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Results for “THYROID DISEASES”

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PubMed1972

Thyroid disease and other maternal factors in mongolism.

One hundred women, who at the age of 35 years or more had had a child with mongolism, were investigated to discover any relation between thyroid disease and autoimmunity and mongolism and to search for other possible etiological factors. They were compared with 100 matched controls. The mothers of mongoloid children had a higher incidence of thyroid disease, either hypo- or hyperactivity (11 compared with three in the control group). The proportion with thyroglobulin antibodies was the same (18.8%) in both groups and mean serum protein-bound iodine levels were similar. There was no difference in reproductive history, diseases other than of the thyroid, frequency of previous pelvic and abdominal x-rays or incidence of infectious hepatitis during the year prior to conception.

Adult↗
PubMed2001

Clustering of autoimmune thyroid diseases in children and adolescents: a study of 66 families.

Autoimmune thyroid diseases (AITD) are known to be clustered in families, but to what extent this occurs in childhood and adolescence is not well defined. In order to establish the prevalence of AITD in the siblings of affected children and adolescents, we examined 73 siblings from 66 families selected on the basis of a pediatric index patient. Sixty-six families, including a total of 146 offspring, were selected on the basis of diagnosis of chronic lymphocytic thyroiditis (CLT) (n = 55) or Graves' disease (GD) (n = 11). Among the 73 siblings examined, 20 new cases of CLT (27%) were detected. L-Thyroxine therapy was required in 4/20. History of AITD was recorded in 24/66 mothers (36%), and in two fathers. Overall in these families, considering both the index patients and the new patients, 86/141 (61%) children and adolescents were affected with AITD, with a female/male ratio of 3.3:1. Our study confirms that AITD clusters in families with a high prevalence in the siblings of affected children and adolescents. These children should be followed in order to avoid undiagnosed hypothyroidism. Prospective studies are warranted to identify predictive factors for overt thyroid disease.

Adolescent↗
PubMed2005

[Surgical treatment of thyroid gland diseases].

Thyroid gland surgery is a treatment of choice for morphological changes of the gland, although patients with some functional problems, indicated from endocrynologist, underwent surgery. The goal is to analyze retrospectively patients with thyroid gland diseases according to incidence and surgery. We analyzed surgically treated patients with thyroid gland disease at ENT clinic in Sarajevo in last 5 years. There were 339 patients, 312 (92%) were patients with benign diseases, and 17 (8%) patients with malignant disease. Malignant diseases of thyroid gland were treated in two acts and benign forms in one act. Injury of recurrent nerve was not encountered, neither was postoperative hypoparathyroidism.

Adult↗
PubMed2001

[Surgical treatment of thyroid diseases at the Surgical Clinic of the University Hospital of Plzen 1994-2000].

The authors operated in 1994-2000 at the Surgical Clinic, Faculty Hospital Plzen a total of 793 patients on account of thyroid disease. This group comprised 57 patients with malignant thyroid disease. The mean age of the operated patients was 48.8 years (range 12-89 years). Three patients (0.38%) died within 30 days after operation. The postoperative morbidity was 6.1%. A lesion of the recurrent nerve was recorded during the postoperative period in 24 patients (3.03%) and had a declining trend. Postoperative hypoparathyroidism was recorded in 5.8% (n = 46) injuries of the neighbouring organs in 1.02% (n = 8), oedema of the larynx in 18 patients, i.e. 2.3%. On the whole the authors observed a decline of postoperative complications during the investigation period, the number being lowest in 2000 associated with the number of performed thyroid operations and a change of the surgical strategy.

Adolescent↗
PubMed2002

Thyroid disease and lipids.

