortality risk. Better control of comorbidities may
reduce this risk.
© 2020 Published by Elsevier Inc.

Introduction (SMR) of 1.62 (95% confidence interval (CI): 1.21-2.12) in PsA


patients compared to the general population, in a longitudinal
Psoriasis is a chronic inflammatory skin disease, affecting 2-3% of observational cohort study conducted at the University of Toronto
the world's population. Psoriatic arthritis (PsA) is an inflammatory between 1978 and 1993. A follow up study from the same centre
musculoskeletal disease that affects 20-30% of psoriasis patients and 10 years later, reported overall increased SMR of 1.36 (95% CI: 1.12-
can lead to significant joint damage and disability. PsA is considered 1.64) for the period of 1978-2004, and an estimated life-years loss
a systemic disease with well-established comorbidities such as of 2.99 (95% CI: 1.14 -4.77). An improved trend in mortality risk was
depression, obesity, type 2 diabetes, hypertension, metabolic syn- observed in patients entering the cohort in a later calendar period,
drome, fatty liver, and cardiovascular events. [1] [3] with SMRs of 1.89, 1.83, and 1.21 for follow-up periods
Data regarding mortality in psoriatic disease have been pub- 1978 1986, 1987 1995, and 1996 2004, respectively. The
lished since the end of the last century, with inconsistent results. improved survival was attributed to earlier diagnosis and more
Wong et al. [2] reported an increased standardized mortality ratio aggressive treatment in the more recent follow up period. Others
have reported conflicting results about mortality risk in patients
with PsA. [4, 5]
* Corresponding author: Institute of Medical Science, University of Toronto, Toronto,
ON Canada The aims of this study were to: 1. Estimate the mortality over a
E-mail address: dafna.gladman@utoronto.ca (D.D. Gladman). 40-year period; 2. Estimate the risk for different causes of death, and

https://doi.org/10.1016/j.semarthrit.2020.04.001
0049-0172/© 2020 Published by Elsevier Inc.
572 O. Elalouf et al. / Seminars in Arthritis and Rheumatism 50 (2020) 571 575

for age- and sex-specific SMRs among these patients; 3. Identify fac- Descriptive tables were constructed using SAS (version 9.3; SAS
tors associated with mortality. Institute, Cary, NC, USA) while SMR calculations and Cox regression
analysis were performed using R version 3.5.1 (2018).
Patients and methods

