PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “THYROID DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1991

Thyroid disease and pregnancy.

Thyroid disease is common in younger women and may be a factor in reproductive dysfunction. This probably only applies to severe cases of hyper- or hypothyroidism. Once adequately treated, neither of these disorders significantly impacts on fertility. The key is to recognize and to treat thyroid disorders in the reproductive-age woman before conception. Thyroxine therapy and even antithyroid drug therapy should be continued during pregnancy as necessary. Pregnancy is a euthyroid state that is normally maintained by complex changes in thyroid physiology. The fetal and neonatal hypothalamic-pituitary-thyroid system develops independently, but it may be influenced by thyroid disease in the mother. Early pregnancy is characterized by an increase in maternal T4 secretion stimulated by hCG and an increase in TBG, resulting in the elevated total serum T4 in pregnancy. The debate continues as to whether maternal T4 is important in early or late fetal brain development. If so, the physiologic changes in thyroid hormone secretion and transport in early pregnancy would help to ensure that a sufficient amount of thyroid hormone was available. There is new evidence in human subjects that substantial maternal T4 can cross the placenta during pregnancy, and this may be particularly important when fetal thyroid function is compromised as a result of congenital hypothyroidism. Maternal and fetal/neonatal outcomes in pregnancy are adversely affected if severe hypothyroidism is undiagnosed or inadequately treated. Thyroid function tests should be obtained during gestation in women taking T4 and appropriate dose adjustments should be made for TSH levels outside a normal range. The TSH-receptor blocking antibodies from the mother are a recognized cause of congenital hypothyroidism in the fetus and neonate that can be permanent or transient. If neonatal hypothyroidism is detected through neonatal screening programs, and prompt and adequate T4 replacement therapy is instituted as soon as possible following delivery, subsequent growth and development are usually normal. Paradoxically, pregnancy often has a favorable effect on the course of maternal Hashimoto's disease, although there is the risk of relapse postpartum. Pathophysiologic conditions of hCG secretion such as gestational trophoblastic disease and hyperemesis gravidarum may present as thyrotoxicosis in pregnancy, but the main cause of this syndrome is Graves' disease. The mainstay of treatment is antithyroid drugs and either propylthiouracil or methimazole may be used safely. Subtotal thyroidectomy, after medical control, is the alternative treatment, but radioiodine ablation is contraindicated.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1985

Activation, proliferation, and differentiation of circulating B cells in autoimmune thyroid disease.

Several studies of thyroid autoantibody production in vitro have been reported with the use of pokeweed mitogen, but the conclusions that have resulted regarding the immunoregulation of B cell function in thyroid disease are difficult to interpret due to the relatively nonphysiologic nature of pokeweed mitogen stimulation. We have therefore examined the responses of circulating B cells in Graves' disease and Hashimoto's thyroiditis by using a combination of lymphokines and other stimuli that act at various stages of the B cell cycle. In patients with autoimmune thyroid disease, nonspecific B cell proliferation and differentiation into IgG-secreting cells were both normal. However, a previously unsuspected heterogeneity among patients was found in their ability to produce autoantibodies in vitro. B cells of certain patients produced maximal autoantibody in response to pokeweed mitogen, some in response to Staphylococcus aureus Cowan strain I, and some in response to the lymphokines contained in the supernatants of stimulated T cell cultures. There was no correlation between serum autoantibody levels and those achieved in vitro. Attempts to stimulate antibody production by autoantigen (thyroglobulin) were unsuccessful, even when B cells were cultured with purified autologous OKT4+ T cells to avoid potential suppressor effects in the OKT8+ population. However, OKT4+ T cells enhanced pokeweed mitogen-driven autoantibody production. Our results show that several different functional stages of B cells exist in the circulation of patients with autoimmune thyroid disease, and that circulating B cells from such patients do not manifest a uniform response to B cell stimulators. This is presumably the result of differences in migration of circulating B cells and in their level of activation at the major sites of autoantibody production, such as the thyroid gland itself. In the light of these findings, caution is required in interpreting the results obtained from studies of circulating B cells as a means of elucidating the pathophysiology of autoimmune thyroid disease.

Autoantibodies↗
PubMed1988

Screening for thyroid disease in a primary care unit with a thyroid stimulating hormone assay with a low detection limit.

