Efficacy of pharmacotherapy in depressed patients with and without personality disorders: A systematic review and meta-analysis

Kool, Simone; Schoevers, Robert A.; Maat, Saskia de; Van, Rien; Molenaar, Pieter J.; Vink, Aukje; Dekker, Jack

doi:10.1016/j.jad.2005.05.017

Cited by 84 publications

(55 citation statements)

References 21 publications

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“…It is a very common phenomenon 33 and a recent meta-analysis reported that it has been considered a possible clinical negative predictor of response to treatment, 34 consistently with early studies [35][36][37][38] whereas others reported a similar outcome for people with and without personality disorders comorbidity using only well-designed study 39 consistent with some recent studies. [40][41][42] Apart from specific personality disorders, also temperament traits have been associated with response, generally in the direction of a poorer response in subjects with high harm avoidance.…”

Section: Clinical Features Of Comorbid Disorders: Axis IIsupporting

confidence: 83%

Pharmacogenetic studies in depression: a proposal for methodologic guidelines

2007

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Pharmacogenetic studies in mood disorders are rapidly proliferating after the initial reports linking gene variants to treatment outcomes. However, a considerable range of methodologies has been used, making it difficult to compare results across studies and limiting the representativeness of findings. Specification of sampling source (inpatients vs outpatients, primary vs tertiary settings), standardization of diagnostic systems and treatments, adequate monitoring of compliance through plasma levels, sufficient length of observation (at least 6 weeks for acute antidepressant treatments, though 3-6 months are preferable), the use of a range of response criteria and the inclusion of possible environmental confounding variables (life events, social support, temperament) are all potentially important issues when planning pharmacogenetic studies. We reviewed the state-of-the-art methodology and suggested possible guideline for future studies.

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Section: Clinical Features Of Comorbid Disorders: Axis IIsupporting

confidence: 83%

Pharmacogenetic studies in depression: a proposal for methodologic guidelines

2007

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“…Second, although most of the relevant sociodemographic characteristics were ascertained, such as gender, race-ethnicity, income and employment, and marital status, others, such as social support or religiosity, that have been previously linked to antidepressant outcome were not included in STAR * D (22). Personality disorders have been reported as potential confounders of antidepressant treatment outcome in some studies, including recent meta-analyses (23), but not all (24,25). STAR * D did not assess personality traits; however, it is important to note the well-known inaccuracy of assessment of trait characteristics, such as personality disorders, in the context of depressive states (26).…”

Section: What Are the Limitations Of Star*d As A Pharmacogenetics Study?mentioning

confidence: 99%

Pharmacogenetics Studies in STAR*D: Strengths, Limitations, and Results

Laje

Perlis²,

Rush³

et al. 2009

Psychiatric Services

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Several lines of evidence support an important genetic contribution to the wide individual variation in therapeutic response to antidepressant medications. The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study provided the largest cohort assembled to date of DNA from patients with nonpsychotic major depressive disorder, uniformly treated with citalopram and followed prospectively for up to 12 weeks. This pivotal study changed the face of pharmacogenetics research by increasing the sample size by an order of magnitude as well as by providing detailed prospective information about antidepressant response and tolerability. Several groups have identified markers in genes and tested the replication of previous findings of genes associated with outcome and side effects of antidepressant treatment. Variants in HTR2A, GRIK4, and KCNK2 were associated with citalopram treatment outcome. Replication was achieved in markers in the FKBP5 gene. Other findings in PDE11A and BDNF were not successfully replicated, and reports of potential confounders in previous associations with serotonin transporter variation (SLC6A4) were identified. Polymorphisms in pharmacokinetic genes involved in metabolism and transmembrane transport were also not associated with antidepressant response. Adverse events were also tested. Treatment-emergent suicidal ideation was associated with GRIK2, GRIA3, PAPLN, IL28RA, and CREB1. Sexual dysfunction was linked with variation in GRIN3A, GRIA1 GRIA3, and GRIK2. Reported and future findings of pharmacogenetics studies in STAR*D could help elucidate pathways involved in major depression and those pertinent to antidepressant outcome and side effects. Replication of these findings in independent samples could lead to the development of new treatments and to optimization of available treatments.

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“…It is of note, however, that the randomized control trials in this investigation suggested a smaller association of PD with poor treatment response than the case series. Moreover, a meta-analysis of six methodologically rigorous randomized control trials by Kool, Schoevers, de Maat, Van, Molenaar, Vink & Dekker (2005) demonstrated no difference in remission rates between the depressed patients with and without co-morbid PD. This result is in line with the conclusions of Mulder's (2002) narrative review, in which the most methodologically sound studies demonstrated the least evidence of an association between PD and (poor) treatment outcome.…”

mentioning

confidence: 98%

“…This result is in line with the conclusions of Mulder's (2002) narrative review, in which the most methodologically sound studies demonstrated the least evidence of an association between PD and (poor) treatment outcome. Kool et al (2005) and Mulder (2002) proposed that the better outcomes from carefully controlled treatment studies suggests that depressed patients with co-morbid PD may be less likely to receive adequate treatment in everyday clinical practice; nevertheless, recent naturalistic studies con tinue to reveal equivocal results regarding the impact of PD on treatment outcome (Mulder, Joyce, Frampton, Luty, & Sullivan, 2006).…”

mentioning

confidence: 99%