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PubMed1999

Amiodarone compared with iodine exhibits a potent and persistent inhibitory effect on TSH-stimulated cAMP production in vitro: a possible mechanism to explain amiodarone-induced hypothyroidism.

Amiodarone (AMD) is a powerful anti-arrhythmic drug used for the treatment of a wide variety of cardiac arrhythmias and its most striking feature is its high iodine content. Thyroid dysfunction is a limiting side-effect of the drug and both AMD-induced hypothyroidism (AIH) and AMD-induced thyrotoxicosis (AIT) are reported. To examine the hypothesis that altered bioavailability of iodine is a contributing event in the pathogenesis of AIH, we compared the effects of AMD and inorganic iodine in vitro on events involved in the process of thyroid autoregulation. FRTL-5 cells and JP26 CHO cells (transfected with the human TSH receptor) were exposed to AMD or NaI in the presence of TSH, and cAMP production was measured as an indicator of cellular function. Forskolin and cholera toxin were also used to determine the possible target sites of AMD and iodide. Our results indicated that there was a difference between the effects of AMD versus those of physiological doses of iodide. The inhibitory effects of AMD occurred at lower concentrations of iodide than those seen in the NaI-treated cells. The effects of AMD were irreversible indicating a possible persistence of the Wolff-Chaikoff effect due to a constant high intracellular iodide level. The inhibitory effects of AMD (also seen at supraphysiological doses of iodide) were partially overcome by forskolin but not by cholera toxin indicating an effect on TSH receptor interactions with the other signal transduction elements such as G proteins and adenylate cyclase. The persistence of the Wolff-Chaikoff effect through loss of autoregulation may be a mechanism of the observed hypothyroidism in some patients taking AMD. The combined effects of the constant release of iodide together with the drug toxicity may be the mechanism for the observed effects.

Amiodarone↗
PubMedDate not supplied

[Current evaluation of the classical Werner test and its correlation with current in vitro E.T.R. technics].

The authors evaluated the current standing of the classical 131I uptake test, together with its subsidiary stimulation and suppression tests, and its correlation to clinical diagnosis and the in vitro ETR (Effective Thyroxine Ratio) technique. In the 349 cases studied, a good correlation was found between the previous diagnosis--made by means of 131I uptake test--and the clinics and symptomatology, and very particularly, the in vitro ETR test. The authors conclude that the combination of both tests is sufficiently reliable for the diagnosis of thyroid dysfunction.

Adolescent↗
PubMed1989

[Iodine overload in newborn infants caused by the use of PVP-iodine for perineal preparation of the mother in vaginal delivery].

The high incidence of transient thyroid dysfunction in newborns from our hospital (0.6%), led us to investigate whether povidone perineal prep. during delivery and daily postpartum antisepsis, induced iodine overload in the newborn, and whether breast milk was the vehiccle. In a controlled randomized trial we used either povidone-iodine or clorhexidine in 36 mothers, and we investigated in them and in their newborns iodine levels and thyroid function. Iodine levels in cord blood, maternal urine and newborn urine were significantly higher in povidone treated group (p less than 0.001) up to the 4th postpartum day. These levels were also significantly higher in breast fed than in formula-fed babies within the group of povidone-iodine-treated mothers. Maternal prepartum urine iodine, and thyroid function in mothers and newborns were not significantly different in both groups.

Delivery, Obstetric↗
PubMed1983

Association of chronic urticaria and angioedema with thyroid autoimmunity.

Seventeen patients, constituting 12.1% of 140 consecutively seen cases of chronic urticaria, demonstrated thyroid autoimmunity with thyroid microsomal antibodies (TMAs) in serum titers greater than or equal to 1:1,600. Eight of these 17 patients had goiter or thyroid dysfunction. In a control group of 477 consecutively seen patients, only 27 (5.6%) had similar TMA titers. Routine and special immunologic test results in this group of 17 patients did not differ from those found in other patients with chronic urticaria and angioedema (CUA), and the only notable clinical feature was that all 17 had angioedema. The age and sex distribution and thyroid features of these 17 patients were similar to those described in autoimmune thyroiditis. Patients (especially women) with CUA should be tested for the presence of TMAs. In this subgroup, CUA may have an autoimmune basis.

Adolescent↗
PubMed1985

Antithyroid antibodies in depressed patients.

