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At least 379 records · Page 21Linked to original sources
PubMed2001

Thyroid function and anti-thyroid antibodies in MS patients screened for interferon treatment. A multicenter study.

Interferon beta (IFNB) treatment for multiple sclerosis (MS) has been associated with thyroid disorders (TD), in particular in patients with subclinical TD or anti-thyroid (AT) autoantibodies (autoAb) before starting treatment. TD and AT autoAb frequency was reported increased in MS. To determine whether MS patients have subclinical thyroid function abnormalities or anti-thyroid autoimmunity predisposing to develop TD, we performed a prospective multicenter screening of thyroid function and autoimmunity in 152 relapsing-remitting (RR) MS patients selected to receive IFNB treatment and in 437 healthy normothyroidal controls. Thyroid-related hormones and anti-thyroid microsomal antigen (anti-TMA) autoAb were tested with sensitive immunoradiometric or chromatographic assays. Cases were stratified for different progressively decreasing or increasing cutoff values of thyroid-stimulating hormone (TSH) (0.3, 0.2, 0.1, 3 and 5 mIU/l), and odds ratios (OR) with 95% confidence intervals (CI) calculated using logistic regression adjusted for gender, age, and anti-TMA autoAb positivity. The frequency of cases below or above the TSH cutoff values was not significantly different in MS patients and controls, and the risk to have an abnormal TSH level was not significantly increased in MS patients (OR ranging 0.37-0.84; CI, 0.05-3.01), even if anti-TMA autoAb positive (OR ranging 0.35-0.85; CI, 0.04-3.00). Frequencies of subclinical hypothyroidism and of anti-TMA autoAb positivity were, however, trending higher in MS men (ranging 5-7%) than in controls (3%). MS patients do not have an increased risk of subtle thyroid function abnormalities, subclinical TD, or anti-TMA autoAb positivity that may predispose to develop thyroid dysfunction during IFNB treatment. The positive trend for subclinical hypothyroidism and anti-TMA autoAb positivity, however, advises a longitudinal study of thyroid function and autoimmunity during IFNB treatment to see whether patients with baseline subclinical thyroid dysfunction develop clinically significant alteration during treatment.

Adolescent↗
PubMed1998

[Non-thyroid indications of treatment with thyroid hormones].

INTRODUCTION: The use of thyroid hormone is currently strictly limited to thyroid diseases. Several recent papers have examined the effects of thyroid hormone in non-thyroidal diseases. These studies examined either the use of the pharmacological properties of thyroid hormone or the effect of the correction of the decrease in triiodothyronine (T3) associated with non-thyroid illnesses. CURRENT KNOWLEDGE AND KEY POINTS: Intravenous administration of T3 improves the cardiac index during ongoing cardiac surgery, with a paradoxical decrease in the incidence of atrial fibrillation. T3 administered by the oral route also improves the cardiac index in the medium term in dilated cardiomyopathy. No benefit on survival has been demonstrated in non-thyroidal diseases when using the pharmacological properties of thyroid hormone. Other situations, such as transplantation or neural rescue after cardiac arrest, are currently under study. In non-thyroidal diseases, administration of thyroxine (T4) has no effect because of the deeply disturbed metabolism of thyroid hormones. FUTURE PROSPECTS AND PROJECTS: Adverse metabolic effects of T4 and T3 therapy have probably been overestimated and may depend on the dose and on the time of administration in the course of the disease. Indications in cardiac surgery and cardiac diseases need to be clarified. To further understand the value of thyroid hormones in non-thyroidal diseases, placebo-controlled studies using small doses of T3 are required.

Animals↗
PubMed2005

Questionnaire on management of nodular thyroid disease (Annual Meeting of the Thyroid Section of the German Society of Endocrinology 2003).

