The pharmacologic meaning of successful antipsychotic-antidepressant combinations.
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Antidepressive Agents↗
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The TRH test and urinary MHPG in unipolar depression.
Twenty-five men and 26 women with major unipolar depression were evaluated by the TRH test and urinary MHPG excretion. A significant positive correlation between TSH response to TRH and urinary MHPG was found in the men, though not in the women. These findings suggest that at least for depressed men, central norepinephrine deficiency may be the neurobiological substrate of blunted TSH responses to TRH.
Adolescent↗
Comparative pharmacokinetics of zimelidine and desipramine in man following acute and chronic administration.
Single dose and steady-state pharmacokinetics of zimelidine and desipramine were compared in eight depressed patients who were subjects in a double-blind crossover study. Within the same patient, there was no relationship between the pharmacokinetics of desipramine (pharmacokinetically similar to all other tricyclic antidepressants) and those of zimelidin, a bicyclic antidepressant. The weight-corrected dose of zimelidine gives a reasonable index of the concentration of its active metabolite norzimelidine, which predominates over zimelidine by a ratio of approximately 3 to 1. The variation in steady-state concentration of norzimelidine for a given dose of zimelidine in adults is about twofold and can be reduced by correcting for weight.
Adolescent↗
Dopamine-mediated behavior produced by the enkephalin analogue FK 33-824.
Intraperitoneal injection of FK 33-824 produced apomorphine-like stereotyped behavior in rats. Antagonism of this stereotypy by naloxone and neuroleptics suggests that FK 33-824 can activate opiate and dopamine receptors in the brain. Because increased dopaminergic neuronal activity is thought to be involved in schizophrenia and dopamine-mediated stereotypy has been used as an animal model for this illness, these results are consistent with an involvement of endogenous opiate-like peptides in schizophrenia. This involvement provides a possible mechanism for the reported improvement in schizophrenic psychosis produced by naloxone.
Animals↗
Changes in lymphocyte beta-adrenergic receptors in depression and mania.
The beta-adrenergic receptors were studied in vitro in lymphocytes obtained from patients with major affective disorders and controls. Specific L-[3H]-dihydroalprenolol binding was decreased in both depressed and manic patients compared to controls and euthymic patients. Isoproterenol-stimulated, but not prostaglandin El-stimulated, cyclic adenosine-3',5'-monophosphate production was decreased in manic and depressed patients. These results suggest decreased lymphocyte beta-receptor functioning in depression and mania. This decrease may be an index of changes in brain beta-receptors in mania and depression, or may simply reflect homeostatic regulation of peripheral beta-receptors in response to stress-induced increases in circulating catecholamines.
Adult↗
The thyroid-stimulating hormone response to thyrotropin-releasing hormone in mania and bipolar depression.
The release of thyroid-stimulating hormone (TSH) from the pituitary after infusion of 500 microgram of thyrotropin-releasing hormone (TRH) was decreased (p < 0.01) in manic patients and increased (p < 0.01) in bipolar depressed patients compared to a control group of patients with personality disorders. These results suggest that the TRH test may be useful in the diagnosis of psychiatric disorders and in the prediction of response to pharmacotherapy. We discuss the role of central monoaminergic systems in changes in the TSH response to TRH.
Affective Disorders, Psychotic↗
Serum prolactin and opiate withdrawal.
To evaluate the dopamine hyperactivity hypothesis for opiate withdrawal, we measured serum prolactin (PRL) in 21 male methadone addicts during significant opiate withdrawal and after clonidine suppression of opiate withdrawal signs and symptoms. We also measured serum PRL in these addicts 4 weeks after they were free of clonidine and opiates. Serum PRL was significantly decreased during opiate withdrawal and after clonidine reversal of withdrawal symptoms when compared to serum PRL measured in the drug-free baseline samples. These data suggest that dopaminergic hyperactivity is present in opiate withdrawal, but may not be related to the signs and symptoms of withdrawal. A noradrenergic hyperactivity hypothesis is proposed to explain the neurobiological system that becomes activated in withdrawal, generates symptoms, and is inhibited after clonidine administration.
Clonidine↗
Relationship of thyrotropin-releasing hormone test and dexamethasone suppression test abnormalities in unipolar depression.
