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Ghazala Zaidi Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Vijayalakshmi Bhatia Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Saroj K Sahoo Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Aditya Narayan Sarangi Departments of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Niharika Bharti Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Li Zhang Department of Immunology, Barbara Davis Centre for Childhood Diabetes, Denver, USA

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Liping Yu Department of Immunology, Barbara Davis Centre for Childhood Diabetes, Denver, USA

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Daniel Eriksson Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden

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Sophie Bensing Department of Molecular Medicine and Surgery, Karolinska Institutet, and Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden

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Olle Kämpe Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden

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Nisha Bharani Department of Endocrinology, Amrita Institute of Medical Sciences, Kochi, India

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Surendra Kumar Yachha Departments of Paediatric Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Anil Bhansali Department of Endocrinology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

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Alok Sachan Department of Endocrinology, Sri Venkateshwara Institute of Medical Sciences, Tirupathi, India

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Vandana Jain Department of Paediatrics, All India Institute of Medical Sciences, New Delhi, India

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Nalini Shah Department of Endocrinology, King Edward Memorial Hospital, Seth GS Medical College, Mumbai, India

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Rakesh Aggarwal Departments of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Amita Aggarwal Departments of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Muthuswamy Srinivasan Departments of Medical Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Sarita Agarwal Departments of Medical Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Eesh Bhatia Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Objective

Autoimmune polyendocrine syndrome type 1 (APS1) is a rare autosomal recessive disorder characterized by progressive organ-specific autoimmunity. There is scant information on APS1 in ethnic groups other than European Caucasians. We studied clinical aspects and autoimmune regulator (AIRE) gene mutations in a cohort of Indian APS1 patients.

Design

Twenty-three patients (19 families) from six referral centres in India, diagnosed between 1996 and 2016, were followed for [median (range)] 4 (0.2–19) years.

Methods

Clinical features, mortality, organ-specific autoantibodies and AIRE gene mutations were studied.

Results

Patients varied widely in their age of presentation [3.5 (0.1–17) years] and number of clinical manifestations [5 (2–11)]. Despite genetic heterogeneity, the frequencies of the major APS1 components (mucocutaneous candidiasis: 96%; hypoparathyroidism: 91%; primary adrenal insufficiency: 55%) were similar to reports in European series. In contrast, primary hypothyroidism (23%) occurred more frequently and at an early age, while kerato-conjunctivitis, urticarial rash and autoimmune hepatitis were uncommon (9% each). Six (26%) patients died at a young age [5.8 (3–23) years] due to septicaemia, hepatic failure and adrenal/hypocalcaemic crisis from non-compliance/unexplained cause. Interferon-α and/or interleukin-22 antibodies were elevated in all 19 patients tested, including an asymptomatic infant. Eleven AIRE mutations were detected, the most common being p.C322fsX372 (haplotype frequency 37%). Four mutations were novel, while six others were previously described in European Caucasians.

Conclusions

Indian APS1 patients exhibited considerable genetic heterogeneity and had highly variable clinical features. While the frequency of major manifestations was similar to that of European Caucasians, other features showed significant differences. A high mortality at a young age was observed.

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Lia Ferreira Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

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João Silva Department of Endocrinology, Hospital das Forças Armadas, Lisboa, Portugal

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Susana Garrido Department of Endocrinology, Centro Hospitalar Tâmega e Sousa, Porto, Portugal

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Carlos Bello Department of Endocrinology, Centro Hospitalar Lisboa Ocidental, Lisboa, Portugal

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Diana Oliveira Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

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Hélder Simões Department of Endocrinology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Isabel Paiva Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

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Joana Guimarães Department of Endocrinology, Centro Hospitalar do Baixo Vouga, Aveiro, Portugal

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Marta Ferreira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

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Teresa Pereira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

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Rita Bettencourt-Silva Department of Endocrinology, Centro Hospitalar de São João, Porto, Portugal

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Ana Filipa Martins Department of Endocrinology, Centro Hospitalar Lisboa Norte, Lisboa, Portugal

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Tiago Silva Department of Endocrinology, Hospital Garcia da Orta, Lisboa, Portugal

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Vera Fernandes Department of Endocrinology, Hospital de Braga, Braga, Portugal

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Maria Lopes Pereira Department of Endocrinology, Hospital de Braga, Braga, Portugal

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Adrenal Tumors Study Group of the Portuguese Society of Endocrinology Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

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Introduction

Primary adrenal insufficiency (PAI) is a rare but severe and potentially life-threatening condition. No previous studies have characterized Portuguese patients with PAI.

