Predictors of Depression in a Multiethnic Cohortof Patients With Rheumatoid ArthritisM. MARGARETTEN,1 E. YELIN,1 J. IMBODEN,2 J. GRAF,2 J. BARTON,1 P. KATZ,1 AND L. JULIAN1

Objective. Patients with rheumatoid arthritis (RA) who experience depression have worse health outcomes. This studyidentifies predictors of depression in an ethnically and racially diverse population of patients with RA.Methods. Patients with RA in a prospective cohort at the San Francisco General Hospital outpatient rheumatology clinicwere included if they were age >18 years, met the American College of Rheumatology classification criteria for RA, hada Health Assessment Questionnaire (HAQ) score collected, and had the RA-specific Disease Activity Score performed bya rheumatologist. The outcome variable was a depression score measured by the Patient Health Questionnaire 9 (PHQ-9),a self-report questionnaire validated to correlate with a diagnosis of major depression.Results. Three hundred forty-nine clinical visits for 172 patients were included in the analysis. Forty percent of patientsscored >10 on the PHQ-9 during at least one clinic visit, which corresponds to a symptom severity of at least moderatedepression. The mean PHQ-9 score was 7, corresponding to a symptom severity of mild depression. In the multivariateanalysis, higher HAQ scores were associated with depression, and Asians had lower depression scores compared withHispanic, white, and African American subjects.Conclusion. Identifying associated predictors of depression in a diverse population of patients with RA can help guidetreatment, which should include preventing disability and decreased function as well as targeting depressive symptomsmore specifically in patients with RA.

INTRODUCTION

Of the 1.3 million adults in the US (0.6%) with rheumatoidarthritis (RA) (1,2), most will develop progressive func-tional limitation and physical disability (3). Depression, afrequent disorder among patients with RA, is often unrec-ognized or undertreated (4,5). The prevalence of major

depressive disorder is 13–42% in patients with RA (6–13),which is at least double that in the general population.

In patients with RA, poor clinical characteristics andfunction are associated with subsequent depression. Thereare more RA-related physician visits and hospitalizationsin patients with depression, as well as negative health andfunctional outcomes and increased health service use (14).Patients with rheumatic diseases and depression are lesslikely to be adherent with their medications (15) and morelikely to discontinue anti–tumor necrosis factor � (anti-TNF�) therapy when compared with patients without de-pression (16), which may then have a negative effect ontheir health status. Furthermore, comorbid depression isan independent risk factor for death in patients with RA,with a hazard ratio of 2.2 (95% confidence interval [95%CI] 1.2, 3.9; P � 0.01) (17,18).

Studies have shown that disability and decreased func-tion as measured by the Health Assessment Questionnaire(HAQ) are associated with depression in white popula-tions (19–22), but have not addressed potential predictorsof depression in an ethnically diverse group of patientswith RA. A recent study identified Hispanics with RA asmore likely to have symptoms of depression than non-Hispanic subjects (23); however, important covariatessuch as disease activity and disease duration were nottaken into account. Furthermore, patients of other races/ethnicities (African Americans, Asians) were not included

Because Drs. Yelin and Katz are Editors of Arthritis Care& Research, review of this article was handled by the Editorof Arthritis & Rheumatism.

Supported by the Arthritis Foundation, the American Col-lege of Rheumatology Research and Education Foundation“Within our Reach” Grant, the National Institute of Arthri-tis and Musculoskeletal and Skin Diseases (grant P60-AR-053308), the Rosalind Russell Medical Research Center forArthritis, University of California, San Francisco, and theUniversity of California, San Francisco School of MedicineResearch Evaluation & Allocation Committee.

1M. Margaretten, MD, E. Yelin, PhD, J. Barton, MD, P.Katz, PhD, L. Julian, PhD: University of California, SanFrancisco; 2J. Imboden, MD, J. Graf, MD: University of Cal-ifornia, San Francisco and San Francisco General Hospital,San Francisco, California.

Address correspondence to M. Margaretten, MD, ArthritisResearch Group, University of California, San Francisco,3300 California Street, Suite 270, San Francisco, CA 94143.E-mail: mary.margaretten@ucsf.edu.

Submitted for publication March 27, 2009; accepted inrevised form July 1, 2009.

