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)

Patients who have undergone thyroidectomy for thyroid carcinoma are frequently subjected to periods of induced severe hypothyroidism in preparation for 131I whole body scanning and measurement of serum TG. These two tests are crucial in evaluating the patient's clinical status and determining administration of 131I or other necessary treatment. Severe hypothyroidism produces fatigue, weight gain, depression, inability to carry out usual activities, and occasionally significant illness. We compared the efficacy of inducing moderate hypothyroidism by cutting replacement therapy in half, to a standard method. In the standard preparation, patients substituted triiodothyronine for thyroxine replacement over a 3-week period, and then omitted hormone therapy for 3 weeks. For the subsequent scan, 6 to 12 months later, the thyroxine dosage was cut in half. TSH levels were assessed 4 weeks later, and if adequately elevated, whole body scanning was conducted at the end of the fifth week. Pulse, weight, clinical symptoms, thyroid hormone levels, and some clinical chemistries were evaluated prior to each scan, and some of the tests were also carried out during the interval between scans. Moderate hypothyroidism induced by the half-dose protocol induced TSH elevations above the target level (25-30 microU/mL) at 5 weeks in most patients. Typically TSH of 15 microU/mL in the previous week predicted adequate elevation of TSH at the time of scan. Half dose therapy can be prolonged, if necessary, especially in patients who begin with extreme suppression of TSH, or if a higher TSH is desired. Pulse, weight gain, and cholesterol were significantly different in the two protocols, and the patient's subjective evaluation of hypothyroid symptoms was significantly reduced. Reduction of thyroxine replacement dosage to half the usual amount, in patients with thyroid cancer, allows after 5 weeks in most patients sufficient elevation of TSH for whole body scanning and measurement of TG levels. This simple and economical procedure drastically reduces symptomatology of hypothyroidism and makes this key procedure much more tolerable to patients.
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PMID:Moderate hypothyroidism in preparation for whole body 131I scintiscans and thyroglobulin testing. 1566 27

Depression is associated with abnormalities of the thyroid axis, but the role of thyroid hormone therapy is controversial. In patients presenting with depression, the thyroid status should be carefully evaluated since hypothyroidism can cause depression. Frank hypothyroidism should be treated in the usual fashion with L-thyroxine, which may reverse the depressive state. If subclinical hypothyroidism and/or autoimmune thyroiditis are present, T3 adjuvant administration (25 micrograms/day) should be seriously considered in patients resistant to tricyclic antidepressant (TCA) (and probably also) serotonin selective reuptake inhibitor (SSRI) medication. The possible efficacy of adjuvant T4 in reversing the depression of such subjects appears less than T3. In depressed patients with TCA or SSRI resistance and no evidence of hypothyroidism, the data available do not establish the therapeutic role of T3 in this situation. Multicenter controlled studies of T3 adjuvant therapy are required. The possible mechanisms through which T3 adjuvant therapy might be efficacious are discussed.
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PMID:Does thyroid hormone have a role as adjunctive therapy in depression? 877 87

Decreased turnover of thyroid indices and blunting of TSH release after TRH administration has been associated with depressive disorder. A further decrease in plasma thyroid hormone; during antidepressant treatment has been reported. However, the putative association between the plasma thyroid indices' concentration and response has not been addressed. In the present study 21 depressed inpatients underwent a four-week double blind antidepressant with amitriptyline and mianserin; their plasma thyroid hormone indices (total thyroxine [TT4], free thyroxine [FT4], total triiodothyronine [TT3], free triiodothyronine [FT3], thyrotropin [TSH], and thyroglobulin [TBG]) were quantified to elucidate their involvement in depression and during antidepressant drug treatment. Depressed patients' plasma TSH, when corrected for age, was significantly lower than that of healthy subjects. During antidepressant treatment the entire patient cohort showed a significant decrease in plasma TT4 and FT4 concentrations. Responders showed a significant drop in TT4 FT4, FT3, and T4/TBG, but nonresponders only a decrease in FT4. During mianserin treatment, a decrease was observed in TT4, FT4, FT3, and T4/TBG. FT4 and FT3 baseline levels correlated positively with the improvement in the Hamilton Depression Rating Score (HDRS). These findings show that depressed inpatients' serum TSH levels are within the reference range, but significantly lower than those of healthy subjects, and those patients who turn out to be nonresponders have potentially lower availability of thyroid hormones than responders. Therefore, we hypothesize that in order to assure clinical improvement in depression, an adequate capacity of the thyroid hormone pool is necessary to compensate for the additional antidepressant-provoked decrease in serum thyroid hormone availability.
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PMID:Low plasma thyroid indices of depressed patients are attenuated by antidepressant drugs and influence treatment outcome. 889 43