Aims

To characterize the clinical presentation, diagnostic workup, treatment and follow‐up of Portuguese patients with confirmed PAI.

Methods

This multicentre retrospective study examined PAI patients in 12 Portuguese hospitals.

Results

We investigated 278 patients with PAI (55.8% were females), with a mean age of 33.6 ± 19.3 years at diagnosis. The most frequent presenting clinical features were asthenia (60.1%), mucocutaneous hyperpigmentation (55.0%) and weight loss (43.2%); 29.1% of the patients presented with adrenal crisis. Diagnosis was established by high plasma ACTH and low serum cortisol in most patients (43.9%). The most common aetiology of PAI was autoimmune adrenalitis (61.0%). There were 38 idiopathic cases. Autoimmune comorbidities were found in 70% of the patients, the most frequent being autoimmune thyroiditis (60.7%) and type 1 diabetes mellitus (17.3%). Seventy-nine percent were treated with hydrocortisone (mean dose 26.3 ± 8.3 mg/day) mostly in three (57.5%) or two (37.4%) daily doses. The remaining patients were treated with prednisolone (10.1%), dexamethasone (6.2%) and methylprednisolone (0.7%); 66.2% were also on fludrocortisone (median dose of 100 µg/day). Since diagnosis, 33.5% of patients were hospitalized for disease decompensation. In the last appointment, 17.2% of patients had complaints (7.6% asthenia and 6.5% depression) and 9.7% had electrolyte disturbances.

Conclusion

This is the first multicentre Portuguese study regarding PAI. The results emphasize the need for standardization in diagnostic tests and etiological investigation and provide a framework for improving treatment.

Open access
Elinor Chelsom Vogt Department of Clinical Science, University of Bergen, Bergen, Norway
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Francisco Gómez Real Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Gynecology and Obstetrics, Haukeland University Hospital, Bergen, Norway

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Eystein Sverre Husebye Department of Clinical Science, University of Bergen, Bergen, Norway
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Sigridur Björnsdottir Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden

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Bryndis Benediktsdottir Medical Faculty, University of Iceland, Reykjavik, Iceland
Department of Sleep, Landspitali University Hospital Reykjavík, Reykjavik, Iceland

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Randi Jacobsen Bertelsen Department of Clinical Science, University of Bergen, Bergen, Norway

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Pascal Demoly University Hospital of Montpellier, IDESP, Univ Montpellier-Inserm, Montpellier, France

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Karl Anders Franklin Department of Surgical and Perioperative Sciences, Surgery, Umeå University, Umeå, Sweden

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Leire Sainz de Aja Gallastegui Unit of Epidemiology and Public Health, Department of Health, Basque Government, Vitoria-Gasteiz, Spain

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Francisco Javier Callejas González Department of Respiratory Medicine, Albacete University Hospital, Albacete, Spain

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Joachim Heinrich Institute and Clinic for Occupational, Social and Environmental Medicine, University Hospital, LMU Munich, Munich, Germany
Allergy and Lung Health Unit, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia

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Mathias Holm Occupational and Environmental Medicine, School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Nils Oscar Jogi Department of Clinical Science, University of Bergen, Bergen, Norway

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Benedicte Leynaert Université Paris-Saclay, Inserm U1018, Center for Epidemiology and Population Health, Integrative Respiratory Epidemiology Team, Villejuif, France

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Eva Lindberg Department of Medical Sciences, Respiratory, Allergy and Sleep Medicine, Uppsala University, Uppsala, Sweden

