Celiac disease and autoimmune thyroid disease

Celiac disease (CD) or gluten sensitive enteropathy is relatively common in western populations with prevalence around 1%. With the recent availability of sensitive and specific serological testing, many patients who are either asymptomatic or have subtle symptoms can be shown to have CD. Patients with CD have modest increases in risks of malignancy and mortality compared to controls. The mortality among CD patients who comply poorly with a gluten-free diet is greater than in compliant patients. The pattern of presentation of CD has altered over the past three decades. Many cases are now detected in adulthood during investigation of problems as diverse as anemia, osteoporosis, autoimmune disorders, unexplained neurological syndromes, infertility and chronic hypertransaminasemia of uncertain cause. Among autoimmune disorders, increased prevalence of CD has been found in patients with autoimmune thyroid disease, type 1 diabetes mellitus, autoimmune liver diseases and inflammatory bowel disease. Prevalence of CD was noted to be 1% to 19% in patients with type 1 diabetes mellitus, 2% to 5% in autoimmune thyroid disorders and 3% to 7% in primary biliary cirrhosis in prospective studies. Conversely, there is also an increased prevalence of immune based disorders among patients with CD. The pathogenesis of co-existent autoimmune thyroid disease and CD is not known, but these conditions share similar HLA haplotypes and are associated with the gene encoding cytotoxic T-lymphocyte-associated antigen-4. Screening high risk patients for CD, such as those with autoimmune diseases, is a reasonable strategy given the increased prevalence. Treatment of CD with a gluten-free diet should reduce the recognized complications of this disease and provide benefits in both general health and perhaps life expectancy. It also improves glycemic control in patients with type 1 diabetes mellitus and enhances the absorption of medications for associated hypothyroidism and osteoporosis. It probably does not change the natural history of associated autoimmune disorders.     

Immunoregulatory genes in autoimmune thyroid disease]

Autoimmune thyroid diseases (AITD) has a strong genetic basis. Although several candidate genes have been studied, the AITD causing genes are still unknown. Major candidate immune regulatory genes include human leukocyte antigen (HLA) gene, Ig heavy chain genes, T cell receptor genes, IL-1 receptor antagonist gene, IL-1 alpha gene and cytotoxic T lymphocyte antigen-4 (CTLA-4) gene. The relation between HLA and AITD has extensively been studied. In addition, polymorphism of the 3'-untranslated region and codon 17 of the CTLA-4 gene has been reported to associate positively with AITD. However, no linkage analyses have showed positive relation between AITD and these candidate genes except for HLA.     

Animal models for autoimmune thyroid disease]

Animal models for chronic thyroiditis include (1) experimental autoimmune thyroiditis induced by immunizing rabbits or rodents with thyroid extracts or thyroglobulin and (2) spontaneous thyroiditis in certain species of rodents and chickens. For Graves' disease, no spontaneous animal models are reported. An animal model for Graves' disease has been developed by xenotransplantation of Graves' thyroid tissue plus autologous immune cells to immunodeficient mice. Another animal model for Graves' disease is made by immunizing TSH receptor-peptide or protein to mice. Animal models are very useful for studying etiology of autoimmune thyroid diseases, although no current animal models are satisfactory for human autoimmune thyroid disease.     

维生素D与自身免疫性甲状腺疾病的研究进展

自身免疫性甲状腺疾病(AITD)是一种T淋巴细胞介导的器官特异性自身免疫性疾病,主要包括桥本甲状腺炎(HT)和Grave病(GD),其发病机制尚不明确,可能与遗传、环境及免疫等有关。维生素D除具有调节骨和钙磷代谢,防治骨质疏松外,近年研究发现维生素D可能通过影响T淋巴细胞的增殖与分化,参与免疫调节,维持免疫内稳态。本文综述维生素D与AITD相关性的研究进展,旨在为AITD的预防与治疗提供新的思路。     

Serum interferon gamma levels in autoimmune thyroid disease

The lymphokine, interferon gamma (IFN gamma) is considered to play an important role in the development of autoimmune thyroid disease (AITD); the main source of IFN gamma has been shown to be CD4 cells when stimulated by soluble antigen. We have measured the serum IFN gamma concentration in 42 patients with AITD (24 Graves' disease and 18 Hashimoto's thyroiditis) and 9 normal control subjects, using a sandwich enzyme-linked immunosorbent assay (ELISA) (detectable limit, 1 IU/ml). One of normal controls, 14 of the 24 patients with Graves' disease, and 5 of the 18 patients with Hashimoto's thyroiditis had detectable IFN gamma levels. Patients with Graves' disease were found to have higher concentrations of serum IFN gamma (11.6 +/- 15.8 IU/ml, mean +/- SD) than normal controls (1.1 +/- 0.3 IU/ml). However, the values in patients with Hashimoto's thyroiditis (9.4 +/- 15.5 IU/ml) were not significant when compared to those in normal controls. Serum IFN gamma values in patients with AITD did not correlate with serum anti thyroid autoantibodies (antithyroglobulin, antithyroid microsomal antibody, or TSH binding inhibitory immunoglobulin activity) or with thyroid function. Thus, increased in vivo production of IFN gamma in Graves' disease as evidenced in these serum concentrations might reflect T cell activity, but does not appear to be an accurate reflection of intrathyroidal events.     

