scholarly journals Impact of Abdominal Obesity on Thyroid Auto-Antibody Positivity: Abdominal Obesity Can Enhance the Risk of Thyroid Autoimmunity in Men

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Jazyra Zynat ◽  
Suli Li ◽  
Yanrong Ma ◽  
Li Han ◽  
Fuhui Ma ◽  
...  

Background. The interrelation between obesity and autoimmune thyroid diseases is complex and has not been confirmed. The aim of the present study was to observe the relationship between thyroid autoimmunity and obesity, especially abdominal obesity, in a large population. Methods. A total of 2253 residents who had lived in Xinjiang for more than 3 years were enrolled. Serum thyroid hormone concentration, thyroid autoantibodies, lipid parameters, Weight, height, and waist and hip circumference were measured. Results. The prevalence of thyroid peroxidase antibody (TPOAb) and/or thyroglobulin antibody (TgAb) positive was 32.1% (21.2% in men and 37% in women, P<0.01). Compared with women, men had significantly higher TG levels, waist circumference, and hip circumference levels (P<0.01), while women showed higher TSH, TPOAb, and TgAb levels (P<0.01). The prevalence of overweight and obesity was 71.1% in men and 63.5% in women. Men had a higher prevalence of abdominal obesity than women (56.6% in men and 47.6% in women, P<0.01). TPOAb correlates positively with waist circumference (r = 0.100, P<0.05) in men. Binary logistic analysis showed that TPOAb positivity had increased risks of abdominal obesity in men, and the OR was 1.1044 (95% CI 1.035, 1.151, P<0.05). Conclusion. Our results indicate that men had higher lipid levels, thicker waist circumference, and higher prevalence of overweight, obesity, and abdominal obesity. Abdominal obesity is a risk factor for TPOAb positivity in men, suggesting that abdominal obesity can enhance the risk of thyroid autoimmunity in men.

2012 ◽  
Vol 153 (26) ◽  
pp. 1013-1022 ◽  
Author(s):  
Csaba Balázs

Autoimmune thyroid diseases are the most common organ-specific autoimmune disorders affecting 5% to 10% of the population in Western countries. The clinical presentation varies from hyperthyroidism in Graves’ disease to hypothyroidism in Hashimoto’s thyroiditis. While the exact etiology of thyroid autoimmunity is not known, the interaction between genetic susceptibility and environmental factors appears to be of fundamental importance to initiate the process of thyroid autoimmunity. The identified autoimmune thyroid disease susceptibility genes include immune-modulating genes, such as the major histocompatibility complex, and thyroid-specific genes, including TSH receptor, thyroglobulin and thyroid peroxidase. The majority of the anti-TSH-receptor antibodies have a stimulating capacity and are responsible for hyperthyroidism. The anti-thyroglobulin- and anti-thyroid peroxidase antibodies belonging to the catalytic type of antibodies destroy the thyrocytes resulting in hypothyroidism. The appearance of anti-thyroid peroxidase antibodies precedes the induction of thyroiditis and the manifestation of hypothyroidism. The molecular analysis of thyroglobulin gene polymorphism is important in the mechanism of autoimmune thyroiditis. The autoantigen presentation by major histocompatibility complex molecules is a key point of the autoimmune mechanism. It has been shown that a HLA-DR variant containing arginine at position 74 of the DRβ1 chain confers a strong genetic susceptibility to autoimmune thyroid diseases, Graves’ disease and Hashimoto’s thyroiditis, while glutamine at position DRβ1-74 is protective. Human thyroglobulin 2098 peptide represents a strong and specific DRβ1-Arg74 binder, while a non-binding control peptide, thyroglobulin 2766 fails to induce this response. Moreover, thyroglobulin 2098 stimulated T-cells from individuals who were positive for thyroglobulin antibodies, demonstrating that thyroglobulin 2098 is an immunogenic peptide capable of being presented in vivo and activating T-cells in autoimmune thyroid diseases. Taken together these findings suggest that thyroglobulin 2098, a strong and specific binder to the disease-associated HLA-DRβ1-Arg74, is a major human T-cell epitope and it participates in the pathomechanism of the autoimmune thyroid disease. The exact nature of the role of environmental factors in the autoimmune thyroid disease is still not well known, but the importance of several factors such as iodine, drugs and infections has been reported. Further knowledge of the precise mechanisms of interaction between environmental factors and genes in inducing thyroid autoimmunity could result in the development of new strategies for diagnosis, prevention and treatment. Orv. Hetil., 2012, 153, 1013–1022.


