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PubMed2001

Serum Tg--a sensitive marker of thyroid abnormalities and iodine deficiency in epidemiological studies.

Serum Tg is widely used in the control of thyroid cancer but also in the diagnosis of certain other thyroid diseases. Serum Tg may be useful in the characterization of the iodine status of a population, but little is known about determinants of serum Tg levels. We examined a random selection of 4,649 subjects from 2 regions in Denmark with different iodine status. Thyroid volume and structure were determined with ultrasonography, and thyroid function tests and Tg analysis were performed. The factor with the closest association with serum Tg levels was thyroid volume at ultrasonography (P < 0.001). Also thyroid nodularity (P < 0.001) and iodine excretion (P < 0.001) had close associations to serum Tg, even after adjusting for the influence of the other parameters. Thyroid dysfunction had a less pronounced but still highly significant association with serum Tg (P < 0.001), but no relation was found to serum TSH in general. The association with age seemed to rely on differences in the prevalence of thyroid abnormalities, and men had lower Tg levels than women of the same age. There was a marked difference in serum Tg between the two regions with slightly different iodine excretion also after adjusting for the other factors. In conclusion, serum Tg reflects thyroid abnormalities and thyroid function and is a sensitive marker of iodine deficiency in a population.

Adolescent↗
PubMed1996

Follicular Carcinoma Associated with Minocycline-Induced Black Thyroid.

Grossly evident black pigmentation of the thyroid has been observed in a number of patients, most of whom have a history of chronic ingestion of minocycline. In the majority of reported cases, no thyroid dysfunction or lesion has been noted, although rare instances of papillary carcinoma have been described. We describe a patient with a history of chronic minocycline ingestion, who presented with a neck mass of recent onset. Histologic examination of the thyroid revealed diffuse pigment deposition, typical for that seen in association with minocycline ingestion. Also present was a 3.2-cm follicular neoplasm with capsular and vascular permeation, consistent with minimally invasive follicular thyroid carcinoma. This represents the first report of follicular carcinoma associated with minocycline-induced black thyroid (MIBT).

Journal Article↗
PubMed1986

Thyroid status and thermogenesis in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Several key aspects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity resemble the effects of hypothyroidism, while in other ways the toxic responses are characteristics of hyperthyroidism. Whether thyroid dysfunction plays a role in TCDD toxicity remained unknown, however. We therefore determined the dose-related effects of TCDD treatment on plasma concentrations of L-thyroxine (T4), 3,5,3'-triiodo-L-thyronine (T3), and thyroid-stimulating hormone (TSH), and compared these changes with signs of TCDD toxicity. We also determined whether indices of functional thyroid status (and thermogenesis) were altered in response to TCDD treatment. Young adult male Sprague-Dawley rats were given single oral doses of TCDD (6.25-100 micrograms/kg) and evaluated 1 week later. Toxicity, measured by decreases in feed intake and body weight, ranged from minimal to severe. Plasma concentrations of T4 were greatly reduced at all doses tested, while T3 was increased in a dose-related fashion (up to 35%). TSH was elevated but was inversely proportional to dose. Thyroid histology was unremarkable, and TCCD treatment had little effect on the ability of rats to raise serum T4, T3, and TSH concentrations in response to acute cold stress. TCDD treatment caused a slight (8%) decrease in basal metabolic rate, yet comparable decreases were seen in pair-fed control animals. Thermogenesis, as measured by O2 consumption and colonic temperatures in rats exposed to various ambient temperatures, was only marginally affected. In summary, although thyroid hormone concentrations were markedly altered, rats given doses of TCDD sufficient to cause overt toxicity appeared to be essentially euthyroid. These results do not support proposals by other researchers that altered thyroid status is a major contributor to TCDD toxicity and/or a key response to TCDD exposure.

Animals↗
PubMed2002

Epidemiology and prevention of thyroid disease in pregnancy.

