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Tian Zhou School of Clinical Medicine, GuiZhou Medical University, Guiyang, Guizhou, China
Department of Breast Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

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Dai-wei Zhao School of Clinical Medicine, GuiZhou Medical University, Guiyang, Guizhou, China
Department of Surgery, Second People's Hospital of Guizhou Province, Guiyang, Guizhou, China

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Ning Ma School of Clinical Medicine, GuiZhou Medical University, Guiyang, Guizhou, China

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Xue-ying Zhu School of Clinical Medicine, GuiZhou Medical University, Guiyang, Guizhou, China

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Xing-hong Chen Department of Surgery, Second People's Hospital of Guizhou Province, Guiyang, Guizhou, China

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Xue Luo Department of Breast Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

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Song Chen School of Clinical Medicine, GuiZhou Medical University, Guiyang, Guizhou, China

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Qing-jun Gao Department of Thyroid Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

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Objective

Thyroid cancer (THCA) is the most common endocrine cancer in the world. Although most patients with THCA have a good prognosis, the prognosis of those with THCA who have an extra-glandular invasion, vascular invasion, and distant metastasis is poor. Therefore, it is very important to find potential biomarkers that can effectively predict the prognosis and progression of highly aggressive THCAs. It has been identified that forkhead box P4 (FOXP4) may be a new biomarker for the proliferation and prognosis for tumor diagnosis. However, the expression and function of FOXP4 in THCA remain to be determined.

Methods

In the present study, the function of FOXP4 in cells was investigated through the comprehensive analysis of data in The Cancer Genome Atlas and combined with experiments including immunohistochemistry (IHC), colony formation, Cell Counting Kit-8 assay, wound scratch healing, and transwell invasion assay.

Results

In the present study, relevant bioinformatic data showed that FOXP4 was highly expressed in THCA, which was consistent with the results of the IHC and cell experiments. Meanwhile, 10 FOXP4-related hub genes were identified as potential diagnostic genes for THCA. It was found in further experiments that FOXP4 was located in the nucleus of THCA cells, and the expression of FOXP4 in the nucleus was higher than that in the cytoplasm. FOXP4 knockdown inhibited in vitro proliferation of the THCA cells, whereas overexpression promoted the proliferation and migration of THCA cells. Furthermore, deficiency of FOXP4 induced cell-cycle arrest.

Conclusion

FOXP4 might be a potential target for diagnosing and treating THCA.

Open access
Kaili Yang Department of Medical Oncology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

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Jiarui Li Department of Gastrointestinal Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China

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Yuejuan Cheng Department of Medical Oncology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

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Chunmei Bai Department of Medical Oncology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

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Background

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are heterogenous malignancies that require well-designed trials to develop effective management strategies. This cross-sectional study aimed to illustrate the current landscape of clinical trials in GEP-NENs to provide insights for future research.

Materials and methods

We reviewed all clinical trials registered on ClinicalTrials.gov between 1 January 2000 and 31 December 2021 with GEP-NEN in the ‘condition or disease’ field.

Results

We included 206 eligible trials. Most trials enrolled less than 50 patients (59.8%) and were sponsored by institutions other than government or industry (67.0%). Most trials were conducted in high-income countries (86.6%) and countries located in Europe (30.1%) or Northern America (29.6%). The overall result reporting rates of GEP-NEN trials was 41.4%, and the median time from primary completion to result reporting was 101 months. Characteristics that improved the reporting of results included larger sample size, tumor differentiation specification for inclusion, progression-free survival as primary endpoint, industry sponsorship, and multicenter or multinational participation (all P < 0.05). Compared with trials registered between 2000 and 2011 (n = 28), trials registered between 2012 and 2021 (n = 178) were more likely to specify the Ki-67 index for inclusion (68.0% vs 35.7%, P = 0.002) and to be conducted outside Europe or Northern America (16.4% vs 3.7%, P = 0.02), while the sample size and the sponsorship did not change significantly.

Conclusions

Novel management options have been explored for GEP-NENs with more specific inclusion criteria during the past two decades. More efforts are needed to promote international collaborations in clinical trials and enhance timely result dissemination.