Nodular thyroid disease is highly prevalent in iodine deficient areas. In Germany it affects approximately 30 % of the adult population. Differential diagnosis of thyroid nodules is directed at exclusion of rare thyroid malignancy and assessment of the nodules' functional characteristics in order to determine the best treatment approach. In 2003 the annual meeting of the Sektion Schilddrüse, a thyroid specialist group of the German Society of Endocrinology addressed the topic of "management of benign nodular thyroid disease". To assess the current diagnostic and therapeutic approach to nodular thyroid disease by German thyroid experts we designed a questionnaire, which was sent to all members of the Thyroid Section before the meeting and was answered by 70 % of the participants. We here report the results of the questionnaire, which show a considerable national heterogeneity in the management of thyroid nodules as well as diagnostic and treatment preferences for different thyroid specialist subgroups, e.g. endocrinologists and nuclear medicine specialist. This is in agreement with results of previous questionnaires assessing state-of-the-art practise among members of the European and American Thyroid Associations and underlines the definite need for a consensus process and for carefully planned randomized trials to answer the many unresolved questions in diagnosis and therapy of nodular thyroid disease.

Biopsy, Needle↗
PubMed1997

Quality-of-life changes in patients with thyroid cancer after withdrawal of thyroid hormone therapy.

Quality of life (QOL) is an important consideration as patients survive longer with cancer and is an area of increasing interest in patients with thyroid cancer who undergo long-term cancer surveillance. However, there are few disease-specific QOL tools available to evaluate QOL in patients with thyroid cancer. The purposes of this longitudinal, repeated-measures study were to: (1) test a new instrument, the QOL-Thyroid Scale, during thyroid hormone withdrawal; and (2) to evaluate the impact of thyroid hormone withdrawal on patients' perceived changes in quality of life. The sample included 34 subjects (mean age 40 years) undergoing thyroid hormone withdrawal in preparation for scanning procedures. Subjects completed three instruments (demographic data tool, the QOL-Thyroid, and the FACT-G) at four specific time points in relationship to scanning. The results demonstrated that the QOL-Thyroid tool is a reliable and valid measure of QOL. Cronbach's alpha coefficient of r = .78 between QOL-Thyroid and FACT-G indicated good concurrent validity. Second, the impact of thyroid hormone withdrawal on QOL showed significant changes in physical, psychological, and social well-being across the four testing points. The greatest changes occurred between peak hormone withdrawal and thyroxine (T4) therapy. While it is generally known that patients suffer troublesome physical symptoms relating to thyroid hormone withdrawal, the negative psychological, family, and work sequelae are less apparent. In conclusion, the QOL-Thyroid is a reliable and valid measure for use in evaluating patients undergoing scanning procedures and may be used to identify and target teaching and support for high-risk areas in patients lives that are negatively affected by hormone withdrawal.

Adult↗
PubMed1994

Thyroid function and thyroid size in normal pregnant women living in an iodine replete area.

OBJECTIVE: The interpretation of the changes in thyroid hormone concentrations during normal pregnancy is a matter of debate involving, in some geographical regions, enhanced thyroid activity in early pregnancy and a hypothyroid state in the third trimester. A clinically detectable increase in thyroid size has been found in areas of mild iodine deficiency ('goitre of pregnancy'), but not in iodine replete areas. DESIGN: A prospective study. We have studied thyroid size and function in normal pregnant women living in an iodine replete area. PATIENTS: Healthy women before and during a normal pregnancy resulting from artificial insemination (n = 10) and other women during the normal menstrual cycle (n = 11), in the iodine replete area of Amsterdam. MEASUREMENTS: Thyroid volume was measured by ultrasonography. Plasma T4, free T3, free reverse T3, TSH, thyroxine binding globulin, hCG, progesterone and thyroid autoantibodies were measured. RESULTS: Thyroid volume did not change during pregnancy (data given before pregnancy and during 1st, 2nd and 3rd trimesters, respectively: 10.3 +/- 5.1, 10.6 +/- 4.4, 9.6 +/- 3.8 and 9.4 +/- 3.0 ml, NS). Free T4 and free T3 levels declined during pregnancy (13.7 +/- 2.0, 13.5 +/- 4.1, 11.2 +/- 2.8, 10.2 +/- 1.6 pmol/l, P = 0.005; 4.55 +/- 0.63, 4.64 +/- 0.88, 3.72 +/- 0.67 and 4.01 +/- 0.75 pmol/l, P = 0.003), whereas free reverse T3 levels increased during pregnancy (0.16 +/- 0.04, 0.19 +/- 0.07, 0.14 +/- 0.03 and 0.20 +/- 0.07 pmol/l, P = 0.001). Thyroglobulin levels remained unchanged. Thyroid hormones and thyroid volume did not differ between follicular and luteal phases of the menstrual cycle. CONCLUSION: Thyroid volume does not increase during pregnancy in iodine-replete areas. The decrease in free T4 and free T3 and the increase in free reverse T3 concentrations during pregnancy resemble the changes in thyroid hormones seen in non-thyroidal illness. This could be a physiological adaptation enabling energy conservation during the high metabolic demands of pregnancy.

