Earlier vs. later time period of COVID-19 infection and emergent autoimmune signs, symptoms, and serologies.

OBJECTIVE: Autoantibodies and autoimmune diseases after SARS-CoV-2 infection are widely reported. Given evolving variants, milder infections, and increasing population vaccination, we hypothesized that SARS-CoV-2 infection earlier in the pandemic would be associated with more autoimmune connective tissue disease (CTD) symptoms and immunologic abnormalities. METHODS: Patients ≥18 years old with COVID-19 3/1/2020-8/15/2022 completed the CTD Screening Questionnaire and were tested for 27 autoimmune serologies, SARS-CoV-2 serologies, cell-bound complement activation products (CB-CAPs), and T and B lymphocyte immunophenotypes by flow cytometry. We assessed relationships between symptoms, serologies, and immunophenotypes in earlier (3/1/2020-1/31/2021) vs. later (2/1/2021-8/15/2022) periods, with different predominating SARS-CoV-2 viruses. RESULTS: 57 subjects had earlier and 23 had later pandemic COVID-19. 35 % of earlier vs. 17 % of later pandemic patients had CTD symptoms (p 0.18). More patients were antinuclear antibody (ANA) positive (44 % vs. 13 %, p 0.01) and had lupus anticoagulant (11 % vs. 4 %, p 0.67). After adjustment for age, race, and sex, earlier (vs. later) COVID-19 was associated with increased ANA positivity (OR 4.60, 95%CI 1.17, 18.15). No subjects had positive CB-CAPs. T and B cell immunophenotypes and SARS-CoV-2 serologies did not differ by group. In heatmap analyses, higher autoantibody variety was seen among those with infection in the early pandemic. CONCLUSION: In this sample, having COVID-19 infection in the earlier (pre-2/1/2021) vs. later pandemic was associated with more CTD symptoms, ANA positivity, and autoantibody reactivities. Earlier SARS-CoV-2 variants circulating in a less vaccinated population with less natural immunity may have been more immunogenic.

Real-world application of the pediatric Glucocorticoid Toxicity Index in childhood-onset lupus.

OBJECTIVES: The pediatric Glucocorticoid Toxicity Index (pGTI) is a new, pediatric-specific tool to quantify glucocorticoid (GC)-related morbidity in children. We evaluated the feasibility and construct validity of retrospective pGTI scoring in patients with pediatric-onset systemic lupus erythematosus (pSLE) and identified risk factors for cumulative toxicity. METHODS: We conducted a retrospective cohort study of patients with pSLE treated with GCs at two pediatric centers (1999-2023). GC exposure was estimated using interval-averaged oral prednisone-equivalent dose and cumulative prednisone-equivalent dose. We scored change in GC toxicity every 6 months (±2) using a modified pGTI including 7 of 10 domains. We calculated the Cumulative Worsening Score (CWS), a continuous summation of toxicity accrued. Mixed effects linear regression was used to identify factors associated with CWS. RESULTS: There were 126 patients with pSLE, including 88 with nephritis, with a median of 6 visits/patient. Nearly half (47 %) experienced toxicity in the Blood Pressure domain. Other common toxicities were mood disturbance (25 %), followed by increased body mass index (BMI), striae, and sleep disturbance (21 % each). Decreased growth velocity was observed in 18 %. There was modest correlation between cumulative GC dose and CWS (rho 0.3; p < 0.01). Greater cumulative toxicity was associated with younger age, elevated BMI, and rituximab use at the time of GC initiation, albeit indications for the latter were not captured. CONCLUSIONS: Patients with pSLE experience a high burden of GC toxicity, particularly related to blood pressure, BMI, sleep, and growth. Standardized, pediatric-specific GC toxicity assessment is feasible in real-world settings and can facilitate evaluation of strategies to reduce morbidity in children requiring chronic GC treatment.

Barriers, Facilitators, and Preferences for Mental Health Services Among Patients With Systemic Lupus Erythematosus: A Qualitative Study.