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Andrei Malinovschi Department of Medical Sciences, Clinical Physiology, Uppsala University, Uppsala, Sweden

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Jesús Martínez-Moratalla Pneumology Service of the General University Hospital of Albacete, Albacete, Spain
Albacete Faculty of Medicine, Castilla-La Mancha University, Albacete, Spain

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Raúl Godoy Mayoral Department of Respiratory Medicine, Albacete University Hospital, Albacete, Spain

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Anna Oudin Section of Sustainable Health, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

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Antonio Pereira-Vega Juan Ramón Jiménez University Hospital in Huelva, Huelva, Spain

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Chantal Raherison Semjen INSERM, EpiCene Team U1219, University of Bordeaux, Talence, France

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Vivi Schlünssen Department of Public Health, Environment, Work and Health, Danish Ramazzini Centre, Aarhus University, Aarhus, Denmark
The National Research Center for the Working Environment, Copenhagen, Denmark

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Kai Triebner Department of Clinical Science, University of Bergen, Bergen, Norway

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Marianne Øksnes Department of Clinical Science, University of Bergen, Bergen, Norway
K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Objective

To investigate markers of premature menopause (<40 years) and specifically the prevalence of autoimmune primary ovarian insufficiency (POI) in European women.

Design

Postmenopausal women were categorized according to age at menopause and self-reported reason for menopause in a cross-sectional analysis of 6870 women.

Methods

Variables associated with the timing of menopause and hormone measurements of 17β-estradiol and follicle-stimulating hormone were explored using multivariable logistic regression analysis. Specific immunoprecipitating assays of steroidogenic autoantibodies against 21-hydroxylase (21-OH), side-chain cleavage enzyme (anti-SCC) and 17alpha-hydroxylase (17 OH), as well as NACHT leucine-rich-repeat protein 5 were used to identify women with likely autoimmune POI.

Results

Premature menopause was identified in 2.8% of women, and these women had higher frequencies of nulliparity (37.4% vs 19.7%), obesity (28.7% vs 21.4%), osteoporosis (17.1% vs 11.6%), hormone replacement therapy (59.1% vs 36.9%) and never smokers (60.1% vs 50.9%) (P < 0.05), compared to women with menopause ≥40 years. Iatrogenic causes were found in 91 (47%) and non-ovarian causes in 27 (14%) women, while 77 (39%) women were classified as POI of unknown cause, resulting in a 1.1% prevalence of idiopathic POI. After adjustments nulliparity was the only variable significantly associated with POI (odds ratio 2.46; 95% CI 1.63–3.42). Based on the presence of autoantibodies against 21 OH and SCC, 4.5% of POI cases were of likely autoimmune origin.

Conclusion

Idiopathic POI affects 1.1% of all women and almost half of the women with premature menopause. Autoimmunity explains 4.5% of these cases judged by positive steroidogenic autoantibodies.

Open access
Sriharsha Gunna Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Mahaveer Singh Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Rakesh Pandey Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Rungmei S K Marak Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Amita Aggarwal Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Bibhuti Mohanta Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Liping Yu Barbara Davis Centre for Diabetes, School of Medicine University of Colorado, Aurora, Colorado, USA

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Eesh Bhatia Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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The etiology, presentation and mortality of patients with primary adrenal insufficiency (PAI) in developing countries may differ from economically developed nations. However, information in this regard is scanty. The aim of this study was to determine the etiology and compare the clinical characteristics and mortality in infectious and autoimmune causes of PAI in Indian patients. All eligible (n = 89) patients (ages 15–83 years) diagnosed with PAI between 2006 and 2019 were studied. Patients were followed for a median duration of 5.9 (range 0.1–15.7) years. Eighty-six subjects underwent an abdominal computerized tomography scan or ultrasonography, and adrenal biopsy was performed in 60 patients. The most frequent etiologies of PAI were adrenal histoplasmosis (AH, 45%), adrenal tuberculosis (AT, 15%), autoimmunity (AI, 25%) and primary lymphoma (6%). Forty-two percent of patients presented with an acute adrenal crisis. AH and AT could not be differentiated on the basis of clinical features, except for a greater frequency of hepatomegaly–splenomegaly and type 2 diabetes mellitus (63% vs 15%, P < 0.01) in the former. Patients with an autoimmune etiology had a higher frequency of 21-hydroxylase antibodies (41% vs 3%) and autoimmune thyroid disease (46% vs 5%) vs those with infectious etiologies. Mortality was significantly higher in AH (45%) compared with AT (8%) or AI (5%) (P = 0.001). Causes of death included adrenal crises, progressive AH and unexplained acute events occurring at home. In conclusion, infections, especially AH, were the most frequent cause of PAI in north India. Despite appropriate therapy, AH had very high mortality as compared with AT and AI.

