METHODS : The study included 17 female patients, aged 30-60 years, with treatment-resistant depressive episode in the course of unipolar or bipolar mood disorder. All patients had no history of thyroid axis disturbances and had T3, T4, and thyroid-stimulating hormone (TSH) values within the normal range.2. Literature Search A PubMed search was performed through the English literature from 1969 to present using the keywords: acceleration, antidepressant treatments, augmentation, brain, depression, hyperthyroidism, hypothyroidism, and mood disorder. 3.
The efficacy of augmentation did not show any correlation with laboratory tests' results performed before (T3, T4, TSH and TSH stimulation test) as well as with any clinical factors (age, diagnosis, duration of illness, duration of episode).Furthermore, thyroid hormones are reported by many authors to be an effective adjunct treatment for depression. In this paper, we will present an overview of thyroid hormone metabolism in the brain, reexamine the different observations and clinical studies assessing the relationship between thyroid and depression, and shed light on the advances in neuroimaging approaches in.
Most of the T4 enter the brain via a number of transporters including transthyretin (TTR a thyroid hormone transport protein synthesized by the choroid plexus and secreted into the cerebrospinal fluid 5, 6.CONCLUSIONS : The addition of moderate dose of l-thyroxine may be a successful augmentation strategy in female depressed patients in whom the effect of serotonergic antidepressant had been unsatisfactory. It may be efficient despite of the lack of disturbances of thyroid axis in such patients.
The antidepressants preceding thyroxine augmentation were serotonergic antidepressants (clomipramine - 11 patients, paroxetine - 5 patients, fluoxetine - 1 patient). l-thyroxine was added in the dose of 100 microm daily for 4 weeks.Mutations in MCT8 have also been recognized to cause isolated brain hypothyroidism by blocking T3 transport into neurons 8, 31. 6. Peripheral Thyroid Hormone Concentrations 6.1. Thyroxine (T4) Studies examining total and free plasmatic T4 levels in patients with depression have shown inconsistent results.
However, the mechanisms underlying the interaction between thyroid function and depression remain to be further clarified. Recently, advances in biochemical, genetic, and neuroimaging fields have provided new insights into the thyroid-depression relationship.Feb 7, 2007. L-thyroxine augmentation of serotonergic antidepressants in female patients with refractory depression. ojko D(1 Rybakowski JK).
1. Introduction The association between thyroid function and psychiatric disorders particularly mood disorders has long been recognized. Historically, this association has been described more than 200 years ago. Parry in 1825 reported an increased incidence of nervous affectations in thyroid disorders.A state of brain hypothyroidism in the setting of systemic euthyroidism has been suggested. This could result from a defect in the thyroid hormone receptor 26, or in the thyroid hormone transport and uptake into the brain and neuronal cells 7, 27.
On the other hand, hypothyroid patients frequently demonstrate features of depression, cognitive dysfunction, apathy, and psychomotor slowing. In severe forms of hypothyroidism, clinical symptoms may mimic that of melancholic depression and dementia 12.Augmentation Strategies in Resistant Depression - Some Are Effective and Well. or thyroxine (T4; 100 g/day) appear to be well tolerated when administered.
Treatment resistant depression is discussed separately, as is the initial treatment of depression and treatment of hypothyroidism. (See "Unipolar major depression in adults: Choosing initial treatment" and "Treatment of hypothyroidism" and "Unipolar depression in adults: Treatment of resistant depression".) INDICATIONS Indications for treating nonpsychotic, unipolar major depression with triiodothyronine (T3) include 4 : Augmenting response.In addition, it has been shown that elevated serum T4 levels fall after successful treatment of depression. A direct effect of antidepressants on the TRH neuron has been demonstrated resulting in an inhibition of TRH secretion 34.
Serum T4 levels in the upper range of normal or slightly higher have been reported in depressed patients as compared to healthy or psychiatric controls. These levels have been found to regress after successful treatment of depression 32.Primary thyroid disorders including both hypothyroidism and hyperthyroidism may be accompanied by various neuropsychiatric manifestations ranging from mild depression and anxiety to overt psychosis. Dysphoria, anxiety, irritability, emotional lability, and impairment in concentration constitute the classical neuropsychiatric symptoms occurring in hyperthyroidism or thyrotoxicosis.