Arthritis & Rheumatism (Arthritis Care & Research)Vol. 61, No. 11, November 15, 2009, pp 1586–1591DOI 10.1002/art.24822© 2009, American College of Rheumatology

ORIGINAL ARTICLE

1586

in this study for comparison. Since concomitant depres-sive symptoms are known to worsen health outcomes andconfer independent risk for mortality in RA, it would beuseful to discover associations between depression andRA in diverse populations.

Our objective was to identify demographic and disease-related predictors of depressive symptoms in a socioeco-nomically and ethnically distinct population of patientswith RA at an urban public hospital. The independenteffects of race/ethnicity on depressive symptoms were ofspecial interest in this multiethnic cohort of patients withRA.

SUBJECTS AND METHODS

Study population. The study subjects were patientsfrom the University of California, San Francisco (UCSF)RA cohort at the San Francisco General Hospital (SFGH)outpatient rheumatology clinic. The SFGH is the majorprovider to the poor, minority population of the City andCounty of San Francisco. Patients were consecutively en-rolled when they presented for their initial or return visitbetween November 2006 and December 2008, and the datawere gathered at regular clinical visits. Patients were in-cluded in the analysis if they were age �18 years, met theAmerican College of Rheumatology (formerly the Ameri-can Rheumatism Association) classification criteria for RA(24), had a depression score measured by the PatientHealth Questionnaire 9 (PHQ-9), had the RA-specific Dis-ease Activity Score in 28 joints (DAS28) performed by arheumatologist at the same clinical visit, and had a HAQscore collected within 6 months before or after the depres-sion measure. The UCSF Committee on Human Researchapproved the study. Written informed consent was ob-tained and patients were interviewed in the language oftheir choice (English, Cantonese, Mandarin, or Spanish).

Assessment of clinical data. In addition to sociodemo-graphic characteristics (age, sex, self-reported ethnicity)and disease duration, a wide range of clinical data wascollected at enrollment and at regular intervals thereafterduring routine clinical encounters. Disease activity wasassessed with the DAS28, calculated at each clinic visit.The DAS28 includes scores of tender and swollen jointcounts, patient global disease activity rating scale, anderythrocyte sedimentation rate (ESR) (25,26). Functionallimitation was evaluated with the 20-item HAQ score (27),which is a reliable and valid assessment of functionallimitations in RA. HAQ scores collected within 6 monthsof the depression scores were included, since HAQ scoresare generally stable over a 1-year period among patientswith RA (28–30). The HAQ has been translated and vali-dated in Mandarin/Cantonese (31) and Spanish (32). Treat-ment-related variables were prednisone use and other dis-ease-modifying antirheumatic drugs (DMARDs) such asmethotrexate, hydroxychloroquine, sulfasalazine, azathio-prine, leflunomide, anti-TNF� medications, or other bio-logic medications.

Ascertainment of depression. The outcome variable wasdepressive symptoms measured by the PHQ-9. This self-

report depression questionnaire yields a 27-point scalethat correlates with a diagnosis of major depression(33,34). The PHQ-9 is composed of 10 items correspondingto the 9 diagnostic criteria of major depressive disorder,plus 1 item to assess functional impairment secondary todepression. A score of 5–9 is consistent with mild depres-sive symptoms, 10–14 with moderate depressive symp-toms, 15–19 with moderate to severe depressive symp-toms, and �20 with severe depressive symptoms. ThePHQ-9 has established reliability and validity in white,African American, Asian, and Hispanic populations(35,36). To classify patients with at least moderate symp-toms of depression, we used a clinically useful cut point of10, which distinguishes between no/mild and moderate/severe depressive symptoms for the univariate analysis.The term “depressed” will be used from this point forwardto refer to participants meeting this threshold of symptomseverity.

Data collection. Study research staff who were not thepatient’s physician administered standardized question-naires (PHQ-9, HAQ) and interviews in English, Spanish,or Chinese. Research staff and treating physicians wereblind to PHQ-9 scores and HAQ scores because scoreswere tabulated independently.