2019 ◽  
Vol 51 (12) ◽  
pp. 765-769 ◽  
Author(s):  
Marlena Godlewska ◽  
Damian Gawel ◽  
Ashley M. Buckle ◽  
J. Paul Banga

AbstractThyroid peroxidase (TPO) is an enzyme that participates in thyroid hormone biosynthesis. TPO is also a major autoantigen in autoimmune thyroid diseases (AITD). In this review, we summarize the latest developments in the field of TPO research. We present the current understanding of immunodominant serologic determinants, frequency of TPO-specific autoantibodies in the population, as well as genetic and environmental factors contributing to their development. Moreover, we report recent progress in the clinical utilities of TPO autoantibody testing, including thyroid dysfunctions and extra-thyroidal disorders.


2002 ◽  
Vol 54 (3) ◽  
pp. 141-157 ◽  
Author(s):  
Thierry Chardès ◽  
Nicolas Chapal ◽  
Damien Bresson ◽  
Cédric Bès ◽  
Véronique Giudicelli ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Maria Segni ◽  
Ida Pucarelli ◽  
Simona Truglia ◽  
Ilaria Turriziani ◽  
Chiara Serafinelli ◽  
...  

Background. Antinuclear antibodies (ANA) are a hallmark of many autoimmune diseases and can be detected many years before disease onset. Autoimmune thyroid diseases (AITD) are frequently associated with other organ- and non-organ-specific autoimmune disorders.Objectives. To assess the prevalence of ANA in pediatric patients with AITD and their clinical correlations.Methods. Ninety-three consecutive pediatric patients with AITD were enrolled (86 children with chronic lymphocytic thyroiditis and 7 with Graves’ disease). ANA, anti-double DNA (anti-dsDNA) antibodies, anti-extractable nuclear antigen (anti-ENA), anti-cyclic citrullinated peptide antibodies (anti-CCP), and rheumatoid factor (RF) was obtained. Signs and symptoms potentially related to rheumatic diseases in children were investigated by a questionnaire.Results. ANA positivity was found in 66/93 children (71%), anti-ENA in 4/93 (4.3%), anti-dsDNA in 1/93 (1.1%), RF in 3/93 (3.2%), and anti-CCP in none. No significant differences were found between the ANA-positive and ANA-negative groups with respect to age, sex, L-thyroxine treatment, or prevalence of other autoimmune diseases. Overall, parental autoimmunity was found in 23%.Conclusions. ANA positivity was demonstrated in 71% of children with AITD. ANA positivity was not related to overt immune-rheumatic diseases. However, because the positivity of ANA can occur even many years before the onset of systemic autoimmune diseases, prospective studies are warranted.


2011 ◽  
Vol 96 (6) ◽  
pp. 1859-1863 ◽  
Author(s):  
Alessandro Antonelli ◽  
Silvia Martina Ferrari ◽  
Silvia Frascerra ◽  
Andrea Di Domenicantonio ◽  
Andrea Nicolini ◽  
...  