Setting Results

Patients who were enrolled into the University of Toronto PsA During the period of January 1, 1978 through December 31, 2017,
Clinic between January 1, 1978 and December 31, 2017 were 1490 patients were enrolled into the University of Toronto PsA clinic. Of
included in the study. these 1490 patients, 830 (56%) were males and 660 (44%) were females.
Patients are referred from family doctors, rheumatologists, der- There were 225 (15%) confirmed deaths among 111 female and 114
matologists and other medical specialists. The clinic serves as a pri- male individuals. Patients’ characteristics are presented in Table 1.
mary, secondary, and tertiary referral center and provides clinical Assuming these lost to follow up patients were still alive at the end
care to patients with a broad spectrum of disease severity. of 2017, the number of years of follow-up was 15062.8 (8482.6 for
men, and 6580.2 for women). The mean age of the patients entering
Assessments the clinic was 44.5 years (SD 13.2). Mean age at psoriasis onset was
28.7 years (SD 14.7), while mean age at PsA onset was 38.2 years (SD
Patients are evaluated at the initial clinic visit and subsequently 13.7). Mean PsA duration at entry to the clinic was 6.3 years (SD 7.9).
every 6-12 months according to a standard protocol. [6] The prospec- Causes of death are presented in Table 2. The leading causes were
tively collected data are stored in a web-based database that include malignant neoplasm (n=61), acute myocardial infarction (n=32) and
demographics, personal and family medical history, smoking and pneumonia (n=14). The cause of death could not be retrieved in 25
alcohol drinking habits, medications, skin and musculoskeletal dis- cases. The overall SMR comparing the mortality of the PsA cohort to
ease activity, imaging, and laboratory findings. [7] Most of the the general population of Ontario for the study period between 1978
patients (98%) fulfill the ClASsification for Psoriatic ARthritis (CAS- and 2017 was 0.92 (95% CI: 0.80-1.05). The sex-specific SMRs for the
PAR) criteria for classification of PsA. [8, 9] same period were 1.08 (95% CI: 0.89-1.30) for females, and 0.81 (95%
CI: 0.66-0.97) for males. Overall SMRs throughout the years as pre-
Death and Causes of Death sented by 10-year rolling SMRs (Fig. 1A) show a declining trend from
the 1980s until the present time. A similar trend is seen for the male
Information on patient deaths and causes of death was collected population, while the female population displayed an initial
prospectively through notifications by family members and physi- increased mortality risk, which later decreased as well. Fig. 1B dis-
cians, daily checks of death notices in the newspaper, through linkage plays the 5-year rolled SMRs which show similar patterns for the
with the provincial cancer registry and death registry, and through overall, male and female populations.
telephone interviews and correspondence with family physicians Looking at age-specific SMRs, there is a significant increased mor-
and patients’ relatives. Death certificates, and hospital admission tality in the 20-39 year group with SMR of 3.36 (95% CI: 1.61-6.18),
records were used, where possible, to verify patient death and to while in the other age groups of 40-59 (SMR=0.97, 95% CI: 0.68-1.34),
identify the primary cause of death. 60-79 (SMR=0.88, 95% CI: 0.73-1.06), and above 80 (SMR=0.86, 95%
CI: 0.66-1.11), the rates are similar to the mortality rate of the general
Statistical Analysis
Table 1
Characteristics of the study patients at first presentation.
A descriptive table was constructed of demographic, disease fea-
tures, drug intake and comorbidities for both the deceased and sur- Overall Alive Deceased (n=225)
viving individuals. Crude mortality rates (reported per 1000 person), (n=1490) (n=1265)
as well as SMRs, were computed by comparing the mortality rate in Age in years, mean (SD) 44.5 (13.2) 42.8 (12.5) 54.3 (12.6)
the diseased individuals with the mortality rate in the general popu- Age at Psoriasis onset in 28.7 (14.7) 27.5 (13.9) 35.4 (17.2)
lation of Ontario, Canada. The mortality data of the general popula- years, mean (SD)
Age at PsA onset in years, 38.2 (13.7) 37.1 (13.3) 44.2 (14.5)
tion after 2013 could not be obtained from Statistics Canada.
mean (SD)
Mortality data for the general population of Ontario, stratified by 5- PsA duration in years, mean 6.3 (7.9) 5.6 (7.1) 10.2 (10.6)
year age bands, sex, and calendar year (from 1978 to 2013), were (SD)
used to calculate the reference mortality rates. Our cohort was Follow up duration in years, 10.4 (9.7) 10.4 (9.7) 8.7 (8.7)
divided into four age groups by 20-year age bands: 20-39, 40-59, 60- mean (SD)
Smoking ever, n (%) 663 (44%) 579 (46%) 84 (37%)
79, and above 80 years of age. Overall SMRs were calculated by Sex, n (%)
adjusting for age, sex, and calendar year, and SMRs were also * Female 660 (44%) 549 (43%) 111 (49%)
reported by sex, by age, as well as by cause-specific SMRs. In addition, Alcohol consumption, n (%)
we performed a trend analysis by using 5-year “rolling-average” * None 510 (41%) 456 (40%) 54 (50%)
* Social 630 (50%) 592 (52%) 38 (35%)
SMRs analysis from 1981 to 2017. All analyses performed were based
* Daily 109 (9%) 93 (8%) 16 (15%)
on the assumption that any patient lost to follow-up was still alive at Ethnicity, n (%)
the end of 2017. * Caucasian 1281 (87%) 1070 (85%) 211 (94%)
Cox regression models with time-dependent covariates were used Marital status, n (%)
to identify factors associated with increased risk of death among * Single 285 (23%) 269 (24%) 16 (14%)
* Married/Common law 824 (66%) 751 (66%) 73 (65%)
patients with PsA while adjusting for two fixed covariates such as * Divorced and other 134 (11%) 111 (10%) 23 (21%)
duration of PsA at clinic entry and sex. Time-dependent covariates Decade of entry, n (%)
included marital status, education level (college or above), actively * 1978-1987 326 (22%) 185 (15%) 141 (63%)
inflamed joint count, dactylitis count, enthesitis count, psoriasis area * 1988-1997 238 (16%) 199 (16%) 39 (17%)
* 1998-2007 427 (29%) 389 (31%) 38 (17%)
severity index (PASI) score, nail lesions, acute phase reactants, pres-
* 2008-2016 499 (33%) 492 (39%) 7 (3%)
ence of comorbidities such as diabetes, heart disease, depression and
PsA = Psoriatic arthritis.
cancer, medications, radiographic damage and axial disease.
O. Elalouf et al. / Seminars in Arthritis and Rheumatism 50 (2020) 571 575 573