Celiac disease occurring in a patient with hypoparathyroidism and autoimmune thyroid disease

Patients with an underlying autoimmune endocrine disorder are at an increased risk of developing other autoimmune diseases. We describe a patient with idiopathic autoimmune hypoparathyroidism who developed hyperthyroidism due to Graves disease and subsequently was diagnosed with celiac disease. Malabsorption of L-thyroxine was the only clue regarding the presence of celiac disease. This particular association of these three autoimmune disorders occurring in the same patient has not, to our knowledge, been previously reported. The presentation, investigations performed, and treatment provided are discussed and the literature pertaining to similar cases is reviewed.     

Ultrasonography of the thyroid gland in pregnancies complicated by autoimmune thyroid disease

Thyroid function and ultrasonographically determined thyroid volume were studied in nine pregnant women with diagnosed autoimmune thyroid disease at regular intervals during pregnancy and two months after delivery. The results were compared to the findings in ten healthy pregnant women. In ultrasound examinations seven of the patients showed definite morphological changes such as hypoechogeneity and inhomogeneity of the thyroid gland, which did not change during the course of pregnancy nor during the post-partum period of eight weeks. There were no morphological changes in the thyroid glands of the control group. The mean thyroid volume did not significantly change during pregnancy and after delivery in both the patient group and controls. The mean thyroid volume was smaller in the study group, with 7.55 ml (SD 6.01) compared to the controls with 11.29 ml (SD 5.61), a difference which was not statistically significant. Neither course of pregnancy nor fetal outcome was influenced by inactive autoimmune disease of the thyroid. © 1993 John Wiley & Sons, Inc.     

调节性T细胞亚群与自身免疫性甲状腺疾病发病机制的关系

自身免疫性甲状腺疾病(autoimmune thyroid disease,AITD)是人类常见的器官特异性自身免疫性疾病之一。多年来,对于AITD有过很多的基础和临床研究,其发病机制不仅与遗传环境因素有关,且与免疫调节关系更为密切,但其具体的发病机制目前尚未得到完整的解释。调节性T细胞(regulatory T cells,Treg)和Th17细胞均属CD4+T细胞亚     

甲状腺自身抗体在自身免疫性甲状腺疾病诊断中的应用价值

目的 探究甲状腺自身抗体在自身免疫性甲状腺疾病(AITD)诊断中的应用价值.方法 选择2019年5月至2020年5月我院收治的80例AITD患者作为AITD组,其中34例为桥本甲状腺炎(HT),46例为毒性弥漫性甲状腺肿(Graves病);另选取同期我院50例健康体检者作为对照组.比较各组的促甲状腺激素受体抗体(TRA...     

Apoptosis in the pathogenesis of autoimmune thyroid disease]

Apoptosis is a physiological process of cell death that occurs as part of normal development and in response to a variety of physiological and pathophysiological stimuli. The effector mechanisms, which carry out the death program, are well preserved across species and evolution. This article summarizes the recent studies on apoptosis in view of its molecular mechanism and the relation to autoimmune thyroid diseases. In Hashimoto's thyroiditis, which is a typical organ-specific autoimmune disease, Fas-FasL-mediated apoptosis has been demonstrated as the mechanism of follicular epithelial cell death. In Graves' disease, Anti TSH receptor antibody inhibits Fas antigen-mediated apoptosis of thyrocytes through the inhibitory effect of Fas antigen expression, resulting in the promotion of growth of the thyroid gland.     

血清甲状腺球蛋白抗体、甲状腺微粒体抗体、甲状腺过氧化物酶抗体对自身免疫性甲状腺疾病的诊断价值

目的探讨血清甲状腺球蛋白抗体（TGAb）、甲状腺微粒体抗体（TMAb）、甲状腺过氧化物酶抗体（TPOAb）对自身免疫性甲状腺疾病（AITD）的诊断价值。方法100例甲状腺功能异常患者根据血清中三碘甲状腺原氨酸（B）、甲状腺素（Td）、促甲状腺激素（TSH）水平分为甲亢组和甲减组,每组50例;另选择50例甲状腺功能正常人群作为对照组。各组患者均采集静脉血5mL,分离血清,放射免疫法测定患者血清中TGAb、TMAb、TPOAb、L、T4、TSH水平。观察各组患者血清中TGAb、TMAb、TPOAb阳性率;比较各组TGAb、TMAb、TPOAb阳性患者血清水平。结果甲亢组和甲减组血清TPOAb阳性率均明显高于血清TGAb、TMAb阳性率;甲亢组、甲减组患者血清TGAb、TMAb、TPOAb阳性率均明显高于对照组;甲减组患者血清TGAb、TMAb、TPOAb阳性率均明显高于甲亢组。甲亢组和甲减组患者血清TGAb、TMAb、TPOAb水平均明显高于对照组。甲减组患者血清中TGAb、TMAb、TPOAb水平均明显高于甲亢组。结论TPOAb在AITD的诊断中具有重要意义,为AITD的诊断、治疗及预后评估提供了重要依据。     

Clinical application of ultrasonography to the autoimmune thyroid disease]

US images can detects exactly the size of thyroid gland. B-mode images with high resolution USG shows fine structure of thyroid gland. Furthermore, recent progress of ultrasonography can clarify the vascularity of thyroid gland using 3D-images. The thyroid gland of Graves' disease shows diffuse and remarkably increased vascularity. On the other hand, that of destructive thyroiditis reveals hypovascularity in hypoechoic lesion. There is the possibility that ultrasonographic images is useful tool to clarify the pathogenesis of autoimmune thyroid disease.     