The presence of antithyroid (antimicrosomal and antithyroglobulin) antibodies was assessed in 45 psychiatric inpatients with prominent depressive symptoms (28 with DSM-III major depression). Nine patients (20%) had detectable titers of antithyroid antibodies, a rate considerably higher than the 5%-10% observed in the normal population. Each of these nine patients with symptomless autoimmune thyroiditis had normal baseline serum thyrotropin concentrations and normal thyroid function (as assessed by T4, T3 uptake, and free thyroxine index). These findings support the hypothesis of subtle thyroid dysfunction in a sizable sample of psychiatric inpatients with prominent depressive symptoms.

Adolescent↗
PubMed1977

Studies on thyroid and hypophysary thyrotrophic hormone (TSH) in Down syndrome.

Serum TSH was studied in 22 patients with Down syndrome, from 4 to 15 years old. In 6 of these patients radioidine uptake by thyroid gland after 2 and 24 hours of administration and clearance rates before and after TSH stimulus (10 mul-IM) were measured. Results show that serum TSH was normal in 17 patients and above normal limits in 5 patients. Thyroid uptake after 2 hours as well clearance rates, both below normal, had a response to TSH stimulus with normal or below values. These data along with previous reports, suggest, that in children with Down syndrome, there is a thyroid dysfunction in which a slow response no TSH stimulus seems to be the basic defect.

Adolescent↗
PubMed1986

A quantitative assessment of thyroid histopathology of herring gulls (Larus argentatus) from the Great Lakes and a hypothesis on the causal role of environmental contaminants.

Thyroids from 213 adult herring gulls of both sexes were collected during incubation from nine colonies in the Great Lakes basin of eastern North America between 1974 and 1983, and from a single colony in the Bay of Fundy from 1977 to 1982. Qualitative and quantitative histological assessment revealed that the majority of the gulls from the Great Lakes basin suffered from goiter. These thyroids had a greater mass than those from the Bay of Fundy, and were microfollicular and frequently hyperplastic. The histopathology was similar to that previously observed in Pacific salmon from the Great Lakes. These findings are consistent wit a forage fish-borne goitrogenic etiology other than, or in addition to, iodine deficiency. Temporal and spatial differences in the severity of thyroid dysfunction are consistent with the hypothesis that polyhalogenated hydrocarbons are responsible for the goiter development and thyrotoxic effects observed in herring gulls from the Great Lakes area.

Animals↗
PubMed1999

[Therapy of amiodarone-induced thyrotoxicosis and hypothyroidism].

Pathogenesis, diagnostic procedures and therapy of amiodarone-induced thyrotoxicosis (AIT) and hypothyroidism (AIH) are briefly discussed. Diagnosis of AIT and AIT is based on the classical signs and symptoms of thyroid dysfunction, although oligosymptomatic cases may occur, and on laboratory tests such as TSH, fT4 und fT3. In AIT, radioiodine therapy usually is no option due to the high iodine content of amiodarone. Besides withdrawal of amiodarone, medical and surgical treatment remain the only modalities. If arrhythmia can be controlled by an alternative treatment, amiodarone should be discontinued although this will not immediately restore normal thyroid function. For medical treatment, thionamides, perchlorate (not available in Switzerland), steroids (mainly for type II and mixed forms of AIT) and lithium (only for severe cases) are available. Surgery is a valid therapeutical option for severe forms of AIT which cannot be controlled adequately by medical treatment. The main advantage of surgical therapy of AIT is the rapid correction of thyrotoxicosis combined with the possibility to continue amiodarone, if it is necessary and effective. With AIH, amiodarone does not have to be stopped, if indicated and effective, and L-thyroxine is the therapy of choice.

Algorithms↗
PubMed2001

Thyroid function test abnormalities in newly admitted psychiatric patients residing in an iodine-deficient area: patterns and clinical significance.

