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At least 649 records · Page 36Linked to original sources
PubMed1978

Occult thyroid disease in an elderly hospitalized population.

Measurements of thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), and T3 talc uptake (T3TU) were performed on 425 hospitalized patients over 60 years of age. Unsuspected thyroid disease was found in 10 patients (2.4%); 9 were hypothyroid and 1 hyperthyroid. Another 11% of the population had abnormal T4 or TSH levels but were not proved to have thyroid disease. Repeat measurements in 10 of 40 patients with low serum T4 concentrations showed a return of the tests to normal. The low T4 levels occurred in patients who were seriously ill and were usually associated with low T3TU values. Low serum T3 concentrations were observed in 32 of the patients. Although we found TSH to be the most useful test in the diagnosis of hypothyroidism, it is a relatively expensive test and is not helpful in screening for hyperthyroidism. The present results suggest that the best single test for screening for occult thyroid disease is a serum T4 measurement. We recommend a T4 test on all hospitalized patients over age 60 years. Serum should be held in the laboratory for measurement of TSH concentration if the T4 result is below 6.5 micrograms/dl. A T3 resin or talc uptake and a serum T3 measurement should be performed to rule out hyperthyroidism if the serum T4 concentration is elevated. This regimen will identify virtually all cases of occult thyroid disease.

Age Factors↗
PubMed1991

[Interferon-alpha and gamma product in peripheral blood of patients with thyroid diseases].

To investigate the immunological process in various thyroid disease, we measured interferon-alpha, -gamma (IFN-alpha,-gamma, natural killer (NK) activity, and lymphocyte subsets in the peripheral blood of 27 patients with Basedow's disease (BD) (M:F = 9:18), 8 with Hashimoto's thyroiditis (HT) (2:6), 5 with idiopathic hypothyroidism (1HT) (1:4), and normal controls (C). IFN-alpha, -gamma levels were measured by bioassay with Dye-uptake method, and NK activity was measured by the LDH method. The mean +/- SD levels of IFN-gamma in BD, HT, IHT, and C (N = 217) were 173.9 +/- 88.0, 288.0 +/- 134.9, 120.4 +/- 38.0 and 173.9 +/- 88.01U/ml, respectively. The IFN-gamma level was higher in HT (p less than 0.05) than in controls, and lower in BD (p less than 0.02). Moreover, this IFN-gamma level did not correspond with the titers of thyroid hormones; TSH, anti-microsome antibody, and anti-TSH-receptor antibody in peripheral blood. However, IFN-alpha levels and NK activity in the patients of every group were similar to those in controls. The ratios of lymphocyte subsets of peripheral blood were measured by cytofluorometry with monoclonal antibodies. The mean +/- SD levels of T cells in BD, HT, IHT and C were 75.9 +/- 7.0, 83.4 +/- 7.2, 85.2 +/- 5.7, 82.3 +/- 5.8%, and those of B cells were 17.5 +/- 6.1, 10.9 +/- 4.2, 8.0 +/- 5.8, 10.9 +/- 5.0%, respectively. The ratio of T cells was higher in IHT (p less than 0.05) and lower in BD (p less than 0.01) than in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Analysis of MHC genes in a Tunisian isolate with autoimmune thyroid diseases: implication of TNF -308 gene polymorphism.

Autoimmune thyroid diseases (AITDs), which include Hashimoto thyroiditis (HT), Graves' disease (GD) and primary idiopathic myxoedema (PIM), are recognized as multifactorial diseases. In this study, we have examined single and haplotypic genetic variation across the major histocompatibility complex (MHC) in a Tunisian isolate with a high prevalence of AITDs (62 patients: 32 with GD, 9 with HT and 21 with PIM). Genotyping was performed for HLA class I and II alleles as well as polymorphisms within tumor necrosis factor (TNF), lymphotoxin alpha (TLalpha) and heat shock protein (HSP70-02 and HSP70-hom) genes. Our results showed association of HLA-A2-B50-TNF 2 haplotype with AITDs (p = 0.045). Linkage analysis using Simwalk2 program has shown significant result with TNF -308 gene polymorphism (p = 0.03). The FBAT has given evidence for genetic association with TNF -308 and HLA-DR gene polymorphisms. TNF 2 allele was associated with GD (p = 0.0011), whereas TNF 1, HLA-DR11 and DR12 (p = 0.0039, p = 0.00089 and p = 0.0056, respectively) were rather implicated in HT pathogenesis. Results found by TDT-STDT have confirmed the involvement of the TNF -308 gene polymorphism in AITD pathogenesis (p < 10(-9)).

