Association of Antipsychotic Use With Mortality Risk in Patients With Parkinson Disease.
Ontology highlight
ABSTRACT:
SUBMITTER: Weintraub D
PROVIDER: S-EPMC5157923 | biostudies-literature | 2016 May
REPOSITORIES: biostudies-literature
Publications
Association of Antipsychotic Use With Mortality Risk in Patients With Parkinson Disease.
Weintraub Daniel D Chiang Claire C Kim Hyungjin Myra HM Wilkinson Jayne J Marras Connie C Stanislawski Barbara B Mamikonyan Eugenia E Kales Helen C HC
JAMA neurology 20160501 5
<h4>Importance</h4>As many as 60% of patients with Parkinson disease (PD) experience psychosis, 80% develop dementia, and the use of antipsychotics (APs) in the population with PD is common. The use of APs by patients with dementia in the general population is associated with increased mortality, but whether this risk extends to patients with PD remains unknown.<h4>Objective</h4>To determine whether AP use in patients with PD is associated with increased mortality.<h4>Design, setting, and partic ...[more]
Similar Datasets
Project description:BackgroundNeuroinflammation may contribute to the pathogenesis of Parkinson disease (PD). Use of nonsteroidal anti-inflammatory drugs (NSAID) in general, and possibly ibuprofen in particular, has been shown to be related to lower PD risk in previous epidemiologic studies.MethodsWe prospectively examined whether use of ibuprofen or other NSAIDs is associated with lower PD risk among 136,197 participants in the Nurses' Health Study (NHS) and the Health Professionals Follow-up Study (HPFS) free of PD at baseline (1998 for NHS and 2000 for HPFS). NSAIDs use was assessed via questionnaire. Results were combined in a meta-analysis with those of published prospective investigations.ResultsWe identified 291 incident PD cases during 6 years of follow-up. Users of ibuprofen had a significantly lower PD risk than nonusers (relative risk [RR], adjusted for age, smoking, caffeine, and other covariates = 0.62; 95% confidence interval [CI] 0.42-0.93; p = 0.02). There was a dose-response relationship between tablets of ibuprofen taken per week and PD risk (p trend = 0.01). In contrast, PD risk was not significantly related to use of aspirin (RR = 0.99; 95% CI 0.78-1.26), other NSAIDs (RR = 1.26; 95% CI 0.86-1.84), or acetaminophen (RR = 0.86; 95% CI 0.62-1.18). Similar results were obtained in the meta-analyses: the pooled RR was 0.73 (95% CI 0.63-0.85; p < 0.0001) for ibuprofen use, whereas use of other types of analgesics was not associated with lower PD risk.ConclusionsThe association between use of ibuprofen and lower PD risks, not shared by other NSAIDs or acetaminophen, suggests ibuprofen should be further investigated as a potential neuroprotective agent against PD.
| S-EPMC3059148 | biostudies-literature
Project description:ImportanceParkinson disease (PD) is an increasingly common neurodegenerative disorder in many aging societies. Although comorbidities with mental disorders are common in PD, whether PD is associated with an increased risk of suicide is unclear.ObjectiveTo use a large national representative PD cohort to compare the risk of suicide in patients with PD and control participants and identify potential risk factors.Design, setting, and participantsThis nationwide population-based cohort study used linked data from Taiwan's National Health Insurance data set and Taiwan Death Registry between January 2002 and December 2016. Patients with incident PD diagnosed between January 2005 and December 2014 were followed up until December 2016. Four control participants from the general population were randomly selected by risk set sampling and were matched on age, sex, and residence to each affected individual. Data analysis occurred from June 2019 to October 2020.ExposuresDiagnosis of PD retrieved from the National Health Insurance data set.Main outcomes and measuresSuicide was recorded in the Taiwan Death Registry. Cox proportional models and hazard ratios (HRs) were used to estimate the association between PD and the risk of suicide over the follow-up period.ResultsOver 11 years, 35 891 patients with PD were followed up (17 482 women [48.7%]; mean [SD] age, 72.5 [10.1] years) and matched to 143 557 control participants (69 928 women [48.7%]; mean [SD] age, 72.5 [10.1] years). A total of 151 patients with PD (cumulative incidence, 