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)

Cell-mediated immune responses were studied in autoimmune diseases of thyrogastric type, Hashimoto's thyroiditis and autoimmune pernicious anaemia-type gastritis. Specific cell-mediated immunity was investigated by the leucocyte migration inhibition procedure, and general cell-mediated immunity (T-cell performance) was studied by standard in vivo and in vitro tests. In thyrogastric autoimmune diseases inhibition of migration of leucocytes was induced by thyroglobulin and gastric parietal cell microsomes; under conditions of presumably low cellular sensitization, stimulation of migration was observed. There was no depression of general cell-mediated immunity, in contrast to what occurs in systemic lupus erythematosus and related autoimmune diseases. A weak association of autoimmune gastritis with HL-A3 and HL-A7 (P LESS THAN 0.05) lost significance when an appropriate correction was applied; this weakness with HL-A clearly does not explain the strong genetic component in thyroid and gastric autoimmunity.
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PMID:Thyrogastric autoimmune disease. Studies on the cell-mediated immune system and histocompatibility antigens. 108 89

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

Postpartum thyroid dysfunction (PTD) occurs in approximately 5% to 10% of all women within 1 year following delivery and is usually due to intrinsic thyroid disease rather than hypothalamic or pituitary lesions. The most common etiology of PTD, which may resemble postpartum depression, is autoimmune thyroid disease (chronic or Hashimoto's thyroiditis). Women with Graves' disease who experience symptom exacerbation in the postpartum period account for a small percentage of cases. Clues to PTD include nonspecific symptoms such as tiredness, fatigue, depression, palpitations, and irritability. On physical examination, tachycardia may be noted. Goiters are detected in the majority of cases. The disease course varies; most patients experience a phase of hypothyroidism that takes 2 to 6 months to resolve, but some develop permanent hypothyroidism within 5 years of the diagnosis.
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PMID:Evaluating and Managing Postpartum Thyroid Dysfunction. 974 99

Natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) against k562 human tumor cell targets was studied in patients with Graves' disease and Hashimoto's thyroiditis. NK activity was measured in a standard 4-hour 51chromium (Cr) release assay. Cytotoxicity was expressed as lytic units (LU)/10(6) PBL. Significantly decreased NK cell activity was demonstrated in both groups of patients, with mean (+/- SE) lytic units of 10.3 (+/- 9.1) and 13.3 (+/- 10.3) for patients with Graves' disease and Hashimoto's thyroiditis, respectively, compared with 36.0 (+/- 26.3) for age- and sex-matched normal subjects. When patients with Graves' disease were analyzed according to their thyroid status; NK activity was significantly depressed in (1) hyperthyroid patients before treatment; (2) hyperthyroid patients receiving antithyroid therapy; and (3) euthyroid patients receiving antithyroid therapy, compared with normal subjects. Graves' disease patients who were hypothyroid after radioactive iodine therapy or thyroidectomy had normal NK activity. No significant differences between hyperthyroid and euthyroid patients or between hypothyroid patients and normal subjects were demonstrated. NK activity in patients with Graves' disease did not correlate with serum levels of thyroxine, the presence or severity of ophthalmopathy, or titers of serum thyroid antibodies. In patients with Hashimoto's thyroiditis there was no correlation between NK activity and goiter size, titers of antithyroid antibodies, or thyroid status. These findings suggest that depression of NK activity in both disorders is secondary to abnormalities of thyroid hormone secretion, although an effect of the underlying autoimmune reactions has not been excluded.
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PMID:Natural killer cell activity in patients with Graves' disease and Hashimoto's thyroiditis. 984 16