Statistical analysis. The analysis accommodated the re-peated measures from an individual’s multiple clinicalencounters and was conducted using STATA, version 10.0(StataCorp, College Station, TX). The unit of analysis wasa subject’s clinical visit, in which the patient had a PHQ-9score collected. A total of 46 visits (12%) involving 22patients were excluded because of incomplete informa-tion. Most of these visits were dropped because a compo-nent of the DAS28 was not collected and therefore couldnot be calculated. Differences in baseline characteristicsbetween depressed and non-depressed subjects were as-sessed using a 2-sided t-test with equal variance or thePearson’s chi-square test, as appropriate. For the multivar-iate analysis, we used generalized estimating equations(GEEs) with robust standard errors of the estimate (SEEs)to assess associations with depression scores, while takinginto account within-subject correlations between measure-ments over time and to account for the influence of poten-tial confounding covariates (37). The PHQ-9 score wasused as a continuous outcome for the multivariate analy-sis. For the multivariate analysis, independent variableswere determined a priori with a forward inclusion strat-egy. Variables were selected based on face validity andbiologic plausibility to obtain a minimally confoundedestimate of their effect and identify important independentpredictors of depression in patients with RA. Given themodestly sized data set and the number of predictors,bootstrapping (re-sampling of subjects, not observations)was employed to check the reliability of the SEEs and CIs.

RESULTS

Three hundred forty-nine clinical visits for 172 patientswere included in the analysis. The average number of

Depression in a Multiethnic RA Cohort 1587

outpatient rheumatology clinic visits per patient was 2(range 1–5). In this study, 89% of included patients werewomen, with a mean age of 52 years (Table 1). In regard torace/ethnicity, 54% of the patients were Latino/Hispanic,34% were Asian/Pacific Islander, 7% were African Amer-ican, and 4% were white. Eighty-four percent of thepatients were rheumatoid factor positive and 81% wereanti–cyclic citrullinated peptide (anti-CCP) positive.Eighty-three percent of patients were taking a DMARD,24% were taking anti-TNF� medications, and 62% of pa-tients were taking prednisone, with a mean dose of 4 mg.Fifteen percent of patients were prescribed an antidepres-sant medication. The mean HAQ score was 1.25 and themean DAS28 was 4.1, which is indicative of fairly highlevels of functional impairment and disease activity, re-spectively.

With regard to the prevalence of depressive symptomsin our cohort, 40% of patients scored �10 on the PHQ-9during at least one clinic visit (n � 138 clinic visits),which corresponds to a symptom severity of at least mod-erate depression. The mean PHQ-9 score was 7, corre-sponding to symptom severity of mild depression.

In univariate analyses of baseline data, there were nostatistically significant differences between depressed andnon-depressed patients with regard to age, ethnicity, dis-ease duration, antibody status, or prednisone treatmentand dose. However, depressed participants had higherHAQ and DAS28 scores, and were less likely to be treatedwith a DMARD (Table 1).

After adjusting for age, sex, race/ethnicity, disease du-

ration and activity, prednisone treatment, and RA disease-modifying medications in a GEE model (Table 2), higherHAQ scores were significantly associated with higherPHQ-9 scores. A clinically meaningful change in HAQscore is 0.24 (38), so the GEE coefficient, which representsassociations with a 1-point difference in HAQ score, wasdivided by 4. With each 0.24-unit increase in the HAQscore, there was an increase in the PHQ-9 score of 0.98(95% CI 0.73, 1.3). Asian ethnicity was associated withlower depression scores, specifically a decrease in PHQ-9score of 1.6 (95% CI �3.0, �0.28) as compared with thereference group, Latinos/Hispanics (Table 2). The CIs fromthis multivariate model remained similar when bootstrap-ping was employed. The effects of HAQ score and race/ethnicity on PHQ-9 scores did not differ when modeled forpossible interactions.

DISCUSSION

To our knowledge, this is the first study evaluating thepredictors of depressive symptoms in an underserved, eth-nically diverse cohort of patients with rigorously definedRA that includes measures of functional disability anddisease status as measured by the DAS28. Several conclu-sions stem from our data.