The haemodynamic effects of thyroid hormones are well known and include those on heart rate, contractility and myocardial oxygen consumption. Cardiopulmonary bypass produces various alterations in endocrine homoeostasis and may exert important haemodynamic effects postoperatively. The purpose of this prospective study was to determine the relation of cardiopulmonary bypass to changes in thyroid function. Blood samples were obtained from 20 patients preoperatively, at specific times before, during and after cardiopulmonary bypass. Total thyroxin (TT4), total triiodothyronine (TT3), free thyroxin (fT4), free triiodothyronine (fT3), thyroid-stimulating hormone (TSH), thyroid-binding globulin (TBG) and albumin were measured by radioimmunoassay and competitive immunoassay. Values of TT4, TT3 and fT3 were significantly depressed up to 24 h after cardiopulmonary bypass (P < 0.05). TSH and fT4 levels remained within normal ranges at all sampling times. It is increasingly evident that cardiopulmonary bypass affects thyroid hormone metabolism, leading to a transient depression characterized by low levels of circulating TT4, TT3 and fT3.
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PMID:Thyroid hormone alterations during and after cardiopulmonary bypass. 890 19

Hormones of the thyroid axis have been used to treat patients with any of several mental illnesses. However, in recent decades interest has focused almost exclusively on depression, though thyroid hormones, mainly thyroxine (T4), are used with lithium in rapid cycling bipolar disorder, a condition in which depression and mania rapidly alternate. In depression L-triiodothyronine (T3) has been used in preference to T4 because of its rapid onset and offset of action. In women starting treatment, T3 hastens the onset of therapeutic action of standard antidepressant drugs. It fails to do so in depressed men, who anyway respond faster than women to standard antidepressants. Standard drugs fail to produce satisfactory improvement in one-quarter to one-third of depressed patients. Then, in both men and women, T3 converts about two-thirds of drug failures to successes in rapid fashion. Lithium, which has antithyroid properties, produces a similar conversion rate. The majority of depressed patients are grossly euthyroid, but many show one or another subtle change in thyroid axis activity. However, the thyroid state of patients has not been matched systematically with their response to thyroid hormone augmentation. It seems likely that a tendency toward hypothyroidism can predispose to depression, but when depression occurs in a euthyroid patient, the thyroid axis is often invoked in the process of restitution.
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PMID:Novel uses of thyroid hormones in patients with affective disorders. 893 85

The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiac function in patients with hypothyroidism or hyperthyroidism. Triiodothyronine (T3)-induced changes in cardiac function can result from direct or indirect T3 effects. Direct T3 effects result from T3 action in the heart itself and are mediated by nuclear or extranuclear mechanisms. Extranuclear T3 effects, which occur independently of nuclear T3 receptor binding and increases in protein synthesis, influence primarily the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T3 effects are mediated by the binding of T3 to specific nuclear receptor proteins, which results in increased transcription of T3-responsive cardiac genes. The T3 receptor is a member of the ligand-activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. T3 increases the heart transcription of the myosin heavy chain (MHC) alpha gene and decreases the transcription of the MHC beta gene, leading to an increase of myosin V1 and a decrease in myosin V3 isoenzymes. Myosin V1, which is composed of two MHC alpha, has a higher myosin ATPase activity than myosin V3, which contains two MHC beta. The globular head of myosin V1, with its higher ATPase activity, leads to a more rapid movement of the globular head of myosin along the thin filament, resulting in an increased velocity of contraction. T3 also leads to an increase in the speed of diastolic relaxation, which is caused by the more efficient pumping of the calcium ATPase of the sarcoplasmic reticulum (SR). This T3 effect results from T3-induced increases in the level of the mRNA coding for the SR calcium ATPase protein, leading to an increased number of calcium ATPase pump units in the SR. Overall, T3 leads to an increase in ATP consumption in the heart. In addition, less chemical energy of ATP is used for contractile purposes and more of it goes toward heat production, which causes a decreased efficiency of the contractile process in the hyperthyroid heart. The pathophysiologic basis for myxedema is the opposite of that discussed for the hyperthyroid heart. In addition to decreased direct effects of thyroid hormone in cardiac myocytes, indirect effects occur through decreases in peripheral oxygen consumption and changes in hemodynamic parameters. Myofibrillar swelling with loss of striation and interstitial fibrosis occurs on histologic examination of hypothyroid hearts. In addition, accumulation of mucopolysaccharide substances (Glycosaminoglycans) can be demonstrated. On electron microscopic examination, mitochondria show disruption and lipid inclusion. Cardiac papillary muscle obtained from animals with hypothyroidism shows a depression of the force velocity curve and reduced rate of tension development, indicating significant contractile abnormalities. In patients with hypothyroidism, a true enhanced incidence of hypertension (increased peripheral vascular resistance) has been found. In addition, hypercholesterolemia and impairment of fatty acid mobilization are associated with myxedema and present additional risk factors for the development of atherosclerotic cardiovascular disease.
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PMID:[Cardiovascular effects of thyroid hormones]. 906 69