Pregnancy has variable effects on thyroid hormone concentrations throughout pregnancy as well as being associated with goiter. The latter is largely preventable by ensuring optimal iodine intake of at least 200 microg/d. Immunologic changes in pregnancy include a so-called T(H)2 shift that reverts to T(H)1 status around birth or early in the postpartum period. Hyperthyroidism during gestation, usually caused by Graves' disease, is rare (0.2%) and is best managed medically with propylthiouracil; thyroid-stimulating antibodies should be measured. Prevention of the deleterious effects of Graves' disease includes adequate preconception advice, adequate monitoring during pregnancy, and total avoidance of (131)I therapy during pregnancy. Hypothyroidism during pregnancy has an incidence of 2.5% although there is a 10% incidence of thyroid peroxidase (TPO)-antibody positivity in early gestation. There are convincing epidemiologic data to show that suboptimal thyroid function in pregnancy is associated with impaired neurointellectual development (e.g., 19% with IQ < 85 compared to 5% in one study). Therefore, there is a case for screening for thyroid function in early pregnancy with thyroxine (T(4)) intervention therapy. Maintenance of optimal iodine intake is critical to prevent nonautoimmune gestational maternal hypothyroxinaemia. Postpartum thyroid dysfunction (PPTD) occurs in 5%-9% of women and in up to 50% of TPO-antibody positive women (as ascertained in early pregnancy). Prevention of PPTD at this time could only be achieved by pregestational ablation of the thyroid. Another approach is to at least improve the prediction of postpartum thyroid disease (PPT) because the TPO antibody has a sensitivity of only 50%.

Child↗
PubMed1994

High CTG repeat number in nodular thyroid tissue from a myotonic dystrophy patient.

CTG triplet expansion was studied in lymphocytes and thyroid tissue in a patient with myotonic dystrophy (DM) and associated thyroid nodular disease. An approximately 7 fold larger amplification was found in abnormal thyroid tissue compared to lymphocytes, suggesting that anomalies in the putative DM kinase gene might contribute to thyroid dysfunction.

Adult↗
PubMed1995

Longitudinal study of antibodies against thyroid in patients undergoing interferon-alpha therapy for HCV chronic hepatitis.

Seventy-five patients (50 M, 25 F), affected by chronic hepatitis caused by hepatitis C virus (HCV), without clinically overt thyroid disease, underwent r-interferon (IFN)-alpha-2a treatment (3-6 MU, 3 times/week) for 12 months. They were tested for thyroid function and for thyroid autoantibodies before (A), 6 (B) and 12 (C) months after the beginning of treatment and after 6 (D) months off therapy. Antithyroglobulin antibodies (Tg-Ab) and TSH were measured by IRMA, antiperoxidase antibodies (TPO-Ab), free T3 (FT3) and free T4 (FT4) by RIA, thyrotropin receptor antibodies (TR-Ab) by RRA. None of the patients showed TR-Ab positivity throughout the study. The number of the patients with one or both antithyroid antibodies progressively increased during treatment (A 10.7%; B 26.7%; C 45.3%) and decreased when off therapy (D 22.7%) with none of them positive for Tg-Ab alone (TPO-Ab 6.7%; Tg-Ab+TPO-Ab 16%). Tg-Ab increased during rIFN (median: A 29.0; B 35.0; C 73.0 U/ml) but decreased when off therapy (D 29.0 U/ml). Instead, TPO-Ab significantly increased throughout the study (A 1.0; B 3.0; C 6.0; D 7.0 U/ml). However, some patients showed for the first time an appearance of antibodies when off therapy. Five patients showed both antibodies and thyroid dysfunction: 2 at B, 2 at C, and 1 at D. Only 1 developed mild transient hyperthyroidism while the other 4 developed hypothyroidism, persistent however only in 1 case. Our study confirms that rIFN-alpha-2a frequently induces thyroid autoimmunity. TPO-Ab seems more useful than Tg-Ab in monitoring the immunological response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Neonatal thyroid disease: differential expression in three successive offspring.

Neonatal thyroid disease, manifested as either hyperthyroidism or hypothyroidism, has been described in the offspring of women with autoimmune thyroid disorders. We report clinical and laboratory observations in a mother with autoimmune thyroiditis who gave birth to three children with different forms of thyroid dysfunction. The first child was clinically normal, the second child had transient neonatal hyperthyroidism, and the third child had neonatal hypothyroidism. After the birth of the second child, the mother was found to be biochemically hypothyroid. Long-acting thyroid stimulator and antithyroid microsomal antibodies were detected in her serum. She was treated with L-T4 (0.15 mg/day). After the birth of her third child, the mother was found to have thyroid-stimulating immunoglobulins and TSH-blocking inhibitory immunoglobulins in her serum. The latter also were detected in the third newborn. Six weeks later, TSH-blocking inhibitory immunoglobulins were not detected in the child, but they persisted in the mother. This report further expands the spectrum of neonatal thyroid disease and suggests that differing disease syndromes in the newborn can occur depending on whether stimulating or blocking antibodies predominate in the mother.

