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Biomedical subjects

S T Sokolov

Publications and source records attributed to S T Sokolov.

12 recordsLinked to original sources

Does the chronological relationship between the onset of dysthymia and major depression influence subsequent response to antidepressants?

OBJECTIVE: To determine whether the chronological relationship between the onset of dysthymia and the onset of the first major depression influences treatment outcome in patients with double depression (DD). METHOD: Clinical and outcome measures previously collected in 77 consecutive outpatients who presented with major depression and who had pre-existing dysthymia (i.e. DD) were reviewed for the current retrospective analysis. Subjects had been administered the Schedule for Affective Disorders and Schizophrenia, Lifetime Version (SADS-LV), and the Hamilton Rating Scale for Depression (HAM-D) prior to open antidepressant treatment and after 5 and 12 weeks of therapy. Response was defined as a 50% decline in HAM-D to score +/-8. Subjects were divided into those with the onset of dysthymia before the first major depression (DysB; n = 47), onset of dysthymia after major depression (DysA; n = 12) and those with onset of both condition within 2 years of each other (INDIST; n = 18). RESULTS: There were no significant differences between these three groups in baseline HAM-D. However, DysA subjects had significantly higher mean HAM-D scores than the DysB subjects at week 5 and the INDIST subjects at week 12. Response rates at week 12 were lower in subjects with DysA (33%) as compared with DysB (57%; Fisher's exact test, P = 0.06) and INDIST (78%; Fisher's Exact test P = 0.02). CONCLUSIONS: These findings suggest that the onset of the first episode of dysthymia after the first major depressive episode (i.e. DysA) may adversely affect response to subsequent treatments in patients with DD.

Adolescent↗

Thyroid hormone levels before unsuccessful antidepressant therapy are associated with later response to T3 augmentation.

Thyroid function was measured in 24 patients before antidepressant treatment, and following failure of acute desipramine treatment but before triiodothyronine (T3) augmentation. While all measures of thyroid function were within the euthyroid range, eventual T3 augmentation responders were found to have, prior to any antidepressant treatment, lower levels of TSH and higher levels of thyroxine (T4) and free thyroxine index (FTI) than non-responders. This suggests that T3 augmentation may be of particular importance in subjects with comparatively elevated levels of serum FTI.

Adult↗

Co-administration of fluoxetine and sumatriptan: the Canadian experience.

Major depression and migraine are commonly comorbid. Therefore, there is considerable opportunity for serotonin reuptake inhibitors, which are commonly prescribed for the treatment of depression, to be used at the same time as sumatriptan, an anti-migraine treatment. As both of these drugs increase serotonin transmission, the potential for drug interaction is considerable. Adverse event reports were obtained from the post-marketing surveillance of fluoxetine in Canada. Of 22 adverse event reports obtained six showed varying degrees of evidence of a drug interaction between fluoxetine and sumatriptan, suggesting that this combination is not entirely free of side-effects and should be used with caution when indicated.

Canada↗

Changes in thyroid hormone levels associated with desipramine response in adolescent depression.

1. The authors recently reported that acutely ill depressed adolescents have elevated plasma T4 and fT4 compared to controls. Studies in adult depression suggest antidepressant response is associated with decreases in these elevated levels. The effect of antidepressant treatment on adolescent thyroid indices has not been examined. 2. Thyroid indices were examined in 12 adolescent patients (4 male, 8 female; age 14-19y) in the active treatment arm of a double-blind, placebo-controlled desipramine trial (200 mg/day for 6 weeks). Antidepressant responders had higher pre-treatment levels of T4 and larger decreases were observed responders vs. nonresponders. 3. These results replicate findings observed in adult depressed patients and suggest similar alterations in the hypothalamic-pituitary-thyroid (HPT) axis function in adolescent depression.

Adolescent↗

Response to an open trial of a second SSRI in major depression.