OBJECTIVE: Although patients with systemic lupus erythematosus (SLE) experience high levels of depression and anxiety disorders, evidence concerning patient perceptions of facilitators and barriers to effective uptake of mental health services (eg, referral to therapists and psychiatrists, psychoeducational interventions, or support groups) is limited. METHODS: We conducted semistructured qualitative interviews with 15 adults with SLE to explore patient experiences and perceptions of mental health services to identify facilitators and barriers to accessing mental health care among patients with SLE. Qualitative interviews were conducted via telephone and audio recorded for transcription and directed content analysis using NVivo software by two coders. RESULTS: The median age of the 15 participants was 48 years, 87% were female, 33% identified as Black or African American, and 33% identified as Hispanic or Latino. Qualitative themes were organized into three domains: barriers, facilitators, and preferences for mental health services. Barriers to the use of mental health services include mental health stigma, sociodemographic factors, lack of autonomy, and time commitment. Facilitators to the use of mental health services included strong relationships with their rheumatologists and mental health care clinician experience with patients with SLE. Preferences for mental health services included education-based formats, mental health providers who work with patients with SLE, peer group formats, demographically and disease-matched psychological resources, and an emphasis on non-disease-related activities. CONCLUSION: In the setting of persistent unmet psychosocial needs of patients living with SLE, data from this qualitative study will inform the development and refinement of mental health interventions that bolster psychological wellbeing in the SLE population.

Incidence and Risk Factors for Eosinophilia and Lung Disease in Biologic-Exposed Children With Systemic Juvenile Idiopathic Arthritis.

OBJECTIVE: Although interleukin-1 (IL-1)/IL-6 inhibitors are effective therapies for systemic juvenile idiopathic arthritis (JIA), some patients develop eosinophilia and lung disease during treatment. This study was undertaken to retrospectively evaluate incidence and risk factors for eosinophilia and describe lung disease outcomes in IL-1/IL-6 inhibitor-exposed patients with systemic JIA. METHODS: Among JIA patients at our institution exposed to interleukin-1 (IL-1)/IL-6 inhibitors (1995-2022), we compared incidence rate of eosinophilia in systemic JIA compared to other JIA, stratified by medication class (IL-1/IL-6 inhibitors, other cytokine inhibitors, methotrexate). We used Cox models to identify predictors of eosinophilia during IL-1/IL-6 inhibitor use and summarized treatment changes and outcomes after eosinophilia, including lung disease. HLA typing was performed on a clinical or research basis. RESULTS: There were 264 new medication exposures in 75 patients with systemic JIA and 41 patients with other JIA. A total of 49% of patients with systemic JIA with HLA typing (n = 45) were positive for HLA-DRB1*15 alleles. Eosinophilia was common during IL-1/IL-6 inhibitor use and did not differ by systemic JIA compared to other JIA (0.08 and 0.07 per person-year, respectively; P = 0.30). Among systemic JIA patients, pretreatment macrophage activation syndrome (MAS) was associated with a higher rate of subsequent eosinophilia on biologic therapy (unadjusted hazard ratio 3.2 [95% confidence interval 1.2-8.3]). A total of 4 of 5 patients who switched therapy within 10 weeks of eosinophilia experienced disease flare compared to none of the patients who continued the original therapy. A total of 8 of 25 patients with pulmonary evaluations had lung disease, and all had severe manifestations of systemic JIA (MAS, intensive care unit stay). One death was attributed to systemic JIA-lung disease. CONCLUSION: Eosinophilia is common in JIA patients using IL-1/IL-6 inhibitors. Severe disease may be associated with eosinophilia and lung disease in systemic JIA.

The link between post-traumatic stress disorder and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a heterogeneous, multisystem autoimmune disorder characterized by unpredictable disease flares. Although the pathogenesis of SLE is complex, an epidemiologic link between posttraumatic stress disorder (PTSD) and the development of SLE has been identified, suggesting that stress-related disorders alter the susceptibility to SLE. Despite the strong epidemiologic evidence connecting PTSD and SLE, gaps remain in our understanding of how the two may be connected. Perturbations in the autonomic nervous system, neuroendocrine system, and at the genomic level may cause and sustain immune dysregulation that could lower the threshold for the development and propagation of SLE. We first describe shared risk factors for SLE and PTSD. We then describe potential biological pathways which may facilitate excessive inflammation in the context of PTSD. Among those genetically predisposed to SLE, systemic inflammation that accompanies chronic stress may fan the flames of smoldering SLE by priming immune pathways. Further studies on the connection between trauma and inflammation will provide important data on pathogenesis, risk factors, and novel treatments for SLE.

Posttraumatic Stress Disorder and Risk of Systemic Lupus Erythematosus Among Medicaid Recipients.

