Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:"Symptomless" autoimmune thyroiditis in depression. 681 Apr 1

The circadian variation of serum thyrotropin (thyroid-stimulating hormone; TSH) was studied in nine patients with endogenous depression before and after recovery. Depressed state did not appear to influence the pattern of TSH. When 2 mg of dexamethasone was administered, serum TSH was significantly reduced for 18 hours, whereafter the effect leveled off. The TSH response to thyrotropin-releasing hormone (TRH) was evaluated 25 hours after the administration of dexamethasone and the response was found to be unchanged.
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PMID:Circadian variation of serum thyrotropin in endogenous depression. 681 Apr 2

Severe intercurrent nonthyroidal illnesses (diabetic ketoacidosis, myocardial infarction, fulminant hepatitis and bacterial pneumonia) in four thyrotoxic patients were associated with depression of total serum thyroxine (T(4)) and triiodothyronine (T(3)) values into the normal or even subnormal range. A diagnosis of hyperthyroidism was established by a combination of elevated radioactive iodine uptake, absent thyroid-stimulating hormone response to thyrotropin-releasing hormone or an elevated free T(4) by dialysis values. In the two of four cases that had a fatal outcome, there was a progressive decline in total T(4) and total T(3) values. In contrast, the two surviving patients had a progressive increase of total T(3) and total T(4) values into the hyperthyroid range as their underlying illness resolved. As has been seen with severe nonthyroidal illnesses, pronounced depression of total T(3) and total T(4) levels in hyperthyroid patients may also portend a poor prognosis.
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PMID:Influence of nonthyroidal illnesses on serum thyroid hormone indices in hyperthyroidism. 688 Jan 82

To evaluate the relationship between hypothyroidism and depression, thyroid function was evaluated in 250 consecutive patients referred to a psychiatric hospital for treatment of depression or anergia. Twenty of the 250 patients had some degree of hypothyroidism. Two patients (less than 1%) were identified with grade 1 (overt); nine patients (3.6%), grade 2 (mild); and ten patients (4%), grade 3 (subclinical) hypothyroidism. These results suggest that a significant proportion of patients with depression and anergia may have early hypothyroidism, the cases of about half of which are detected only by thyrotropin-releasing hormone (TRH) testing. Because hypothyroidism can produce signs and symptoms of depression and can coexist as a second illness in depressed patients, patients with early hypothyroidism may be candidates for thyroid replacement therapy. Clinical examination and measurement of triiodothyronine resin uptake thyroxine and baseline thyroid-stimulating hormone (TSH) levels, and TSH response to TRH are necessary to identify candidates for thyroid replacement among cases diagnosed by descriptive criteria as having either major or minor depression, particularly those that are atypical or treatment resistant.
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PMID:Hypothyroidism and depression. Evidence from complete thyroid function evaluation. 723 Mar 83

Since there have been reports of elevated CSF concentrations of thyrotropin-releasing hormone (TRH) in depression, the authors compared the TRH levels of 17 depressed patients and 19 normal subjects. All subjects underwent lumbar punctures after fasting overnight, and CSF concentrations of TRH were determined by radioimmunoassay. CSF concentrations of norepinephrine and monoamine metabolites were also measured. There was no significant difference between the two groups on any measure, and in the depressed patients there was no significant relation between CSF concentrations of TRH and thyrotropin-stimulating hormone responses to TRH infusion.
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PMID:Differences in CSF concentrations of thyrotropin-releasing hormone in depressed patients and normal subjects: negative findings. 751 76

The interaction of serotonin and thyrotropin-releasing hormone (TRH) on monosynaptic reflex (MSR) in isolated neonatal spinal cords was examined. Superfusion of serotonin (1-30 microM) in untreated cords, depressed the MSR in a dose-dependent manner. The depression was about 25% at 10 microM of serotonin, in either control or vehicle-treated groups. While for the same concentration of serotonin, the depression was 97 +/- 2.1% of the control in cords from 5,7 dihydroxytryptamine (5,7-DHT)-treated animals. The inhibition of the reflex seen in cords obtained from 5,7-DHT-treated animals could not be reversed by washing with normal physiological solution (> 60 min) or in presence of serotonin antagonists. TRH (0.03-1.0 microM) reversed the depression in a concentration-dependent manner and complete reversal could be seen with 1 microM of TRH. These observations indicate that, serotonin and TRH act dissimilarly on the spinal synaptic transmission though they are known to coexist in the descending bulbospinal tracts.
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PMID:Thyrotropin-releasing hormone reverses the supersensitively depressed monosynaptic transmission by serotonin in 5,7-dihydroxytryptamine-treated neonatal rats in vitro. 781 85