Adolescent↗
PubMed1992

Proliferative responses of peripheral blood mononuclear cells from patients with autoimmune thyroid diseases to synthetic peptide epitopes of human thyroid peroxidase.

In order to analyze T cell epitopes of human thyroid peroxidase (TPO), 60 peptides based on the sequence of TPO were synthesized and used as antigens in a peripheral blood mononuclear cell (PBMC)-proliferation assay. PBMCs were obtained from 19 patients with Graves' disease, 19 patients with Hashimoto's thyroiditis, and 24 normal subjects. Significant proliferation of PBMC to these peptides occurred only among the autoimmune thyroid disease (AITD) patients, whereas normal subjects did not respond to any of the peptides with a stimulation index over 2. Many peptides induced isolated positive responses and eight produced stimulation of PBMCs from multiple patients on comparison to control PBMC responses. To confirm the significance of reactivity to the peptides PBMCs from four patients were studied on two occasions, and the proliferative responses found to be reproducible. Four peptides, designated according to the amino acid sequence as p110-129, p211-230, p842-861, and p882-901, stimulated patients' PBMCs in a dose-dependent manner. The optimal concentration was 10 micrograms/ml. An anti-HLA-DR monoclonal antibody directed against a monomorphic determinant of the DR molecule was able to block the responses. A significant correlation was found between the PBMC responses to these peptides and responses to microsomal antigen (McAg)/TPO. These data suggest that four peptides corresponding to the amino acid sequences 110-129, 211-230, 842-861 and 882-901 are T cell epitopes of TPO.

Adult↗
PubMed1984

Autoimmune thyroid disease: an integrated concept of Graves' and Hashimoto's diseases.

Graves' disease and Hashimoto's thyroiditis have been previously considered separate clinical and pathologic entities. Current knowledge of the autoimmune cause of specific systemic syndromes has been applied to these seemingly dissimilar diseases and now permit evolution of a unified integrated concept for considering them as two subsets of a single pathologic process. Experimental and clinical data now support the thesis that autoimmune thyroid disease is a genetically conditioned immunologic dysfunction, perhaps an abnormality of suppressor lymphocytes that results in production of humoral and tissue antibodies directed against thyroid gland cells and receptors of other somatic tissues. Thyroid autoantibodies possess hormonally stimulatory qualities and cytotoxic (inflammatory or destructive) properties. They may be present singly or together in the same individual with resulting diverse clinical and biochemical patterns depending upon the predominance or concordance of specific antibodies. Further, antibodies in autoimmune thyroid disease may be directed against other somatic structures such as ocular muscle, skin, hair, pigment cells, hematologic organs, or other endocrine glands. The immune etiology appears to predispose to nonendocrine systemic autoimmune disorders that coincide with thyroid disease. It is not clear at this time how genetic factors influence the onset, course, or ultimate outcome of autoimmune thyroid disease or why certain associated immunopathies tend to cluster with one or the other of these syndromes. Our understanding of the immune etiology common to Graves' and Hashimoto's diseases permits a more precise definition of the terms hyperthyroidism and thyrotoxicosis, the former denoting a pathologic goitrous phenomenon and the latter, a peripheral tissue manifestation of cellular receptor site excess of thyroid hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Childhood thyroid diseases around Chernobyl evaluated by ultrasound examination and fine needle aspiration cytology.