In a study at a primary care centre in a predominantly rural area of Sweden the records of all patients with established thyroid disease were scrutinised and 2000 consecutive adult patients screened with an immunoenzymometric thyroid stimulating hormone assay. The aims of the study were fourfold: firstly, to assess the total burden of thyroid disease in primary care centres in Sweden; secondly, to assess the efficacy of clinical diagnosis of the disease in unselected populations of patients; thirdly, to assess the efficacy of clinical evaluation of treatment with thyroxine; and, lastly, to see whether a single analysis of the serum thyroid stimulating hormone concentration by recent methods would be enough to identify an abnormality of thyroid function. Of the roughly 17,400 adults in the study community, 111 women and 10 men were being treated for thyroid disease. Screening detected 68 patients (3.5%) not receiving thyroxine who had a serum thyroid stimulating hormone concentration of 0.20 mU/l or less, all of whom were followed up clinically. Fifty of these patients were also studied biochemically during follow up. Only nine of the 68 patients had thyroid disease (three with thyrotoxicosis requiring treatment), no evidence of the disease being found in the remainder. Sixteen patients had spontaneous hypothyroidism requiring treatment, and neither these nor three patients with thyrotoxicosis had been detected at the preceding clinical examination. Of 35 patients in whom thyroid disease was suspected clinically at screening, none had laboratory evidence of thyroid dysfunction. In this series 1.3% of all women in the study community (2.6% of all 50-59 year olds) and 0.1% of the men were being treated for thyroid disease at the primary care centre, roughly 1.0% of adults subjected to screening were found to have thyroid disease requiring treatment, and most patients with a thyroid stimulating hormone concentration of 0.20 mU/l or less did not have thyroid dysfunction. It is concluded that measuring the basal serum thyroid stimulating hormone concentration by present methods is insufficient for the biochemical assessment of thyroid dysfunction in unselected populations.

Cross-Sectional Studies↗
PubMed1998

Usefulness of surface phenotype study of intrathyroidal lymphocytes obtained by fine needle aspiration cytology in autoimmune thyroid disease and malignant lymphoma of the thyroid.

OBJECTIVES: The surface phenotypes of intrathyroidal lymphocytes have been studied in various thyroid diseases. In most of the previous reports, intrathyroidal lymphocytes were obtained by surgical operation. We evaluated the usefulness of surface phenotype study of intrathyroidal lymphocytes obtained by fine needle aspiration in the diagnosis of Graves' disease, chronic thyroiditis, and malignant lymphoma of the thyroid. PATIENTS AND DESIGN: Eighty-seven untreated patients including 24 with Graves' disease, 59 with chronic thyroiditis, and 4 with malignant lymphoma of the thyroid, and 2 treated patients with malignant lymphoma of the thyroid were studied. Surface phenotypes of the peripheral lymphocytes and the intrathyroidal lymphocytes obtained by fine needle aspiration were analyzed using a FACScan and the monoclonal antibodies: anti-Leu5b/CD2, Leu4/CD3, Leu3a/CD4, Leu2a/CD8, and Leu12/CD19. Percentages of cells positive for each monoclonal antibody were calculated. In one case with malignant lymphoma, monoclonal antibodies to surface-immunoglobulin markers were also studied. RESULTS: In peripheral lymphocytes, the percentage of positive cells in each phenotype was almost normal in each disease. In intrathyroidal lymphocytes, the percentage of CD19 positive cells was increased, and the percentage of CD2 and CD3 positive cells was reduced compared to those of peripheral lymphocytes in each disease. The percentage of intrathyroidal CD19 positive cells was remarkably high in malignant lymphoma, constituting more than 70% of cells. In Graves' disease, a relative decrease in the percentage of intrathyroidal CD4 positive cells and an increase in CD8 positive cells compared to peripheral lymphocytes were observed. In 2 treated patients with malignant lymphoma of the thyroid, the intrathyroidal CD19 positive cells almost disappeared in a patient shortly after successful treatment, and reappeared to constitute 76% of cells in a patient in relapse. In one case with malignant lymphoma in which monoclonal antibodies to surface-immunoglobulin markers were studied, the clonality of the affected cells could be demonstrated; more than 70% of the cells were positive for kappa light-chain and mu and delta heavy-chain. This finding was proved by subsequent immunohistochemical study based on open biopsy. CONCLUSIONS: Surface phenotype study of intrathyroid lymphocytes obtained by fine needle aspiration has limited utility in the evaluation or diagnosis of Graves' disease and chronic thyroiditis. However, this simple rapid method is very helpful in the diagnosis and follow up of malignant lymphoma of the thyroid.

Adult↗
PubMed2002

Autoimmunity in thyroid disease.