Open access
M A Webb NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK

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H Mani Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK
Department of Diabetes and Endocrinology, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester, UK
Diabetes and Endocrinology Department, Kettering General Hospital NHS Foundation Trust, Kettering, UK

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S J Robertson The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK

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H L Waller Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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D R Webb NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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C L Edwardson NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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D H Bodicoat NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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T Yates NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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K Khunti NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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M J Davies NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit, University Hospitals of Leicester, Leicester General Hospital, Leicester, UK
The Leicester Diabetes Centre, University Hospitals of Leicester NHS Trust, Leicester General Hospital, Leicester, UK
Diabetes Research Centre, University of Leicester, Leicester General Hospital, Leicester, UK

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Aims

Physical activity has been proposed to be an effective non-pharmacological method of reducing systemic inflammation and therefore may prove particularly efficacious for women with polycystic ovary syndrome (PCOS) who have been shown to have high levels of inflammation and an increased risk of type 2 diabetes (T2DM) and cardiovascular disease (CVD). Therefore, the aim of the present study was to assess whether modest changes in daily step count could significantly reduce levels of inflammatory markers in women with PCOS.

Subjects and Methods

Sixty-five women with PCOS were assessed at baseline and again at 6 months. All had been provided with an accelerometer and encouraged to increase activity levels. Multivariate linear regression analyses (adjusted for age, ethnicity, baseline step count, change in BMI and change in accelerometer wear-time) were used to assess changes in daily step count against clinical and research biomarkers of inflammation, CVD and T2DM.

Results

Mean step count/day at baseline was 6337 (±270). An increase in step count (by 1000 steps) was associated with a 13% reduction in IL6 (β: −0.81 ng/L; 95% CI, −1.37, −0.25, P = 0.005) and a 13% reduction in CRP (β: −0.68 mg/L; 95% CI, −1.30, −0.06, P = 0.033). Additionally, there was a modest decrease in BMI (β: 0.20 kg/m2; 95% CI, −0.38, −0.01, P = 0.038). Clinical markers of T2DM and CVD were not affected by increased step count.

Conclusions

Modest increases in step count/day can reduce levels of inflammatory markers in women with PCOS, which may reduce the future risk of T2DM and CVD.

Open access
Milica Popovic Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland

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Fahim Ebrahimi Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland

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Sandrine Andrea Urwyler Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland

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Marc Yves Donath Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Biomedicine, University of Basel, Basel, Switzerland

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Mirjam Christ-Crain Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland
Department of Clinical Research, University of Basel and University Hospital Basel, Basel, Switzerland