Context: Recently, CXCL9 and CXCL11 have been shown to be involved in autoimmune thyroid disorders; however, no data are present about CXCL9 and CXCL11 circulating levels in thyroid autoimmunity. Objective: Our objective was to evaluate circulating CXCL9 and CXCL11 in autoimmune thyroiditis (AIT). Design and Patients or Other Participants: Serum CXCL9 and CXCL11 have been measured in 141 consecutive patients with newly diagnosed AIT (AIT-p), 70 euthyroid controls, and 35 patients with nontoxic multinodular thyroid. The three groups were similar in gender distribution and age; among the AIT-p, 26% had subclinical hypothyroidism. Results: Serum CXCL9 and CXCL11 levels were significantly (P &lt; 0.0001 for both) higher in AIT-p (143 ± 164 and 121 ± 63 pg/ml, respectively) than in controls (68 ± 37 and 65 ± 19 pg/ml, respectively) or patients with multinodular thyroid (87 ± 43 and 71 ± 20 pg/ml, respectively). Among AIT-p, CXCL9 and CXCL11 levels were significantly higher in patients older than 50 yr or those with a hypoechoic ultrasonographic pattern or with hypothyroidism. In a multiple linear regression model including age, thyroid volume, hypoechogenicity, hypervascularity, TSH, anti-thyroglobulin, and anti-thyroid peroxidase, only age and TSH were significantly (P &lt; 0.05) related to serum CXCL9 or CXCL11 levels. In a multiple linear regression model of CXCL9 vs. age, TSH, and CXCL11, TSH (P = 0.032) and CXCL11 (P = 0.001) were significantly and independently related to CXCL9. Conclusions: We first show that circulating CXCL9 and CXCL11 are increased in patients with thyroiditis and hypothyroidism and are related to each other. These results underline the importance of a Th1 immune attack in the initiation of AIT.


2001 ◽  
Vol 22 (5) ◽  
pp. 605-630 ◽  
Author(s):  
Alex F. Muller ◽  
Hemmo A. Drexhage ◽  
Arie Berghout

Abstract Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of the thyroid. The prevalence ranges from 5–7%. We discuss the role of antibodies (especially thyroid peroxidase antibodies), complement, activated T cells, and apoptosis in the outbreak of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an acute phase of autoimmune thyroid destruction in the context of an existing and ongoing process of thyroid autosensitization. From pregnancy an enhanced state of immune tolerance ensues. A rebound reaction to this pregnancy-associated immune suppression after delivery explains the aggravation of autoimmune syndromes in the puerperal period, e.g., the occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve due to autoimmune thyroiditis is increasingly recognized as a serious health problem. 1) Thyroid autoimmunity increases the probability of spontaneous fetal loss. 2) Thyroid failure due to autoimmune thyroiditis—often mild and subclinical—can lead to permanent and significant impairment in neuropsychological performance of the offspring. 3) Evidence is emerging that as women age subclinical hypothyroidism—as a sequel of postpartum thyroiditis—predisposes them to cardiovascular disease. Hence, postpartum thyroiditis is no longer considered a mild and transient disorder. Screening is considered.


2008 ◽  
Vol 39 (5) ◽  
pp. 801-810 ◽  
Author(s):  
S. E. Saarni ◽  
S. I. Saarni ◽  
M. Fogelholm ◽  
M. Heliövaara ◽  
J. Perälä ◽  
...  

BackgroundThe literature suggests an association between obesity and schizophrenia but fat mass and fat-free mass, which have been shown to be more predictive of all-cause mortality than only waist circumference and obesity [body mass index (BMI) ⩾30 kg/m2], have not been reported in psychotic disorders. We examined the detailed body composition of people with different psychotic disorders in a large population-based sample.MethodWe used a nationally representative sample of 8082 adult Finns aged ⩾30 years with measured anthropometrics (height, weight, waist circumference, fat percentage, fat-free mass and segmental muscle mass). Psychiatric diagnoses were based on a consensus procedure utilizing the Structured Clinical Interview for DSM-IV (SCID)-interview, case-notes and comprehensive register data.ResultsSchizophrenia (including schizo-affective disorder) was associated with obesity [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.5–3.6], abdominal obesity (waist circumference ⩾88 cm for women, ⩾102 cm for men) (OR 2.2, 95% CI 1.3–3.6) and with higher fat percentage (mean difference 3.8%, 95% CI 2.0–5.7%), adjusted for age and gender, than in the remaining sample. The associations between schizophrenia and low fat-free mass and decreased muscle mass on trunk and upper limbs became statistically significant after adjusting for BMI. After further adjusting for current antipsychotic medication, education, diet and smoking, schizophrenia remained associated with obesity (OR 1.9, 95% CI 1.1–3.6) and abdominal obesity (OR 3.8, 95% CI 1.5–9.4). Participants with affective psychoses did not differ from the general population.ConclusionsIndividuals with schizophrenia have metabolically unfavorable body composition, comprising abdominal obesity, high fat percentage and low muscle mass. This leads to increased risk of metabolic and cardiovascular diseases.