First, the prevalence of clinically significant depressivesymptoms in an urban, multiethnic sample of patientswith RA is 40%. Although this is within the range ofpreviously reported results (13–42%), it is on the higher

Table 1. Baseline characteristics of the San Francisco General Hospital rheumatoid arthritis cohort by depression*

All subjects(n � 172)

PHQ-9 score<10 at any visit

(n � 103)

PHQ-9 score>10 at any visit

(n � 69) P

Sex 0.68Women 153 (89) 92 (89) 61 (88)Men 19 (11) 11 (11) 8 (12)

Age, mean � SD years 52 � 13 51 � 14 53 � 13 0.26Ethnicity 0.17

Latino/Hispanic 93 (54) 54 (52) 37 (54)African American 12 (7) 8 (8) 4 (6)Asian/Pacific Islander 58 (34) 35 (34) 25 (36)White 7 (4) 6 (6) 1 (1)American Indian/other 2 (1) 0 (0) 2 (3)

DAS28, mean � SD† 4.1 � 1.4 4.0 � 1.3 4.3 � 1.6 0.04Disease duration, mean � SD years 7.5 � 8.0 6.9 � 7.5 8.4 � 8.9 0.08HAQ score, mean � SD 1.25 � 0.81 1.1 � 0.68 1.4 � 0.92 �0.0001Antibody positive

Rheumatoid factor 144 (84) 87 (84) 57 (83) 0.92Anti-CCP 139 (81) 83 (81) 56 (82) 0.66

DMARDs‡ 143 (83) 89 (86) 54 (78) 0.03Methotrexate 105 (61) 66 (64) 39 (56) 0.11Prednisone 107 (62) 66 (64) 41 (60) 0.65Prednisone dose, mean � SD mg 4 � 4.8 4.1 � 4.4 4.3 � 5.3 0.76Anti-TNF� 41 (24) 24 (23) 17 (25) 0.84

* Values are the number (percentage) unless otherwise indicated. PHQ-9 � Patient Health Questionnaire 9; DAS28 � Disease Activity Score in 28joints; HAQ � Health Assessment Questionnaire; anti-CCP � anti–cyclic citrullinated peptide; anti-TNF� � anti–tumor necrosis factor �.† Includes tender and swollen joint counts, patient global rating scale, and erythrocyte sedimentation rate.‡ Includes any disease-modifying antirheumatic drug (DMARD) other than prednisone (i.e., methotrexate, hydroxychloroquine, sulfasalazine, aza-thioprine, leflunomide, anti-TNF� medications, and rituximab).

1588 Margaretten et al

end of the spectrum compared with white populationswith RA and depression.

Second, those with more disability are at greater risk fordepression. These findings in a previously unstudied pop-ulation corroborate with the literature. Given the highprevalence of depression in our subjects and the strongassociation with decreased function, this raises the ques-tion of whether depression is a product of increased dis-ability as measured by the HAQ. A mean HAQ score of1.25 is well above the previously reported mean HAQscore of 0.71 in a population-based cohort of patients withRA (28). Why is there a higher mean HAQ score in ourstudy sample? The most obvious answer is that healthdisparities in the RA cohort at the SFGH associated withrace/ethnicity and socioeconomic status lead to worseoutcomes (39); in this case, a higher mean HAQ score.Identifying pathways and mechanisms by which socioeco-nomic status and race/ethnicity affect HAQ scores wouldprovide more options for intervention to eliminate disabil-ity and subsequent depression in patients with RA.

Third, it is surprising that disease activity as measuredby swollen, tender joints, patient global disease activityscale, and the ESR is not associated with higher depressionscores, given previous research in this area (40,41). In themultivariate analysis, the upper limit for the GEE coeffi-cient of the DAS28 is 0.45. The SD for the DAS28 in thecohort is 1.4, and a 2-point change in the DAS28 would bequite large clinically. Therefore, the maximum change inthe depression score associated with a 2-point increase inDAS28 is only 0.9, which is quite a small clinical change.This suggests that it is not the acute pain or clinical man-ifestations of RA disease activity, but more the long-termdisability and joint damage associated with arthritis thatlead to depression in patients with RA.

Finally, Asians in the SFGH RA cohort had lower de-pression scores compared with Latino/Hispanic, white,and African American subjects. To our knowledge, this isthe first study to find an association between depressivesymptoms and Asian race/ethnicity in patients with RA.This finding is supported by previous literature other thanthat specific to RA, which substantiates that there is a lowlevel of reporting depressive symptoms in Asians (42),owing to the stigma of mental illness, implications ofweakness of character, and factors that may protect againstdepression such as stoicism and cultural support systems(43).

