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)

Thyroid function and presence of thyroid autoantibodies were assessed in a group of 75 consecutive female patients with mood disturbances and in a group of 38 healthy women of similar age recruited as controls. Nine patients suffered from major (endogenous) depression and 66 from minor (neurotic) depression. The individual patients had normal values of circulating thyroid hormones. Nevertheless, endogenously depressed patients had total serum triiodothyronine (M +/- SE = 1.49 +/- 0.09 nmol/l) and both total (83.9 +/- 4.3 nmol/l) and free serum thyroxine (13.9 +/- 1.1 pmol/l) lower than in the group of minor depressed and in the group of controls (p < 0.01, in both comparison). The median value of serum thyrotropin was 5.22 mU/l in the major depressed patients versus 1.72 mU/l in the minor depressed and 1.69 mU/l in the controls. Thyroid function test results in the minor depressed group did not significantly differ from those in the controls. Five of the 9 endogenously depressed patients were subclinically hypothyroid, while none of the 66 patients with minor depressive disorder showed thyroid dysfunction. Antibodies against thyroglobulin and/or thyroid peroxidase were positive in all the 5 endogenously depressed women with subclinical hypothyroidism, revealing a symptomless autoimmune thyroiditis, which was also confirmed by ultrasonography in all cases and histopathologically demonstrated in one case. None of the endogenously depressed women without thyroid dysfunction and none of the 66 minor depressives were seropositive for thyroid autoantibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subclinical hypothyroidism resulting from autoimmune thyroiditis in female patients with endogenous depression. 786 3

We studied relationships between shyness and health during a health screening survey of older adults (ages 50-88) living in an active retirement community in the southwestern United States (n = 232). As in previous studies of infants, older individuals with hay fever, insomnia and constipation were more shy than those without these problems. Shy persons overall showed higher sitting systolic blood pressure and a larger fall in orthostatic systolic blood pressure on standing; shy men had a greater prevalence of hypertension histories than did low-shy men. Shy subjects of both sexes had lower HDL cholesterol and higher triglycerides than did low-shy subjects; shy women tended to have higher LDL cholesterol than did low-shy women. In contrast with findings of elevated salivary cortisol in extremely inhibited children of both sexes, only shy women had higher 24 h urinary free cortisol excretion than did low-shy women; men showed the opposite pattern, possibly related to suppression of aggression. Shy men also tended to report a higher prevalence of thyroid disease history than did low-shy men (20% versus 6%). Notably, autoimmune thyroiditis has previously been linked with panic and depression, disorders which in turn have been associated with shyness. Taken together with previous work in shy children and their families, the data raise the possibility of (a) increased risk for arteriosclerotic vascular disease; and (b) increased risk of adrenal- and/or thyroid-related diseases in certain shy older adults.
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PMID:Vascular disease risk factors, urinary free cortisol, and health histories in older adults: shyness and gender interactions. 843 51

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

From an endocrine outpatient clinic and psychiatric outpatient clinic in Kaunas, Lithuania, 41 women with major depression were selected for study. Three groups of depressed women were established: 15 with autoimmune thyroiditis (AIT); 13 with diffuse non-toxic goiter (DNG); 13 with no thyroid disease (NTD). Standard biochemical tests were used to exclude patients with overt hypothyroidism or overt hyperthyroidism. At baseline the three groups were similar in age and almost identical in severity of depression. In part because of exclusion criteria, all baseline biochemical measures were similar. However, a slight elevation of thyroid-stimulating hormone (TSH) in the AIT group was noted and considered to indicate a tendency toward subclinical hypothyroidism. After thyrotropin-releasing hormone (TRH) administration, six AIT women and six DNG women, but no NTD women, showed blunted TSH responses. As a group DNG women showed smaller TRH responses than other women. Four AIT women showed exaggerated TSH responses. In all three groups basal TSH correlated positively with TSH response to TRH. Basal prolactin (PRL) responses to TRH infusion were similar in all three groups. However, the four AIT women with enhanced TSH responses also showed enhanced PRL responses. Indeed, in the AIT group, but only in this group, PRL responses were correlated with both TSH and basal TSH. In all groups of women the PRL response was unrelated to basal PRL.
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PMID:Pituitary responses to thyrotropin releasing hormone stimulation in depressed women with thyroid gland disorders. 904 46

Alpha interferons have been used widely to treat chronic hepatitis C virus infection. These include recombinant interferons, purified natural leukocyte, and lymphoblastoid interferons. Alpha interferon is administered by subcutaneous or intramuscular injection either daily or three times weekly for a period of 6 to as long as 24 months. A wide array of adverse effects of alpha interferon have been described. Several side effects such as fever, headache fatigue, arthralgias, and myalgias are common, especially with the initial injections. These early side effects of interferon are predictable and are encountered in the majority of patients. These may not require dose modification, but can be problematic for a significant proportion of patients. Other adverse events effects may require dose modification or even discontinuation of therapy in 2% to 10% of patients. Neuropsychiatric side effects such as depression and irritability can be most troublesome; their mechanisms are not well understood. Granulocytes, platelets, and red blood cell counts decrease during treatment, but the decreases are usually mild, although they can be dose limiting if cell counts are low initially. Interferon has important immunomodulatory properties, and treatment can induce autoimmune phenomena, the most frequent being autoimmune thyroiditis with either hypothyroidism or hyperthyroidism, especially in predisposed patients. Other autoimmune disease can be aggravated by interferon therapy. Severe and even life-threatening side effects of interferon occur in 0.1% to 1% of patients; these include thyroid, visual, auditory, renal, and cardiac impairment, and pulmonary interstitial fibrosis. Some of these side effects may be irreversible. Higher doses of interferon (above 5 million units three times weekly) cause higher rates of adverse events than standard doses. Contraindications to alpha interferon have been recognized.
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PMID:Side effects of alpha interferon in chronic hepatitis C. 930 75