The thyrotropin-releasing hormone (TRH) test and the dexamethasone suppression test (DST) were administered to 50 inpatients with unipolar depression. Of the patients tested, 64% had a blunted thyroid-stimulating hormone (TSH) response to TRH and 50% failed to suppress on the DST. There was no significant association between these two abnormalities by chi-square test. This lack of association suggests that the blunted TSH response to TRH is not an artifact of hypothalamic-pituitary-adrenal hyperactivation. The TRH test and the DST complemented each other as biological markers for active unipolar depression: 30% of the patients were identified by both tests, 34% by the TRH test only, 20% by the DST only, and 16% by neither test. The two tests may be useful in developing a nosology for major unipolar depression that is based on both descriptive and neurobiological information.
Adult↗
The thyrotropin-releasing hormone test in the diagnosis of unipolar depression.
The establishment of criteria for a blunted thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) may prove useful in distinguishing patients with major unipolar depression from patients with nonmajor depressions and controls. To this end, we administered the TRH test to a group of depressed, euthyroid inpatients diagnosed by Research Diagnostic Criteria and 20 normal volunteer controls. The mean maximal TSH response (delta TSH) to infusion of 500 micrograms of TRH of 7.3 +/- SD 4.6 microIU/ml in the 105 patients with major depressive disorder, primary unipolar subtype was significantly lower than that of 13.4 +/- SD 4.4 in the 20 controls and 10.9 +/- SD 4.4 in the 40 patients with nonmajor depressions. The differences were not explainable by differences in baseline thyroid function, age, or sex. When a delta TSH less than or equal to 7.0 microIU/ml was used as a diagnostic test for unipolar depression, the sensitivity of the TRH test was 56%, the specificity 93%, and the predictive value 91%. These results suggest that the TRH test may be useful in confirming the diagnosis of major unipolar depression and hence identifying patients likely to respond to antidepressant medications or electroconvulsive therapy.
Adult↗
Thyroid-stimulating hormone response to thyrotropin-releasing hormone in unipolar depression before and after clinical improvement.
Fourteen patients with unipolar depression who had a blunted thyroid-stimulating hormone (TSH) response to infusion of 500 micrograms of thyrotropin-releasing hormone (TRH) and who showed marked clinical improvement after pharmacotherapy and/or electroconvulsive therapy had the TRH test repeated after improvement. The mean (+/- SD) maximal TSH response to TRH (delta TSH) increased significantly from 4.0 +/- 1.9 to 9.1 3.5 micro IU/ml. The number of patients with delta TSH less than 7.0 micro IU/ml increased significantly from 0 to 9 of 14 after improvement. Eleven of the patients were followed for 5 to 19 months, and none showed clear relapse. The results suggest that the blunted TSH response to TRH has features of both a state marker for active unipolar depression and a trait marker for vulnerability to this illness, and support the suggestion that the TRH test may be useful in diagnosis and treatment planning.
Depressive Disorder↗
"Symptomless" autoimmune thyroiditis in depression.
The magnitude of the thyroid-stimulating hormone (TSH) response induced by thyrotropin-releasing hormone (TRH) helps identify patients whose thyroid is failing. Many of these patients have been found to have Hashimoto's thyroiditis, symptomless autoimmune thyroiditis (SAT), and subclinical hypothyroidism. While patients with SAT are clinically euthyroid, what might be "symptomless" for the endocrinologist might be a syndrome presenting with psychiatric symptoms to the psychiatrist. As a preliminary test of this hypothesis, we tested 100 consecutive admissions to a psychiatric hospital who complained of depression or lack of energy. Fifteen (15%) of 100 patients were identified from the baseline thyroxin (T4), triiodothyronine (T3) resin uptake (RU), T3 radioimmunoassay (T3RIA), TSH, and TRH test who met criteria for either subclinical, mild, or overt hypothyroidism. Of these 15 patients, 9 (60%) had positive thyroid microsomal antibodies with titers of greater than or equal to 1:10. Our data suggest that SAT is not symptomless and may be an important diagnosis to consider in the evaluation of depressed, anergic, or atypical patients.
Depressive Disorder↗
The thyrotropin-releasing hormone and dexamethasone suppression tests in the familial classification of depression.