Screening by ultrasound examination and fine-needle aspiration cytological biopsy (FNA) was conducted in five regions in Belarus, Ukraine, and Russia to investigate the prevalence of childhood thyroid diseases around Chernobyl. Gomel, Zhitomir, Kiev, and the western area of Bryansk are the administrative regions where severe radioactive contamination occurred. The subjects from Mogilev, where contamination was relatively low, served as controls. Among 55,054 subjects (26,406 boys and 28,648 girls), the prevalence of ultrasonographic thyroid abnormalities such as nodule, cyst, and abnormal echogenity was significantly higher in the regions with severe contamination than in Mogilev. Of the 1,396 children showing echographic thyroid abnormalities 197 were selected for FNA, and a sample was successfully obtained for diagnosis from 171 (51 boys and 120 girls) of the 197 subjects. The aspirate was insufficient for diagnosis in the remaining 26 subjects. Thyroid cancer was encountered in four children (2.3%) from the contaminated regions, two children being from Gomel. The other thyroid diseases were follicular neoplasm, 6.4%; adenomatous goiter, 18.7%; chronic thyroiditis, 31.0%; and cyst, 24.0%, suggesting that a major cause of thyroid nodularity is nonneoplastic changes, mainly chronic thyroiditis and cysts. These results will serve as an important data base for further analyses and suggest that childhood thyroid diseases, including both neoplasms and immunological disorders, are consequences of radioactive fallout.

Adenocarcinoma, Follicular↗
PubMed1977

[Iatrogenic thyroid diseases].

The authors investigated the patients of an ambulant dispensary for patients with diseases of the thyroid gland in the endemic district Dresden for cause, kind and frequency of iatrogenic diseases of the thyroid gland and in 13.1% of the patients they found such lesions which above all are conditioned by wrong use of thyroid hormones and thyreostatics. The foundation of special dispensaries is demanded.

Dose-Response Relationship, Drug↗
PubMed1987

Amylase in thyroid tissues from normal and various thyroid diseases. Biochemical and immunohistochemical study.

Amylase activity was measured in thyroid tissues of various thyroid diseases and was analysed electrophoretically. Normal thyroid tissues contained significant amounts of amylase (mean +/- SD; 2.71 +/- 1.15 IU/g of tissue), and their amylase isozyme was composed of a majority of salivary type isoamylase and other peculiar isoamylase. The statistical decrease of amylase activities in tissues of Graves' disease under hyperthyroidism, thyroid carcinoma, and most of thyroid adenomas were found (Graves' disease; 1.04 +/- 0.41, carcinoma; 1.49 +/- 1.10, adenoma (except five cases with high activity); 0.88 +/- 0.49 IU/g tissue). Five of 18 cases of adenoma showed strikingly higher amylase activity in their tissues. Electrophoretical patterns of amylase isoenzymes in these five adenoma tissue were different from those of normal thyroid tissues. The cellular localization of amylase in the normal thyroid tissues and the adenoma tissues was also demonstrated immunohistochemically.

Adenoma↗
PubMed1984

Autoimmune thyroid disease: purification and phenotypic analysis of intrathyroid T cells.

A phenotypic analysis of T cells infiltrating the thyroid of patients with autoimmune thyroid disease (both Graves' disease and Hashimoto's thyroiditis) was performed. T lymphocytes were purified from mononuclear cells extracted from surgically removed tissue. The following markers were evaluated: la antigens, MLR4 antigen (expressed on activated T cells) 5/9 antigen (expressed on a subset of lymphocytes containing the whole "helper-inducer" activity in vitro), Fc gamma-receptors, B9 antigen (expressed by cytotoxic, or precursor of cytotoxic, T cells). We observed increased percentages of 5/9-, MLR4- and la-positive T cells with respect to peripheral blood in both HT and GD: on the contrary, in specimens from nonautoimmune thyroid diseases mononuclear infiltrate was minimal, and even T cell evaluation was not possible. In addition, B9- and Fc gamma-positive T cells were increased in Hashimoto's, but not in Graves' thyroid tissue, thus suggesting a different role of cytotoxic effector mechanisms in the two diseases.