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Arginine vasopressin (AVP) was suggested to contribute to cardiovascular risk and type 2 diabetes in patients with metabolic syndrome. The proinflammatory cytokine interleukin (IL)-1 is able to induce AVP secretion and plays a causal role in cardiovascular mortality and type 2 diabetes. We investigated in two studies whether copeptin levels – the surrogate marker for AVP – are regulated by IL-1-mediated chronic inflammation in patients with metabolic syndrome. Study A was a prospective, interventional, single-arm study (2014–2016). Study B was a randomized, placebo-controlled, double-blind study (2016–2017). n = 73 (Study A) and n = 66 (Study B) adult patients with metabolic syndrome were treated with 100 mg anakinra or placebo (only in study B) twice daily for 1 day (study A) and 28 days (study B). Fasting blood samples were drawn at day 1, 7, and 28 of treatment for measurement of serum copeptin. Patients with chronic low-grade inflammation (C-reactive protein levels ≥2 mg/L) and BMI >35 kg/m2 had higher baseline copeptin levels (7.7 (IQR 4.9–11.9) vs 5.8 (IQR 3.9–9.3) pmol/L, P inflamm = 0.009; 7.8 (IQR 5.4–11.7) vs 4.9 (IQR 3.7–9.8) pmol/L, P BMI = 0.008). Copeptin levels did not change either in the anakinra or in the placebo group and remained stable throughout the treatment (P = 0.44). Subgroup analyses did not reveal effect modifications. Therefore, we conclude that, although IL-1-mediated inflammation is associated with increased circulating copeptin levels, antagonizing IL-1 does not significantly alter copeptin levels in patients with metabolic syndrome.

Open access
Xiao-Shan Huang Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Ning Dai Zhejiang Chinese Medical University, Hangzhou, China

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Jian-Xia Xu Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Jun-Yi Xiang Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Xiao-Zhong Zheng Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Tian-Yu Ke Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Lin-Ying Ma Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Qi-Hao Shi Zhejiang Chinese Medical University, Hangzhou, China

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Shu-Feng Fan Department of Radiology, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China

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Objective

Hashimoto’s thyroiditis is an inflammatory disease, and research suggests that a low-carbohydrate diet may have potential anti-inflammatory effects. This study aims to utilize Dixon-T2-weighted imaging (WI) sequence for a semi-quantitative assessment of the impact of a low-carbohydrate diet on the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis.

Methods

Forty patients with Hashimoto’s thyroiditis were recruited for this study and randomly divided into two groups: one with a normal diet and the other with a low-carbohydrate diet. Antibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb) were measured for all participants. Additionally, thyroid water content was semi-quantitatively measured using Dixon-T2WI. The same tests and measurements were repeated for all participants after 6 months.

Results

After 6 months of a low-carbohydrate diet, patients with Hashimoto’s thyroiditis showed a significant reduction in thyroid water content (94.84 ± 1.57% vs 93.07 ± 2.05%, P < 0.05). Concurrently, a decrease was observed in levels of TPOAb and TgAb (TPOAb: 211.30 (92.63–614.62) vs 89.45 (15.9–215.67); TgAb: 17.05 (1.47–81.64) vs 4.1 (0.51–19.42), P < 0.05). In contrast, there were no significant differences in thyroid water content or TPOAb and TgAb levels for patients with Hashimoto’s thyroiditis following a normal diet after 6 months (P < 0.05).

Conclusion

Dixon-T2WI can quantitatively assess the degree of thyroid inflammation in patients with Hashimoto’s thyroiditis. Following a low-carbohydrate diet intervention, there is a significant reduction in thyroid water content and a decrease in levels of TPOAb and TgAb. These results suggest that a low-carbohydrate diet may help alleviate inflammation in patients with Hashimoto’s thyroiditis.

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Borros Arneth Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, University Hospital of the Universities of Giessen and Marburg, UKGM, Justus Liebig University, Giessen, Giessen, Germany

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Background

The origin of autoimmune disease type 1 diabetes is still unknown.

Aim

This study assessed the activation of CD4+ and CD8+ T-lymphocytes by human insulin and human glutamate decarboxylase (GAD) in patients with type 1 or type 2 diabetes mellitus (DM) and healthy volunteers.

Materials and methods

The expression of CD69, a marker of T-lymphocyte activity, was determined in whole blood samples by flow cytometry after 12 h of incubation with or without insulin or GAD. The analysis included samples from 12 type 1 DM patients, 14 type 2 DM patients and 12 healthy volunteers.

Results

Significant increases in the number of activated CD4+ and CD8+ T-lymphocytes following pre-incubation of whole blood samples with human insulin or GAD were observed in samples from patients with type 1 DM, whereas no activation of these cells was detected in samples from either type 2 DM patients or healthy subjects.