Environment↗
PubMed1987

Epidermal growth factor decreases thyroid hormone receptors and attenuates thyroid hormone responses in GH4C1 cells.

The present study was undertaken to examine the effect of long term exposure to epidermal growth factor (EGF) on thyroid hormone responses as well as the concentration of specific nuclear thyroid hormone receptors in GH4C1 rat pituitary tumor cells. GH4C1 cells were first incubated for 48 h in medium with 5% fetal calf serum depleted of thyroid hormones by ion exchange resin. EGF had no effect on thyroid hormone receptors after 2 h, but decreased [125I]T3 binding to 56% of control values at 24 h and 68% at 48 h. L-T3 (0.5 nM) caused down-regulation of thyroid hormone receptors, and addition of EGF caused a further decrease. T3 alone (0.5 nM) caused a 2- to 3-fold induction of GH after 48 h, and GH induction was significantly inhibited by the addition of 10 nM EGF. Scatchard analysis of specific nuclear [125I]T3 binding showed that 48-h incubation with 10 nM EGF decreased T3 receptors from a Bmax of 2.35 to 1.26 pmol/mg DNA in thyroid hormone-depleted medium without affecting receptor affinity (Kd, 80 pM). The decrease in nuclear thyroid hormone receptors caused by EGF was dose dependent, with half-maximal inhibition at 0.10 nM EGF. EGF attenuated the GH response to T3 with similar dose-response characteristics. When cells were incubated for 48 h with different concentrations of T3, EGF (10 nM) decreased thyroid hormone receptors to 56-72% of control values regardless of the dose of T3, and EGF shifted the ED50 for T3 stimulation of GH from 0.1 to 1.2 nM. EGF also reduced from 5- to 1.8-fold the increase in cell number caused by thyroid hormone over 2 weeks. In contrast, EGF stimulation of PRL synthesis was changed only slightly by thyroid hormone at all times. In conclusion, we demonstrate that low concentrations of EGF decrease nuclear thyroid hormone receptors and thyroid hormone responses; this may be the mechanism by which EGF suppresses T3-induced GH production in GH4C1 cells.

Animals↗
PubMed1996

Interleukin-6 (IL-6) inhibits thyroid function in the presence of soluble IL-6 receptor in cultured human thyroid follicles.