Table 2 Table 3
Causes of death. Standardized mortality ratios along with
age- and sex-specific mortality ratios.
Cause of Death Cases
SMR (95% CI)
Malignant neoplasm 61
Acute myocardial infarction 32 Overall SMR 0.92 (0.80,1.05)
Pneumonia 14 Age specific SMR
Injuries / Poisoning 13 * 20-39 3.36 (1.61,8.18)
Cirrhosis / liver failure 10 * 40-59 0.97 (0.68,1.34)
Stroke 9 * 60-79 0.88 (0.73,1.06)
Respiratory diseases 8 * 80 + 0.86 (0.66,1.10)
Alzheimer’s disease 8 Sex specific SMR
Congestive heart failure 7 * Female 1.08 (0.89,1.30)
Renal failure 6 * Male 0.80 (0.66,0.97)
Infections 5
Atherosclerosis 5
Gastrointestinal bleeding 4
Other 17
Unknown 25 Table 4
Total 224 Cause specific SMRs.

Cause of death Cause specific SMR (95% CI)


population (Table 3). When analyzing age- and sex-specific SMRs, the
Alzheimer’s disease 0.43 (0.01,2.44)
male population showed increased mortality for the 20-39-year-old
Atherosclerosis 1.01 (0.27,2.58)
patients (SMR 3.3, 95% CI: 1.32-6.80), while the older groups of 60-79 CHF 2.57 (0.94,5.59)
and above 80 showed better survival (SMR=0.75, 95% CI: 0.57-0.97 Cirrhosis* 3.62 (1.65,6.88)
and SMR=0.56, 95% CI: 0.32-0.90, respectively). For the female popu- CVA* 0.38 (0.10,0.97)
GIB 5.01 (0.60,18.11)
lation, increased mortality was seen for young patients, that later
Infections* 5.32 (2.13,10.96)
decreased, and this trend was similar to the general population. Injury/Poisoning 0.82 (0.4,1.4)
Malignant neoplasm (Table 4) was the leading cause of death with Malignancy 0.97 (0.72,1.28)
61 cases (27%), although the rate was similar to the general population MI 1.11 (0.74,1.58)
(SMR=0.97, 95% CI: 0.72-1.28). Thirty-two patients (14.3% with Pneumonia* 2.46 (1.27,4.31)
Renal Diseases* 11.88 (7.53,17.8)
SMR=1.11, 95% CI: 0.74-1.58) died from acute myocardial infarctions.
Respiratory Disease* 98.5 (36.1,214.4)
The cause of death could not be identified for 25 deceased patients
*significant increase in mortality.

although it is known that they did not die of malignancy. Although


there was no increase in overall mortality, cause- specific SMRs dem-
onstrated increase rates for liver cirrhosis (SMR=3.62, 95% CI: 1.65-
6.88), infections (SMR=5.32, 95% CI: 2.13-10.96), particularly pneumo-
nia (SMR=2.46, 95% CI: 1.27-4.31), renal disease (SMR=11.88, 95% CI:
7.53-17.8), and respiratory disease (SMR=98.5, 95% CI: 36.1-214.4).