OBJECTIVE: The prevalence of abnormal in-vitro thyroid function tests in psychiatric in-patients may be as high as 24%. Thus far, however, there is only limited data addressing the underlying causes of these abnormal test results, i.e. how often they can be attributed to genuine thyroid disease. METHOD: We conducted an observational study of all in-patients admitted to our institution during 1 calendar year running analyses of total thyroxin (T4), free thyroxin index (FTI) and thyroid-stimulating hormone (TSH). Patients with abnormal test results were classified according to an algorithm which had been established previously. RESULTS: In 243 of 880 patients with in-vitro thyroid function analysis, at least one concentration of either T4, FTI or TSH was found to be outside the reference range. Work-up according to the algorithm was completed in 848 patients; alterations were classified as representing thyroid dysfunction in 100 (41% of patients with abnormal test results), non-specific findings in 92 (38%), influence of ingested drugs in 18 (7%) and of severe physical disease in 1 (0.4%). As measures of T4 and/or FTI provided no essential information in 854 patients (97% of tested), we found that in most cases the determination of TSH alone was sufficient for demonstrating normal thyroid function. CONCLUSION: In 27.6% of newly admitted patients living in an iodine-deficient area, at least one abnormal result in either T4, FTI or TSH values was found. Genuine thyroid disease was found in slightly less than half the patients with an abnormal value.

Adolescent↗
PubMed2006

Thyroid disorders during interferon alpha therapy in 625 patients with chronic hepatitis C: a prospective cohort study.

AIM: to report the prevalence, risk factors, management and long-term outcome of thyroid disorders caused by INFalpha in patients with chronic hepatitis C. PATIENTS AND METHODS: From January 1991 to December 2004, 625 patients with chronic hepatitis C underwent INFalpha therapy. TSH assay was normal and antithyroperoxidase antibodies (anti-TPO) was performed before onset antiviral treatment; then TSH was performed every 2 months in all patients during therapy, and every 3 months after treatment. RESULTS: 58 patients developed thyroid disorder (8.9%). Mean age was 50.6+/-13 years; sex ratio: 1 M/2 F; the anti-TPO antibodies were positive before onset antiviral treatment in 9 patients (13.8%). 26 patients developed hypothyroidism (44.8%), 9 patients developed hyperthyroidism (15.5%) and among them 3 cases of Grave's disease. Biphasic thyroiditis occurred in 21 patients (36.2%), anti-TPO increase during treatment in 2 patients (3.5%) without hypothyroidism. The dysthyroidism was more frequent in risk in female gender (p<0.05) and in the group with positive antiTPO antibodies before treatment (p<0.02). CONCLUSION: Female gender and positive antiTPO antibodies are the predictive factors of development of the thyroid dysfunction during INFalpha therapy.

Antiviral Agents↗
PubMed2006

Cardio-protective role of terazosin is possibly mediated through alteration in thyroid function.

An investigation was made to reveal the possible involvement of thyroid hormones, if any, in terazosin (an alfa-1 adrenergic receptor blocker) induced alterations in tissue lipid peroxidation (LPO) and in the concentration of different serum lipids. We determined the impact of terazosin on the changes in hypercholesterolemic (CCT) diet induced thyroid dysfunction; cardiac, renal and hepatic LPO and on serum glucose concentration in female Wister rats. Simultaneously levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), creatinine, alkaline phosphatase (ALP) activity, hepatic glycogen synthesis and total daily food consumption were studied as supporting parameters. While a decrease in the level of serum thyroid hormones, HDL-C and in hepatic glycogen content, was observed in CCT diet fed animals; it increased the concentration of other serum lipids, glucose and creatinine; ALP activity; tissue and serum LPO. However, following terazosin administration for 15 days to CCT diet fed animals, status of thyroid hormones and all other thyroid dependent parameters were reversed suggesting that the drug might be acting through an alteration in the thyroid functions.

Adrenergic alpha-Antagonists↗
PubMed1983

Alzheimer's disease: genetic aspects and associated clinical disorders.

Genetic aspects and associated clinical disorders were studied in a consecutive series of 68 men and women in whom Alzheimer's disease appeared at or before age 70. Secondary cases of dementia were found in 17 (25%) of the families, affecting 22 of the probands' siblings and parents. The cumulative incidence of Alzheimer's disease in these relatives was approximately 14% at age 75. An increased frequency of Down's syndrome was observed among relatives of the probands: a rate of 3.6 per 1,000, as compared with an expected rate of 1.3 per 1,000. A history of thyroid disease was established in 9 (19.6%) of the 46 female probands, a frequency greater than that reported in the general population. There was no excess of hematological malignancies among the blood relatives, and parental age at the time of birth of the probands did not differ from the norm. The results of this study indicate that early-onset Alzheimer's disease is associated with a genetic factor manifested in a substantial familial aggregation of dementia, a probable excess of Down's syndrome in the probands' relatives, and a possible association with thyroid dysfunction in women with this form of dementia.