66.6 per 100 000 [95% confidence limits [CL], 78.1-91.7]) and 300 control participants (cumulative incidence, 32.3 per 100 000 [95% CL, 36.2-40.5]) died by suicide. The risk of suicide was higher (HR, 2.1 [95% CL, 1.7-2.5]) in patients with PD than control participants, after adjustment for markers of socioeconomic position, medical comorbidities, and dementia. After controlling for mental disorders, the association between PD and suicide risk remained (HR, 1.9 [95% CL, 1.6-2.3]). Compared with control participants who died by suicide, those who died by suicide in the PD group were slightly younger (mean [SD] age: patients with PD, 74.0 [10.4] years vs control participants, 76.0 [10.2] years; P = .05) and more likely to be urban dwelling (medium urbanization, 39 patients with PD [25.8%] vs 115 control participants [38.3%]; high urbanization, 84 patients with PD [55.6%] vs 136 control participants [45.3%]; P = .03), have mental disorders (depression, 15 of 151 patients with PD [9.9%] vs 15 of 300 control participants [5.0%]; other mental disorders, 12 patients with PD [8.0%] vs 11 control participants [3.7%]; P = .02), and adopt jumping as a method of suicide (21 patients with PD [13.9%] vs 16 control participants [5.3%]; P < .01).Conclusions and relevanceIn this population-based cohort study, Parkinson disease, a common neurodegenerative disorder common in elderly persons, was independently associated with an increased risk of suicide. Integrating mental health care into primary care and PD specialty care, along with socioenvironmental interventions, may help decrease the risk of suicide in patients with PD.
| S-EPMC7745139 | biostudies-literature
Project description:BACKGROUND:Recent data showed that melanoma was more common among patients with Parkinson disease than individuals without Parkinson disease and vice versa. It has been hypothesized that these two diseases may share common genetic and environmental risk factors. METHODS:We evaluated the association between single-nucleotide polymorphisms (SNP) selected on the basis of recent genome-wide association studies (GWAS) on Parkinson disease risk and the risk of melanoma using 2,297 melanoma cases and 6,651 controls. RESULTS:The Parkinson disease SNP rs156429 in the chromosome 7p15 region was nominally associated with melanoma risk with P value of 0.04, which was not significant after the Bonferroni correction for multiple comparisons. No association was observed between the remaining 31 Parkinson disease SNPs and the risk of melanoma. The genetic score based on the number of Parkinson disease risk allele was not associated with melanoma risk [OR for the highest genetic score quartile (30-35) vs. the lowest (15-20), 1.13, 95% confidence interval (CI), 0.47-2.70]. CONCLUSION:The Parkinson disease SNPs identified in published GWAS do not seem to play an important role in melanoma development. IMPACT:The Parkinson disease susceptibility loci discovered by GWAS contribute little to the observed epidemiologic association between the Parkinson disease and melanoma.
| S-EPMC3253945 | biostudies-literature
Project description:ImportanceCaregivers are integral to Parkinson disease (PD) care, but little information exists regarding how caregivers impact patient outcomes.ObjectiveTo assess the association between caregivers reporting depression symptoms and patient quality of life (QOL), emergency department (ED) visits, and hospitalizations.Design, setting, and participantsThis retrospective cohort study was conducted at 15 Parkinson's Foundation Centers of Excellence within the US. The Parkinson's Foundation Parkinson Outcomes Project registry was used to collect baseline data from January 1, 2016, to December 31, 2018, with subsequent annual study visits through July 31, 2020. Data were analyzed from August 5, 2020, to June 9, 2023. A convenience sample of 454 patients with PD and their caregivers was recruited during routine clinical visits with movement disorder specialists. Patients with a physician diagnosis of idiopathic PD who lived at home and had 1 or more follow-up study visits were included.ExposureCaregiver depression symptoms using the Center for Epidemiologic Studies Depression Scale.Main outcomes and measuresPatient health-related QOL (measured by the 39-item Parkinson Disease Questionnaire), number of annual ED