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At least 19 recordsLinked to original sources
PubMed2000

The quantitative measurement of autoantibodies to thyroglobulin and thyroid peroxidase by automated microparticle based immunoassays in Hashimoto's disease, Graves' disease and a follow-up study on postpartum thyroid disease.

The aim of this study was to investigate the association between various autoimmune thyroid diseases and the presence of anti-TPO and anti-Tg antibodies using two novel automated microparticle based immunoassays developed for the AxSYM analyzer. Serum samples from 65 individuals with Hashimoto's Disease, 38 with Graves' Disease and 80 UK blood donors were assayed. In addition, samples were taken from 50 women known to be positive for TPO antibodies, for up to 24 weeks following delivery. Precision for both assays ranges from 5.7-9.1% CV, while analytical sensitivity was determined to be 1.0 IU/ml for Anti-Tg and 0.3 IU/ml for Anti-TPO. The Anti-TPO test showed positive results in 86% of Hashimoto's Disease and 87% of Graves' Disease. The figures obtained for Anti-Tg were 58% and 73% respectively. Specificity was 94% with Anti-TPO and 99% with Anti-Tg. The postpartum women were divided into 2 groups, group A remained symptomless while group B developed thyroid dysfunction. Within the 2 groups, medians calculated at each time point were compared between and within groups using the Mann-Whitney Rank Sum Test or the Kruskal-Wallis One Way ANOVA on Ranks. Anti-TPO baseline levels (week 6) were statistically different between both groups (median 36 vs. 167 IU/ml, p = 0.002). In group A, the median values increased from 36 to 87 IU/ml within the observation period, although the difference was not statistically significant. In group B, antibody titres showed a statistically significant increase from 168 IU/ml (week 6) up to 676 IU/ml after 20 weeks (p < 0.001). Anti-Tg baseline levels were not statistically different between the two groups. In group A, the median values did not change significantly over time (range: 47-86 IU/ml) whereas antibody titres in group B showed a statistically significant increase from 79 IU/ml (week 6) to 276 IU/ml after 24 weeks (p = 0.002). Results obtained indicate that these assays provide useful tools for the quantitative determination of autoantibodies in both primary diagnosis as shown with the Hashimoto's disease and Graves' disease samples and patient follow-up as demonstrated with the postpartum samples. The automation and high precision of the assays make them perfectly suited to routine diagnostic use.

Autoanalysis↗
PubMed2005

Autoimmune thyroid disease (Graves' disease and hashimoto's thyroiditis) in two patients with Crohn's disease: case reports and literature review.

An increased prevalence of the association between autoimmune thyroid diseases and ulcerative colitis has been suggested, however, not with Crohn's disease, as only 7 cases of thyroid disease coexisting with Crohn's disease have been reported. Herein, we describe 2 patients with Crohn's disease complicated with Graves' disease or autoimmune thyroiditis, and also review other cases with those complications. Some immunological processes are suggested to be implicated in the pathogenesis of this association, however, the exact mechanism remains unclear.

Adult↗
PubMed2005

The role of cytokeratin 19 in the differential diagnosis of true papillary carcinoma of thyroid and papillary carcinoma-like changes in Graves' disease.

Graves' disease is an autoimmune disease predominantly seen in females. All types of thyroid cancers may co-exist with Graves' disease but papillary carcinoma is the most frequent. Vesicular nuclei, nuclear grooves, and papillary formations that may be seen in Graves' disease may lead the pathologist to an overdiagnosis of papillary carcinoma. The differential diagnosis between a true papillary carcinoma and foci mimicking papillary carcinoma in Graves' disease may be challenging by light microscopic features only. This study is designed to determine whether CK19 is effective in the discrimination between the true papillary carcinoma of thyroid and foci resembling papillary carcinoma in Graves' disease. Twenty-five cases with papillary carcinoma and 25 cases with Graves' disease containing foci resembling papillary carcinoma were included in the study. All 25 cases with papillary carcinoma stained positive with CK19, whereas only six of 25 cases with Graves' disease showed weak staining, and the remaining 19 cases were completely negative. It is known that CK19 may show faint staining in benign thyroid lesions such as adenomas. Staining pattern with CK19 together with histopathological findings may be helpful in the differential diagnosis between foci mimicking papillary carcinoma and true papillary carcinoma in Graves' disease.