Factor associated with mortality

The Cox regression analysis included 1398 patients who had com-
plete covariate information among whom there were 212 deaths. This
analysis revealed that elevated acute phase reactants, presence of
heart disease and presence of cancer increased the risk of death,
whereas higher education was “protective” (Table 5). Sensitivity analy-
ses (results not shown in tables) which included only those patients
who had all covariates available, including smoking, provided broadly
similar findings. When HLA alleles known to be associated with PsA
were included, the modeling identified similar prognostic factors.

Discussion

In our first mortality study in PsA patients, which reflected the


period from 1978 to 1994, we demonstrated an increased risk of mor-
tality in patients with PsA compared to the general population. [2]
We subsequently demonstrated improved survival among PsA
patients in the 1990s compared to previous decades but still found
an increased mortality risk with SMR of 1.36. [3] Subsequent studies
also found lower mortality risk in more recent decades. [5]
Comparing mortality data between different studies might be
problematic from several aspects. First, studies based on national reg-
istries or medical record registries as opposed to clinical databases do
not define precisely the disease phenotype, for instance, patient
Fig. 1. (A) Unadjusted standardized mortality ratios. Overall rates in 1490 study selection based only on medical record diagnosis might misclassify
patients, as well as sex-specific rates (B) SMR over 5 years gap. PsA patients as psoriasis patients and vice versa, and as a
574 O. Elalouf et al. / Seminars in Arthritis and Rheumatism 50 (2020) 571 575

Table 5
Factors associated with mortality in patients with PsA.

Covariate Univariate Multivariate

Full model Reduced model

HR (95% CI) P value HR (95% CI) P value HR (95% CI) P value

Fixed Covariates
PsA duration (per 1 year) 1.00 (0.99, 1,02) 0.51 1.00 (0.99, 1.02) 0.31
Gender (Male vs female) 1.19 (0.89, 1.59) 0.25 1.13 (0.86, 1.50) 0.38
Time-dependent covariates
Married 0.65 (0.48, 0.89) 0.006 0.75 (0.53, 1.06) 0.10
College or above 0.54 (0.39, 0.75) 0.0002 0.53 (0.37, 0.77) 0.0007 0.46 (0.34, 0.64) <0.0001
Active joint counts 1.01 (1.00, 1.03) 0.11 1.00 (0.98, 1.02) 0.96
Dactylitis counts 1.11 (1.00, 1.23) 0.05 1.03 (0.92, 1.16) 0.61
Enthesitis counts 0.89 (0.60, 1.31) 0.54 0.90 (0.61, 1.35) 0.62
PASI score 1.00 (0.98, 1.02) 0.94 1.00 (0.97, 1.02) 0.67
Nail lesions (yes vs. no) 1.35 (0.99, 1.84) 0.06 1.34 (0.95, 1.89) 0.10
High acute phase reactant 1.60 (1.17, 2.17) 0.003 1.53 (1.11, 2.11) 0.009 1.56 (1.14, 2.13) 0.005
Axial disease (yes vs no) 0.94 (0.70, 1.26) 0.67 0.88 (0.65, 1.20) 0.43
Arthritis mutilans (yes vs no) 1.08 (0.77, 1.50) 0.66 1.06 (0.75, 1.49) 0.76
Damage joints (yes vs no) 1.21 (0.83, 1.77) 0.32 1.19 (0.81, 1.75) 0.38
Diabetes (yes vs no) 1.51 (0.98, 2.33) 0.07 1.54 (0.96, 2.47) 0.07
Heart disease (yes vs. no) 1.79 (1.23, 2.50) 0.002 1.64 (1.07, 2.51) 0.02 1.67 (1.12, 2.49) 0.01
Depression (yes vs. no) 1.30 (0.87, 1.95) 0.20 1.19 (0.76, 1.87) 0.44
Cancer (yes vs. no) 1.75 (1.22, 2.50) 0.002 1.84 (1.24, 2.72) 0.002 1.79 (1.22, 2.61) 0.003
Strongest medication
NSAIDs vs. none 0.82 (0.44, 1.52) 0.53 0.83 (0.44, 1.55) 0.43
csDMARDs vs none 0.90 (0.51, 1.60) 0.72 0.85 (0.47, 1.54) 0.59
Biologics vs none 0.75 (0.39, 1.49) 0.42 0.84 (0.41, 1.73) 0.64
HR hazard ratio; CI confidence interval, PASI psoriasis area severity index, NSAIDs nonsteroidal anti-inflammatory drugs,
csDMARD conventional synthetic disease modifying anti-rheumatic drugs.