visits, and number of annual hospitalizations were measured. The independent association between caregivers reporting depression symptoms and patient outcomes was assessed using linear mixed-effects and Poisson regression models. The a priori hypotheses were that a greater number of depression symptoms reported via the Center for Epidemiologic Studies Depression Scale would be associated with worse patient QOL and a greater number of ED visits and hospitalizations.ResultsAmong 454 patient-caregiver dyads (patients: mean [SD] age, 67.3 [8.4] years; 320 men [70.5%]; caregivers: mean [SD] age, 65.9 [8.7] years; 326 women [71.8%]), the mean (SD) follow-up was 2.0 (1.4) study visits. Greater depression symptoms among caregivers were associated with worse patient QOL as measured by the Parkinson Disease Questionnaire (mean [SD] score, 33.78 [17.71], on a scale of 0-100, with higher scores indicating worse QOL, among patients with caregivers who had depression symptoms vs 24.50 [14.19] among patients with caregivers who did not have depression symptoms; β = 0.43; 95% CI, 0.28-0.58; P < .001) and more annual ED visits (β = 0.02; 95% CI, 0 to 0.04; P = .03) but not more hospitalizations (β = 0.02; 95% CI, -0.01 to 0.03; P = .10).Conclusions and relevanceIn this cohort study, patients with PD who had caregivers at higher risk of depression were more likely to have worse QOL and higher ED use than patients who had caregivers not at higher risk of depression. Additional caregiving resources and interventions to reduce caregiver depression symptoms could potentially improve patient outcomes.
| S-EPMC10422183 | biostudies-literature
Project description:BackgroundAntipsychotics are used in Parkinson disease (PD) to treat psychosis, mood, and behavioral disturbances. Commonly used antipsychotics differ substantially in their potential to worsen motor symptoms through dopaminergic receptor blockade. Recent real-world data on the use and continuation of antipsychotic therapy in PD are lacking. The objectives of this study are to (1) examine the continuation of overall and initial antipsychotic therapy in individuals with PD and (2) determine whether continuation varies by drug dopamine receptor blocking activity.MethodsWe conducted a retrospective cohort study using U.S. commercially insured individuals in Optum 2001-2019. Adults aged 40 years or older with PD initiating antipsychotic therapy, with continuous insurance coverage for at least 6 months following drug initiation, were included. Exposure to pimavanserin, quetiapine, clozapine, aripiprazole, risperidone, or olanzapine was identified based on pharmacy claims. Six-month continuation of overall and initial antipsychotic therapy was estimated by time to complete discontinuation or switching to a different antipsychotic. Cox proportional hazards models evaluated factors associated with discontinuation.ResultsOverall, 38.6% of 3566 PD patients in our sample discontinued antipsychotic therapy after the first prescription, 61.4% continued with overall treatment within 6 months of initiation. Clozapine use was too rare to include in statistical analyses. Overall therapy discontinuation was more likely for those who initiated medications with known dopamine-receptor blocking activity (adjusted hazard ratios 1.76 [95% confidence interval 1.40-2.20] for quetiapine, 2.15 [1.61-2.86] for aripiprazole, 2.12 [1.66-2.72] for risperidone, and 2.07 [1.60-2.67] for olanzapine), compared with serotonin receptor-specific pimavanserin. Initial antipsychotic therapy discontinuation also associated with greater dopamine-receptor blocking activity medication use - adjusted hazard ratios 1.57 (1.28-1.94), 1.88 (1.43-2.46), 2.00 (1.59-2.52) and 2.03 (1.60-2.58) for quetiapine, aripiprazole, risperidone, and olanzapine, respectively, compared with pimavanserin. Similar results were observed in sensitivity analyses.ConclusionsOver one-third of individuals with PD discontinued antipsychotic therapy, especially if the initial drug has greater dopamine-receptor blocking activity. Understanding the drivers of antipsychotic discontinuation, including ineffectiveness, potentially inappropriate use, clinician inertia, patient adherence and adverse effects, is needed to inform clinical management of psychosis in PD and appropriate antipsychotic use in this population.