Adolescent↗
PubMed1994

Analysis of a Chinese population suggests that the TNFB gene is not a susceptibility gene for Graves' disease.

Graves' disease is associated with different HLA genes in different races. The TNFB gene lies between the class I and class II HLA genes and has two alleles, TNFB*1 and TNFB*2. Studies in Caucasians have suggested that the TNFB gene might be a susceptibility gene for Graves' disease. To investigate further the role of TNFB in predisposition to Graves' disease, we determined whether the TNFB disease associations in the Chinese were similar to those in Caucasians. A total of 57 patients with Graves' disease (32 male) were studied. A TNFB gene fragment was amplified from genomic DNA by using the polymerase chain reaction and digested with Nco I to distinguish the TNFB alleles (TNFB*1 and TNFB*2). Genotype frequencies were compared with those in a racially matched group of 92 controls. TNFB*1 homozygosity occurred in 15 (26%) Graves' and 22 (24%) control subjects. TNFB*1/TNFB*2 heterozygosity occurred in 29 (51%) and 48 (52%) and TNFB*2 homozygosity in 13 (23%) and 22 (24%), respectively (NS). There were gender differences in the frequencies of TNFB*1 homozygosity (13 male [41%], 2 female [8%]). TNFB*1/TNFB*2 heterozygosity (13 male [41%], 16 female [64%]) (chi 2 = 7.3, p = 0.02), and TNFB*2 frequency (19 male [59%], 23 female [92%]; pc = 0.04) in Graves' patients. We conclude that the TNFB associations with Graves' disease in the Hong Kong Chinese differ between the genders and from those described in Caucasians. The TNFB gene is not a susceptibility gene for Graves' disease.

Asian People↗
PubMed1999

[An elevation of serum immunoglobulin E provides a new aspect of hyperthyroid Graves' disease].

Graves' disease is an autoimmune disorder characterized by circulating TSH receptor antibodies (TRAb), the majority of which lies in the immunoglobulin G (IgG) class. However, there may be a role of other immunoglobulins in the induction and maintenance of hyperthyroid Graves' disease. We focus on the role of IgE on these issues. One third of hyperthyroid Graves' disease shows IgE elevation (greater than 170 U/mL). This prevalence is significantly higher than other thyroid diseases and controls, suggesting IgE elevation appears associated with autoimmune Graves' disease. Half of Graves' patients with IgE elevation have hereditary and/or allergic conditions such as bronchial asthma and pollen allergy. There is a significantly smaller decrease in TRAb in patients with IgE elevation than in those with normal IgE during methimazole treatment. The remission rate is significantly less in patients with IgE elevation than in those with normal IgE. These findings suggest that TRAb synthesis is increased when IgE synthesis is stimulated. There is an elevation of interleukin (IL)-13, but not of IL-4, in two thirds of patients with IgE elevation in the absence of detectable helper T-cell-1 marker, IFN gamma. It seems that TH2 cells are stimulated in hyperthyroid Graves' disease to secrete excess IL-13, following stimulation of B cells to secrete TRAb and IgE. IgE elevation as a result of aggravating complex (IL-13-IgE synthesis), thus, may play a role in the participation of thyroid autoimmunity rather than its pathogenesis.

Graves Disease↗
PubMed1997

Polymorphisms of TAP1 and TAP2 genes in Graves' disease.

