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Renea A Taylor Department of Physiology, Cancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia

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Jennifer Lo Department of Physiology, Cancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia

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Natasha Ascui Department of Physiology, Cancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia

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Matthew J Watt Department of Physiology, Cancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia

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The global epidemic of obesity is closely linked to the development of serious co-morbidities, including many forms of cancer. Epidemiological evidence consistently shows that obesity is associated with a similar or mildly increased incidence of prostate cancer but, more prominently, an increased risk for aggressive prostate cancer and prostate cancer-specific mortality. Studies in mice demonstrate that obesity induced by high-fat feeding increases prostate cancer progression; however, the mechanisms underpinning this relationship remain incompletely understood. Adipose tissue expansion in obesity leads to local tissue dysfunction and is associated with low-grade inflammation, alterations in endocrine function and changes in lipolysis that result in increased delivery of fatty acids to tissues of the body. The human prostate gland is covered anteriorly by the prominent peri-prostatic adipose tissue and laterally by smaller adipose tissue depots that lie directly adjacent to the prostatic surface. We discuss how the close association between dysfunctional adipose tissue and prostate epithelial cells might result in bi-directional communication to cause increased prostate cancer aggressiveness and progression. However, the literature indicates that several ‘mainstream’ hypotheses regarding obesity-related drivers of prostate cancer progression are not yet supported by a solid evidence base and, in particular, are not supported by experiments using human tissue. Understanding the links between obesity and prostate cancer will have major implications for the health policy for men with prostate cancer and the development of new therapeutic or preventative strategies.

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Elizabeth Yan Zhang Department of Pharmacology, Department of Biology, Toxicology and Therapeutics, School of Medicine, University of Kansas Medical Center, Room 4061 of KLSIC Building, 2146 West 39th Street, Kansas City, Kansas 66160, USA

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Bao-Ting Zhu Department of Pharmacology, Department of Biology, Toxicology and Therapeutics, School of Medicine, University of Kansas Medical Center, Room 4061 of KLSIC Building, 2146 West 39th Street, Kansas City, Kansas 66160, USA
Department of Pharmacology, Department of Biology, Toxicology and Therapeutics, School of Medicine, University of Kansas Medical Center, Room 4061 of KLSIC Building, 2146 West 39th Street, Kansas City, Kansas 66160, USA

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The endogenous estrogens are important modulators of the immune system and its functions. However, their effects are rather complex and many aspects have not been studied. In this study, we used the 1-chloro-2,4-dinitrobenzene (DNCB)-induced contact dermatitis as a disease model and investigated the effect of estriol (E3), along with two other estrogens, 17β-estradiol and estrone, on the pathogenesis of contact hypersensitivity. A series of parameters, such as ear swelling, skin inflammation, antigen-specific immunoglobulins, and lymphocyte compositions in peripheral lymphoid organs, were evaluated in mice following development of contact dermatitis. We found that administration of all three estrogens elicited strong inhibition of DNCB-induced dermatitis, while E3 exerted the strongest suppressive effect. Administration of E3 alleviated dermatitis, and this effect was accompanied by decreases in serum DNCB-specific immunoglobulins, such as IgA, IgG1, IgG2a, and IgG2b. Besides, treatment with E3 reduced B cell population, especially IgG-producing cells in the peripheral lymphoid organs following the induction of dermatitis. These observations consistently suggest that the antibody (Ab)-mediated humoral immune reactions play a critical role in the pathogenesis of DNCB-induced contact dermatitis. The results from this study demonstrate, for the first time, that estrogen administration has a strong suppressive effect on the pathogenesis of contact dermatitis. These findings offer important insights concerning the pathogenic role of antigen-specific Abs in contact dermatitis and the treatment of chemical-induced, Ab-mediated skin hypersensitivity reactions in humans.