There are limitations to this study. Like other chronicconditions, assessing depressive symptoms in patientswith RA can be difficult. It is well understood that somaticsymptoms of depression (e.g., fatigue or decreased energy)overlap with symptoms of RA. Consequently, there is arisk that depression in RA may be overestimated (44).Conversely, there is also some evidence to suggest thatusing conventional assessments of depression does notoverestimate depression in similar chronic conditions(45). In our approach to the assessment of depressivesymptoms, we chose the PHQ-9 as a measure for depres-sion because it was developed for primary care, is inwidespread use for a range of acute and chronic medicalconditions, and was developed to closely parallel the di-agnostic symptoms of major depressive disorder(33,34,46).

Our study design was cross-sectional, and therefore cau-sality between greater HAQ scores and the associated in-creased depressive symptoms cannot be established. Fu-ture studies should examine this relationship in aprospective manner. Also, as a cross-sectional study, thereis a limit to the information that can be produced about thewaxing and waning nature of depressive symptoms overtime. The high prevalence of depressive symptoms in thiscohort is either because they occur more frequently orbecause the depressive symptoms last longer.

Another potential limitation to this study is that detec-tion bias or medical surveillance bias could influence theassociation between depressive symptoms and clinicalpredictors if depressed patients with RA were less likely toattend clinical appointments. To investigate this possibil-ity, we compared the mean number of clinical visits ofpatients with and without depressive symptoms andfound no significant difference.

Finally, the question of how applicable our results are toother RA patients must be asked. The high percentage ofsubjects with positive anti-CCP (81%), which portends apoor prognosis, is greater than reported in other clinicalcohorts. Furthermore, our study population has relativelyhigh disease activity, with a mean DAS28 of 4.1 and amean HAQ score of 1.25. The fact that our study popula-tion has more erosive and disabling disease is likely areflection of referral practices to a public urban hospitalclinic as well as our precise definition of RA for entry intothe study. Although our cohort was skewed toward moresevere disease and included an ethnically diverse patientpopulation, we believe that the heterogeneity of our cohortis a benefit and not a limitation.

Given that patients in this cohort are comprised of mi-

Table 2. Multivariate model of predictorsof depression*

Characteristic

GEEcoefficient(95% CI) P

Female sex �0.41 (�2.6, 1.7) 0.70Age, years �0.31 (�0.09, �0.02) 0.27Ethnicity

Latino/Hispanic ReferenceAfrican American �0.20 (�2.7, 2.4) 0.88Asian/Pacific Islander �1.6 (�3.0, �0.28) 0.02White 0.37 (�2.1, 2.8) 0.77American Indian/other �1.8 (�6.1, 2.6) 0.43

DAS28† 0.08 (�0.31, 0.45) 0.70Disease duration, years �0.02 (�0.10, 0.05) 0.50HAQ score 0.98 (0.73, 1.3) �0.0001DMARDs‡ �0.76 (�2.6, 1.1) 0.43Prednisone �0.42 (�1.7, 0.83) 0.51

* GEE � generalized estimating equation; 95% CI � 95% confi-dence interval; DAS28 � Disease Activity Score in 28 joints; HAQ �Health Assessment Questionnaire.† Includes tender and swollen joint counts, patient global ratingscale, and erythrocyte sedimentation rate.‡ Includes any disease-modifying antirheumatic drug (DMARD)other than prednisone (i.e., methotrexate, hydroxychloroquine, sul-fasalazine, azathioprine, leflunomide, anti–tumor necrosis factor �medications, and rituximab).

Depression in a Multiethnic RA Cohort 1589

norities who struggle with poverty and often have pooreducation, future studies should directly compare thispopulation with those with higher socioeconomic status todetermine associations between depression, disease activ-ity, disability, and health disparities in patients with RA.Since depression is known to confer risk of poor healthoutcomes, identifying associated predictors of depressionin all patients with RA, not just whites, is useful. Theabove findings can help guide treatment to include pre-venting disability and decreased function as well as tar-geting depressive symptoms more specifically in a vulner-able population of patients with RA.

AUTHOR CONTRIBUTIONS

All authors were involved in drafting the article or revising itcritically for important intellectual content, and all authors ap-proved the final version to be submitted for publication. Dr. Mar-garetten had full access to all of the data in the study and takesresponsibility for the integrity of the data and the accuracy of thedata analysis.Study conception and design. Margaretten, Yelin, Imboden, Graf,Julian.Acquisition of data. Margaretten, Yelin, Imboden, Graf, Barton,Julian.Analysis and interpretation of data. Margaretten, Yelin, Imboden,Katz.

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