Adult↗
PubMed1996

Carboxy-terminal propeptide of type 1 procollagen (P1CP) and carboxy-terminal telopeptide of type 1 collagen (1CTP) as sensitive markers of bone metabolism in thyroid disease.

We measured serum levels of the carboxy-terminal propeptide of type 1 procollagen (P1CP) as a marker of bone formation and the carboxy-terminal telopeptide of type 1 collagen (1CTP) as a marker of bone resorption by RIA in sera from 40 Graves' disease patients and 14 Hashimoto's disease patients before and during treatment. The serum P1CP levels of the untreated Graves' disease were significantly higher than in the controls (176.8 +/- 93.5 vs. 107 +/- 35 ng/ml, P < 0.01), and these levels decreased significantly during treatment with antithyroid drugs. There was a significant statistical correlation between serum P1CP levels and serum total alkaline-phosphatase activity (r = 0.61, P < 0.01) in the patients with Graves' disease and Hashimoto's disease as a whole. 1CTP levels were also significantly increased in untreated Graves' patients (6.5 +/- 2.8 compared with 2.7 +/- 1.1 ng/ml in normal subjects, P < 0.01). The P1CP/1CTP ratio, which reflects the relative ratio of bone formation to bone resorption, was lower than normal in untreated Graves' disease, but increased following the normalization of thyroid function. The results of this study suggest that the measurement of serum P1CP and 1CTP levels may be useful in evaluating bone metabolism in thyroid disease.

Adult↗
PubMed1978

Thyroid disease and function in breast cancer patients and non-hospitalized controls evaluated by determination of TSH, T3, rT3 and T4 levels in serum.

Investigations concerning a possible influence of thyroid disease and function on the risk for breast cancer have given contradictory results--although a slight hypothyroidism was repeatedly suggested and supported by increased thyrotropin concentrations and exaggerated TRH-responses. The selection of proper controls was stressed and in this study 179 consecutively diagnosed breast cancer patients were compared with 179 age-matched controls chosen from a computerized population register. The prevalence of thyroid disease and thyroxine treatment showed no differences between the groups. Slight but significant differences were found in the patient group--with a higher mean value for thyrotropin, reverse triodothyronine and T3-resin uptake and a lower mean value for triiodothyronine. No difference was found concerning thyroxine. This pattern of changes was inconsistent with a hypothyroidism, but has recently been found in many non-thyroidal diseases. It is suggested that it may represent a secondary and probably extrathyroidal metabolic change, most likely due to an altered peripheral conversion of the thyroxine.

Adult↗
PubMedDate not supplied

Thyroid disease and its treatment: short- and long-term consequences.

Thyroid dysfunction is common, with up to 5% of the population affected by hyper- or hypothyroidism. Short-term effects of overt thyroid dysfunction are well recognised: for example, effects of hyperthyroidism on pulse rate or blood pressure and effects of hypothyroidism on lipids. There is now also increasing evidence for long-term morbidity and mortality associated with thyroid dysfunction. This includes an increased likelihood of cardiovascular and cerebrovascular mortality in subjects with previous thyrotoxicosis treated with radioiodine, and of osteoporotic fracture of the femur in those with previous thyrotoxicosis. Subclinical or mild thyroid dysfunction may also be associated with long-term effects, with evidence for increased risk of atrial fibrillation in those with subclinical hyperthyroidism. Treatment for thyroid disease may also cause long-term problems. The cancer risk associated with therapeutic radioiodine for hyperthyroidism has been investigated extensively. Our own studies reveal no increase in cancer diagnoses or deaths, apart from a small increase in thyroid cancer risk which may be associated with the underlying thyroid disease.

Bone Diseases↗
PubMedDate not supplied

Arterial stiffness in type 1 diabetes mellitus is aggravated by autoimmune thyroid disease.