Adult↗
PubMed2007

Barriers in the quest for quality drug information: salutary lessons from TGA-approved sources for thyroid-related medications.

Product information (PI) for thyroid-related medications endorsed by the Therapeutic Goods Administration, as reproduced in the commonly used compilation publications June 2006 MIMS (Monthly index of medical specialties) annual, MIMS Online and the Australian prescription products guide 2006, was evaluated to see whether it reflects contemporary therapeutic practice. Compared with current medical literature, these PI-based sources provide inadequate, inaccurate or outdated therapeutic directives. Examples include: Incorrect advice that thyroxine therapy should always begin at very low dosage. Failure to recommend increased thyroxine dosage early in pregnancy (thus placing the offspring of women being treated for hypothyroidism at risk of impaired fetal brain development). Incorrect and potentially unsafe advice to treat thyrotoxicosis with stable iodide in late pregnancy. Failure to advise serial adjustment of antithyroid drug dosage until after a patient becomes euthyroid (this can result in iatrogenic thyroid dysfunction). Outdated advice that antithyroid drugs are not compatible with breastfeeding. Recent initiatives to upgrade consumer medicine information (CMI) appear to accept PI-based sources as a reliable benchmark for CMI. That inference is not warranted for thyroid-related medications. Accountability for the updating of clinical information in PI needs to be defined, and the process for updating PI may need to be modified. Quality drug information, both PI and CMI, depends on fluent, evidence-based collaboration between suppliers, regulators, prescribers, specialist clinicians and consumers.

Antithyroid Agents↗
PubMed1999

Transplacental passage of anti-thyroid auto-antibodies in a pregnant woman with auto-immune thyroid disease.

We report the intra-uterine and postnatal thyroid status of a newborn, whose mother, affected with Hashimoto's thyroiditis superimposed on a previous Graves' disease, again became hyperthyroid during the third trimester of pregnancy. The mother had very high levels of anti-thyroid auto-antibodies, including TSH receptor auto-antibodies (TRAb) measured as TSH-binding inhibiting auto-antibodies (TBIAb). In order to exclude fetal thyroid dysfunction due to passive transplacental transfer of TRAb, fetal blood samples were obtained by cordocentesis at 21, 27 and 32 weeks of gestation. A transplacental transfer of TRAb was already seen at 21 weeks, but no alteration of fetal thyroid function was present at that time. In the following weeks, a rise in TRAb and circulating thyroid hormones was observed both in the fetus and mother, accompanied by overt hyperthyroidism in the mother and by growth retardation in the fetus. At birth, TRAb were shown to have stimulating activity both in the newborn and mother. This report documents the early transplacental passage of thyroid auto-antibodies and underlines the importance of close follow-up of pregnant women with auto-immune thyroid disorders.

Adult↗
PubMed2002

Thyroid autoimmunity in chronic idiopathic urticaria: implications for therapy.

The association between thyroid autoimmunity and chronic idiopathic urticaria has long been recognized, although prevalence rates differ in the studies reported to date (from 12 to 29%). There is, therefore, a strong indication to screen patients affected by chronic urticaria of unknown origin for thyroid antibodies (antithyroperoxidase and antithyroglobulin) and, when positive, for serum thyrotropin to assess thyroid functional status. Less clear is the implication of thyroid autoimmunity for therapy, as most patients with urticaria who have associated thyroid autoimmunity are euthyroid. There is no doubt that cases with clinical or subclinical thyroid dysfunction should undergo treatment with either levothyroxine or antithyroid drugs for hypo- or hyper-function, respectively. Although the best remission rates for symptoms of urticaria have so far been obtained with levothyroxine in patients who are euthyroid, monitoring of thyroid function through serum thyrotropin determination is highly recommended because of the risk of hyperthyroidism, especially in the elderly.