The autoimmune thyroid diseases, Graves' disease and autoimmune hypothyroidism, represent the two ends of a disease spectrum where an immune response is directed against the thyroid gland. In Graves' disease, antibodies directed against the thyrotropin receptor (TSH-R) lead to the development of glandular overactivity, while in autoimmune hypothyroidism, cell-mediated and humoral thyroid injury leads to destruction of thyroid tissue and thyroid hormone deficiency. The mechanisms by which these diseases develop are unknown, although it is likely that both diseases occur in genetically susceptible individuals exposed to a permissive environment. A number of environmental factors have been postulated to be involved in the development of autoimmune thyroid disease. There is, however, no direct evidence to support clear causality. Susceptibility loci within immune response genes have been identified although a significant component of the genetic predisposition to disease remains unknown. This review will focus on some of the studies designed to identify genes that confer susceptibility to the autoimmune disease process within the thyroid gland.

Abatacept↗
PubMed1991

Evidence of limited variability of antigen receptors on intrathyroidal T cells in autoimmune thyroid disease.

BACKGROUND: Patients with autoimmune thyroid diseases, including Graves' disease and Hashimoto's disease, have marked lymphocytic infiltration in their thyroid glands. We examined the gene for the variable regions of the alpha-chain of the human T-cell receptor (the V alpha gene) in intrathyroidal T cells to determine whether the infiltration is a secondary heterogeneous immune response or a more restricted, and therefore primary and presumably pathogenetic, reaction to thyroid autoantigens. METHODS: We used the polymerase chain reaction to detect small numbers of T cells expressing the variable region of the V alpha gene. Different oligonucleotides were used to amplify complementary DNA for the 18 known families of the V alpha gene in intrathyroidal T cells from 9 patients with autoimmune thyroid disease. We compared the findings with the results in patients with nonautoimmune thyroid disease as well as those in normal subjects. RESULTS: We found marked restriction in the expression of T-cell-receptor V alpha genes by T cells from the thyroid tissue of patients with autoimmune thyroid disease. An average of only 5 of the 18 V alpha genes were expressed in such samples, as compared with 17 V alpha genes expressed in peripheral-blood T cells from the same patients. No such restriction was found in thyroid tissue from patients with nonautoimmune thyroid disease. The predominantly expressed V alpha genes differed from patient to patient, however, with no clear association with the type of disease. CONCLUSIONS: Intrathyroidal T-cell accumulation in autoimmune thyroid disease is highly restricted and points to the primacy of T cells in causing thyroid disorders. These results present the possibility of using antibodies to the T-cell receptor for the specific inhibition of abnormal T-cell function in autoimmune thyroid disease.

Antigens, CD↗
PubMed2004

Family history of benign thyroid disease and cancer and risk of thyroid cancer.

In a population-based study of 313 case-control pairs in Kuwait, we evaluated whether a family history of benign thyroid disease (BTD) and thyroid or other cancers was associated with an increased risk of thyroid cancer, the second most common neoplasm among women in this and several other Arab countries in the Gulf region. Family history of BTD was reported by 78 (24.9%) cases and 40 (12.8%) controls in 132 and 57 relatives, respectively. There was an approximately 2-fold increased risk of thyroid cancer in individuals who had a mother (Odds Ratio (OR)=2.3; 95% Confidence Intervals (95% CI): 1.1-5.1), sister(s) (OR=2.6; 95% CI: 1.3-5.3) or aunt(s) (OR=2.1; 95% CI: 0.9-5.3) with BTD; there was also a significant trend in increasing risk with an increasing number of affected female relatives (P<0.0001). Stratification by age at diagnosis of the case showed that individuals aged </= 35 years, who had an affected first- or second/third-degree relative(s), had an approximately 3-fold increased risk of the cancer. Family history of thyroid cancer was reported by 9 (2.9%) cases in 13 relatives (11 females, 2 males) and by 3 controls in 3 relatives (all females) (OR=3.0; 95% CI: 0.8-11.1). The OR for all hormone-related cancers combined was 1.5 (95% CI: 0.8-2.6). There was no clear association with family history of breast or any other common cancer. Our data suggest that a family history of BTD is associated with an increased risk of thyroid cancer, and point to the role of familial susceptibility to BTD and thyroid cancer in the Kuwaiti population.

Adolescent↗
PubMedDate not supplied

[Thyroid diseases in pregnancy].

The thyroid diseases are more frequent in women, which is probably related to the fact that many thyroid diseases are of the autoimmune type, secondary to the effects of sexual steroids in the immunological system; although it had never been completely cleared up, it seems that estrogens and progestogens may modulate the lymphocyte differentiation as well as the induction of the autoimmune response. After delivery, the thyroid dysfunction of autoimmune type often occurs, even in women without previous history of thyroid disease. Some authors assume that the cytokines, produced by the mother, fetus or placenta, inhibit the autoimmune reaction during pregnancy. The subsequent reduction in the inhibiting cytokines, after delivery, allows the aggravation or the beginning of the autoimmune disease. Although autoimmunity is traditionally considered as a major cause for thyroid disease during pregnancy, recent studies indicate that the most common aetiology of disturbance of thyroid tests during pregnancy is the hyperthyroidism due to the inadequate production of human chorionic gonadotropin (hCG). However, from the clinical point of view, the hyperthyroidism caused by Graves' disease is the most important cause for maternal and fetal morbidity.

