ABSTRACT
In an evaluation of the possible role of dopamine on TRH test results, 21 depressed patients were given TRH before and after one week of treatment with a low dose of haloperidol. Haloperidol significantly increased serum prolactin (both basal and after TRH) and cortisol levels, decreased body temperature, and had no effect on serum TSH, growth hormone, or thyroid hormone levels. Five of six patients with initial TSH blunting were retested with TRH; in four patients the TSH response remained blunted. These data render it unlikely that dopamine exerts a major inhibitory input on TSH secretion in depression.
Subject(s)
Brain/physiopathology , Depressive Disorder/physiopathology , Dopamine/physiology , Haloperidol , Thyrotropin-Releasing Hormone , Adult , Depressive Disorder/drug therapy , Female , Haloperidol/therapeutic use , Humans , Male , Middle Aged , Pituitary Gland, Anterior/metabolism , Prolactin/metabolism , Thyrotropin/metabolismABSTRACT
Leukopenia, a rare but serious side effect of many psychotropic agents including monoamine oxidase inhibitors (MAOIs), has not been reported in the literature in association with phenelzine. The authors report such a case and suggest a toxic etiology independent of MAOI activity.
Subject(s)
Leukopenia/chemically induced , Phenelzine/adverse effects , Adult , Depressive Disorder/drug therapy , Female , Humans , Obsessive-Compulsive Disorder/drug therapyABSTRACT
Chronic alcoholics who had been abstinent from alcohol for more than 2 years were evaluated with the thyrotropin-releasing hormone (TRH) test. The findings suggest the following profound disturbances in the hypothalamic-pituitary-thyroid axis: 1) a "euthyroid sick syndrome," evidenced by low levels of triiodothyronine (T3), high levels of reverse T3, and normal levels of thyroxine (T4) (this syndrome implies a decreased 5'-deiodination of T4 to T3 and of reverse T3 to its lesser iodinated metabolites), 2) an increased binding capacity for thyroid hormones, evidenced by a decreased T3-uptake value and an increased level of T4-binding globulin, and 3) thyroid-stimulating hormone (TSH) blunting in 31% of patients. Paradoxically, there was a positive correlation between basal T4 and delta max TSH in subjects with blunted TSH, but baseline TSH levels were reduced in subjects with and without blunted TSH.
Subject(s)
Alcohol Drinking , Alcoholism/blood , Thyrotropin-Releasing Hormone , Thyrotropin/blood , Adult , Aged , Alcoholism/complications , Alcoholism/diagnosis , Depressive Disorder/diagnosis , Depressive Disorder/etiology , Depressive Disorder/genetics , Growth Hormone/blood , Humans , Male , Middle Aged , Prolactin/blood , Thyroxine/blood , Triiodothyronine/blood , Triiodothyronine, Reverse/bloodABSTRACT
Fifteen patients with a primary diagnosis of borderline personality disorder were studied with the thyrotropin-releasing hormone (TRH) test. Twelve carried the additional diagnosis of depression, substance abuse, or both. A blunted thyroid-stimulating hormone (TSH) response to TRH was found in seven patients, two of whom were neither depressed nor had the additional diagnosis of depression and/or substance abuse. TSH blunting was unrelated to such factors as thyroid status, serum cortisol, weight, height, or body surface. Since TSH blunting occurs in about 25% of patients with major depression but not in schizophrenia, the findings suggest that some patients with borderline personality disorder share a neuroendocrine abnormality with some affective disorder patients.