The composition and the transport of lipoproteins are seriously disturbed in thyroid diseases. Overt hypothyroidism is characterized by hypercholesterolaemia and a marked increase in low-density lipoproteins (LDL) and apolipoprotein B (apo A) because of a decreased fractional clearance of LDL by a reduced number of LDL receptors in the liver. The high-density lipoprotein (HDL) levels are normal or even elevated in severe hypothyroidism because of decreased activity of cholesteryl-ester transfer protein (CETP) and hepatic lipase (HL), which are enzymes regulated by thyroid hormones. The low activity of CETP, and more specifically of HL, results in reduced transport of cholesteryl esters from HDL(2) to very low-density lipoproteins (VLDL) and intermediate low-density lipoprotein (IDL), and reduced transport of HDL(2) to HDL(3). Moreover, hypothyroidism increases the oxidation of plasma cholesterol mainly because of an altered pattern of binding and to the increased levels of cholesterol, which presents a substrate for the oxidative stress. Cardiac oxygen consumption is reduced in hypothyroidism. This reduction is associated with increased peripheral resistance and reduced contractility. Hypothyroidism is often accompanied by diastolic hypertension that, in conjunction with the dyslipidemia, may promote atherosclerosis. However, thyroxine therapy, in a thyrotropin (TSH)-suppressive dose, usually leads to a considerable improvement of the lipid profile. The changes in lipoproteins are correlated with changes in free thyroxine (FT(4)) levels. Hyperthyroidism exhibits an enhanced excretion of cholesterol and an increased turnover of LDL resulting in a decrease of total and LDL cholesterol, whereas HDL are decreased or not affected. The action of thyroid hormone on Lp(a) lipoprotein is still debated, because both decrease or no changes have been reported. The discrepancies are mostly because of genetic polymorphism of apo(a) and to the differences between the various study groups. Subclinical hypothyroidism (SH) is associated with lipid disorders that are characterized by normal or slightly elevated total cholesterol levels, increased LDL, and lower HDL. Moreover, SH has been associated with endothelium dysfunction, aortic atherosclerosis, and myocardial infarction. Lipid disorders exhibit great individual variability. Nevertheless, they might be a link, although it has not been proved, between SH and atherosclerosis.

Humans↗
PubMed1989

Total thyroidectomy for benign thyroid disease: when and why.

Surgical complications after total thyroidectomy (TT) and subtotal thyroidectomy (STT) are analysed in a series of 364 patients operated on over a 36-month period. All operations were carried out because of the following 3 groups of disease: malignant tumors, multinodular goiter and Graves' disease. The difference among the incidence of surgical complications resulted to be not statistically significant when as discriminating factors the type of surgery or disease were used, while the difference was statistically significant when the results obtained in the 2 groups of patients operated only once or undergoing reoperative surgery for recurrence, were compared. Based on these observations, the surgical approach consistent with the above mentioned types of thyroid disease is reported, and the preference for total thyroidectomy is justified to a larger extent by what has been done to-date also in case of benign thyroid disease. The choice of the type of surgery should always be made, based on a careful clinical and intraoperative assessment of each case.

Adult↗
PubMed1995

Anti 70 kDa heat shock protein antibodies in sera of patients affected by autoimmune and non-autoimmune thyroid diseases.

Twenty eight patients (25F, 3M) affected by autoimmune and non-autoimmune thyroid diseases were studied. HSP 70 antibodies were present in 21.4% of patients. Five of them were affected by Graves' disease and one by De Quervain's thyroiditis. The HSP 70 antibodies mean values of patients were significantly higher than the normals (p < 0.05). This datum was confirmed by Western blotting. The presence of HSP 70 antibodies in the sera of those patients may support the link between the protein and the thyroid autoimmune processes.

Adult↗
PubMed2003

Association study of autoimmune thyroid disease at 5q23-q33 in Japanese patients.

As part of a genome scan to locate familial Graves' disease (GD) and Hashimoto's thyroiditis (HT) genes, an autoimmune thyroid disease (AITD) susceptibility locus has recently been identified at 5q31-q33 in a Japanese population. We performed an association study using six microsatellite markers located at this locus in a set of 440 unrelated Japanese AITD patients and 218 Japanese controls. We found significant allelic association between AITD and three markers located in 5q23-q33. GD demonstrated significant associations with two of these markers, while HT did not show significant associations with any markers. Further, when patients with GD were stratified according to clinical manifestations, the association was significantly different from the other subgroup of each category. These findings suggest the presence of susceptible genes of AITD, especially distinct subgroups of GD, in or near 5q23-q33.

Alleles↗
PubMedDate not supplied

[Proceedings: Peroxydase activity in benign thyroid diseases and in experimental rat goiters (author's transl)].

Peroxydase activity in various benign thyroid diseases has been investigated. In hyperthyroid patients treated with antithyroid drugs, the observed increase in iodide-peroxydase activity (7 times that of normal tissue) is double than that of the DNA content. In goiter, the activity is 3 times that of normal tissue while the DNA content is unchanged. These results are in agreement with those obtained in rats maintained on a low iodine diet suggesting that high cellular enzymatic activity is due to specific enzyme induction in excess of cell proliferation and protein synthesis.

Animals↗
PubMed2004

Quality specifications in thyroid diseases.

BACKGROUND: Laboratory tests to support the diagnosis and management of thyroid diseases have undergone significant changes with the introduction of highly sensitive assays for thyroid stimulating hormone (TSH) and free T4 and T3 concentrations in plasma. Given the importance of these measurements, quality specifications are needed to ensure accurate results. Goals for precision and accuracy are available based on known intraindividual and interindividual biological variation. METHODS: Results of external quality assurance (EQA) schemes are sufficient to document precision goals but survey materials are not commutable for use in determining bias or detect the presence of unusual antibodies on a case-by-case basis. Because TSH concentrations are inversely related to free T4, this physiologic relationship can be exploited for quality assurance purposes. RESULTS: Significant discordance between this relationship can be caused by subclinical and potentially unrecognized disease, dysequilibrium caused by recent therapy, the presence of abnormal binding proteins or protein binding competitor drugs, and antibody interferences such as human antimouse antibody (HAMA) or rheumatoid factor. CONCLUSION: A mechanism to automatically track discordances for subsequent follow and investigation can be an effective part of a quality assurance program for thyroid hormone measurements.