Female↗
PubMed1992

Cutaneous manifestations of thyroid disease.

Cutaneous manifestations of thyroid disease are protean in nature and affect all age groups. This review focuses on normal thyroid gland physiology, specific cutaneous/thyroid lesions such as the thyroglossal duct cyst and metastatic thyroid malignancies, nonspecific cutaneous alterations of the hyperthyroid and hypothyroid states, and the numerous associations of thyroid disease with other cutaneous and/or systemic disorders.

Humans↗
PubMed1998

Thyroid disease in women.

Thyroid diseases occur more commonly in women than men, in part because of the autoimmune nature of many thyroid disorders. Hypothyroidism, and thyroid nodules occur frequently in both pre- and postmenopausal women. Pregnancy is also associated with changes in thyroid function. The goal of this article is to review the current information on the pathophysiology and treatment of thyroid disorders which are common in women.

Chorionic Gonadotropin↗
PubMed2006

Frequency of rheumatic diseases in patients with autoimmune thyroid disease.

We aimed to investigate the frequency of rheumatic diseases in patients suffering from autoimmune thyroid diseases (ATD). Sixty-five patients (56 F, 9 M), who were followed by diagnosis of ATD, were questioned and examined for the presence of rheumatic disease. Basic laboratory tests and antithyroid antibodies, antinuclear antibody and rheumatoid factor (RF) levels were also measured by appropriate methods. Various rheumatic diseases were detected in 40 (62%) of patients with ATD. The most frequent rheumatic conditions were fibromyalgia, recurrent aphthous stomatitis, osteoarthritis, keratoconjunctivitis sicca and xerostomia and carpal tunnel syndrome which were detected in 20 (31%), 13 (20%), 10 (15%), 9 (14%) and 8 (12%) of patients, respectively. Autoimmune diseases, except Sjogren's syndrome, which were detected in ten patients with ATD, are as follows-vitiligo: two; autoimmune hepatitis: two; oral lichen planus: one, ulcerative colitis: one, inflammatory arthritis in four patients (two of them had rheumatoid arthritis, one had psoriasis and psoriatic arthritis and one had mixed collagen tissue disease). RF was positive in two patients, one of them had rheumatoid arthritis and FANA was positive in six (9%) patients; all of them had hypothyroidism. The frequency of rheumatic diseases seems to be higher in patients suffering from ATD. Initial evaluation and a regular checking for rheumatic diseases in patients suffering from ATD were recommended.

Adolescent↗
PubMed1994

[Clinical aspects of autoimmune thyroid diseases].

AITD (autoimmune thyroid disease) comprise atrophic thyroiditis (AT), hypertrophic Hashimoto's thyroiditis (HT), and immunogenic hyperthyroidism (Graves' disease, GD). Combinations with other types of autoimmune disorders frequently occur and are called polyglandular autoimmune syndrome. Familial disposition may be documented by genetic markers: GD and AT are associated with HLA-B8 and DR3 respectively, while HT associates with DR5. Pathogenesis of the fore-mentioned 3 AITD may be explained on the one hand by an immunological balance and on the other hand by a predominance of either stimulating or destructive/blocking immune processes. In diagnosing AITD the determination of antibodies against thyroglobulin or thyroidal peroxidase have been in use for quite some times. Antibodies directed against TSH receptors (TRAb) are determined by means of a radioligand assay which will not distinguish between stimulating or blocking antibodies, so that clinical symptoms and thyroid function parameters are essential in evaluating hyper- oder hypothyroid function. TRAb are transferred via the placenta and should therefore be determined in patients with AITD within the 3rd trimester of pregnancy. The prevalence of AITD is far higher in iodine rich countries and is 4 times more frequent in women, with a general age peak between the 5th and 6th decade. The rare AT mostly presents as primary myxoedema and is discovered less frequently during the exploration of an unclear hypercholesterolemia. In HT we differentiate between the chronic fibrous and the juvenile oxiphilic variant. In the former fibrosis is predominant with plasmacellular infiltration producing extremely high titers of antibodies enabling diagnosis without fine needle biopsy (FNB). In the latter, the oxiphilic variant, titers of antibodies are mostly low or even missing so that a reliable diagnosis will require a FNB. However, two thirds of adolescent goitres are caused by HT.

Autoantibodies↗