Graves' disease is an autoimmune disorder in which HLA DQA1*0501 and DQB1*0201 confer predisposition. The genes for transporters associated with antigen processing (TAP1 and TAP2) locate near to HLA DQ coding regions and display only a limited degree of polymorphism. Since polymorphisms of TAP might influence susceptibility to Graves' disease by a possibly different selection of antigenic peptides, we investigated sequence variants of TAP1 and TAP2 genes in 235 patients with Graves' disease and 218 random healthy controls by polymerase chain reaction (PCR) followed by sequence specific oligonucleotide analysis (SSO), single strand conformational polymorphism (SSCP) analysis and amplification refractory mutation system (ARMS). TAP1*0301 (Val-333/Asp-637: 71% vs. 55% in controls, p < 0.008, RR = 2.05) and TAP2*0101 (Val-379/Ala-565/Thr-665/stop-687: 83% vs. 69% in controls, p < 0.03, RR = 2.20) showed a positive association with Graves' disease whereas TAP1*0401 a negative (Ile-333/Gly-637: 4% vs. 13% in controls, p < 0.01, RR = 0.25). After selection of patients and controls for HLA DQA1*0501 a similar association was found for TAP1*0301 (72% vs. 50% in controls, p < 0.02, RR = 2.63) and TAP1*0401 (4% vs. 16% in controls, p < 0.04, RR = 0.22), when matching for HLA DQB1*0201 as well as for TAP1*0401 (3% vs. 16% in controls, p < 0.05, RR = 0.18). Our findings indicate that the positive association of TAP1*0301 and the negative of TAP1*0401 with Graves' disease cannot only be explained by linkage disequilibrium between TAP alleles and HLA DQ. Therefore, these TAP alleles contribute to genetic susceptibility in Graves' disease as additional permissive and protective factors.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Morbidity after total thyroidectomy for benign thyroid disease: comparison of Graves' disease and non-Graves' disease.

The purpose of this study was to review the safety of total thyroidectomies for benign thyroid disease, with special emphasis on the comparison between Graves' disease and non-Graves' disease. In this study, 107 patients who underwent total thyroidectomies for clinically benign thyroid disease performed by the same surgeon between January 1987 and December 2004 were enrolled; 48 had Graves' disease and 59 had non-Graves' disease. The rates of temporary vs. permanent hypoparathyroidism, hematoma requiring surgical intervention, and temporary vs. permanent recurrent laryngeal nerve palsy (RLNP) after total thyroidectomy for benign thyroid disease were 34.6% vs. 3.7%, 6.5%, and 6.5% vs. 1.85%, respectively. The rates of permanent hypoparathyroidism and temporary RLNP in the Graves' disease group were significantly different when compared with the non-Graves' disease group (8.3% vs. 0% and 11.5% vs. 2.5%, respectively). However, comparing the rates of temporary hypoparathyroidism, permanent RLNP, and postoperative hematoma, there was no statistically significant difference. Compared with total lobectomy, the rates of postoperative hematoma increased significantly for total thyroidectomy (6.5% vs. 0.48%). Total thyroidectomy for non-Graves' benign thyroid disease may be performed with minimal morbidity as has been advocated by many authors. For patients with Graves' disease in this study, however, the complication rates of permanent hypoparathyroidism and temporary RLNP were significantly increased. Therefore, we suggest that total thyroidectomy for Graves' disease should be performed by an experienced surgeon.

Graves Disease↗
PubMedDate not supplied

Etiopathogenesis of Graves' disease.

Graves' disease is an autoimmune disorder, caused by thyroid-stimulating antibodies, which bind to and activate the thyrotropin receptor on thyroid cells, inducing the synthesis and release of thyroid hormones. It is a polygenic and multifactorial disease that develops as a result of complex interaction between genetic susceptibility and environmental and/or endogenous factors. Graves' disease differs from other autoimmune diseases of the thyroid by specific clinical features, including hyperthyroidism, vascular goitre, ophthalmopathy and--less commonly--infiltrative dermopathy. This article discusses current theories, regarding the etiology and pathogenesis of Graves' disease, including possible predisposing factors, autoimmune aspects of Graves' disease, ophthalmopathy, and dermopathy.

Autoimmunity↗
PubMed2007

beta-2-adrenergic receptor gene polymorphism confers susceptibility to Graves disease.