Eighty-eight depressed patients who had received a dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test were divided into four subgroups based on family history of psychiatric illness. Nonsuppression on the DST was found in 46% of familial pure depressive disease (FPDD) patients, 38% of sporadic depressive disease (SDD) patients, 38% of depressive spectrum disease (DSD) patients, and 50% of mixed depressive disease patients (patients with both a first degree relative with alcoholism and one with depression). A blunted thyroid-stimulating hormone response to TRH was found in 50% of FPDD patients, 56% of SDD patients, 47% of DSD patients, and 56% of mixed depressive disease patients. Neither the DST nor TRH test was found to distinguish significantly among the four familial subgroups of depression.
Adult↗
The TRH test in the diagnosis of major and minor depression.
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Alcoholism↗
The dexamethasone suppression and thyrotropin-releasing hormone tests in depressed borderline patients.
Borderline patients can be both a diagnostic and a therapeutic enigma. We investigated a group of 24 depressed women with borderline personality disorder or strong borderline features by DSM III criteria for the presence of either an abnormal dexamethasone suppression test (DST) or a blunted TSH response to TRH, abnormalities which have been reported in major depression. Thirteen of the 24 borderlines failed to suppress on the DST, compared with one of 14 normal women (p less than 0.01). Nine of the 24 borderlines had a blunted TSH response to TRH, compared with one of 11 normal women. Neuroendocrine abnormalities were found in a total of 75% of the borderline women, independent of whether or not they met DSM III criteria for major depressive disorder. The results of this study support the notion that many borderline patients with depression have a genuine affective component to their illness, perhaps biologically similar to major depression in non-borderlines.
Adolescent↗
Number of cortisol time-points and dexamethasone suppression test sensitivity for major depression.
Failure to suppress cortisol secretion after administration of dexamethasone has been reported to be a diagnostic marker for major depression and to have prognostic implications when repeated after antidepressant treatment. The pulsatile pattern of cortisol secretion suggested to us that increasing the number of post-dexamethasone cortisol determinations might significantly increase the sensitivity of the dexamethasone suppression test (DST) for major depression. With a conventional two-point DST (1600 h and midnight), 5% of 20 normal volunteers, 8% of 13 inpatients with non-major depressions, and 31% of 65 inpatients with primary major depression failed to suppress. With six post-dexamethasone points (0800 h, 1200 h, 1600 h, 2000 h, 2200 h, midnight), the respective percentages were 10, 15 and 44%. The additional points increased the sensitivity from 31 to 44%, mostly by identifying more major depressives with a "late escape" pattern. If a clinician is using the DST to establish a marker for major depression that can be repeated to monitor response to treatment and the likelihood of relapse, then perhaps the increased sensitivity of the six-point DST would be helpful, despite a modest decrease in specificity from 94 to 88%.
Adjustment Disorders↗
Opiate detoxification with lofexidine.
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Clonidine↗
Evidence for an endorphin dysfunction in methadone addicts: lack of ACTH response to naloxone.
Chronic exogenous opiate administration might be responsible for the acute and protracted abstinence syndrome by producing a prolonged decrease in the availability of endogenous opioids (endorphins). However, the hypothesis that potent exogenous opiates may have anti-endorphin effects has been difficult to test. We have been investigating this hypothesis with neuroendocrine test paradigms which have provided preliminary evidence of anti-endorphin effects for chronic methadone. Naloxone-induced ACTH response data from chronic methadone addicts offers preliminary support for the hypothesis that chronic exogenous opiate administration has anti-endorphin effects. The subjects were 7 male methadone addicts who had been addicted to greater than or equal to 40 mg of methadone and 7 male healthy opiate-naive volunteers. Naloxone failed to produce a significant increase in ACTH in methadone addicts while opiate-naive normal volunteers demonstrated a significant naloxone-induced release of ACTH. Five of the seven methadone addicts ahd no demonstrable ACTH response to naloxone. These impaired naloxone response data reported here for recently detoxified addicts suggest that chronic methadone administration comprises the functional integrity of the endorphin system. Prolonged abstinence, post-detoxification depression and other affective symptoms which contribute to relapse may result from a prolonged endorphin derangement.
Adrenocorticotropic Hormone↗
Identifying depression secondary to lithium-induced hypothyroidism.
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Bipolar Disorder↗