| S-EPMC8223332 | biostudies-literature
Project description:Purpose of reviewThe prevalence of diabetes is 2-3-fold higher in people with severe mental illness than the general population. There are concerns that antipsychotics increase the risk of diabetes. This review will examine the latest epidemiological studies linking antipsychotics and diabetes, as well as the mechanisms underlying the association and the clinical implications to minimise the impact of antipsychotics on metabolic health.Recent findingsAlthough there is an increased risk of diabetes in people with first-episode psychosis, the prevalence increases rapidly after antipsychotics are started. Antipsychotics likely increase the risk of diabetes through weight gain and directly by adversely affecting insulin sensitivity and secretion. It is important to implement measures to prevent diabetes, to screen for diabetes to ensure prompt diagnosis and to provide effective diabetes care. Further research is needed to understand how antipsychotics cause diabetes and to improve the clinical management of diabetes in people with severe mental illness.
| S-EPMC6718373 | biostudies-literature
Project description:ObjectiveTo identify biotypes in patients with newly diagnosed Parkinson disease (PD) and to test whether these biotypes could explain interindividual differences in longitudinal progression.MethodsIn this longitudinal analysis, we use a data-driven approach clustering PD patients from the Parkinson's Progression Markers Initiative (n = 314, age 61.0 ± 9.5, years 34.1% female, 5 years of follow-up). Voxel-level neuroanatomic features were estimated with deformation-based morphometry (DBM) of T1-weighted MRI. Voxels with deformation values that were significantly correlated (p < 0.01) with clinical scores (Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale Parts I-III and total score, tremor score, and postural instability and gait difficulty score) at baseline were selected. Then, these neuroanatomic features were subjected to hierarchical cluster analysis. Changes in the longitudinal progression and neuroanatomic pattern were compared between different biotypes.ResultsTwo neuroanatomic biotypes were identified: biotype 1 (n = 114) with subcortical brain volumes smaller than heathy controls and biotype 2 (n = 200) with subcortical brain volumes larger than heathy controls. Biotype 1 had more severe motor impairment, autonomic dysfunction, and much worse REM sleep behavior disorder than biotype 2 at baseline. Although disease durations at the initial visit and follow-up were similar between biotypes, patients with PD with smaller subcortical brain volume had poorer prognosis, with more rapid decline in several clinical domains and in dopamine functional neuroimaging over an average of 5 years.ConclusionRobust neuroanatomic biotypes exist in PD with distinct clinical and neuroanatomic patterns. These biotypes can be detected at diagnosis and predict the course of longitudinal progression, which should benefit trial design and evaluation.
| S-EPMC7116258 | biostudies-literature
Project description:ObjectiveTo characterize how disease progression is associated with mortality in a large cohort of patients with Parkinson disease (PD) with long-term follow-up after subthalamic nucleus deep brain stimulation (STN-DBS).MethodsMotor and cognitive disabilities were assessed before and 1, 2, 5, and 10 years after STN-DBS in 143 consecutive patients with PD. We measured motor symptoms "off" and "on" levodopa and STN-DBS and recorded causes of death. We used linear mixed models to characterize symptom progression, including interactions between treatment conditions and time to determine how treatments changed efficacy. We used joint models to link symptom progression to mortality.ResultsMedian observation time was 12 years after surgery, during which akinesia, rigidity, and axial symptoms worsened, with mean increases of 8.8 (SD 6.5), 1.8 (3.1), and 5.4 (4.1) points from year 1-10 after surgery ("on" dopamine/"on" STN-DBS), respectively. Responses to dopaminergic medication and STN-DBS were attenuated with time, but remained effective for all except axial symptoms, for which both treatments and their combination were predicted to be ineffective 20 years after surgery. Cognitive status significantly declined. Forty-one patients died, with a median time to death of 9 years after surgery. The current level of axial disability was the only symptom that significantly predicted death (hazard ratio 4.30 [SE 1.50] per unit of square-root transformed axial score).ConclusionsWe quantified long-term symptom progression and attenuation of dopaminergic medication and STN-DBS treatment efficacy in patients with PD and linked symptom progression to mortality. Axial disability significantly predicts individual risk of death after surgery, which may be useful for planning therapeutic strategies in PD.