OBJECTIVE: We studied posttraumatic stress disorder (PTSD), a severe trauma-related mental disorder, and systemic lupus erythematosus (SLE) risk in a large, diverse population enrolled in Medicaid, a US government-sponsored health insurance program for low-income individuals. METHODS: We identified SLE cases and controls among patients ages 18-65 years enrolled in Medicaid for ≥12 months in the 29 most populated US states from 2007 to 2010. SLE and PTSD case statuses were defined based on validated patterns of International Classification of Diseases, Ninth Revision codes. Index date was the date of the first SLE code. Controls had no SLE codes but had another inpatient or outpatient code on the index date and were matched 1:10 to cases by age, sex, and race. Conditional logistic regressions calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for the association of PTSD with incident SLE, adjusting for smoking, obesity, oral contraceptive use, and other covariates. RESULTS: A total of 10,942 incident SLE cases were matched to 109,420 controls. The prevalence of PTSD was higher in SLE cases, at 10.74 cases of PTSD per 1,000 person-years (95% CI 9.37-12.31) versus 7.83 cases (95% CI 7.42-8.27) in controls. The multivariable-adjusted OR for SLE among those with PTSD was 2.00 (95% CI 1.64-2.46). CONCLUSION: In this large, racially and sociodemographically diverse US population, we found patients with a prior PTSD diagnosis had twice the odds of a subsequent diagnosis of SLE. Studies are necessary to clarify the mechanisms driving the observed association and to inform possible interventions.

An Evidence-Based Guideline Improves Outcomes for Patients With Hemophagocytic Lymphohistiocytosis and Macrophage Activation Syndrome.

OBJECTIVE: To compare clinical outcomes in children with hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) who were managed before and after implementation of an evidence-based guideline (EBG). METHODS: A management algorithm for MAS-HLH was developed at our institution based on literature review, expert opinion, and consensus building across multiple pediatric subspecialties. An electronic medical record search retrospectively identified hospitalized patients with MAS-HLH in the pre-EBG (October 15, 2015, to December 4, 2017) and post-EBG (January 1, 2018, to January 21, 2020) time periods. Predetermined outcome metrics were evaluated in the 2 cohorts. RESULTS: After the EBG launch, 57 children were identified by house staff as potential patients with MAS-HLH, and rheumatology was consulted for management. Ultimately, 17 patients were diagnosed with MAS-HLH by the treating team. Of these, 59% met HLH 2004 criteria, and 94% met 2016 classification criteria for MAS complicating systemic juvenile idiopathic arthritis. There was a statistically significant reduction in mortality from 50% before implementation of the EBG to 6% in the post-EBG cohort (P = 0.02). There was a significant improvement in time to 50% reduction in C-reactive protein level in the post-EBG vs pre-EBG cohorts (log-rank P < 0.01). There were trends toward faster time to MAS-HLH diagnosis, faster initiation of immunosuppressive therapy, shorter length of hospital stay, and more rapid normalization of MAS-HLH-related biomarkers in the patients post-EBG. CONCLUSION: While the observed improvements may be partially attributed to advances in treatment of MAS-HLH that have accumulated over time, this analysis also suggests that a multidisciplinary treatment pathway for MAS-HLH contributed meaningfully to favorable patient outcomes.

Joint-Specific Memory and Sustained Risk for New Joint Accumulation in Autoimmune Arthritis.

OBJECTIVE: Inflammatory arthritides exhibit hallmark patterns of affected and spared joints, but in each individual, arthritis affects only a subset of all possible sites. The purpose of this study was to identify patient-specific patterns of joint flare to distinguish local from systemic drivers of disease chronicity. METHODS: Patients with juvenile idiopathic arthritis followed without interruption from disease onset into adulthood were identified across 2 large academic centers. Joints inflamed at each visit were established by medical record review. Flare was defined as physician-confirmed joint inflammation following documented inactive disease. RESULTS: Among 222 adults with JIA, 95 had complete serial joint examinations dating from disease onset in childhood. Mean follow-up was 12.5 years (interquartile range 7.9-16.7 years). Ninety (95%) of 95 patients achieved inactive disease, after which 81% (73 patients) experienced at least 1 flare. Among 940 joints affected in 253 flares, 74% had been involved previously. In flares affecting easily observed large joint pairs where only 1 side had been involved before (n = 53), the original joint was affected in 83% and the contralateral joint in 17% (P < 0.0001 versus random laterality). However, disease extended to at least 1 new joint in ~40% of flares, a risk that remained stable even decades after disease onset, and was greatest in flares that occurred while patients were not receiving medication (54% versus 36% of flares occurring with therapy; odds ratio 2.09, P = 0.015). CONCLUSION: Arthritis flares preferentially affect previously inflamed joints but carry an ongoing risk of disease extension. These findings confirm joint-specific memory and suggest that prevention of new joint accumulation should be an important target for arthritis therapy.

