The Impact of Treatment-Resistant Depression on Health Care Utilization and Costs

Crown, William H.; Finkelstein, Stan N.; Berndt, Ernst R.; Ling, Davina C.; Poret, Amy W.; Rush, A. John; Russell, James M.

doi:10.4088/jcp.v63n1102

Cited by 323 publications

(191 citation statements)

References 0 publications

Supporting

Mentioning

168

Contrasting

Unclassified

Order By: Relevance

“…Treatment-resistant MDD contributes substantially to the costs and disability associated with MDD (Crown et al, 2002). In the STAR*D clinical cohort as a whole, individuals who did not adequately benefit from the first two treatments had less than a 15% likelihood of responding to subsequent interventions .…”

Section: Discussionmentioning

confidence: 99%

Pharmacogenetic Analysis of Genes Implicated in Rodent Models of Antidepressant Response: Association of TREK1 and Treatment Resistance in the STAR*D Study

Perlis

Moorjani

Fagerness

et al. 2008

Neuropsychopharmacol

View full text Add to dashboard Cite

Recent rodent models of antidepressant response implicate a novel set of genes in mechanisms of antidepressant action. The authors examined variants in four such genes (KCNK2 (TREK1), SLC18A2 (VMAT2), S100A10, and HDAC5) for association with remission in a large effectiveness trial of antidepressant treatments. Subjects were drawn from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, a multicenter, prospective, effectiveness trial in major depressive disorder (MDD). Outpatients with nonpsychotic MDD were initially treated with citalopram for up to 14 weeks; those who did not remit with citalopram were sequentially randomized to a series of next-step treatments, each for up to 12 weeks. Single-nucleotide polymorphisms in four genes were examined for association with remission, defined as a clinician-rated Quick Inventory of Depressive Symptomatology (QIDS-C 16 ) score p5. Of 1554 participants for whom DNA was available, 565 (36%) reached remission with citalopram treatment. No association with any of the four genes was identified. However, among the 751 who entered next-step treatment, variants in KCNK2 were associated with treatment response (Bonferroni-corrected, gene-based empirical po0.001). In follow-up analyses, KCNK2 was also associated with effects of similar magnitude for third-step treatment among those with unsatisfactory benefit to both citalopram and one next-step pharmacotherapy (n ¼ 225). These findings indicate that genetic variation in KCNK2 may identify individuals at risk for treatment resistance. More broadly, they indicate the utility of animal models in identifying genes for pharmacogenetic studies of antidepressant response.

show abstract

Section: Discussionmentioning

confidence: 99%

Pharmacogenetic Analysis of Genes Implicated in Rodent Models of Antidepressant Response: Association of TREK1 and Treatment Resistance in the STAR*D Study

Perlis

Moorjani

Fagerness

et al. 2008

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Crown et al [69] in a database analysis showed that patients with treatment-resistant depression incurred Gunther et al [65] (Germany, N 5 104)…”

Section: Response Definitionsmentioning

confidence: 99%

Nonresponse, partial response, and failure to achieve remission: humanistic and cost burden in major depressive disorder

et al. 2009

View full text Add to dashboard Cite

Objective: To characterize the spectrum of clinical outcomes achieved with depression treatment and the associated impact on quality of life (QOL), functional status, overall well-being, health-care costs, and productivity. Sources: Electronic databases including Medline were searched for English language sources between 1995 and 2007 using key words of depression, nonresponse, partial response, and remission and QOL, functional status, utility, cost, and productivity. Study selection: Relevant abstracts were obtained for 488 references and full-text articles were reviewed that included primary data and compared outcomes by treatment response. Data were abstracted from 26 full-text articles. Data abstraction: Detailed evidence tables were prepared with the relevant data as well as information on the study design. All data abstracted were checked for accuracy. Synthesis: Treatment remitters and partial responders reported clinically and statistically significant improvements in QOL, functional status, and overall well-being compared to nonresponders. Annual health-care costs and productivity losses were significantly lower for remitters and partial responders compared to nonresponders. Conclusions: The reduced disease burden for remitters and partial responders compared to nonresponders indicates that new treatment strategies that improve the rates of response/remission with initial treatment might have value to patients and to society. Depression and Anxiety 26:83-97, 2009.

show abstract

“…These databases are derived primarily from employer health insurance plans and have been used widely for diverse health economics research studies. [7][8][9][10] The data sources contain the inpatient, outpatient, and outpatient prescription drug claims of approximately 14 million individuals of all ages who are covered under a variety of feefor-service, point-of-service, and capitated benefit plans. Approximately 1 million of the covered lives are from the Medicare database, which consists of individuals with Medicare coverage who have supplemental, employer-funded coverage.…”

Section: Data Sourcementioning

confidence: 99%

Economic burden of metastatic bone disease in the U.S.

Schulman

Kohles

2007

Cancer

200

135

View full text Add to dashboard Cite

BACKGROUNDPrevious research has documented the prevalence of primary bone cancer; however, there are few data available regarding the impact of metastatic bone disease (MBD) on national expenditure. In this study, the authors quantified the prevalence and direct medical care costs of patients with MBD and the resulting cost impact on U.S. oncology expenditure.METHODSAnonymous, patient‐level data on health care utilization and cost were obtained from the Thomson Medstat MarketScan research databases. In total, 396,200 patients who were diagnosed with cancer between 2000 and 2004 were selected for the study. Patients with MBD were matched subsequently to non‐MBD controls. A 2‐part linear regression model was used to compare cases with controls to quantify the incremental cost associated with the disease.RESULTSCancer prevalence in the U.S. during the study period was estimated at 4,861,987 cases annually, and 5.3% (n = 256,137) of those patients had MBD. Rates of MBD were highest in patients with multiple myeloma (28.8%) and lung cancer (15.6%). The mean direct medical cost for all cancers combined was $75,329 for patients with MBD and $31,382 for controls. Regression‐adjusted, incremental costs were $44,442 (P < .001) across all cancer types. The incremental cost was highest for patients with multiple myeloma ($63,455) and lowest for patients with lung cancer ($24,946).CONCLUSIONSThe national cost burden for patients with MBD was estimated at $12.6 billion, which is 17% of the $74 billion in total direct medical cost estimated by the National Institutes of Health, suggesting that MBD is a significant driver of overall oncology cost. Cancer 2007. © 2007 American Cancer Society.

show abstract

The Impact of Treatment-Resistant Depression on Health Care Utilization and Costs

Cited by 323 publications

References 0 publications

Pharmacogenetic Analysis of Genes Implicated in Rodent Models of Antidepressant Response: Association of TREK1 and Treatment Resistance in the STAR*D Study

Pharmacogenetic Analysis of Genes Implicated in Rodent Models of Antidepressant Response: Association of TREK1 and Treatment Resistance in the STAR*D Study

Nonresponse, partial response, and failure to achieve remission: humanistic and cost burden in major depressive disorder

Economic burden of metastatic bone disease in the U.S.

Contact Info

Product

Resources

About