Open access
A J Clark Endocrine Connections Editor-in-Chief, Emeritus Professor of Endocrinology, University of London, London, United Kingdom of Great Britain and Northern Ireland

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Sarah Ying Tse Tan Department of Endocrinology, Singapore General Hospital, Singapore

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Hong Chang Tan Department of Endocrinology, Singapore General Hospital, Singapore

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Ling Zhu Department of Endocrinology, Singapore General Hospital, Singapore

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Lih Ming Loh Department of Endocrinology, Singapore General Hospital, Singapore

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Dawn Shao Ting Lim Department of Endocrinology, Singapore General Hospital, Singapore

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Du Soon Swee Department of Endocrinology, Singapore General Hospital, Singapore

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Yoke Ling Chan Department of Speciality Nursing, Singapore General Hospital, Singapore

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Huee Boon Lim Department of Speciality Nursing, Singapore General Hospital, Singapore

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Shiau Lee Ling Department of Speciality Nursing, Singapore General Hospital, Singapore

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En Jun Ou Department of Speciality Nursing, Singapore General Hospital, Singapore

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Wynn Ee Teo Department of Speciality Nursing, Singapore General Hospital, Singapore

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Xiao Ping Zhang Department of Speciality Nursing, Singapore General Hospital, Singapore

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Hui Fen Goh Department of Speciality Nursing, Singapore General Hospital, Singapore

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Peng Chin Kek Department of Endocrinology, Singapore General Hospital, Singapore

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Background

Adrenal insufficiency (AI) is potentially life-threatening, and accurate diagnosis is crucial. The first-line diagnostic test, the adrenocorticotrophic hormone (ACTH) stimulation test, measures serum total cortisol. However, this is affected in states of altered albumin or cortisol-binding globulin levels, limiting reliability. Salivary cortisol reflects free bioactive cortisol levels and is a promising alternative. However, few studies are available, and heterogenous methodologies limit applicability.

Methods

This study prospectively recruited 42 outpatients undergoing evaluation for AI, excluding participants with altered cortisol-binding states. Serum (immunoassay) and salivary (liquid chromatography tandem mass spectrometry) cortisol levels were sampled at baseline, 30 min, and 60 min following 250 µg synacthen administration. AI was defined as a peak serum cortisol level <500 nmol/L in accordance with guidelines.

Results

The study recruited 21 (50%) participants with AI and 21 without AI. There were no significant differences in baseline characteristics, blood pressure, or sodium levels between groups. Following synacthen stimulation, serum and salivary cortisol levels showed good correlation at all timepoints (R 2 = 0.74, P < 0.001), at peak levels (R 2 = 0.72, P < 0.001), and at 60 min (R 2 = 0.72, P < 0.001). A salivary cortisol cut-off of 16.0 nmol/L had a sensitivity of 90.5% and a specificity of 76.2% for the diagnosis of AI.

Conclusion

This study demonstrates a good correlation between serum and salivary cortisol levels during the 250 µg synacthen test. A peak salivary cortisol cut-off of 16.0 nmol/L can be used for the diagnosis of AI. It is a less invasive alternative to evaluate patients with suspected AI. Its potential utility in the diagnosis of AI in patients with altered cortisol-binding states should be further studied.

Open access
Tristan Avril Pediatric Endocrinology Department, CHU Bicetre, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR DevGen, Le Kremlin Bicêtre, Paris, France

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Quentin Hennocq Datascience platform, Imagine Institute, Université Paris Cité, Paris, France

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Anne-Sophie Lambert Pediatric Endocrinology Department, CHU Bicetre, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR DevGen, Le Kremlin Bicêtre, Paris, France

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Juliane Leger Pediatric Endocrinology Department, CHU Robert Debré, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR de la Croissance et du Développement, Paris, France
Université Paris Cité, Faculté de Santé, UFR de Médecine, Paris, France

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Dominique Simon Pediatric Endocrinology Department, CHU Robert Debré, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR de la Croissance et du Développement, Paris, France

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Laetitia Martinerie Pediatric Endocrinology Department, CHU Robert Debré, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR de la Croissance et du Développement, Paris, France
Université Paris Cité, Faculté de Santé, UFR de Médecine, Paris, France
Inserm UMR1185, Le Kremlin Bicetre, Paris, France

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Claire Bouvattier Pediatric Endocrinology Department, CHU Bicetre, Assistance Publique-Hôpitaux de Paris, Reference Center for Rare Disease CRMR DevGen, Le Kremlin Bicêtre, Paris, France
Inserm UMR1185, Le Kremlin Bicetre, Paris, France
Paris-Saclay University, Paris, France

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Objective

Newborns with congenital hypogonadotropic hypogonadism (CHH) have an impaired postnatal activation of the gonadotropic axis. Substitutive therapy with recombinant gonadotropins can be proposed to mimic physiological male mini-puberty during the first months of life. The aim of this study was to compare the clinical and biological efficacy of two treatment modalities of gonadotropins administration during mini-puberty in CHH neonates.