OBJECTIVE: The aim of our study was to measure arterial stiffness in patients with Type 1 diabetes mellitus, its contributing factors and its relation to macrovascular arterial changes. MATERIALS AND METHODS: Thirty-one female Type 1 diabetic patients were studied; 11 had concomitant autoimmune thyroid disease although euthyroid during the study period. Stiffness was studied using applanation tonometry and pulse wave analysis for evaluation of systolic arterial pressure augmentation secondary to arterial stiffening and early wave reflection. Results were compared to 24 healthy individuals. In all patients, endothelium-related flow-mediated dilation (FMD) of the brachial artery and intima-media thickness (IMT) of the carotid artery were measured. RESULTS: Augmentation pressure (AP) and augmentation index (AI) were higher in Type 1 diabetic patients suggesting stiffer arteries compared to controls (AP: 5.8 +/- 3.6 vs 2.8 +/- 2.2 mmHg, p < 0.001; and AI:18.3 +/- 9 vs 11.1 +/- 8.8%, p = 0.004). The subgroup of diabetic patients with autoimmune thyroid disease presented stiffer arteries than those without (AP: 6.5 +/- 2.9 vs 5.5 +/- 3.9 mmHg, p < 0.05; and AI: 21.3 +/- 5.4 vs 16.7 +/- 10.3%, p < 0.05), though the two groups did not differ statistically by means of age, disease duration, hemoglobin A1c (HbA1c), lipid levels, FMD and IMT. In multiple regression analysis, variables independently associated to AI in the diabetes group were: age (p = 0.028), IMT of the carotid artery bifurcation (p = 0.045), disease duration (p = 0.031) and autoimmune thyroid disease (p = 0.015). No correlation was observed between AI and metabolic control, blood pressure, microalbuminuria, presence of retinopathy and endothelial function (FMD). CONCLUSIONS: Women with Type 1 diabetes have increased arterial stiffness, which indicates macroangiopathy. An independent correlation between these indices and carotid IMT was observed. Concomitant autoimmune thyroid disease seems to aggravate arterial compliance in these patients, a finding that merits further investigation.

Arteries↗
PubMed2006

Benign thyroid disease: what is the role of nuclear medicine?

Nuclear medicine is directly involved in both the diagnosis and treatment of benign thyroid disease, which requires an understanding of the pathophysiology and management of thyroid disorders in addition to expertise in nuclear methodology. Thyroid uptake and imaging, the principal nuclear tests in thyroid disease, may be used as follows: (1) Differential diagnosis of hyperthyroidism: A very low thyroid uptake suggests destructive ("subacute") thyroiditis, a self-limited disorder, whereas a normal or elevated uptake is consistent with toxic nodular goiter and Graves' disease. Scintigraphic characteristics also help differentiate between nodular and Graves' disease. (2) Function of thyroid nodules: Fine-needle aspiration biopsy with cytological examination (FNAB) is used routinely to assess for malignancy in thyroid nodules. Scintigraphy may be of assistance before FNAB. "Hot" nodules are generally benign and do not require FNAB, while "cold" nodules may be malignant. (3) Differential diagnosis of congenital hypothyroidism: Scintigraphy combined with ultrasound examination may be used to identify such conditions as thyroid agenesis, dyshormonogenesis, and incomplete thyroid descent. Treatment of Graves' disease and toxic nodular disease with (131)I may require greater clinical involvement and decision analysis compared with thyroid uptake and imaging. The following aspects of treatment are particularly important: (1) Risk: Radioiodine treatment may occasionally aggravate hyperthyroidism, Graves' ophthalmopathy, and airway obstruction caused by large, nodular goiters. Alternative treatments, including the temporary use of antithyroid drugs, and surgery for nodular goiters, may be considered. (2) Radioiodine dose: Cure of hyperthyroidism with a single (131)I treatment is desirable, though not always possible. Such factors as a large goiter, severe hyperthyroidism, and prior propylthiouracil therapy, may contribute to treatment failure. (3) Informed consent: A detailed discussion with the patient regarding the clinical risks, outcomes, and side effects of (131)I is a critical component of successful management.