Whereas clinical relevant hypo- as well as hyperthyreosis are strongly suspected to induce psychiatric symptoms, there is a controversy about the relevance of only subclinical and autoimmune findings. We found autoantibodies (MAK, TAK, TRAK) in a high percentage (100 out of 144 = 70%) in severely depressed inpatients. Also we found a Hashimoto thyreoiditis in 5 patients. In the long run this may lead to relevant hypothyreosis which is regarded to be a risk factor for depression and for possible non-response in medical treatment. We conclude that in cases of repeated depressive episodes especially depression of the elderly and in nonresponders it seems necessary not only to get lab for TSH, T3 and T4 but also to assess the autoimmune status of the thyroid gland (autoantibodies). There is further need for controlled studies whether there is a better outcome in nonresponders to antidepressive medical treatment and positive autoantibody status after supplementation with triiodothyronine.
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PMID:[Thyroid autoantibodies in depressive disorders]. 1052 30

Psychiatric manifestations are infrequent or rarely described in Hashimoto's encephalopathy. It usually begins like a subacute diffuse encephalopathy with confusion, tremor and other neurologic symptoms. A relapsing course is characteristic. Neither biologic nor clinical symptoms are specific but high antithyroid antibodies levels are characteristic. The diagnosis can be seriously delayed by the fact that the different symptoms implicate approaches by psychiatrists, neurologists or endocrinologists. There are two clinical types. The one presented here evaluates progressively to dementia with psychotic episodes, confusion and seizures. An early steroid treatment makes the symptoms regress without aftereffects. We have analysed the clinical and biological findings of a woman who has been admitted to different neurologic and psychiatric departments before her diagnosis was made. First clinical presentation and evolution were that of a depression. Each time the antidepressive treatment was stopped, depression relapsed in spite of an appropriate steroid treatment. Literature shows that a close link exists between depression and antithyroid antibodies whatever thyroid status. This link does still exist after adjustment of psycho-social determinants of depression. The decrease of those antibodies only reflects the decrease of inflammation. So, for the psychiatrist it is important to diagnose Hashimoto's encephalopathy without delay, especially when psychiatric manifestations are in the foreground. Furthermore, a psychiatric report should systematically be added to the clinical and biological findings in order to make a better approach of the existing links between depression and other manifestations of the disease.
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PMID:[Depression, anti-thyroid antibodies and Hashimoto encephalopathy]. 1140 65

Hypothyroidism affects 4% to 10% of women, increasing with age. Symptoms, which are often nonspecific and subtle, can include: lethargy, mild weight gain, edema, cold intolerance, constipation, mental impairment, dry skin, depression, irregular menses, hoarseness, myalgias, hyperlipidemia, and bradycardia. TSH determination is usually warranted when some of these are present. Confirmation of diagnosis is based on laboratory tests, not symptoms. With Hashimoto's thyroiditis, the most common cause, the thyroid is usually firm and irregular to palpation. Screening is recommended by the American Thyroid Association, American Association of Clinical Endocrinologists and ACOG. Studies indicate that even slight hypothyroidism is associated with increased miscarriage, late fetal demise and lower IQ of offspring. Many believe all women intending conception or pregnancy should be screened. Most patients with even slightly elevated TSH should be treated, though controversy remains. Hypothyroidism is usually permanent, and treatment is life-long; postpartum thyroiditis may be transient. Levothyroxine is the standard treatment. Because of variable bioavailability of some levothyroxine preparations, designation of a specific high-quality brand is appropriate; TSH should be monitored to titrate the dose. The third-generation super-sensitive TSH is the most accurate test for both hypo- and hyperthyroidism. Because estrogen increases levels of thyroid binding globulin, women who are on HRT or OCs, or are pregnant, usually have total T4 levels above the reference range.
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PMID:Hypothyroidism and women's health. 1208 Dec 57

Characteristic clinical findings of Hashimoto's encephalopathy (HE) are stroke-like episodes, epileptic seizures, myoclonus, psychosis, and progressive cognitive impairment. Diagnosis of HE is supported by elevated antithyroid antibodies, an abnormal EEG, and by good response to steroids. We report on a 74-year-old female patient with a severe depressive episode who showed no treatment response to citalopram 40 mg/day and venlafaxine 150 mg/day. Diagnostic examination revealed an abnormal EEG, elevated thyroid peroxidase antibodies (TPO-Ab), and older postinflammatory changes in thyroidal sonography. We diagnosed a depression in HE and began treatment with prednisolone 70 mg/day with stepwise dose reduction, continuing treatment with venlafaxine 150 mg/day. Within 4 weeks of treatment, the severe depressive episode disappeared as well as abnormal EEG. In addition, serum values of TPO-Ab decreased. In HE, depressive symptoms can possibly be seen in a subgroup of patients or in the early course of the disease. Diagnosis of HE should be included in diagnostic procedures in cases of therapy-refractory depression because of a good response of HE to steroids.
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PMID:[Depression in Hashimoto's encephalopathy. Successful treatment of a severe depressive episode with a glucocorticoid as an add-on therapy]. 1544 21