Design

Multicenter retrospective analytical epidemiological study comparing two treatments, pump vs injection, between 2004 and 2019.

Methods

Clinical (penile size, testis size, testicular descent) and biological parameters (serum concentrations of testosterone, anti-Müllerian hormone (AMH) and Inhibin B) were compared between the two groups by multivariate analyses.

Results

Thirty-five patients were included. A significantly higher increase in penile length and testosterone level was observed in the injection group compared to the pump group (+0.16 ± 0.02 mm vs +0.10 ± 0.02 mm per day, P = 0.002; and +0.04 ± 0.007 ng/mL vs +0.01 ± 0.008 ng/mL per day, P = 0.001). In both groups, significant increases in penile length and width, testosterone, AMH, and Inhibin B levels were observed, as well as improved testicular descent (odds ratio of not being in a scrotal position at the end of treatment = 0.97 (0.96; 0.99)).

Conclusions

Early postnatal administration of recombinant gonadotropins in CHH boys is effective in stimulating penile growth, Sertoli cell proliferation, and testicular descent, with both treatment modalities.

Open access
Heleen I Jansen Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands
Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam, The Netherlands
Amsterdam UMC location University of Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands

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Marijn M Bult Amsterdam UMC location University of Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands

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Peter H Bisschop Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam, The Netherlands
Amsterdam UMC location University of Amsterdam, Department of Endocrinology and Metabolism, Amsterdam, The Netherlands

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Anita Boelen Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam, The Netherlands
Amsterdam UMC location University of Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands
Amsterdam Reproduction & Development Research Institute, Amsterdam, The Netherlands

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Annemieke C Heijboer Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands
Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam, The Netherlands
Amsterdam UMC location University of Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands
Amsterdam Reproduction & Development Research Institute, Amsterdam, The Netherlands

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Jacquelien J Hillebrand Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam, The Netherlands
Amsterdam UMC location University of Amsterdam, Department of Clinical Chemistry, Endocrine Laboratory, Amsterdam, The Netherlands

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Introduction

In our hospital, physicians noticed high free thyroxine (fT4) concentrations without complete suppression of thyroid-stimulating hormone (TSH) in blood samples of patients at the outpatient clinic, which appeared to occur more often following the introduction of a new fT4 immunoassay. This discordance may be explained by incorrect reference intervals, analytical issues, or patient-related factors. We aimed to establish the contribution of the possible factors involved.

Methods

Reference intervals of both fT4 immunoassays were re-evaluated using blood samples of healthy volunteers and the new immunoassay’s performance was assessed using internal quality controls and external quality rounds. The frequency of discordant fT4 and TSH pairings obtained from laboratory requests were retrospectively analysed using a Delfia (n = 3174) and Cobas cohort (n = 3408). Last, a literature search assessed whether the time of blood draw and the time of levothyroxine (L-T4) ingestion may contribute to higher fT4 concentrations in L-T4 users.

Results

The original reference intervals of both fT4 immunoassays were confirmed and no evidence for analytical problems was found. The Delfia (n = 176, 5.5%) and Cobas cohorts (n = 295, 8.7%) showed comparable frequencies of discordance. Interestingly, 72–81% of the discordant results belonged to L-T4 users. Literature indicated the time of blood withdrawal of L-T4 users and, therefore, the time of L-T4 intake as possible explanations.

Conclusions

High fT4 without suppressed TSH concentrations can mainly be explained by L-T4 intake. Physicians and laboratory specialists should be aware of this phenomenon to avoid questioning the assay’s performance or unnecessarily adapting the L-T4 dose in patients.

Open access
Hong Tang Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Xiaomei Jiang Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Yu Hua Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Heyue Li Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Chunlan Zhu Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Xiaobai Hao Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Minhui Yi Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Linxia Li Departments of Gynaecology and Obstetrics Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Background

Polycystic ovary syndrome (PCOS) is an androgen disorder and ovarian dysfunction disease in women of reproductive age. The cell death of granulosa cells (GCs) plays an important role in the development of PCOS. However, the mechanism of GC death is still unclear.