BACKGROUND: We evaluated the efficacy of a second serotonin selective reuptake inhibitor (SSRI) in patients who had failed to respond to the first SSRI used. METHOD: Fifty-five patients with major depression who had failed one of the SSRIs for their current depressive episode were included. After failing a trial of one SSRI, they received a second SSRI in an open clinical trial. RESULTS: On the basis of the Clinical Global Impression-Improvement scale, 28 of 55 patients had a marked or complete antidepressant response. CONCLUSION: These data provide preliminary clinical evidence that substituting a second SRI may be a useful clinical alternative in depressed patients who fail to respond to an adequate trial of an SSRI.

1-Naphthylamine↗

Augmentation strategies: focus on anxiolytics.

Approximately 20% to 40% of patients will fail to respond to the first antidepressant used for their current major depressive episode. Furthermore, it has been suggested that a further 20% to 30% of patients will have only a partial response. There are four main options to consider in the treatment of these patients: optimization, substitution, augmentation, and combination therapy. Several combination antidepressant treatments have been used in treatment-refractory depression. Moreover, various augmentation strategies have also proved to be successful. Although the empirical data to support these treatment options are limited, augmentation treatment has several potential advantages over the other clinical options available, particularly substitution. These data are reviewed and clinical applications discussed. Particular attention is paid to the role of anxiolytics as augmentation agents in the treatment of major depression.

Anti-Anxiety Agents↗

Thyroid hormone treatment of depression.

The use of thyroid hormones in the treatment of depression is reviewed. The studies examining the use of triodothyronine (T3) alone as well as combination with antidepressants are discussed. The data suggest that there is little evidence that T3 alone has antidepressant efficacy but that this hormone may be used to enhance therapeutic effects of antidepressants in treatment refractory depressed patients. The different theories to explain the antidepressant effects of T3 are summarized.

Antidepressive Agents↗

Basal thyroid indices in adolescent depression and bipolar disorder.

OBJECTIVE: Abnormalities of the thyroid axis are documented in adult mood disorders. The most consistent findings have been observed in major depressive disorder with elevations of thyroxine (T4) or free-T4 (fT4) within the euthyroid range that decrease with treatment. The literature on adolescents is limited, and it is unknown whether similar findings might be present in this population. METHOD: First admissions to a university hospital adolescent psychiatry unit were reviewed. Fourteen depressed and 13 manic patients satisfied inclusion and exclusion criteria. None had a history of thyroid illness or medical illness or were taking medications known to affect thyroid function. Basal serum thyrotropin, T4, fT4, triiodothyronine (T3), reverse-T3, free thyroxine index (FTI), and T3 resin uptake levels were compared with those of a group of adolescent normal controls. RESULTS: T4 (but not fT4) was elevated in depressed and manic patients compared with controls (p < .05). In manic patients, T3 was decreased and reverse-T3 was increased (p < .05). There were no significant differences in relation to age, sex, or suicidality. CONCLUSIONS: We observed significant differences in basal thyroid hormone levels in depressed and manic adolescents. Our results suggest the presence of abnormalities of thyroid function in adolescent mood disorders similar to those described in mood-disordered adults.

Adolescent↗

Thyroid hormones, the brain, and affective disorders.

Clinical thyroid disorders are frequently associated with psychiatric symptomatology, thus supporting a role for thyroid hormones in the biological basis of psychiatric disorders, particularly mood disorders. Despite extensive literature documenting various abnormalities of thyroid function tests in primary major depression, the role of thyroid hormones in the pathophysiology of affective disorders remains to be clarified. In this review, we describe the various abnormalities of thyroid hormone levels reported in primary affective illness. We also review the competing hypothesis to explain the abnormalities of thyroid function observed. Although neither model can fully explain the role of thyroid hormones in depressive illness, they provide working hypotheses for further study. Additional research is required to clarify the regulation of thyroid hormones by mature brain and the role of these hormones in the biological basis of affective illness.

Brain↗