Interleukin-6 (IL-6), a pleiotropic cytokine, is postulated to be involved in the pathogenesis of sick euthyroid syndrome, although the direct in vitro effects of IL-6 on human thyroid function are controversial. Because IL-6 signal can be transduced when the complex of IL-6 and soluble IL-6 receptor (sIL-6R) binds to gp 130, an IL-6 signal transducer, we studied the effects of IL-6 and sIL-6R on thyroid function, using human thyroid follicles obtained from patients with Graves' disease. IL-6 alone had no inhibitory effect on TSH-induced thyroid function (125I incorporation and organic 125I release), even at supraphysiological concentrations. However, in the presence of physiological concentrations of sIL-6R (100 ng/ml), IL-6 inhibited thyroid function dose dependently and completely, accompanied with the decreased ratio of 125I-T3/125I-T4 not only in the thyroid follicles but also in the culture medium. Thyroid follicles did not secrete sIL-6R but produced IL-6 constitutively. Consistent with these findings, sIL-6R inhibited thyroid function slightly at high concentrations. Furthermore, RT-PCR analyses revealed that human thyroid follicles expressed the messenger RNAs for IL-6 and gp130 but scarcely messenger RNA for IL-6R. These in vitro findings suggest that IL-6 alone hardly affects thyroid function in thyroid follicles in which IL-6R gene is scarcely expressed. However, because sIL-6R is present abundantly in serum, IL-6 in vivo would be capable of inhibiting the synthesis and release of T4 and, to a greater extent, T3 from the thyroid gland. These in vitro findings are at least partly related to the development of sick euthyroid syndrome.

Analysis of Variance↗
PubMed1980

[Studies on the thyrotropin receptor and adenylate cyclase activity in various thyroid diseases: I. The properties of TSH receptor and adenylate cyclase in Graves' thyroid and retro-orbital adipose tissues (author's transl)].

Most current etiologic concepts of Graves' disease postulate that this is an autoimmune disorder. A humoral factor, such as thyroid stimulating immunoglobulin, may be the mediator. On the other hand, it has also been suggested that abnormalities in the thyroid gland itself might be responsible for hyperfunction of the gland in Graves' disease. The true etiology of Graves' disease is still unknown. Similarly, the pathogenesis of the ophthalmic changes of Graves' disease is obscure, but immune mechanisms figure prominently in current hypotheses of the pathogenesis. It has been suggested that human adipose cell membranes have TSH receptors and that antibodies reacting with the receptors may stimulate fat cells. In this study, we have evaluated TSH receptor and adenylate cyclase of Graves' thyroid glands. Furthermore, we have investigated those of retro-orbital and the other adipose tissues in the guinea pig and in man. Human thyroid tissues were obtained at surgery and immediately minced homogenized with a loose-fitting Dounce homogenizer. A part of 10,000 g pellet of the homogenate was used for adenylate cyclase assay. The rest of the pellet was further purified by a discontinuous sucrose gradient ultracentrifugation, and the plasma membrane fraction was used for the receptor assay. The 125I-TSH binding to the fraction was measured, and the affinity constant (Ka) and capacity (Ro) were obtained from Scatchard plots using Rosenthal's method of analysis. Normal thyroid tissue contained high affinity (Ka = 2.4 x 10(10) M-1; Ro = 0.9 pmole/mg protein) and low affinity (Ka = 1.9 x 10(8) M-1; Ro = 386 pmole/mg protein) receptors. The two orders of TSH receptor were also found in Graves' thyroid tissue. The affinity constant and capacity of high affinity receptors were identical with those of normal thyroids, but the affinity constant of low affinity receptors was lower in Graves' thyroid (P less than 0.05). The basal adenylate cyclase activity in normal thyroid tissues was 0.35 nmole/10 min/mg protein. The activity rose to 280% of basal with 166 mU/ml of TSH and 680% of basal with 10 mM of NaF. These values obtained in Graves' disease were not significantly different from the values of normal thyroids. It is concluded that thyroid hyperfunction in Graves' disease is probably not the result of an intrinsic abnormality of the TSH receptor-adenylate cyclase system. Human retro-orbital adipose tissue was obtained at surgery from patients of Graves' exophthalmos or malignant neoplasm of accessory sinus. Guinea pigs tissue was obtained from 250g male animals. We were unable to demonstrate high affinity TSH receptor in human retro-orbital fat, perirenal fat or guinea pig retro-orbital fat. In contrast, guinea pig epididymal fat membranes showed TSH receptor characteristics similar to guinea pig thyroid membranes. In human adipose tissue, TSH did not stimulate the adenylate cyclase activity, although NaF definitely stimulated the enzyme...

Adenylyl Cyclases↗