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Depression treatment response

In another study, conducted in the US Veterans Affairs healthcare system, in adults over 60 years with depression, an examination of whether pain severity and interference with normal work activities moderated the effects of depression treatment response was undertaken [9]. In this study, patients were randomized to integrated care (care debvered in the primary care clinic, by a mental health professional) versus enhanced specialty referral care (care delivered in the 344 subspecialty clinic office) and results were examined... [Pg.344]

Pollock, B. G., Ferrell, R. E. et al. (2000). Allelic variation in the serotonin transporter promoter affects onset of paroxetine treatment response in late-life depression. Neuropsychopharmacology, 23(5), 587-90. [Pg.36]

CT showed significantly better treatment responses than the homozygote group (CC + TT genotypes). Major depression Asian... [Pg.70]

Zill, P., Baghai, T. C., Zwanzger, R et al. (2000). Evidence for an association between a G-protein beta3-gene variant with depression and response to antidepressants treatment. Neuroreport, 11, 1893-7. [Pg.86]

Ferrando et al. (1999) conducted an open-label trial of fluoxetine or sertraline in 30 depressed HIV-positive women (including 16 of Puerto Rican or Dominican descent). No differences in treatment response or adverse effects were found between groups. [Pg.98]

Lee, H.-J., Cha, J.-H., Ham, B.-J. etal. (2004). Association between a G-protein boldbeta3 subunit gene polymorphism and the symptomatology and treatment responses of major depressive disorders. Pharmacogenomics J., 4, 29-33. [Pg.167]

Approximately 30-40% of patients will not respond to a given antidepressant and 60-75% may fail to achieve complete remission [16]. Consequently, in its least restricted definition, treatment resistance could be detected in the majority of depressed patients under treatment. Moreover, prior treatment failure negatively influences the response to subsequent antidepressant treatment, decreasing the odds of treatment response by a factor of 15-20% for each failed treatment [17]. The delayed onset of symptom relief (which takes three to eight weeks to occur) and the presence of adverse drug reactions contribute significantly to low treatment compliance. [Pg.386]

Research underway by our group and others on the clinical pharmacogenomics of depression is focused on identifying genetic markers as positive and negative predictors of treatment response. It is necessary that rigorous clinical studies be performed in order to examine closely the relation between genotype and the phe-... [Pg.387]

Dysthymic Disorder. Dysthymic disorder differs from MDD by being more chronic and less severe. Yet, two issues can cloud the distinction. First, some patients experience double depression in which an episode of major depression is superimposed on dysthymia. This can make it difficult to assess treatment response when the baseline mood is dysthymia instead of a normal euthymic mood. Second, a few patients may experience a chronic major depressive episode, which, like dysthymic disorder, lasts 2 years or more. In contrast to dysthymic patients whose insidious onset of symptoms leaves them unable to say exactly when the depression started, most patients with chronic major depression can tell when their depression began. [Pg.42]

Antidepressants have been shown effective in the treatment of major depression with response rates at approximately 60-70%. The only treatment for depression consistently shown to be more effective is ECT with response rates of 80-90%. There is no definitive means of predicting which medication will work best for a given patient nevertheless, the choice of a medication should not be made capriciously. Several factors can guide medication selection and thereby maximize the likelihood of a successful response. [Pg.62]

Sloan DME, Komstein SG. Gender differences in depression and response to antidepressant treatment. Psychiatr Clin North Am 2003 26(3) 581-594. [Pg.96]

The subset of patients with GAD who do not have a comorbid depressive illness can be treated with buspirone in lieu of an antidepressant. Like the antidepressants, the buspirone treatment response is delayed by several weeks however, opting for buspirone is less likely to cause the transient exacerbation of anxiety or the sexual side effects commonly witnessed with antidepressants. Unfortunately, the usefulness of buspirone is severely limited by its requirement that it be administered two to... [Pg.151]

Generalized Sociai Anxiety Disorder, Treatment Resistance. A significant minority of patients will not experience a satisfactory treatment response to antidepressant therapy, even after a trial of adequate duration at full strength doses. For those with comorbid depression who are experiencing no benefit from SSRI treatment for either the anxiety or depression, then switching treatment is advisable. The options include switching to another SSRI, a SNRI (venlafaxine or perhaps dulox-etine), or, when other alternatives fail, phenelzine. [Pg.166]

The term "bipolar disorder" originally referred to manic-depressive illnesses characterized by both manic and depressive episodes. In recent years, the concept of bipolar disorder has been broadened to include subtypes with similar clinical courses, phenomenology, family histories and treatment responses. These subtypes are thought to form a continuum of disorders that, while differing in severity, are related. Readers are referred to the Diagnostic and Statisticial Manual of Mental Disorders of the American Psychiatric Association (DSM-IV) for details of this classification. [Pg.193]

Based on existing findings, there are many important hypotheses in pediatric psychopharmacogenetics. Selective serotonin transporter inhibitors have been shown to have efficacy in double-blind studies in children and/ or adolescents in the treatment of autism, major depression, OCD, and anxiety disorders. Given the association of the serotonin transporter promoter variant with SSRI treatment response in adult depression (Smeraldi et ah, 1998), all of the SSRI-responsive phenotypes should be tested for promoter variant influence on response using family-based or population-based controlled association studies. The report of strong 5-HTTLPR allelic effects on SSRI-induced mania (Mundo et ah, 2000) is of special interest given frequent SSRI-induced activation in children. [Pg.92]

Comorbid anxiety has been associated with differential treatment response. This association predicts at times a better response to CBT and TCAs (Hughes et ah, 1990 Brent et ah, 1998). Treatment of comorbid anxiety, which most often precedes depression, is essential because the treatment contributes to improvement and may prevent future depressive episodes (Ko-vacs et ah, 1989 Hayward et ah, 2000). Fortunately, pharmacotherapy and psychotherapy treatments found useful for the treatment of MDD have also been found to be beneficial for treatment of youths with anxiety disorders (Kendall, 1994 RUPP Anxiety Group, 2001). [Pg.476]

Other comorbid conditions, such as obsessive-compulsive, conduct, eating, and post-traumatic stress disorders, have also been found to affect the treatment response and need to be addressed for the successful treatment of depressed youths (Birmaher et ah, 1996b Goodyer et ah, 1997 Brent et ah, 1998). [Pg.476]

Hughes, C., Preskorn, S., Weller, E., Weller, R., Hassanein, R., and Tucker, S. (1990) The effect of concomitant disorders in childhood depression on predicting treatment response. Psychophar-macol Bull 26 235—238. [Pg.482]


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Depression response

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