Aged↗
PubMed1991

Effects of subclinical hyperthyroidism on renal handling of water and electrolytes in patients with nodular goiter.

Evidence is beginning to accumulate that minor degrees of hyperthyroidism lead to adverse effects in various tissues, even though clinically the patients are euthyroid. To determine whether these anomalies in thyroid function have deleterious effects on renal function and electrolyte metabolism, the plasma concentrations of electrolytes, urea, and creatinine, the renal handling of water and sodium, and the urinary excretion of these substances were measured in patients with nodular goiter who were displaying stable subclinical hyperthyroidism. The studies were carried out before and after correcting the thyroid dysfunction. Restoration of euthyroidism did not modify any of the renal function parameters studied and did not cause changes in blood analyte levels. The data show that treatment of minor degrees of hyperthyroidism does not have any effects on renal function and electrolyte metabolism, and confirm the well-known capacity of the kidney to adjust its functions to changes induced by an abnormal secretion of thyroid hormones.

Adult↗
PubMed1996

Pendred syndrome maps to chromosome 7q21-34 and is caused by an intrinsic defect in thyroid iodine organification.

Exactly 100 years ago, in 1896, Pendred first described the association of congenital deafness with thyroid goitre (MM#274600). The incidence of Pendred syndrome is estimated at 7.5-10/100,000, and may be responsible for as much as 10% of hereditary deafness. The cause of the congenital deafness in Pendred syndrome is obscure, although a Mondini type malformation of the cochlea exists in some patients. The reason for the association between the thyroid and cochlear defects is similarly obscure, leading some investigators to suggest that the two recessive defects may be occurring together by chance in highly consanguineous families. An in vivo defect in thyroid iodine organification in Pendred syndrome patients has been reported. However, the molecular basis of this defect is unknown and the presence of an intrinsic thyroidal defect has not been conclusively demonstrated. We have adopted a genetic linkage study as a first step towards identifying the gene. The availability of an inbred Pendred syndrome kindred allowed us to utilize an efficient DNA pooling strategy to perform a genome-wide linkage search for the disease locus. In this way, we have mapped the disease locus to an approximately 9-cM interval between GATA23F5 and D7S687 on chromosome 7. In addition, we demonstrate an intrinsic thyroid iodine organification defect in a patient's thyroid cells as the cause of the thyroid dysfunction.

Chromosome Mapping↗
PubMed2000

Animal models of Graves' disease.

Graves' disease (GD) is an autoimmune condition in which goitre and hyperthyroidism are induced by thyroid stimulating antibodies (TSAB) which mimic the action of thyrotrophin (TSH). The target of the autoimmune response is the thyrotrophin receptor (TSHR) and, since its cloning, a number of differing approaches have been adopted in an attempt to develop an animal model of GD. Methods in which synthetic peptides or fragments of the receptor produced in bacteria or insect cells have been injected into animals together with immunological adjuvants have had only limited success in inducing some of the signs and symptoms of GD. Genetic immunisation resulted in thyroiditis in the majority, but TSAB formation in only a minority, of treated inbred mice. Transfer of receptor in vitro primed T cells to syngeneic naive recipients, with priming either using a bacterial fusion protein or genetic immunisation, induced destructive thyroiditis in non-obese diabetic (NOD) mice but lymphocytic thyroiditis in BALBc mice. Furthermore, the orbits of 17/22 of the BALBc animals, but not the NOD animals, with thyroiditis had orbital changes similar to those seen in thyroid eye disease. TSAB and elevated thyroxine levels were induced in AKR/N mice injected with fibroblasts expressing the full length human TSHR and murine major histocompatibility complex (MHC) class II homologous to the recipient mice. No thyroiditis was induced but preliminary results from a different group using the same protocol suggest that receptor autoantibodies and thyroid dysfunction could be transferred using T cells primed in vitro with the receptor and MHC-II expressing cells. The majority of the studies described above have studied inbred mouse strains. In a novel departure, the NMR outbred strain has been treated by genetic immunisation with very promising results, including the induction of increased thyroxine levels in 4/30 female mice, accompanied by TSAB in addition to thyroiditis, and with signs of hyperactivity and orbital pathology. This review discusses the various protocols together with the information regarding the pathogenesis of GD which each has contributed, and concludes with an evaluation of how close we are to mimicking this polygenic, multifactorial disease.