Methods

In the current study, NEDD4L was found to be elevated in PCOS GEO (Gene Expression Omnibus) databases and mouse models. The cell viability was analyzed by CCK-8 and FDA staining. The expression of ferroptosis markers was assessed by ELISA and immunofluorescence. The direct interaction of GPX4 and NEDD4L was verified by co-immunoprecipitation assay.

Result

Functionally, results from CCK-8 and FDA staining demonstrated that NEDD4L inhibited the cell viability of KGN cells and NEDD4L increased the levels of iron, malonyldialdehyde, and reactive oxygen species and decreased glutathione levels. Moreover, the cell death of KGN induced by NEDD4L was blocked by ferroptosis inhibitor, suggesting that NEDD4L regulates KGN cell ferroptosis. Mechanistically, NEDD4L directly interacts with GPX4 and promotes GPX4 ubiquitination and degradation.

Conclusion

Taken together, our study indicated that NEDD4L facilitates GC ferroptosis by promoting GPX4 ubiquitination and degradation and contributes to the development of PCOS.

Open access
Pernille H Hellmann Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jonatan I Bagger Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark

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Katrine R Carlander Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark

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Katrine B Hansen Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark

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Julie L Forman Section of Biostatistics, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Joachim Størling Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark

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Elizaveta Chabanova Department of Radiology, Herlev Hospital, University of Copenhagen, Herlev, Denmark

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Jens Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Tina Vilsbøll Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark

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Filip K Knop Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Objectives

Preclinically, curcumin has been shown to protect against glucocorticoid-induced insulin resistance. We evaluated the effect of curcumin administered with prednisolone in healthy overweight or obese men.

Methods

In a double-blind, parallel-group trial, 24 overweight/obese non-diabetic men were randomised to one of three intervention groups (A) prednisolone placebo+curcumin placebo, (B) prednisolone (50 mg/day)+curcumin placebo or (C) prednisolone and curcumin (400 mg/day). Curcumin or curcumin placebo treatment started 1 day prior to 10-day prednisolone or prednisolone placebo treatment. The primary endpoint was change in prednisolone-induced insulin resistance assessed by homeostatic model assessment of insulin resistance (HOMA2-IR). Other endpoints included anthropometric measurements, magnetic resonance spectroscopy-assessed hepatic fat content, blood pressure, circulating metabolic markers and continuous glucose monitoring measures.

Results

Baseline characteristics (mean ± s.d): age 44.2 ± 13.7 years, BMI 30.1 ± 3.5 kg/m2, HbAlc 33.3 ± 3.2 mmol/mol, HOMA2-IR 1.10 ± 0.45 and fasting plasma glucose 5.2 ± 0.4 mmol/L. Prednisolone significantly increased HOMA2-IR (estimated treatment difference 0.36 (95% CI 0.16; 0.57)). Co-treatment with curcumin had no effect on HOMA2-IR (estimated treatment difference 0.08 (95% CI −0.13; 0.39)). Prednisolone increased HbAlc, insulin, C-peptide, glucagon, blood pressure, mean interstitial glucose, time spent in hyperglycaemia and glucose variability, but no protective effect of curcumin on any of these measures was observed.

Conclusions

In this double-blind, placebo-controlled parallel-group study involving 24 overweight or obese men randomised to one of three treatment arms, curcumin treatment had no protective effect on prednisolone-induced insulin resistance or other glucometabolic perturbations.

Open access
Hanna F Nowotny Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Jillian Bryce Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Salma R Ali Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Roberta Giordano Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Division of Endocrinology, Diabetes and Metabolism, Department of Medical Sciences, University of Turin, Turin, Italy

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Federico Baronio Pediatric Unit, Department Hospital of Woman and Child, Endo-ERN Centre IT11, IRCSS AOU S.Orsola-Malpighi University Hospital, Bologna, Italy

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Irina Chifu Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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Lea Tschaidse Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Martine Cools Department of Paediatric Endocrinology, Ghent University Hospital, University of Ghent, Ghent, Belgium

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Erica LT van den Akker Department of Pediatrics, Division of Pediatric Endocrinology, Erasmus MC - Sophia Children’s Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands

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Henrik Falhammar Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden

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Natasha M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Luca Persani Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan Italy

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Guglielmo Beccuti Department of Clinical and Biological Sciences, University of Turin, Turin, Italy

