ABSTRACT
BACKGROUND: The purpose of this study was to determine the influence of the therapeutic alliance on the efficacy of pharmacotherapy for depression. METHOD: The sample consisted of 31 depressed outpatients treated with antidepressants. The alliance was measured by the patient and therapist versions of the California Pharmacotherapy Alliance Scale. Treatment outcome was measured by the Hamilton Rating Scale for Depression and the Beck Depression Inventory, and the Symptom, Sign, Side-Effect Checklist was also completed. RESULTS: The alliance measures accounted for between 21% and 56% of the variance in the three outcome measures. By averaging across outcome measures, therapist perceptions of the alliance predicted 41% of the variance in improvement in depressive symptoms, where patient perceptions predicted 25%. Scores on both alliance measures were lower than those reported in studies of psychotherapy. Patient attitude toward medication was correlated with somatic complaints, but not with depression scores. Therapist perception of patient hostility correlated with patient depression. Patients differed in the way their alliance and outcome interacted, so that the association might be positive or negative. CONCLUSION: Alliance is correlated with outcome in pharmacotherapy management of depression, although there may be interindividual variability across patients. In the pharmacotherapy of depression, therapist perception of alliance is a better predictor of symptom outcome than patient perception, while the reverse is usually found in psychotherapy.
Subject(s)
Antidepressive Agents/therapeutic use , Attitude of Health Personnel , Attitude to Health , Depressive Disorder/drug therapy , Physician-Patient Relations , Adult , Ambulatory Care , Depressive Disorder/psychology , Depressive Disorder/therapy , Female , Hostility , Humans , Imipramine/therapeutic use , Male , Personality Inventory , Psychiatric Status Rating Scales , Psychotherapy , Regression Analysis , Severity of Illness Index , Treatment OutcomeABSTRACT
OBJECTIVE: This paper reviews the evidence linking gonadal hormones and obsessive-compulsive disorder (OCD) symptoms. METHOD: Four case reports of the relationship between obsessive-compulsive disorder symptoms and exogenous sex hormone changes are presented. These cases are reviewed within the context of other case reports and the literature on the relationship between serotonin, gonadal hormones and OCD. RESULTS: The authors suggest that there is a relationship between onset or exacerbation of OCD and changes in gonadal hormones. CONCLUSION: Clinicians should carefully evaluate patients for exogenous and endogenous changes in gonadal hormones when evaluating onset or exacerbation of OCD.
Subject(s)
Gonadal Steroid Hormones/physiology , Obsessive-Compulsive Disorder/physiopathology , Adult , Humans , Male , Obsessive-Compulsive Disorder/diagnosis , PeriodicityABSTRACT
Morris hepatoma 44, whose growth is sensitive to thyroid hormones and prolactin, contains specific receptors for these hormones. In the present experiments, male Buffalo rats bearing Morris hepatoma 7787 were studied to determine the effects of several sex steroid hormones. Castration 1 week postimplantation inhibited tumor growth relative to controls (-53%). Replacement with testosterone propionate (1 mg per day s.c. injection) restored tumor growth to control levels, whereas administration of testosterone (2 mg per day s.c. injection) to castrated controls resulted in significant stimulation. Testosterone administered to control animals at a dose of 1 mg per day stimulated tumor growth (62%), whereas 2 mg per day failed to do so. Progesterone (4-pregnon-3,20-dione) at doses of 125 or 250 micrograms per day (Silastic implants) had no effect on tumor growth, whereas 500 micrograms per day stimulated tumor growth relative to controls. Estrogen (17 beta-estradiol) at doses of 6, 12, or 24 micrograms per day (Silastic implants) did not influence tumor growth. Cytoplasmic testosterone receptors have been demonstrated in tumors (2.2 +/- 0.8 fmoles per mg cytoplasm), although specific cytoplasmic estrogen and progesterone receptors could not be identified in this model. In female rats bearing either Morris hepatoma 44, 7787 or 5123-D, testosterone markedly stimulated tumor growth (226, 328 and 58%, respectively, relative to controls). In conclusion, although Morris hepatoma 7787 appears to be androgen (testosterone) dependent and contains cytoplastic androgen receptors, it lacks specific cytoplasmic receptors for estrogen and progesterone and is not influenced by these hormones except at very high doses of progesterone.