Animals↗
PubMed1999

[The history of science with regard to the thyroid gland (1800-1960)].

UNLABELLED: This review describes the changing medical perspectives from 1800 to 1960 with regard to the thyroid gland. During the XIXth century, clinical medicine identified the different thyroid diseases: goitrous cretinism (1802), Graves disease (1835-1856) and myxedema (acquired or post-surgery 1888). These clinical entities facilitated the construction of the first complete schema of endocrinology: one gland, one internal secretion and one replacement therapy with an organ extract. With the emergence of biochemistry at the beginning of the XXth century, the first thyroid hormone--thyroxin--was identified. Alternative medical treatments aimed at blocking thyroid secretion, were proposed in 1940 leading to the use of radioiodine and antithyroid compounds which were also used in physiological studies. From 1940 to 1970, the application of radioiodine shed a completely new light on thyroid physiopathology. The main transformations brought about by this tool were the knowledge of radioiodine uptake mechanisms, basis of its therapeutic effect, complete identification of thyroid hormonosynthesis, serum transport of thyroid hormones and thyroid imaging. More recently immunological and molecular paradigms changed the understanding of thyroid diseases. In spite of novel definitions, there was no therapeutic revolution like those introduced by iodine treatment (1820) thyroid surgery (1880), thyroid extract (1893) radioiodine and antithyroid drugs (1940), underlining the actual therapeutic stagnation. CONCLUSION: The prevalence of sub-clinical thyroid dysfunction was 8%. No male subject was affected. The prevalence of nodule was close to 15%. Contrary to the literature, we have not found high incidence of immunological abnormalities in this old population.

Goiter↗
PubMed1998

Effect of endotoxin on hormonal responses to thyrotropin and thyrotropin-releasing hormone in dogs.

OBJECTIVE: To determine whether administration of endotoxin affects thyroid gland function in dogs. ANIMALS: 24 Beagles. PROCEDURE: Dogs were given thyrotropin (TSH) or thyrotropin-releasing hormone (TRH) on 2 occasions. Twenty-four hours before the second challenge with TSH or TRH, all dogs were given 5 micrograms of endotoxin/kg of body weight. Serum concentrations of thyroxine (T4), free T4 (fT4), 3,3',5-triiodothyronine (T3), reverse T3, autoantibodies to T3, and plasma concentrations of ACTH and cortisol were determined. RESULTS: Treatment with endotoxin was associated with reduced baseline concentration of serum T3 and increased baseline concentration of reverse T3 and free T4. Endotoxin treatment resulted in reduced peak serum concentration of T4 after TSH and TRH. However, peak serum concentration of fT4 after TSH and TRH were not affected by endotoxin. CONCLUSIONS: A single dose of endotoxin affects several aspects of thyroid gland function in dogs, including T4 binding, deiodinase activity, and the thyroidal response to TSH and TRH. CLINICAL RELEVANCE: Acute or chronic nonthyroidal illness may affect thyroid gland function in dogs. Determination of fT4 concentration may provide a means of differentiating the effects of nonthyroidal illness from those of thyroid dysfunction, because endotoxin treatment was associated with increased baseline serum free T4 concentration and unchanged peak serum fT4 concentration after administration of TSH or TRH.

Adrenocorticotropic Hormone↗
PubMed2001

Of mice and men and elephants: metabolic rate sets glomerular filtration rate.

Allometric scaling deals with the functional consequences of changes in size or scale among geometrically dissimilar animals (ie, animals differing in proportions). For adult mammals ranging in size and proportion from mouse to elephant, the data describe an interdependent set of functions consisting of metabolism (measured as metabolic rate), glomerular filtration rate (GFR), effective renal plasma flow, excretion of nitrogenous waste products, cardiac output, and pulmonary function-related variables. Within this set of functions, evidence indicates that metabolic rate is the primary process. One important design feature is given by the ratio of GFR to metabolic rate. Because this ratio is independent of size, it can be generalized to all mammals in this series. The numeric value of this ratio gives the optimal GFR for each unit of metabolic rate. A simple hypothesis is proposed: metabolic rate, the primary process, sets GFR. This relationship is unidirectional. A decrease in GFR, for example, caused by nephron loss, should not lead to a change in metabolic rate. This hypothesis was tested in four natural experiments: human growth and development, thyroid dysfunction, chronic renal failure, and hibernation. The results are consistent with this hypothesis.

Age Factors↗