This review describes the aetiology of the major thyroid antigens. Iodination of thyroglobulin produces multiple antigen configurations which are functionally active but immunologically distinct. The thyroid stimulating hormone (TSH) receptor is a two-subunit glycoprotein; the extracellular A subunit is recognized by thyroid stimulating antibodies, while those antibodies recognizing the B subunit, located much nearer the cell surface, appear to function as blocking antibodies. Thyroid peroxidase (TPO), originally described as thyroid microsomal antigen, is present on the apical surface of thyroid follicular cells and is the antigen involved in cell-mediated cytotoxicity. Multiple B-cell-reactive epitopes exist, each giving rise to different antibodies. The aetiology and mechanics of the autoimmune cellular and antibody responses involves a combination of human leucocyte antigen (HLA) linkage, genetics and environmental factors to determine the initial and subsequent stages of the development of autoimmune thyroid disease. Depending on the antibody, a combination of enzyme-linked immunosorbent assay for TPO and thyroglobulin and bioassays and/or radioimmunoassay for TSH receptor antibodies are used to estimate their concentrations. The other conditions with which autoimmune thyroid diseases are associated include, for example, pernicious anaemia, connective tissue disorders, diabetes, coeliac disease, mood disorders like depression and fertility-related problems such as miscarriage, infertility, in vitro fertilization failure, pre-term delivery and postpartum thyroiditis. Often, there is no cause-and-effect relationship between them and it is debatable in some cases whether it is worthwhile monitoring patients with autoimmune thyroid disease for other conditions or vice versa. The review also itemizes the circumstances in which it might be useful to measure each antibody (i.e. the use of TPO antibodies in investigation of goitre, diagnosis of Graves' and Hashimoto's disease and the prediction of risk of developing hypothyroidism during subclinical thyroid disease; TSH receptor antibodies in maternal and neonatal hyperthyroidism and thyroglobulin antibodies in the monitoring and treatment of thyroid carcinoma). Finally, taking the current literature into account, an algorithm is recommended for the most effective use of these antibodies in the investigation of autoimmune thyroid disease.
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PMID:Clinical and laboratory aspects of thyroid autoantibodies. 1670 51

Part II of the series on thyroid disorders discusses hypothyroidism and thyroiditis that may be found in dental patients. An overview of the conditions is presented. Presenting signs and symptoms, laboratory tests used to diagnose hypothyroidism and thyroiditis, and their medical management is discussed. The dental management of patients with hypothyroidism is discussed in detail. The dentist by detecting the early signs and symptoms of hypothyroidism and thyroiditis can refer the patient for medical diagnosis and treatment and avoid potential complications of treating patients with uncontrolled disease. Patients with thyroiditis may have a short period of being hyperthyroid and it may be best to avoid routine dental treatment during that period. Patients with suppurative thyroiditis should not receive routine dental treatment during the acute stage of the disease. The end stage of Hashimoto's thyroiditis results in hypothyroidism. Central nervous system depressants, sedatives, or narcotic analgesics must be avoided in patients with severe hypothyroidism because significant respiratory depression may occur. In addition, myxedematous coma, particularly in elderly hypothyroid patients, can be precipitated by central nervous system depressants, infection, and possibly stressful dental procedures. In medically well-controlled patients the dental treatment plan is not affected and most dental procedures can be offered to these patients.
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PMID:Thyroid disorders. Part II: hypothyroidism and thyroiditis. 1687 54


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