Graves disease (GD) is an autoimmune disorder with genetic predisposition. The polymorphisms 47A-->G (Arg16Gly) and 79C-->G (Gln27Glu) of the adrenergic beta-2 receptor (ADRB2) gene in the 5q32 region affect the functional reaction to adrenergic stimulation, which contributes to the regulation of immunological response. The -367T-->C polymorphism within the 5'-leading regulatory sequence affects ADRB2 transcriptional activity. The aim of the present study was to investigate whether ADRB2 gene variants are associated with susceptibility to GD. All polymorphisms were studied in Polish GD patients (n=300) and healthy control subjects without a family history of autoimmune disorders (n=301). Genotypes were determined by the MassARRAY system (Sequenom, San Diego, CA). Gly16 and Gln27 allele frequencies were 61.4% and 55.2% among healthy controls, almost the same as previously reported in 4441 white participants of a cardiovascular health study. We found a higher risk of GD in Gln27 carriers (CC or CG genotypes) than in Glu27 homozygous (GG genotype) participants (OR=1.99, 95% CI: 1.27-3.12, p=0.003, pcorr=0.03). The frequency of the 79GG protective genotype was significantly smaller in the GD patients without symptoms of Graves ophthalmopathy compared to controls (10% vs 22%, OR=0.41, 95% CI: 0.234-0.706, p=0.0017, pcorr=0.015). We didn't find any association of -367T--> or 47A-->G genotypes/alleles with Graves disease, however, haplotype analysis has shown a significant difference in haplotype distribution between patients and controls (the global p=0.001) with increased -367T/47A/79C haplotype frequency in GD patients compared to controls (34% vs 25%, p=0.00073, pcorr=0.0044). In conclusion, Gln27 carriers (79CC or 79GC genotypes) have increased risk of Graves disease. Our results suggest that ADRB2 plays a role in susceptibility to Graves disease in humans.

Adolescent↗
PubMed1975

Eye signs of Graves' disease.

Graves' disease can affect the eyes and orbits in many ways, some seemingly trivial, others obviously devastating to vision. Because of the relative simplicity of diagnosing Graves' disease in the majority of cases, and now with the addition of B-scan ultrasonography, much expense and needless risk is avoidable in most patients with ophthalmopathic Graves' disease. Those patients whose diagnosis cannot be confirmed by noninvasive techniques may not have Graves' disease and deserve more in-depth study.

Diagnosis, Differential↗
PubMed1990

Surgical correction of exophthalmos secondary to Graves' disease.

Graves' disease has been recorded in the medical literature for more than 150 years. Despite introduction of iodine into the diet, Graves' disease still remains the most important disorder of the thyroid gland. Clinically, Graves' disease is a multisystem disorder of unknown etiology characterized by the clinical triad of infiltrative pretibial dermopathy, thyroid glandular hyperplasia, and ophthalmopathy. Expansion of the bony orbital volume is an effective method of treating moderate to severe exophthalmos. Our experience with a simplified version of a three-wall orbital decompression to correct exophthalmos secondary to Graves' disease is presented.

Adult↗
PubMed1977

Hypothyroid Graves' disease.

Graves' disease has recently been shown to exist in a euthyroid form in untreated patients. Sporadic reports of a hypothyroid form are beginning to emerge, thus illustrating the multifaceted nature of this disorder, with thyrotoxicosis at one end of the spectrum and hypothyroidism at the other. Three patients with nonthyrotoxic Graves' disease and concomitant hypothyroidism were seen at Emory University Hospital in one year, and deatailed studies were made to help elucidate the nature of this unusual combination. Results of these studies are reported and briefly discussed. It is suggested that, until more is known about this intriguing aspect of the Graves' disease spectrum, the label "hypothyroid Graves' disease" is justifiable.

Adult↗
PubMed1992

HLA haplotypes and susceptibility to Graves' disease.

Graves' disease is a polygenic disease in which the HLA cluster could play a role. The purpose of our study is to identify HLA haplotypes in a family with closely related susceptibility to Graves' disease and foresee the risk of disease in the youngest daughter. The family studied had included the father (47 years), mother (46 years) and 3 daughters (18, 17 and 13 years). The mother and 2 eldest daughters were affected by Graves' disease. HLA-A, -B, -C, -DR and -DQ were performed with standard microlymphotoxicity techniques. A mother's role in passing susceptibility to Graves' disease to daughters is undisputed; it seems to be due to the B35 HLA allele. Also, the third daughter (at 15 years) has an HLA B35 allele, and actually has an incipient humoral hyperthyroidism.

Adolescent↗