Antithyroid Agents↗
PubMedDate not supplied

Anterior segment ischemia following strabismus surgery.

Anterior segment ischemia (ASI) is a potentially blinding complication of extensive eye muscle surgery. Eyes have been described with this complication following surgery on as few as two rectus muscles, especially in patients with thyroid dysfunction or other medical illnesses. In an attempt to assess the risk of ASI, we have reviewed the records of 34 eyes in 26 patients who underwent surgery on three or four rectus muscles. Seven eyes of six patients with thyroid ophthalmopathy which underwent two-or three-muscle surgery were also studied. Evidence of clinically significant ASI was apparent in only one patient during a follow-up period of seven months to eleven years. This case was mild and no visual loss resulted. Our findings suggest that surgery on three or four rectus muscles in healthy patients is probably safe when performed in a staged fashion.

Adolescent↗
PubMedDate not supplied

[Osteoporosis in thyroid diseases].

Thyroid hormones play the essential role in the regulation of metabolism and bone remodeling in physiological conditions and in the course of thyroid dysfunction. Introduction of densitometry to the diagnostics of osteoporosis has made possible the evaluation of influence of both hyperthyroidism and hypothyroidism and their treatment on bone mineral density. Moreover it became possible to estimate the influence of treatment with exogenous thyroid hormones on the skeletal system. Authors presented mechanisms of the thyroid hormones action on bone tissue and analysed current state of knowledge concerning the influence of the thyroxine treatment with replacement and suppressive doses on the bone mineral density. The influence of thyroid hormones on the skeletal system with respect to premenopausal and postmenopausal period was also discussed. Great discrepancies in literature data and its reasons were underlined.

Age Factors↗
PubMed2003

Prevalence of thyroid disorders in pregnant women with mild iodine deficiency.

To assess the prevalence of thyroid disorders in a region with mild iodine deficiency, this study was undertaken in a randomized sample of pregnant women during different gestational periods. Evaluations were performed in 215 women: thyroid ultrasound scanning, thyroid stimulating hormone (TSH), free thyroxine (T4) and thyroid peroxidase (TPO) antibodies. At the time of participation in the study, some women (90/215) had been receiving 150-200 micrograms iodine. Hypothyroidism was found in four women (1.86%). Positive TPO antibodies were seen in 34 of 215 women (15.8%), and TPO antibody level over 150 mU/l was found in 9.8% (21/215). There was no significant difference between TSH levels in women with positive or negative TPO antibodies. There were no differences in TSH level between the women receiving and those not receiving iodine prophylaxis. The prevalence of goiter in 211 euthyroid women was found to be 24.2% (51/211). in the group with iodine prophylaxis, thyroid volume was found to be significantly lower (t = 2.5; p = 0.02) than in women who had not received it, or had started it during the second trimester. By comparison of history data on the prevalence of aborted pregnancy between the group with positive (26.5%; 9/34) and the group with negative TPO antibodies (14.3%; 26/181), no significant differences were found. We conclude that, in mild iodine deficiency, pregnancy is related to a high risk of goiter, which can be prevented by iodine prophylaxis. TPO antibody carrier status in pregnant women is probably not associated with a significant risk of thyroid dysfunction or spontaneous abortion.

Adult↗
PubMed1990

Increased detection of elevated TSH using immunoradiometric assay.

Using a highly sensitive immunoradiometric assay, the authors detected an increased rate of elevated thyrotropin in 2,099 patients vs 1,789 patients examined with radioimmunoassay. Closer scrutiny of mood disorder patients with elevations found confirmatory evidence of thyroid dysfunction in most.

Feeding and Eating Disorders↗
PubMed2005

Thyroid epithelial cell hyperplasia in IFN-gamma deficient NOD.H-2h4 mice.