Young rats were fed on an essential fatty acid (EFA)-deprived diet for 6 weeks after weaning. Their pituitary was removed and adenohypophyseal cells dispersed and maintained in culture. Membrane lipids were analyzed and basal and stimulated levels of hormone secretion were measured after 4-day incubation in a culture medium containing or not 160 microM arachidonic acid 20:4n-6 (AA) in order to obtain EFA-deficient or EFA-restored pituitary cells, respectively. In EFA-deficient cells membrane phosphoglycerides (PGL) were depleted in AA and adrenic acid 22:4n-6; the deficit was overcome by incubation in the presence of AA. Depletion diversely affected PGL classes. AA was highly depleted in choline phosphoglycerides (ChoPG), only moderately depleted in serine and ethanolamine phosphoglycerides (SerPG and EtnPG) and not depleted at all in inositol phosphoglycerides, suggesting preferential preservation of AA in that class of PGL. Restoration of AA by addition of the fatty acid to the culture medium was complete for ChoPG and EtnPG and only partial for SerPG. Depressed levels of AA and adrenic acid in PGL were compensated for by a concomitant increase in 20:3n-9 and 22:3n-9. Growth hormone and prolactin (PRL) secretion was assessed by radioimmunoassay and possible effects of a membrane AA deficit on hormone regulation were tested in cells challenged by either growth hormone-releasing hormone, thyrotropin-releasing hormone, angiotensin II (AII), vasoactive intestinal peptide (VIP) or dopamine. Neither basal nor stimulated growth hormone secretion was different from controls in EFA-deficient cells. PRL modulation by VIP or dopamine was not affected either in EFA-deficient cells. In contrast, the capacity of AII, but not of thyrotropin-releasing hormone, to release PRL was markedly decreased in EFA-deprived cells. It was restored by addition of AA to the incubation medium. Parallel depression of AII-induced inositol phosphates and cAMP accumulation was also observed after EFA deficiency. When tested on membranes, the paradoxical inhibition of adenylate cyclase by AII documented by previous observations was reinforced in EFA-deficient membranes. In contrast, binding of AII was not affected by EFA deficiency. It is concluded that under our experimental conditions EFA deficiency affects selectively coupling of the AII receptor to its effectors without alteration of binding. The effect could involve changes in receptor interactions with coupling proteins.
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PMID:Selective effect of a diet-induced decrease in the arachidonic acid membrane-phospholipid content on in vitro phospholipase C and adenylate cyclase-mediated pituitary response to angiotensin II. 782 82

Two thyroid axis findings are often reported in depressed patients: autoimmune thyroiditis and abnormal thyrotropin (thyroid stimulating hormone, TSH) responses to thyrotropin-releasing hormone (TRH). The TSH response to TRH can be exaggerated, suggesting subclinical hypothyroidism; it can alternatively be blunted, for reasons poorly understood. We selected 28 women who had been found to have major depression for TRH testing. Fifteen patients had autoimmune thyroiditis and 13 had diffuse nontoxic goiter. The endocrinological diagnoses were verified by fine-needle aspiration biopsy and cytological assessment. Patients with overt hypothyroidism and hyperthyroidism were excluded from the study. There were no differences between the two groups in total triiodthyronine and thyroxine plasma levels or severity of depression. In the autoimmune group, basal TSH and Dmax TSH tended to be higher (p < 0.1); peak TSH was significantly higher (p < 0.05), suggesting that the prevalence of subclinical hypothyroidism was also higher. Blunted TSH responses were found about as often in one group as the other.
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PMID:Thyrotropin response to TRH stimulation in depressed patients with autoimmune thyroiditis. 782 17

Prolyl endopeptidase (PEP) is a serine proteinase, which may cleave peptides that are involved in the pathophysiology of major depression, such as arginine vasopressin, beta-endorphin, luteinizing hormone-releasing hormone, thyrotropin-releasing hormone, and maybe corticotropin-releasing hormone. PEP may be involved in activation of cell-mediated immunity, autoimmune and inflammatory responses, which repeatedly occur in severe depression. The present study investigates serum PEP activity in 33 normal controls, 16 minor, 14 simple major, and 18 melancholic depressed subjects. Pre-dexamethasone and post-dexamethasone (DST) intact adrenocorticotropic hormone (ACTH) and cortisol values were determined in 33 depressed subjects. Serum PEP activity was significantly lower in depressed subjects compared to normal controls and in melancholic depressed subjects compared to minor and simple major depressed subjects. Up to 61.1% of the melancholic patients had serum PEP activities below the mean PEP values of normal controls minus two SDs. In the depressed study group, significant negative correlations between serum PEP activity and severity of illness, post-DST cortisol, and ACTH values were observed. There was a trend toward higher serum PEP activity with increasing age. It is hypothesized that lower serum PEP activity, and lower serum activity of other peptidases, may play a role in the neuroendocrine and immune pathophysiology of major depression.
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PMID:Lower serum prolyl endopeptidase enzyme activity in major depression: further evidence that peptidases play a role in the pathophysiology of depression. 803 98

Rats given five consecutive daily electroconvulsive shock (ECS) treatments and trained to run in the Morris water maze, starting three days posttreatment, showed deficits in learning and memory functions. Treatment before each training session with the thyrotropin-releasing hormone (TRH) analog NS-3 [(CG-3703), (3R),(6R)-6-methyl-5-oxo-3-thiomorphorinyl-l-histidyl-l-prolinamid e tetrahydrate] reversed these behavioral deficits. The possible use of TRH and its analogs as therapeutic treatment for the cognitive dysfunctions resulting from electroconvulsive shock treatment for depression and the possible involvement of central cholinergic systems in the cognitive dysfunctions are discussed.
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PMID:NS-3, a TRH analog, reverses repeated ECS-induced deficits in water maze performance in the rat. 820 65


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