| S-EPMC6556086 | biostudies-literature
Project description:ImportanceRandomized controlled trials have demonstrated increased all-cause mortality in elderly patients with dementia treated with newer antipsychotics. It is unknown whether this risk generalizes to non-elderly adults using newer antipsychotics as augmentation treatment for depression.ObjectiveThis study examined all-cause mortality risk of newer antipsychotic augmentation for adult depression.DesignPopulation-based new-user/active comparator cohort study.SettingNational healthcare claims data from the US Medicaid program from 2001-2010 linked to the National Death Index.ParticipantsNon-elderly adults (25-64 years) diagnosed with depression who after ≥3 months of antidepressant monotherapy initiated either augmentation with a newer antipsychotic or with a second antidepressant. Patients with alternative indications for antipsychotic medications, such as schizophrenia, psychotic depression, or bipolar disorder, were excluded.ExposureAugmentation treatment for depression with a newer antipsychotic or with a second antidepressant.Main outcomeAll-cause mortality during study follow-up ascertained from the National Death Index.ResultsThe analytic cohort included 39,582 patients (female = 78.5%, mean age = 44.5 years) who initiated augmentation with a newer antipsychotic (n = 22,410; 40% = quetiapine, 21% = risperidone, 17% = aripiprazole, 16% = olanzapine) or with a second antidepressant (n = 17,172). The median chlorpromazine equivalent starting dose for all newer antipsychotics was 68mg/d, increasing to 100 mg/d during follow-up. Altogether, 153 patients died during 13,328 person-years of follow-up (newer antipsychotic augmentation: n = 105, follow-up = 7,601 person-years, mortality rate = 138.1/10,000 person-years; antidepressant augmentation: n = 48, follow-up = 5,727 person-years, mortality rate = 83.8/10,000 person-years). An adjusted hazard ratio of 1.45 (95% confidence interval, 1.02 to 2.06) indicated increased all-cause mortality risk for newer antipsychotic augmentation compared to antidepressant augmentation (risk difference = 37.7 (95%CI, 1.7 to 88.8) per 10,000 person-years). Results were robust across several sensitivity analyses.ConclusionAugmentation with newer antipsychotics in non-elderly patients with depression was associated with increased mortality risk compared with adding a second antidepressant. Though these findings require replication and cannot prove causality, physicians managing adults with depression should be aware of this potential for increased mortality associated with newer antipsychotic augmentation.
| S-EPMC7526884 | biostudies-literature
Project description:ObjectivesOlder adults are particularly vulnerable to the negative consequences of antipsychotic exposure and are disproportionally affected by higher mortality from coronavirus disease 2019 (COVID-19). Our goal was to determine whether concurrent antipsychotic medication use was associated with increased COVID-19 mortality in older patients with preexisting behavioral health problems. We also report on findings from post-COVID follow-ups.DesignRetrospective observational study.ParticipantsOutpatients at a geriatric psychiatric clinic in New York City.MeasurementsDemographic and clinical data including medication, diagnosis and Clinical Global Impression Severity (CGI-S) scales on outpatients who had COVID-19 between February 28th and October 1st 2020 were extracted from the electronic health records (EHR) from the hospital.ResultsA total of 56 patients were diagnosed with COVID-19 (mean age 76 years; median age 75 years) and 13 (23.2%) died. We found an increased mortality risk for patients who were prescribed at least one antipsychotic medication at the time of COVID-19 infection (Fisher's exact test P = 0.009, OR = 11.1, 95% confidence interval: 1.4-96.0). This result remains significant after adjusting for age, gender, housing context and dementia (Logistic regression P = 0.035, Beta = 2.4). Furthermore, we found that most patients who survived COVID-19 (88.4%) recovered to pre-COVID baseline in terms of psychiatric symptoms. Comparison of pre- and post-COVID assessments of CGI-S for 33 patients who recovered from COVID-19 were not significantly different.ConclusionWe observed a higher COVID-19 mortality associated with concurrent antipsychotics use in older patients receiving behavioral health services. The majority of patients in our geriatric clinic who recovered from COVID-19 appeared to return to their pre-COVID psychiatric function. More precise estimates of the risk associated with antipsychotic treatment in older patients with COVID-19 and other underlying factors will come from larger datasets and meta-analyses.
| S-EPMC8530340 | biostudies-literature