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Karim Gariani Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition

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Geneviève Drifte Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition
Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition

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Irène Dunn-Siegrist Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition
Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition

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Jérôme Pugin Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition
Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition

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François R Jornayvaz Service of Endocrinology, Laboratory of Intensive Care, Department of Microbiology and Molecular Medicine, Diabetes, Hypertension and Nutrition

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Fibroblast growth factor 21 (FGF21) is a key regulator in glucose and lipid metabolism and its plasma levels have been shown to be increased not only in humans in different situations such as type 2 diabetes, obesity, and nonalcoholic fatty liver disease but also in animal models of sepsis and pancreatitis. FGF21 is considered as a pharmacological candidate in conditions associated with insulin resistance. The aim of this study was to compare FGF21 plasma levels in patients with sepsis, in patients with systemic inflammatory response syndrome (SIRS), and in healthy controls. We measured FGF21 plasma concentrations in 22 patients with established sepsis, in 11 with SIRS, and in 12 healthy volunteers. Here, we show that FGF21 levels were significantly higher in plasma obtained from patients with sepsis and SIRS in comparison with healthy controls. Also, FGF21 levels were significantly higher in patients with sepsis than in those with noninfectious SIRS. FGF21 plasma levels measured at study entry correlated positively with the APACHE II score, but not with procalcitonin levels, nor with C-reactive protein, classical markers of sepsis. Plasma concentrations of FGF21 peaked near the onset of shock and rapidly decreased with clinical improvement. Taken together, these results indicate that circulating levels of FGF21 are increased in patients presenting with sepsis and SIRS, and suggest a role for FGF21 in inflammation. Further studies are needed to explore the potential role of FGF21 in sepsis as a potential therapeutic target.

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Tatsuya Kondo Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Chuo-Ward, Kumamoto, Japan

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Nobukazu Miyakawa Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Sayaka Kitano Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Chuo-Ward, Kumamoto, Japan

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Takuro Watanabe Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Rieko Goto Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Mary Ann Suico Department of Molecular Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Miki Sato Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Yuki Takaki Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Masaji Sakaguchi Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Motoyuki Igata Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, Chuo-Ward, Kumamoto, Japan

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Junji Kawashima Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Hiroyuki Motoshima Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Takeshi Matsumura Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Hirofumi Kai Department of Molecular Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Eiichi Araki Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Chuo-Ward, Kumamoto, Japan

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Nonalcoholic fatty liver disease (NAFLD) is often accompanied by metabolic disorders such as metabolic syndrome and type 2 diabetes (T2DM). Heat shock response (HSR) is one of the most important homeostatic abilities but is deteriorated by chronic metabolic insults. Heat shock (HS) with an appropriate mild electrical stimulation (MES) activates HSR and improves metabolic abnormalities including insulin resistance, hyperglycemia and inflammation in metabolic disorders. To analyze the effects of HS + MES treatment on NAFLD biomarkers, three cohorts including healthy men (two times/week, n = 10), patients with metabolic syndrome (four times/week, n = 40), and patients with T2DM (n = 100; four times/week (n = 40) and two, four, seven times/week (n = 20 each)) treated with HS + MES were retrospectively analyzed. The healthy subjects showed no significant alterations in NAFLD biomarkers after the treatment. In patients with metabolic syndrome, many of the NAFLD steatosis markers, including fatty liver index, NAFLD-liver fat score, liver/spleen ratio and hepatic steatosis index and NAFLD fibrosis marker, aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio, were improved upon the treatment. In patients with T2DM, all investigated NAFLD steatosis markers were improved and NAFLD fibrosis markers such as the AST/ALT ratio, fibrosis-4 index and NAFLD-fibrosis score were improved upon the treatment. Thus, HS + MES, a physical intervention, may become a novel treatment strategy for NAFLD as well as metabolic disorders.

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Ling Zhou Cangzhou Central Hospital, Cangzhou, Hebei, China

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Ruixue Zhang Cangzhou Central Hospital, Cangzhou, Hebei, China

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Shuangyan Yang Cangzhou Central Hospital, Cangzhou, Hebei, China

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Yaguang Zhang Cangzhou Central Hospital, Cangzhou, Hebei, China

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Dandan Shi Cangzhou Central Hospital, Cangzhou, Hebei, China

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Background:

Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM.

Methods:

First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated.

Results:

AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway.

Conclusion:

AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.