Implications of Evolving Disease Classification for Drug Approval in Juvenile Idiopathic Arthritis.

The classification of inflammatory arthritis incorporates a sharp divide between diseases of childhood onset, grouped together as juvenile idiopathic arthritis, and diseases such as rheumatoid arthritis that begin by definition in adulthood. An important consequence of this divide is that regulatory authorities and many rheumatologists regard pediatric and adult arthritides as truly different, with the implication that drugs should be evaluated separately for each category. However, it is now clear that most forms of arthritis transcend the pediatric/adult boundary and that agents generally exhibit comparable success irrespective of age of onset, offering new opportunities in drug development and regulation focused on pharmacology and safety rather than efficacy. This paradigm shift will enable advances in arthritis treatment, originating either with adults or children, to translate more rapidly across the age spectrum.

Disordered T cell-B cell interactions in autoantibody-positive inflammatory arthritis.

T peripheral helper (Tph) cells, identified in the synovium of adults with seropositive rheumatoid arthritis, drive B cell maturation and antibody production in non-lymphoid tissues. We sought to determine if similarly dysregulated T cell-B cell interactions underlie another form of inflammatory arthritis, juvenile oligoarthritis (oligo JIA). Clonally expanded Tph cells able to promote B cell antibody production preferentially accumulated in the synovial fluid (SF) of oligo JIA patients with antinuclear antibodies (ANA) compared to autoantibody-negative patients. Single-cell transcriptomics enabled further definition of the Tph gene signature in inflamed tissues and showed that Tph cells from ANA-positive patients upregulated genes associated with B cell help to a greater extent than patients without autoantibodies. T cells that co-expressed regulatory T and B cell-help factors were identified. The phenotype of these Tph-like Treg cells suggests an ability to restrain T cell-B cell interactions in tissues. Our findings support the central role of disordered T cell-help to B cells in autoantibody-positive arthritides.

COVID-19 in Pediatrics.

This article reviews the diagnosis and treatment of infection with severe acute respiratory syndrome coronavirus 2, which causes coronavirus disease 2019, as well as a new inflammatory syndrome after severe acute respiratory syndrome coronavirus 2 infection, called multisystem inflammatory syndrome in children.

Th1 polarization defines the synovial fluid T cell compartment in oligoarticular juvenile idiopathic arthritis.

Oligoarticular juvenile idiopathic arthritis (oligo JIA) is the most common form of chronic inflammatory arthritis in children, yet the cause of this disease remains unknown. To understand immune responses in oligo JIA, we immunophenotyped synovial fluid T cells with flow cytometry, bulk RNA-Seq, single-cell RNA-Seq (scRNA-Seq), DNA methylation studies, and Treg suppression assays. In synovial fluid, CD4+, CD8+, and γδ T cells expressed Th1-related markers, whereas Th17 cells were not enriched. Th1 skewing was prominent in CD4+ T cells, including Tregs, and was associated with severe disease. Transcriptomic studies confirmed a Th1 signature in CD4+ T cells from synovial fluid. The regulatory gene expression signature was preserved in Tregs, even those exhibiting Th1 polarization. These Th1-like Tregs maintained Treg-specific methylation patterns and suppressive function, supporting the stability of this Treg population in the joint. Although synovial fluid CD4+ T cells displayed an overall Th1 phenotype, scRNA-Seq uncovered heterogeneous effector and regulatory subpopulations, including IFN-induced Tregs, peripheral helper T cells, and cytotoxic CD4+ T cells. In conclusion, oligo JIA is characterized by Th1 polarization that encompasses Tregs but does not compromise their regulatory identity. Targeting Th1-driven inflammation and augmenting Treg function may represent important therapeutic approaches in oligo JIA.

Patient experiences and strategies for coping with SLE: A qualitative study.