Adult↗
PubMed2002

Thyroid disease and pregnancy.

Several important issues must be considered when thyroid disorders occur during pregnancy. These include establishing the diagnosis (including an understanding of the effect of pregnancy and its hormonal changes on the immune system in general and the thyroid function in particular) treatment and uneventful maternal and neonatal outcome. The evaluation and treatment of women with thyroid disease during pregnancy parallels that of nonpregnant women and men, but presents unique problems. In addition some types of thyroid disorders occur only during pregnancy and the postpartum period. Pregnancy complicated by some thyroid disorders is associated with an increased rate of complications to the mother as well as to the fetus. This review will seek to discuss the diagnosis, management of different thyroid disorders during pregnancy and the postpartum period.

Female↗
PubMed1988

Development of thyroid disease in patients with primary and secondary Sjögren's syndrome.

Autoimmune thyroid disease associated to Sjögren syndrome (SS) may be defined by serological and functional abnormalities. We studied the prevalence of serum anti-thyroid autoantibodies and the development of thyroid functional defects by a follow-up investigation in patients with primary (pSS) and secondary SS (sSS). In keeping with previous literature data, our findings confirmed an increased prevalence of thyroid autoimmune phenomena in the whole series of patients with SS. In addition, evidence was provided for a greater incidence of serological and functional thyroid abnormalities in pSS when compared to sSS. Follow-up study also showed that the rate of thyroid autoimmune disease development was higher in pSS than in sSS. The appearance of circulating anti-thyroid antibodies was particularly frequent in patients with preexisting antibodies against extractable nuclear antigens (anti-ENA). These data indicate the need for a careful monitoring of thyroid function in SS patients, with particular regard to those with pSS and positive anti-ENA tests.

Adult↗
PubMed1993

A new classification for human autoimmune thyroid disease.

We propose a new classification for the human autoimmune thyroid diseases including Graves' disease and Hashimoto's disease. The system proposed involves redefining the term "thyroiditis" and recognition that all clinicians need to speak the same language of medicine whatever their specialty and whatever their nationality. Major advances in our understanding of autoimmune mechanisms suggest that a new classification can add considerable clarity to clinical definitions.

Autoimmune Diseases↗
PubMed1988

Alterations in magnesium and zinc metabolism in thyroid disease.

Magnesium (Mg) and zinc (Zn) status was assessed in subjects to evaluate the effects of thyroid diseases on Mg and Zn metabolism. Plasma and red blood cell (RBC) concentration and peripheral blood mononuclear cell (MNC) content of Mg and Zn, and 24-hour urinary excretion of Mg, Zn, creatinine (Cr), calcium (Ca), sodium (Na), and potassium (K) were measured in 11 thyrotoxic, 29 hypothyroid, and 25 euthyroid control subjects. Serum albumin, alpha 2-macroglobulin, and the binding of Zn to albumin were also determined. Plasma and RBC Mg concentrations were low in half of the hyperthyroid subjects, but mean values were not significantly different from controls. Urinary excretion and clearance of Mg were lower in hypothyroid subjects, but differences were removed when expressed relative to Cr excretion and clearance. Similar patterns were noted for urinary Ca, Na, and K, suggesting that their reduced excretion reflects alterations in renal hemodynamics. Plasma Zn was lower in hypothyroid subjects and correlated with serum albumin; MNC Zn and urinary Zn were also low. Plasma Zn concentration was normal and serum albumin significantly lower in the hyperthyroid group than in the control group. Further, RBC Zn content was significantly lower in hyperthyroid subjects, and inversely related to plasma thyroxine concentration. The hyperthyroid group also excreted significantly greater amounts of Zn than controls, indicative of a catabolic process. This increased urinary loss may reflect a shift in the distribution of plasma Zn between ultrafilterable and Zn-albumin complexes. In summary, this study provides evidence for marked alterations in Zn homeostasis in persons with thyroid disease. Whether the observations indicate deficiency states and have clinical implications will require further investigation.

Adolescent↗