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Angelo Maria Patti Department of Internal Medicine and Medical Specialties, University of Palermo, Palermo, Italy

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Kalliopi Pafili Diabetes Centre, Second Department of Internal Medicine, Democritus University of Thrace, University Hospital of Alexandroupolis, Alexandroupolis, Greece

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Nikolaos Papanas Diabetes Centre, Second Department of Internal Medicine, Democritus University of Thrace, University Hospital of Alexandroupolis, Alexandroupolis, Greece

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Manfredi Rizzo Department of Internal Medicine and Medical Specialties, University of Palermo, Palermo, Italy

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Hormonal changes during pregnancy can trigger gestational diabetes (GDM), which is constantly increasing. Its main characteristic is pronounced insulin resistance, but it appears to be a multifactorial process involving several metabolic factors; taken together, the latter leads to silent or clinically evident cardiovascular (CV) events. Insulin resistance and central adiposity are of crucial importance in the development of metabolic syndrome, and they appear to correlate with CV risk factors, including hypertension and atherogenic dyslipidaemia. Hypertensive disease of pregnancy (HDP) is more likely to be an accompanying co-morbidity in pregnancies complicated with GDM. There is still inconsistent evidence as to whether or not co-existent GDM and HDP have a synergistic effects on postpartum risk of cardiometabolic disease; however, this synergism is becoming more accepted since both these conditions may promote endothelial inflammation and early atherosclerosis. Regardless of the presence or absence of the synergism between GDM and HDP, these conditions need to be dealt early enough, in order to reduce CV morbidity and to improve health outcomes for both women and their offspring.

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Stavroula A Paschou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Nektaria Papadopoulou-Marketou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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George P Chrousos Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Christina Kanaka-Gantenbein Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

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Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of β cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the β cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy β cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of β cells that need to be destroyed before overt diabetes become evident.

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Nancy J Olsen Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

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Ann L Benko Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

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William J Kovacs Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

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Clinical and experimental evidence support a role for gonadal steroids in modulating the expression and course of autoimmune diseases such as lupus. Whether or not inherited variation in sensitivity to circulating androgenic hormones could influence the manifestations of such disease is, however, unknown. We sought to determine whether differences in androgen sensitivity conferred by variation in the exon 1 CAG repeat region of the androgen receptor (AR) gene were associated with differences in the clinical or humoral immune manifestations of lupus in a cohort of female subjects. We found that shorter AR CAG repeat lengths in lupus subjects correlated with a higher Systemic Lupus Erythematosus Disease Activity Index score, higher ANA levels, and expression of a broader array of IgG autoantibodies. Our findings of more severe clinical manifestations and more exuberant humoral autoimmunity in women with a shorter AR exon 1 CAG repeat length suggest a role for genetically determined sensitivity to androgens as a modulator of autoimmune processes.

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Weiwei He Department of Endocrinology, Affiliated Hospital of Yanan Medical University, Shaanxi, China

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Bin Wang Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, China

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Kaida Mu Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

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Jing Zhang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

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Yanping Yang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

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Wei Yao Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

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Sheli Li Department of Endocrinology, Affiliated Hospital of Yanan Medical University, Shaanxi, China

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Jin-an Zhang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

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Background

Accumulating data have shown that interleukin-27 (IL27) polymorphisms are linked to the susceptibility of some autoimmune diseases. We assessed whether there was an association between three single-nucleotide polymorphisms (SNPs) of IL27 gene and autoimmune thyroid diseases (AITDs).

Methods

Three SNPs (rs153109, rs17855750 and rs181206) of IL27 gene were genotyped by Hi-SNP high-throughput genotyping in 843 patients with AITDs (516 Graves’ disease (GD) and 327 Hashimoto’s thyroiditis (HT)) and 677 healthy controls in Chinese Han population.

Results

Compared with controls, rs153109 displayed significant associations with GD in allele and genotype frequencies (P = 0.002 and P = 0.008, respectively) and rs17855750 displayed significant associations with HT in allele frequencies (P = 0.02), whereas no differences in genotype or allele frequencies were found between AITD patients and controls at rs181206.

Conclusion

Our study, for the first time, showed the significant association of the IL27 gene SNPs with AITD.

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Aaron Lerner B. Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
AESKU.KIPP Institute, Wendelsheim, Germany

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Patricia Jeremias AESKU.KIPP Institute, Wendelsheim, Germany

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Torsten Matthias AESKU.KIPP Institute, Wendelsheim, Germany

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Autoimmune thyroiditis has an increased prevalence in patients with celiac disease and vice versa. The objective of the current review is to highlight the epidemiological, clinical, serological, pathological, pathophysiological, hormonal, genetic and immunological factors shared between the two entities. They might represent the two ends of the gut-thyroid axis where the cross-talks’ pathways are still unravelled. New observations are reviewed, highlighting some gut-thyroid interrelated pathways that potentially might lead to new therapeutic strategies.

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