Antibodies, Heterophile↗
PubMed1992

Preferential use of T-cell receptor V genes in human autoimmune thyroid disease.

We review here our analyses of hTcR V gene activity within the thyroid glands of patients with autoimmune thyroid disease. Our data, based on thyroid aspiration specimens, indicate that early in the onset of Graves' disease there is a marked restriction in both hTcR V alpha and V beta gene families utilized by intrathyroidal T-cells. Later, however, and as seen in surgical thyroid specimens from patients with long term disease, there appears to be a loss of V beta restriction for unclear reasons. In contrast, patients with Hashimoto's thyroiditis are usually diagnosed later in the natural history of the disease and appear to show much less hTcR V gene family restriction. The mechanisms driving the use of few and many hTcR V genes within the thyroid gland are likely to be complex and may reveal important insights into disease pathogenesis.

Autoimmune Diseases↗
PubMed1995

Proliferative responses of T-cells to thyroid antigens and synthetic thyroid peroxidase peptides in autoimmune thyroid disease.

We studied the immune responses of 33 patients with autoimmune thyroid disease (AITD; including 17 with Hashimoto's thyroiditis and 16 with Graves' disease), 5 patients with non-AITD, 12 control subjects (CS), and 2 subjects with a family history of autoimmunity to the main thyroid antigens. These antigens included thyroid peroxidase (TPO), thyroglobulin (Tg), TSH receptor (TSH-R), and 13 overlapping TPO peptides. T-cell lines (TCL) were isolated from peripheral blood mononuclear cells (PBMC) after incubation with TPO, Tg, or a protein derivative of tuberculin (PPD). PBMC and TCL were used in a 3- to 5-day microproliferation assay. Peripheral lymphocytes from most AITD patients responded with a stimulation index of 3 or more to TPO, Tg, and/or TSH-R (60-88%) as well as to two or more TPO peptides. Lymphocytes from 3 of 5 patients with non-AITD and 2 subjects with a family history of autoimmunity were also reactive to thyroid antigens. TPO TCL showed a high proliferative response to TPO and its peptides, whereas Tg TCL were less reactive and PPD TCL were nonreactive to these antigens. Six of the 13 peptides tested produced highly significant stimulation in PBMC (CS, 0-17%; AITD, 60-92%) and TPO TCL (73-91%). The amino acid sequences of these putative epitopes were located in TPO regions 100-119, 211-223, 261-275, 420-434, 625-644, and 882-901. These results demonstrate T-cell responses to the main thyroid antigens, including TPO, Tg, and TSH-R, and confirm the heterogeneity of TPO T-cell epitopes in patients with AITD. Amino acid residues 100-119, 420-434, 625-644, and 882-901 are the most common sites recognized by TPO TCL, indicating that they may be immunogenic epitopes in AITD.

Adult↗
PubMed1992

A perspective on human autoimmune thyroid disease: is there an abnormality of the target cell which predisposes to the disorder?

It has been suggested recently that autoimmunity could be regarded as a physiological response of the normal immune system to autoantigens caught up in an inflammatory response to viral or bacterial antigen expressed in the target tissue. Other theories to explain autoimmunity include molecular mimicry whereby a viral or microbial hapten similar to an autoantigen initiates the production of autoantibodies that cross react with an autoantigen, with a subsequent immune response reacting with autologous cell structures which are homologous with the particular microorganism. There has also been a suggestion that there may be a genetic abnormality of the target cell which is necessary for the initiation of autoimmune thyroid disease. The present review examines these proposals and provides evidence against an antigen-driven origin for autoimmune thyroid disease (AITD). Currently, there is no valid evidence for viral involvement, and likewise the evidence for molecular mimicry as an initiating factor does not hold up to scrutiny. While a genetic abnormality of the thyrocyte may be important in certain animal models of AITD, in the human there is no evidence for such an abnormality. Evidence that AITD is derived from a disturbance of immunoregulatory mechanisms has been documented elsewhere and would appear to be the most appropriate explanation for these disorders. The immunoregulatory disturbance itself may be related to an abnormality of the mechanism of specific antigen (i.e. normal autoantigen) presentation to appropriately induce T lymphocytes and that theory will require further illumination.

Animals↗