The role of inflammatory cells in thyroid epithelial cell (thyrocyte) hyperplasia is unknown. Here, we demonstrate that thyrocyte hyperplasia in IFN-gamma-/- NOD.H-2h4 mice has an autoimmune basis. After chronic exposure to increased dietary iodine, 60% of IFN-gamma-/- mice had severe thyrocyte hyperplasia with minimal or moderate lymphocyte infiltration, and thyroid dysfunction with reduced serum T4. All mice produced anti-thyroglobulin autoantibody. Some wild-type NOD.H-2h4 mice had isolated areas of thyrocyte hyperplasia with predominantly lymphocytic infiltration, whereas IL-4-/- and 50% of wild-type NOD.H-2h4 mice developed lymphocytic thyroiditis but no thyrocyte hyperplasia. Both thyroid infiltrating inflammatory cells and environmental factors (iodine) were required to induce thyrocyte hyperplasia. Splenocytes from IFN-gamma-/- mice with thyrocyte hyperplasia, but not splenocytes from naïve IFN-gamma-/- mice, induced hyperplasia in IFN-gamma-/- NOD.H-2h4.SCID mice. These results may provide clues for understanding the mechanisms underlying development of epithelial cell hyperplasia not only in thyroids but also in other tissues and organs.

Animals↗
PubMed2002

Thyroid hormone, brain development, and the environment.

Thyroid hormone is essential for normal brain development. Therefore, it is a genuine concern that thyroid function can be altered by a very large number of chemicals routinely found in the environment and in samples of human and wildlife tissues. These chemicals range from natural to manufactured compounds. They can produce thyroid dysfunction when they are absent from the diet, as in the case of iodine, or when they are present in the diet, as in the case of thionamides. Recent clinical evidence strongly suggests that brain development is much more sensitive to thyroid hormone excess or deficit than previously believed. In addition, recent experimental research provides new insight into the developmental processes affected by thyroid hormone. Based on the authors' research focusing on the ability of polychlorinated biphenyls to alter the expression of thyroid hormone-responsive genes in the developing brain, this review provides background information supporting a new way of approaching risk analysis of thyroid disruptors.

Brain↗
PubMed1982

Use of a single TSH-measurement after oral thyrotrophin releasing hormone: an economical and highly sensitive thyroid screening test.

The increment of serum TSH after thyrotrophin-releasing hormone (TRH) is usually considered an extremely sensitive thyroid test, particularly useful in borderline disturbances. We evaluated 195 patients by measuring serum TSH before and 3 h after 40 mg TRH po, and by various other thyroid tests. We found a very tight correlation between the TSH- increment and the 3 h TSH. Thus the TSH-increment can reliably be estimated from the 3 h TSH. The mann-Whitney test confirmed that the 3 h TSH identified thyroid dysfunction as well as the TSH-increment. The basal TSH can therefore be omitted and we propose the measurement of the 3 h TSH as an initial screening test. This single measurement economically excludes the many euthyroid patients sent for thyroid evaluation from further costly tests.

Adolescent↗
PubMed1998

Effect of small doses of iodine on thyroid function in patients with Hashimoto's thyroiditis residing in an area of mild iodine deficiency.

OBJECTIVE: Several studies have suggested that iodine may influence thyroid hormone status, and perhaps antibody production, in patients with autoimmune thyroid disease. To date, studies have been carried out using large amounts of iodine. Therefore, we evaluated the effect of small doses of iodine on thyroid function and thyroid antibody levels in euthyroid patients with Hashimoto's thyroiditis who were living in an area of mild dietary iodine deficiency. METHODS: Forty patients who tested positive for anti-thyroid (TPO) antibodies or with a moderate to severe hypoechogenic pattern on ultrasound received 250 microg potassium iodide daily for 4 months (range 2-13 months). An additional 43 patients positive for TPO antibodies or with hypoechogenicity on ultrasound served as a control group. All patients were TBII negative. RESULTS: Seven patients in the iodine-treated group developed subclinical hypothyroidism and one patient became hypothyroid. Three of the seven who were subclinically hypothyroid became euthyroid again when iodine treatment was stopped. One patient developed hyperthyroidism with a concomitant increase in TBII titre to 17 U/l, but after iodine withdrawal this patient became euthyroid again. Only one patient in the control group developed subclinical hypothyroidism during the same time period. All nine patients who developed thyroid dysfunction had reduced echogenicity on ultrasound. Four of the eight patients who developed subclinical hypothyroidism had TSH concentrations greater than 3 mU/l. In 32 patients in the iodine-treated group and 42 in the control group, no significant changes in thyroid function, antibody titres or thyroid volume were observed. CONCLUSIONS: Small amounts of supplementary iodine (250 microg) cause slight but significant changes in thyroid hormone function in predisposed individuals.

Adult↗