With antidepressant treatment for major depression there are decreases in thyroid hormone levels and increases in pineal function. We have conducted a study to examine whether there is a relationship between pineal and thyroid hormone measures as well as between hormone measures and response to treatment in patients treated with desipramine. Measures of thyroid activity included thyroxine, triiodothyronine, T3 resin uptake, and TSH. Pineal function was determined by measurement of 6-suphatoxymelatonin in three consecutive 8 hour pools. Hormone measures as well as Hamilton depression scores were obtained prior to treatment and at the end of 5 weeks of treatment. As in previous studies, thyroid measures decreased, pineal activity increased, and Hamilton scores decreased significantly with treatment. No correlations were found between these measures, suggesting that if there is a relationship between them it is not a direct one.
Depression 1996
PMID:Lack of association between thyroid and pineal responses to antidepressant treatment. 916 Jun 44

Pre-translational regulation of subunit c has been suggested to control the biosynthesis of mitochondrial ATP synthase (ATPase) in brown adipose tissue (BAT). Subunit c is encoded by the genes P1 and P2, which encode identical mature proteins. We have determined here the levels of P1 and P2 mRNAs in different tissues, in response to cold acclimation in rats, during ontogenic development of BAT in hamsters, and following thyroid hormone treatment in rat BAT and liver. Quantitative ribonuclease protection analysis showed that both the P1 and P2 mRNAs were present in all rat tissues measured. Their total amount in each tissue corresponded well with the ATPase content of that tissue. While the P1/P2 mRNA ratio is high in ATPase-rich tissues, the P2 mRNA dominates in tissues with less ATPase. Cold acclimation affects P1 but not P2 gene expression in rat BAT. A rapid and transient increase in P1 mRNA is followed by sustained depression, which is accompanied by a decrease in ATPase content. Similarly, ontogenic suppression of ATPase content in hamster BAT was accompanied by suppression of the P1 mRNA levels, while P2 expression was virtually unchanged. Furthermore, when hypothyroid rats were treated with thyroid hormone, the steady-state level of P1 but not of P2 mRNA was significantly increased in liver. BAT was unaffected. We conclude that the P1 and P2 genes for subunit c are differentially regulated in vivo. While the P2 gene is expressed constitutively, the P1 gene responds to different physiological stimuli as a means of modulating the relative content of ATP synthase.
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PMID:ATP synthase subunit c expression: physiological regulation of the P1 and P2 genes. 916 27

In the evaluation of treatment-resistant or treatment-refractory depression (TRD), true resistance to antidepressant therapy must be distinguished from inadequate dose, duration, or compliance with past antidepressant therapy. Reassessment of the diagnosis may reveal psychiatric comorbidity, the presence of depressive subtypes, or the possibility of a medical etiology. Management of TRD should consider patient-specific factors; drug therapy may be directed by depressive subtype or the presence of psychiatric comorbidity. Increasing the dose or duration of current antidepressant therapy is appropriate for patients who have received inadequate therapy in the past. Augmentation of tricyclic antidepressant (TCA) or selective serotonin reuptake inhibitor (SSRI) therapy with thyroid hormone (T3) or lithium has been shown to be effective in open and controlled trials. Efficacy of other strategies such as higher-dose antidepressant treatment, venlafaxine therapy, combined antidepressant therapy, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), or augmentation with pindolol or buspirone has been less well established, but emerging data from open studies and case reports are encouraging.
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PMID:Augmentation strategies in patients with refractory depression. 916 49

Polychlorinated biphenyls (PCB) are ubiquitous environmental contaminants that bioaccumulate in avian species. Exposure to PCBs can result in decreased growth. Thyroid hormones and growth hormone (GH) are important for normal growth. The present studies employed the chicken embryo to investigate effects of Aroclor 1242, Aroclor 1254, 2,2',6,6'-tetrachlorobiphenyl (TCB), 3,3',4,4'-TCB, and 3,3',5,5'-TCB on growth and growth-related hormones. The following indices were measured: embryo mortality, body weights, bone length, pituitary GH content, and plasma concentrations of triiodothyronine (T3), thyroxine (T4), GH, and insulin-like growth factor-1 (IGF-1). Fertile eggs were injected with PCBs on Day 0 and indices determined on Day 17 of incubation. Unexpectedly, 3,3',5,5'-TCB or low-dose Aroclor 1242 treatment increased body weight and bone length (P < 0.05), whereas Aroclor 1242 (high dose), 3,3,4,4'-TCB, or Aroclor 1254 treatment reduced body weights and/or bone length (P < 0.05). Aroclor 1242 or 3,3',4,4'-TCB (low-dose treatment) elevated plasma T4 concentrations (P < 0.05). Both growth and pituitary GH content were increased (P < 0.05) by 3,3',5,5'-TCB (low dose) or Aroclor 1242 treatment. Despite marked differences in growth rates, plasma T3, GH, and IGF-I concentrations were unaffected by PCB treatment. Growth-related hormones may not be responsible for the growth depression observed after PCB treatment. Possibly the decrease in growth occurred because of general toxicity. The importance of chlorine position in causing thyroid hormone axis alterations was not clearly established.
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PMID:Effects of polychlorinated biphenyl mixtures and three specific congeners on growth and circulating growth-related hormones. 916 18


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