Discussion

These results indicated that latent pre-activation of CD4+ and CD8+ T-lymphocytes in response to insulin or GAD epitopes occurred in type 1 DM patients.

Conclusion

These findings suggest that pre-immunization against insulin and/or GAD might be associated with the development of type 1 DM. Alternatively, these results might reflect a non-specific, bystander autoimmune response.

Open access
Liangming Li Center for Scientific Research and Institute of Exercise and Health, Guangzhou Sport University, Guangzhou, China
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Yuan Wei Center for Scientific Research and Institute of Exercise and Health, Guangzhou Sport University, Guangzhou, China
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Chunlu Fang Center for Scientific Research and Institute of Exercise and Health, Guangzhou Sport University, Guangzhou, China
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Shujing Liu Center for Scientific Research and Institute of Exercise and Health, Guangzhou Sport University, Guangzhou, China
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Fu Zhou Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Ge Zhao Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Yaping Li Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Yuan Luo Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Ziyi Guo Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Weiqun Lin Department of Clinical Nutrition, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China

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Wenqi Yang Center for Scientific Research and Institute of Exercise and Health, Guangzhou Sport University, Guangzhou, China
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China

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Exercise has been recommended as an important strategy to improve glucose metabolism in obesity. Adipose tissue fibrosis is associated with inflammation and is implicated in glucose metabolism disturbance and insulin resistance in obesity. However, the effect of exercise on the progression of adipose tissue fibrosis is still unknown. The aim of the present study was to investigate whether exercise retarded the progression of adipose tissue fibrosis and ameliorated glucose homeostasis in diet-induced obese mice. To do so, obesity and adipose tissue fibrosis in mice were induced by high-fat diet feeding for 12 weeks and the mice subsequently received high-fat diet and exercise intervention for another 12 weeks. Exercise alleviated high-fat diet-induced glucose intolerance and insulin resistance. Continued high-fat diet feeding exacerbated collagen deposition and further increased fibrosis-related gene expression in adipose tissue. Exercise attenuated or reversed these changes. Additionally, PPARγ, which has been shown to inhibit adipose tissue fibrosis, was observed to be increased following exercise. Moreover, exercise decreased the expression of HIF-1α in adipose fibrosis, and adipose tissue inflammation was inhibited. In conclusion, our data indicate that exercise attenuates and even reverses the progression of adipose tissue fibrosis, providing a plausible mechanism for its beneficial effects on glucose metabolism in obesity.

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Stefano Mangiola Bioinformatics Division, Walter and Eliza Hall Institute, Parkville, Victoria, Australia
Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia

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Ryan Stuchbery Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia

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Patrick McCoy Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia

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Ken Chow Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia

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Natalie Kurganovs Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Australian Prostate Cancer Research Centre Epworth, Richmond, Victoria, Australia
Ontario Institute for Cancer Research, Toronto, Canada
Princess Margaret Cancer Centre, University Health Network, Toronto, Canada

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Michael Kerger Australian Prostate Cancer Research Centre Epworth, Richmond, Victoria, Australia

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Anthony Papenfuss Bioinformatics Division, Walter and Eliza Hall Institute, Parkville, Victoria, Australia
Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Department of Medical Biology, University of Melbourne, Melbourne, Victoria, Australia
Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Victoria, Australia
Department of Mathematics and Statistics, University of Melbourne, Melbourne, Victoria, Australia

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Christopher M Hovens Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia

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Niall M Corcoran Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
Department of Urology, Royal Melbourne Hospital, Parkville, Victoria, Australia
Department of Urology, Frankston Hospital, Frankston, Victoria, Australia

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Prostate cancer is a leading cause of morbidity and cancer-related death worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of these therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between ADT, obesity, inflammation and prostate cancer progression is well established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castration therapies is missing. Here, we investigated the transcriptional changes in periprostatic fat tissue induced by profound ADT in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that the deprivation of androgen is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of therapies based on androgen deprivation may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.

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