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Ian L Ross Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa

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Simona Grozinsky-Glasberg Neuroendocrine Tumor Unit, ENETS Center of Excellence, Department of Endocrinology and Metabolism, Hadassah Medical Organisation and Faculty of Medicine, the Hebrew University, Jerusalem, Israel

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Alberto M Pereira Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Eystein S Husebye Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Department of Medicine, Karolinska Institutet, Stockholm, Sweden

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Stefanie Hahner Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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S Faisal Ahmed Office for Rare Conditions, University of Glasgow, Glasgow, UK
Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom

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Nicole Reisch Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Background

Information on clinical outcomes of coronavirus disease 19 (COVID-19) infection in patients with adrenal disorders is scarce.

Methods

A collaboration between the European Society of Endocrinology (ESE) Rare Disease Committee and European Reference Network on Rare Endocrine Conditions via the European Registries for Rare Endocrine Conditions allowed the collection of data on 64 cases (57 adrenal insufficiency (AI), 7 Cushing’s syndrome) that had been reported by 12 centres in 8 European countries between January 2020 and December 2021.

Results

Of all 64 patients, 23 were males and 41 females (13 of those children) with a median age of 37 and 51 years. In 45/57 (95%) AI cases, COVID-19 infection was confirmed by testing. Primary insufficiency was present in 45/57 patients; 19 were affected by Addison’s disease, 19 by congenital adrenal hyperplasia and 7 by primary AI (PAI) due to other causes. The most relevant comorbidities were hypertension (12%), obesity (n = 14%) and diabetes mellitus (9%). An increase by a median of 2.0 (IQR 1.4) times the daily replacement dose was reported in 42 (74%) patients. Two patients were administered i.m. injection of 100 mg hydrocortisone, and 11/64 were admitted to the hospital. Two patients had to be transferred to the intensive care unit, one with a fatal outcome. Four patients reported persistent SARS-CoV-2 infection, all others complete remission.

Conclusion

This European multicentre questionnaire is the first to collect data on the outcome of COVID-19 infection in patients with adrenal gland disorders. It suggests good clinical outcomes in case of duly dose adjustments and emphasizes the importance of patient education on sick day rules.

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Annalisa Blasetti Department of Paediatrics, University of Chieti, Chieti, Italy

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Valeria Castorani Department of Paediatrics, University of Chieti, Chieti, Italy

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Nella Polidori Department of Paediatrics, University of Chieti, Chieti, Italy

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Ilaria Mascioli Department of Paediatrics, University of Chieti, Chieti, Italy

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Francesco Chiarelli Department of Paediatrics, University of Chieti, Chieti, Italy

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Cosimo Giannini Department of Paediatrics, University of Chieti, Chieti, Italy

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Objective

Linear growth is impaired in children with type 1 diabetes (T1D) and poor metabolic control. A good metabolic control is a key therapeutic goal to prevent vascular complications and also to ensure appropriate anthropometric development during childhood. In this study, we aimed to identify and characterize the effects of glycemic variability on linear growth in children with T1D.

Methods

Data from 144 prepubertal children with T1D were evaluated. Anthropometric measurements (weight, weight-SDS, height, height-SDS, BMI, BMI-SDS) were collected and glycosylated hemoglobin (HbA1c) was measured at admission and every 4 months over a 2-year period. Glycemic variability indexes (glycemic coefficient of variation (CV), glycemic CV percentage (CV%), and the product between HbA1c-mean and HbA1c-SDS/100 (M*SDS-HbA1c/100)) were calculated. According to height-SDS changes after 2 years of follow-up, the study population was divided into three tertile groups and differences across groups were investigated for variables of interest.

Results

The three groups were similar in terms of age, gender, and follow-up period. After 2 years, all prepubertal children showed a significant positive trend of anthropometric data. Across the three tertile groups, HbA1c-SDS, CV, CV%, and M*SDS-HbA1c significantly decreased from the first to the third tertile of height-SDS. During follow-up, children with lower Δheight-SDS values reported higher values of HbA1c-SDS, CV, CV%, and M*SDS-HbA1c than subjects with higher linear growth.

Conclusions

Glycemic variability correlates with linear growth in children with T1D. Low glycemic variability indexes were reported in higher height-SDS tertiles. Δheight-SDS is inversely correlated with glycemic CV, CV%, and M*SDS-HbA1c.

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