OBJECTIVE: This study explored challenges that patients with systemic lupus erythematosus (SLE) and childhood-onset SLE (cSLE) face to identify modifiable influences and coping strategies in patient experiences. METHODS: Participants were recruited from two academic medical centers through a Lupus Registry of individuals ≥18 years old and ≥4 1997 ACR classification criteria for SLE and a centralized data repository of cSLE patients, and participated in three focus groups. Transcripts were coded thematically and adjudicated by two independent reviewers. RESULTS: Thirteen adults, 7 (54%) with cSLE, participated in focus groups. Themes were categorized into two domains: (1) challenges with SLE diagnosis and management; and (2) patient coping strategies and modifiable factors of the SLE experience. Participants identified five primary challenges: diagnostic odyssey, public versus private face of SLE, SLE-related stresses, medication adherence, and transitioning from pediatric to adult care. Coping strategies and modifiable factors included social support, open communication about SLE, and strong patient-provider relationships. Several participants highlighted positive lessons learned through their experiences with SLE, including empathy, resilience, and self-care skills. CONCLUSIONS: Patients with cSLE and SLE identified common challenges, modifying influences and coping strategies based on personal experiences. A strong patient-provider relationship and trust in the medical team emerged as key modifiable factors. Deriving optimism from experiences with SLE was unique to several patients diagnosed as children or young adults. Leveraging factors that improved the participants' experiences living with SLE may be used in future studies to address vulnerabilities in care.

Th17 reprogramming of T cells in systemic juvenile idiopathic arthritis.

Systemic juvenile idiopathic arthritis (sJIA) begins with fever, rash, and high-grade systemic inflammation but commonly progresses to a persistent afebrile arthritis. The basis for this transition is unknown. To evaluate a role for lymphocyte polarization, we characterized T cells from patients with acute and chronic sJIA using flow cytometry, mass cytometry, and RNA sequencing. Acute and chronic sJIA each featured an expanded population of activated Tregs uncommon in healthy controls or in children with nonsystemic JIA. In acute sJIA, Tregs expressed IL-17A and a gene expression signature reflecting Th17 polarization. In chronic sJIA, the Th17 transcriptional signature was identified in T effector cells (Teffs), although expression of IL-17A at the protein level remained rare. Th17 polarization was abrogated in patients responding to IL-1 blockade. These findings identify evolving Th17 polarization in sJIA that begins in Tregs and progresses to Teffs, likely reflecting the impact of the cytokine milieu and consistent with a biphasic model of disease pathogenesis. The results support T cells as a potential treatment target in sJIA.

Adenosine deaminase 2 as a biomarker of macrophage activation syndrome in systemic juvenile idiopathic arthritis.

OBJECTIVE: Macrophage activation syndrome (MAS) is a life-threatening complication of systemic juvenile idiopathic arthritis (sJIA) characterised by a vicious cycle of immune amplification that can culminate in overwhelming inflammation and multiorgan failure. The clinical features of MAS overlap with those of active sJIA, complicating early diagnosis and treatment. We evaluated adenosine deaminase 2 (ADA2), a protein of unknown function released principally by monocytes and macrophages, as a novel biomarker of MAS. METHODS: We established age-based normal ranges of peripheral blood ADA2 activity in 324 healthy children and adults. We compared these ranges with 173 children with inflammatory and immune-mediated diseases, including systemic and non-systemic JIA, Kawasaki disease, paediatric systemic lupus erythematosus and juvenile dermatomyositis. RESULTS: ADA2 elevation beyond the upper limit of normal in children was largely restricted to sJIA with concomitant MAS, a finding confirmed in a validation cohort of sJIA patients with inactive disease, active sJIA without MAS or sJIA with MAS. ADA2 activity strongly correlated with MAS biomarkers including ferritin, interleukin (IL)-18 and the interferon (IFN)-γ-inducible chemokine CXCL9 but displayed minimal association with the inflammatory markers C reactive protein and erythrocyte sedimentation rate. Correspondingly, ADA2 paralleled disease activity based on serial measurements in patients with recurrent MAS episodes. IL-18 and IFN-γ elicited ADA2 production by peripheral blood mononuclear cells, and ADA2 was abundant in MAS haemophagocytes. CONCLUSIONS: These findings collectively identify the utility of plasma ADA2 activity as a biomarker of MAS and lend further support to a pivotal role of macrophage activation in this condition.

Interleukin-6 Blockade With Tocilizumab in Anakinra-Refractory Febrile Infection-Related Epilepsy Syndrome (FIRES).

Febrile infection-related epilepsy syndrome (FIRES) is characterized by new onset refractory status epilepticus in a previously healthy child that is associated with poor cognitive outcomes and chronic epilepsy. Innate immune system dysfunction is hypothesized to be a key etiologic contributor, with a potential role for immunotherapy blocking pro-inflammatory cytokines, such as interleukin-1ß and interleukin-6. We present a case of FIRES refractory to anakinra, an interleukin-1 receptor antagonist, subsequently treated with the ketogenic diet and tocilizumab, an interleukin-6 receptor antagonist, temporally associated with seizure cessation and a favorable 1-year outcome.