consequence, the rates might be affected. Second, comparing mortal- increased mortality with SMR of 1.59 (95% CI: 1.16 2.03). [4] PsA
ity from different centers and different geographical areas might SMR was comparable to rheumatoid arthritis (1.68) and ankylosing
reflect many differences such as disease severity, frequency of comor- spondylitis (1.87), and also comparable to our initial study. [2]
bidities and treatment, access to effective therapies and its usage. The Some other recent studies did not find increased mortality. Buck-
advantage of our study is that the same methodology was used dur- ley et al. assessed survival in a hospital-based cohort of 453 PsA
ing 3 consecutive studies for patient follow up and for mortality data patients between 1985-2007 in Bath, UK and reported SMR of 0.82
retrieval. Reports from other studies showed inconsistent results and (95% CI: 0.57-1.5). [5] Ogdie et al. conducted a large medical record
do not fully support a chronologic association with improved survival database longitudinal cohort study in the UK, assessing the mortality
as was observed in our cohort (Fig. 2). While two earlier studies from of PsA (n=8706), psoriasis (n=138,424) and RA (n=41,742) patients
Olmsted County assessing patients in the period of 1970-1999 could compared to matched controls (n=81 573). [12] PsA patients did not
not establish a correlation between PsA and increased mortality, have an increased risk of mortality (HR=1.06, 95% CI: 0.80-1.10) after
[10, 11] a more recent hospital registry-based study from Hong-Kong controlling for sex and age (even without controlling for common
describing 778 PsA patients between 1999-2008 reported an cardiovascular risk factors which are more common in PsA), while RA
and severe psoriasis (cDMARDs users) patients had a pronounced
increased mortality risk (HR=1.59, 95% CI: 1.52-1.64 and HR=1.75,
95% CI: 1.56-1.95, respectively). Mild psoriasis (no cDMARDs users)
had a mildly elevated mortality risk (HR=1.08, 95% CI: 1.04-1.12).
Fig. 2 summarizes the mortality ratios in the leading studies.
The literature on mortality in psoriasis provides conflicting find-
ings. Gelfand et al. [13] conducted a retrospective cohort study on pso-
riasis patients between 1987-2002, using the General Practice
Research Database which is a medical records databases in the UK.
Hazard ratios of time to death were comparable to the general popula-
tion for patients with mild psoriasis (defined as no systemic therapy)
(HR=1.0; 95% CI: 0.97-1.02), whereas patients with severe psoriasis
(defined as current or past use of any systemic therapy including pho-
totherapy or PUVA) had an increased hazard ratio of 1.5 (95% CI: 1.3-
1.7). The increased risk persisted after controlling for common mortal-
ity risk factors. The authors suggested that severe but not mild psoria-
sis imparts an increased risk of death. Svedbom et al. [14] assessed the
mortality risk as well as cause-specific mortality risk for mild and
severe psoriasis patients in Sweden. The study was based on data from
Swedish administrative registers and reported increased crude risk of
death both for mild psoriasis defined as no psoriasis related admission
and no systemic therapy (HR=1.15, 95% CI: 1.10-1.21) and for severe
disease (HR=1.56, 95% CI: 1.36-1.79). A recent large study from the
Fig. 2. SMRs from PsA mortality studies. Danish National Patient Registry assessed the mortality risk in
O. Elalouf et al. / Seminars in Arthritis and Rheumatism 50 (2020) 571 575 575