Assessment of serum dipeptidyl peptidase-IV levels in autoimmune thyroid disease

ObjectiveDecreased serum dipeptidyl peptidase-IV (sDPPIV) levels have been reported in patients with autoimmune diseases. However, few studies have analyzed the association between sDPPIV levels and autoimmune thyroid disease (AITD). This study aimed to evaluate the association between sDPPIV levels and three types of AITD: Graves’ disease (GD), Graves’ ophthalmopathy (GO), and Hashimoto’s thyroiditis (HT).MethodsPatients newly diagnosed with GD (n = 65), GO (n = 22), and HT (n = 27) and healthy individuals (n = 30) were recruited. Clinical characteristics and thyroid function data were collected. sDPPIV was measured using enzyme-linked immunosorbent assays.ResultsCompared with controls (786.3 ± 46.95), patients with GD and GO had significantly lower sDPPIV levels (662.2 ± 38.81 and 438.4 ± 31.78). Additionally, sDPPIV levels were negatively associated with antithyroid peroxidase antibody (r = −0.20) and antithyroglobulin antibody (r = −0.19), but there was no significant relationship between thyroid hormone and sDPPIV levels. GO cases were divided by proptosis with and without muscle thickening; sDPPIV levels were lower in the muscle thickening group than those in the without muscle thickening group. Logistic regression analysis showed that sDPPIV was negatively correlated with GO and GD.ConclusionssDPPIV concentrations were abnormal in patients with GD and GO, and reduced sDPPIV expression may be involved in the progression of GO and GD.     

Infiltrating T-lymphocyte receptor Vbeta gene family utilization in autoimmune thyroid disease

The expression of T-cell antigen receptor (TCR) Vbeta genes in autoimmune thyroid diseases (AITDs) was investigated. RNA was extracted from the thyroid tissue of 23 patients with early-stage Graves' disease, 19 patients with late-stage Graves' disease and 20 patients with Hashimoto's disease. Peripheral blood lymphocytes from patients and 20 normal subjects (controls) were analysed in parallel. AITD was found to be associated with diminished TCR Vbeta gene family utilization. In addition, AITDs appeared to select for specific TCR Vbeta families. The Vbeta3, Vbeta5 and Vbeta8 families were expressed more frequently in thyroid-infiltrating T-lymphocytes of early-stage Graves' disease than other Vbeta gene families. Selective expression was not observed in infiltrating T-lymphocytes obtained from thyroid tissue of patients with late-stage Graves' disease or Hashimoto's disease. Preferentially expressed TCR Vbeta gene families may be useful as molecular targets for targeted immunotherapy of AITDs.     

系统性红斑狼疮伴自身免疫性甲状腺病的临床分析

目的探讨系统性红斑狼疮(systemic lupus erythematosus,SLE)伴发自身免疫性甲状腺病(autoimmune thyroid-ism disease,AITD)和甲状腺抗体的情况。方法采用放射免疫分析法测定100例SLE患者中甲状腺激素水平及血清甲状腺微粒体抗体(TMAb)和甲状腺球蛋白抗体(TGAb)水平。结果 100例SLE患者有9例(9%)伴发AITD,其中甲状腺功能减退6例,甲状腺功能亢进2例,亚急性甲状腺炎1例;伴发AITD的SLE患者出现甲状腺抗体的阳性率高于未伴发AITD的患者(P=0.000),合并甲状腺功能减退患者TMAb阳性率高于TGAb阳性率。结论 SLE患者甲状腺功能减退的发生率为6%,AITD发生率远高于普通人群0.4%,SLE伴发AITD并不少见,应重视甲状腺功能和甲状腺抗体的检测。     

Complications of extraintestinal endocrine disease associated with ulcerative colitis--association of ulcerative colitis and autoimmune thyroid disease

We experienced a rare case of Basedow's disease followed by ulcerative colitis (UC). The association of UC and autoimmune thyroid disease was reviewed and discussed. A high frequency of endocrine autoimmunity, especially autoimmune thyroid disease, was reported in patients with UC. But prevalence of autoimmune thyroid disease associated with UC varies widely in different studies. Some authors described that it was impossible to say that the observed numbers of UC associated with thyroid disease exceed to those to be expected in a random sample of the general populations. The hypothesis that autoimmunity is important in the pathogenesis of UC and thyroid disease continues to stimulate interest. But the evidence for autoimmunity acting in these diseases is not quite as convinced. Further investigation is warranted to clarify the exact relationships between UC and thyroid disease.