Identification of Racial Inequities in Access to Specialized Inpatient Heart Failure Care at an Academic Medical Center.

BACKGROUND: Racial inequities for patients with heart failure (HF) have been widely documented. HF patients who receive cardiology care during a hospital admission have better outcomes. It is unknown whether there are differences in admission to a cardiology or general medicine service by race. This study examined the relationship between race and admission service, and its effect on 30-day readmission and mortality Methods: We performed a retrospective cohort study from September 2008 to November 2017 at a single large urban academic referral center of all patients self-referred to the emergency department and admitted to either the cardiology or general medicine service with a principal diagnosis of HF, who self-identified as white, black, or Latinx. We used multivariable generalized estimating equation models to assess the relationship between race and admission to the cardiology service. We used Cox regression to assess the association between race, admission service, and 30-day readmission and mortality. RESULTS: Among 1967 unique patients (66.7% white, 23.6% black, and 9.7% Latinx), black and Latinx patients had lower rates of admission to the cardiology service than white patients (adjusted rate ratio, 0.91; 95% CI, 0.84-0.98, for black; adjusted rate ratio, 0.83; 95% CI, 0.72-0.97 for Latinx). Female sex and age >75 years were also independently associated with lower rates of admission to the cardiology service. Admission to the cardiology service was independently associated with decreased readmission within 30 days, independent of race. CONCLUSIONS: Black and Latinx patients were less likely to be admitted to cardiology for HF care. This inequity may, in part, drive racial inequities in HF outcomes.

Older Adults' Recognition of Trade-Offs in Healthcare Decision-Making.

OBJECTIVES: To examine older persons' understanding of healthcare decision-making involving trade-offs. DESIGN: Cross-sectional survey. SETTING: Primary care clinics. PARTICIPANTS: Community-living persons aged 65 and older (N = 50). MEASUREMENTS: After being primed to think about trade-offs with a focus on chronic disease management, participants were asked to describe a decision they had made in the past involving a trade-off. If they could not, they were asked to describe a decision they might face in the future and were then given an example of a decision. They were also asked about communication with their primary care provider about their priorities when faced with a trade-off. RESULTS: Forty-four participants (88%) were able to describe a healthcare decision involving a trade-off; 25 provided a decision in the past, 17 provided a decision they might face in the future, and two provided a future decision after hearing an example. One participant described a nonmedical decision, and two participants described goals without providing a trade-off. Of the healthcare decisions, 26 involved surgery, seven were end-of life decisions, seven involved treatment of chronic disease, and four involved chemotherapy. When asked whether their providers should know their health outcome priorities, 44 (88%) replied yes, and 35 (70%) believed their providers knew their priorities, but only 18 (36%) said that they had had a specific conversation about priorities. CONCLUSION: The majority of participants were able to recognize the trade-offs involved in healthcare decision-making and wanted their providers to know their priorities regarding the trade-offs. Despite being primed to think about the trade-offs involved in day-to-day treatment of chronic disease, participants most frequently described episodic, high-stakes decisions including surgery and end-of-life care.

Relationship between universal health outcome priorities and willingness to take medication for primary prevention of myocardial infarction.

OBJECTIVES: To determine how well universal health outcome priorities represent individuals' preferences in specific clinical situations. DESIGN: Observational cohort study. SETTING: Community. PARTICIPANTS: Community-dwelling adults aged 65 and older (N = 357). MEASUREMENTS: Participants used three tools assessing universal health outcome priorities related to two common trade-offs: quality versus quantity of life and future health versus present inconveniences and burdens of treatment. The tools' ability to identify participants who were unwilling to take a medication that reduced the risk of myocardial infarction but caused dizziness and fatigue was analyzed. RESULTS: There were consistent and significant associations between unwillingness to take the medication and prioritizing quality of life or future health for all three tools in the expected direction (P < .05). Despite these associations, the positive (PPV) and negative predictive values for the tools were generally modest (0.49-0.83). The tool with the most specific statements resembling the medication scenario had the best specificity (0.97) and PPV (0.83). CONCLUSION: Universal health outcome priorities only modestly identified older persons who would be unwilling to take a medication for primary prevention of myocardial infarction that causes adverse effects. Although tools that are the most general in their assessment of priorities have the benefit of being applicable across the widest range of scenarios, tools with greater specificity may be necessary to inform individual treatment decisions.