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Articles by M. H Trivedi
Total Records ( 2 ) for M. H Trivedi
  J. H Kocsis , A. J Gelenberg , B. O Rothbaum , D. N Klein , M. H Trivedi , R Manber , M. B Keller , A. C Leon , S. R Wisniewski , B. A Arnow , J. C Markowitz , M. E Thase and for the REVAMP Investigators
 

Context  Previous studies have found that few chronically depressed patients remit with antidepressant medications alone.

Objective  To determine the role of adjunctive psychotherapy in the treatment of chronically depressed patients with less than complete response to an initial medication trial.

Design  This trial compared 12 weeks of (1) continued pharmacotherapy and augmentation with cognitive behavioral analysis system of psychotherapy (CBASP), (2) continued pharmacotherapy and augmentation with brief supportive psychotherapy (BSP), and (3) continued optimized pharmacotherapy (MEDS) alone. We hypothesized that adding CBASP would produce higher rates of response and remission than adding BSP or continuing MEDS alone.

Setting  Eight academic sites.

Participants  Chronically depressed patients with a current DSM-IV–defined major depressive episode and persistent depressive symptoms for more than 2 years.

Interventions  Phase 1 consisted of open-label, algorithm-guided treatment for 12 weeks based on a history of antidepressant response. Patients not achieving remission received next-step pharmacotherapy options with or without adjunctive psychotherapy (phase 2). Individuals undergoing psychotherapy were randomized to receive either CBASP or BSP stratified by phase 1 response, ie, as nonresponders (NRs) or partial responders (PRs).

Main Outcome Measures  Proportions of remitters, PRs, and NRs and change on Hamilton Scale for Depression (HAM-D) scores.

Results  In all, 808 participants entered phase 1, of which 491 were classified as NRs or PRs and entered phase 2 (200 received CBASP and MEDS, 195 received BSP and MEDS, and 96 received MEDS only). Mean HAM-D scores dropped from 25.9 to 17.7 in NRs and from 15.2 to 9.9 in PRs. No statistically significant differences emerged among the 3 treatment groups in the proportions of phase 2 remission (15.0%), partial response (22.5%), and nonresponse (62.5%) or in changes on HAM-D scores.

Conclusions  Although 37.5% of the participants experienced partial response or remitted in phase 2, neither form of adjunctive psychotherapy significantly improved outcomes over that of a flexible, individualized pharmacotherapy regimen alone. A longitudinal assessment of later-emerging benefits is ongoing.

Trial Registration  clinicaltrials.gov Identifier: NCT00057551

  E. B Binder , M. J Owens , W Liu , T. C Deveau , A. J Rush , M. H Trivedi , M Fava , B Bradley , K. J Ressler and C. B. Nemeroff
 

Context  The corticotropin-releasing factor (CRF, or corticotropin-releasing hormone) and arginine vasopressin systems have been implicated in the pathophysiology of anxiety and depressive disorders and response to antidepressant treatment.

Objective  To study the association of genetic variants in 10 genes that regulate the CRF and arginine vasopressin systems with treatment response to citalopram in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) sample (N = 1768).

Design  Pharmacogenetic association study derived from the STAR*D study, a multicenter, prospective, open, 12-week effectiveness trial.

Setting  Outpatient primary care and psychiatric clinics.

Patients  Individuals with nonpsychotic major depressive disorder for whom DNA was available who were subsequently treated with citalopram hydrobromide for 4 to 12 weeks.

Intervention  Flexible doses of citalopram.

Main Outcome Measure  Association of genetic polymorphisms in genes encoding the CRF system with response and remission to citalopram treatment at exit visit.

Results  One single-nucleotide polymorphism (SNP) (rs10473984) within the CRHBP locus showed a significant association with both remission (P = 6.0 x 10–6; corrected, P = .0026) and reduction in depressive symptoms (P = 7.0 x 10–7; corrected, P = .00031) in response to citalopram. The T allele of this SNP was associated with poorer treatment outcome in 2 of the 3 ethnic subsamples (African American and Hispanic), despite large differences in minor allele frequency. This association was more pronounced in patients with features of anxious depression (P = .008). The nonresponse allele was shown to be associated with overall higher plasma corticotropin levels and more pronounced dexamethasone suppression of corticotropin.

Conclusions  These data indicate that a genetic variant within the CRHBP locus affects response to citalopram in African American and Hispanic patients, suggesting a role for this gene and for the CRF system in antidepressant treatment response.

 
 
 
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