Author(s):  
Tatjana Zaķe ◽  
Sandra Skuja ◽  
Aivars Lejnieks ◽  
Valērija Groma ◽  
Ilze Konrāde

Abstract Autoimmune thyroid diseases (AITD) mainly include Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), which are characterised by the presence of circulating antibodies against various thyroid autoantigens and infiltration of the thyroid gland by autoreactive lymphocytes. Despite the significant advancement in the knowledge of AITD pathogenesis in the last decade, the specific immunological mechanisms responsible for development of the disease are not thoroughly understood. Classically, HT has long been considered as a T helper (Th)1-mediated disease, while a Th2-driven autoimmune response is dominant for GD development. However, this classification has changed due to the description of Th17 lymphocytes, which suggested participation of these cells in AITD, particularly HT pathogenesis. Moreover, a shift in the balance between Th17 and T regulatory (Treg) cells has been observed in thyroid autoimmunity. We have observed overexpression of IL-17, the prominent effector cytokine of Th17, within thyroid tissues from HT and GD patients in our studies. The present review will focus on recent data regarding the role of Treg and Th17 lymphocytes in AITD pathogenesis. In addition, the impact and proposed mechanisms of the predominant environmental factors triggering the autoimmune response to the thyroid will be discussed.


2008 ◽  
Vol 158 (3) ◽  
pp. 367-373 ◽  
Author(s):  
Inge Bülow Pedersen ◽  
Peter Laurberg ◽  
Nils Knudsen ◽  
Torben Jørgensen ◽  
Hans Perrild ◽  
...  

BackgroundAutoimmune thyroid diseases are common and the prevalence of circulating thyroid antibodies (thyroid peroxidase antibody, TPO-Ab and thyroglobulin antibody, Tg-Ab) is high in the population. The knowledge of a possible association between lifestyle factors and circulating thyroid antibodies is limited.AimTo evaluate the correlation between smoking habits and the presence of circulating TPO-Ab and Tg-Ab.Material and methodsIn a cross-sectional comparative population study performed in two areas of Denmark with moderate and mild iodine deficiency, 4649 randomly selected subjects from the population in some predefined age groups between 18 and 65 years were examined. Blood tests were analysed for TPO-Ab and Tg-Ab using assays based on the RIA technique. The participants answered questionnaires, were clinically examined and blood and urine samples collected.ResultsData were analysed in multivariate logistic regression models. There was a negative association between smoking and the presence of thyroid autoantibodies in serum. This association was observed for the presence of TPO-Ab and/or Tg-Ab, TPO-Ab (without respect to Tg-Ab status), Tg-Ab (without respect to TPO-Ab status) and both antibodies together. The association between smoking and thyroid autoantibodies was stronger for Tg-Ab than for TPO-Ab. There was no association between smoking and TPO-Ab measured alone or between smoking and TPO-Ab when Tg-Ab was included in the model as an explanatory variable.ConclusionSmoking was negatively associated with the presence of thyroid autoantibodies with the strongest association between smoking and Tg-Ab. The study design precludes any conclusions as to the cause of the negative association between smoking thyroid autoantibodies.


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