psoriasis and PsA as well as cause mortality risk. [15] Psoriasis patients evidence from several studies from different geographical areas
had lower survival compared to the general population (HR=1.74; mostly showing comparable mortality rates of PsA patients to the
p<0.001), while this correlation was not demonstrated for PsA general population, further support our findings. These encouraging
patients (HR=1.06; p=0.19). findings might be attributable to instituting therapy in earlier stages
of the disease, improved therapeutic options, and better awareness
Causes of death of the importance of treating comorbidities. However, the comorbid-
ities and active disease remain predictors of mortality in patients
Wong et al. [2] reported a total of 53 deaths among 428 patients, with PsA suggesting that we need to do better in controlling the dis-
28% were attributable to cardiovascular reasons, followed by respira- ease and preventing the comorbidities.
tory, cancer, and injuries/poisoning at 21%, 17%, and 15%, respectively.
SMR was elevated from diseases of the respiratory system and from Declaration of Competing Interests
injuries or poisoning (SMR=5.14, 95% CI: 1.67-12.01 and SMR=1.36,
95% CI: 1.62-9.62, respectively). Mortality was not increased from dis- None.
eases of the circulatory system, cancer or from other reasons. In the
subsequent report by Ali et al. [3] cause-specific SMRs were not calcu- Acknowledgments
lated, however the main causes of death were similar with diseases of
the circulatory system (24.5%) and cancer (23%) as the leading causes. The University of Toronto Psoriatic Arthritis Program is supported
In the hospital-based registry study by Mok et al, [4], cause-specific by a grant from The Krembil Foundation. Dr. Ofir Elalouf was
SMRs were not reported, however in this study reporting patients supported by a Psoriatic Disease Research Fellowship from the
from 1999-2008 infection was the leading cause accounting for 33% of National Psoriasis Foundation/USA. This work was presented as a
the deaths in PsA, while cancer and cardiovascular causes were poster at the American College of Rheumatology Annual meeting
responsible for 20% each. Odgie et al. [12], reported cause-specific October 2018.
mortality rates of psoriasis, PsA and RA patients of the same medical All authors were involved in drafting the article or revising it criti-
record database from UK. Leading causes were cardiovascular, fol- cally for important intellectual content, and all authors approved the
lowed by malignancy, respiratory and infections, while none of the final version to be published. All authors were likewise involved in
above was found to be increased compared to the general population. the study conception and design, acquisition of data as well as analy-
Deaths from suicide were reported to be elevated in PsA patients with sis and interpretation of data. Dr. Gladman had full access to all of the
hazard ratio of 3.03 (95% CI: 1.56- 5.90). As opposed to PsA, RA patients data in the study and takes responsibility for the integrity of the data
had increased cause-specific mortality related to cardiovascular dis- and the accuracy of the data analysis.
eases (HR = 1.55, 95% CI: 1.44- 1.66), respiratory diseases (HR = 1.85,
95% CI: 1.72- 2.01), infectious diseases (HR = 2.21, 95% CI: 2.00- 2.44) Role of funding source
and cancer (HR=1.18, 95% CI: 1.08-1.28).
In our cohort, male patients were found to have slightly better None.
survival than females. This finding was noted in the previous study,
but others have not found the same results. Since SMRs reflect mor- References
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