The diagnosis and treatment of subclinical hypothyroidism in mood-disordered patients is complex and somewhat controversial. The psychiatrist must recognize that such subclinical states may contribute to depression, mood cycling, or delayed response to treatment if undetected. Autoimmune thyroiditis, which may ultimately lead to various grades of hypothyroidism, may also be seen in depressed populations, particularly in postpartum females. The author discusses these issues by means of a clinical vignette, then proposes an algorithm for the diagnosis and treatment of hypothyroid states in mood disordered populations.
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PMID:The diagnosis and treatment of subclinical hypothyroid states in depressed patients. 932 79

Hypothyroidism may give rise to frank depression that usually responds to thyroxine therapy. Depressed subjects with subclinical hypothyroidism and/or autoimmune thyroiditis should probably also be treated similarly. Most patients with depression, although generally viewed as chemically euthyroid, have alterations in their thyroid function including slight elevation of the serum thyroxine (T4), blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) stimulation, and loss of the nocturnal TSH rise. These changes are generally reversed following alleviation of the depression. The role of adjuvant triiodothyronine (T3) treatment in resistant depression has not been established, but the data suggest that it will be beneficial in about 25% of cases. However, controlled trials to establish this approach are needed. The underlying mechanism leading to the beneficial response from T3 is unknown, but may reflect brain hypothyroidism in the context of systemic euthyroidism. The hypothalamus in culture, which is analogous to a deafferentated hypothalamus in vivo, shows a paradoxic increase in TRH production after glucocorticoid stimulation. It is known that in human depression there is a functional disconnection of the hypothalamus with impairment of the inhibitory glucocorticoid feedback pathway from the hippocampus to the hypothalamus that results in the typical elevated cortisol levels and impaired dexamethasone suppression. It is postulated that a similar situation prevails with regards to the thyroid axis and that the increased T4 in depression, as well as the blunted TSH response to exogenous TRH, reflects glucocorticoid activation of the TRH neuron leading to increased TRH secretion with resultant down regulation of the TRH receptor on the thyrotrope. Normalization of thyroid function after treatment may result in part from an inhibitory response of the TRH neuron to antidepressant medication, although other effects may also be responsible.
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PMID:The thyroid axis and depression. 982 65

Depressed patients, although viewed as chemically euthyroid, have alterations in the function of hypothalamic-pituitary-thyroid axis including slight elevation of the serum thyroxine (T4), loss of the nocturnal TSH rise, blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) stimulation and predisposition to autoimmune thyroiditis. Both hypothyroid and depressed patients share a number of clinical features in common. This is the reason that some research workers use the "brain hypothyroidism" hypothesis to explain the pathogenesis of depression. They suggest that depression is a state of local hypothyroidism in brain with normal peripheral thyroid hormone concentrations as a result of brain type II deiodinase inhibition and impaired transport T4 across the blood brain barrier. This theory seems to be compatible with the serotonin deficiency hypothesis of depression. Some studies confirm the existence of classical feedback between serotoninergic and hypothalamus-pituitary-thyroid systems. TRH remains under a constant inhibition by serotonin and reduced intracerebral serotonin concentration seen in depression will lead to increased TRH concentration in brain tissue. This mechanism is probably responsible for blunted TSH response to TRH stimulation.
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PMID:[Hypothalamic-pituitary-thyroid axis in depression]. 1204 45

Our objectives were to investigate thyroid abnormalities and autoimmunity in 120 patients affected by fibromyalgia (FM) and to study their relationships with clinical data and symptoms. Thyroid assessment by means of antithyroglobulin antibodies, antithyroid peroxidase antibodies, free triiodo-thyronine, free thyroxine, and thyroid stimulating hormone analyses was carried out. The clinical parameters "Fibromyalgia Impact Questionnaire", pain, tender points, fatigue, and other symptoms, and the presence of depression or anxiety disorders were evaluated. The basal thyroid hormone levels of FM patients were in the normal range, while 41% of the patients had at least one thyroid antibody. Patients with thyroid autoimmunity showed a higher percentage of dry eyes, burning, or pain with urination, allodynia, blurred vision, and sore throat. Correlations found between thyroid autoimmunity and age or with the presence of depression or anxiety disorders were not significant. However, in the cohort of post-menopausal patients, the frequency of thyroid autoimmunity was higher with respect to pre-menopausal patients. In conclusion, autoimmune thyroiditis is present in an elevated percentage of FM patients, and it has been associated with the presence of typical symptoms of the disease.
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PMID:Association between thyroid autoimmunity and fibromyalgic disease severity. 1748 49

Combined pegylated interferon and ribavirin therapy for chronic hepatitis C infection cause a wide range of side effects, including flu-like syndrome, hematological abnormalities, cardiovascular symptoms, gastrointestinal symptoms, pulmonary dysfunction, depression, and retinopathy. Interferon-alpha has been shown to be related to the development of various autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, autoimmune thyroid disease, and type 1 diabetes mellitus (DM). Type 1 DM and thyroid disease respectively develop in 0.08-2.61% and 10-15% of patients treated with combined interferon-alpha and ribavirin for chronic hepatitis C. The coexistence of type 1 DM and autoimmune thyroiditis was rarely reported. We report a case of a 33-year-old female patient with chronic hepatitis C who simultaneously developed diabetic ketoacidosis and autoimmune thyroiditis after treatment with pegylated interferon-alpha 2b and ribavirin.
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PMID:[Occurrence of diabetic ketoacidosis and autoimmune thyroiditis in a patient treated with pegylated interferon-alpha 2b and ribavirin for chronic hepatitis C]. 2060 4


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