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Sara Lomelino Pinheiro Serviço de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Ana Saramago Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Branca Maria Cavaco Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Carmo Martins Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Valeriano Leite Serviço de Endocrinologia e Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Tiago Nunes da Silva Serviço de Endocrinologia e Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Nineteen cases of parathyroid carcinoma in patients with multiple endocrine neoplasia type 1 have been reported in the literature, of which 11 carry an inactivating germline mutation in the MEN1 gene. Somatic genetic abnormalities in these parathyroid carcinomas have never been detected. In this paper, we aimed to describe the clinical and molecular characterization of a parathyroid carcinoma identified in a patient with MEN1. A 60-year-old man was diagnosed with primary hyperparathyroidism during the postoperative period of lung carcinoid surgery. Serum calcium and parathyroid hormone levels were 15.0 mg/dL (8.4–10.2) and 472 pg/mL (12–65), respectively. The patient underwent parathyroid surgery, and histological findings were consistent with parathyroid carcinoma. Analysis of the MEN1 gene by next-generation sequencing (NGS) identified a novel germline heterozygous nonsense pathogenic variant (c.978C>A; p.(Tyr326*)), predicted to encode a truncated protein. Genetic analysis of the parathyroid carcinoma revealed a c.307del, p.(Leu103Cysfs*16) frameshift truncating somatic MEN1 variant in the MEN1 gene, which is consistent with MEN1 tumor-suppressor role, confirming its involvement in parathyroid carcinoma etiology. Genetic analysis of CDC73, GCM2, TP53, RB1, AKT1, MTOR, PIK3CA and CCND1 genes in the parathyroid carcinoma DNA did not detect any somatic mutations. To our knowledge, this is the first report of a PC case presenting both germline (first-hit) and somatic (second-hit) inactivation of the MEN1 gene.

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Laura Hasse Department of Pediatric Dermatology and Allergology, Children’s Hospital Auf der Bult, Hannover, Germany

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Dagmar Jamiolkowski Department of Pediatric Dermatology and Allergology, Children’s Hospital Auf der Bult, Hannover, Germany

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Felix Reschke Department of Pediatric Diabetology, Children’s Hospital Auf der Bult, Hannover, Germany

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Kerstin Kapitzke Department of Pediatric Diabetology, Children’s Hospital Auf der Bult, Hannover, Germany

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Jantje Weiskorn Department of Pediatric Diabetology, Children’s Hospital Auf der Bult, Hannover, Germany

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Olga Kordonouri Department of Pediatric Diabetology, Children’s Hospital Auf der Bult, Hannover, Germany

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Torben Biester Department of Pediatric Diabetology, Children’s Hospital Auf der Bult, Hannover, Germany

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Hagen Ott Department of Pediatric Dermatology and Allergology, Children’s Hospital Auf der Bult, Hannover, Germany

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Objective

Little is known about specific cutaneous findings in children and adolescents with overweight and obesity. This study assessed the association of skin signs with pivotal auxological and endocrinological parameters and their influence on the quality of life (QoL) of young people with obesity.

Study design

All patients initially recruited for a tertiary hospital's weight control program were offered participation in this interdisciplinary, single-center, cross-sectional study. All participants underwent a detailed dermatological examination, anthropometric measurements and laboratory examinations. QoL was assessed with validated questionnaires.

Results

A total of 103 children and adolescents (age 11.6 ±2.5 years, 41% female, 25% prepubertal, BMI SDS 2.6 ± 0.5, homeostatic model assessment (HOMA) score 3.3 ± 4.2; mean ± s.d.) were recruited in a 12-month study period. Skin affections were linearly associated with increasing BMI and higher age. The most common skin findings were (%) striae distensae (71.0), keratosis pilaris (64.7), acanthosis nigricans (45.0), acne vulgaris (39.2), acrochordons (25.5) and plantar hyperkeratosis (17.6). The HOMA score was associated with acanthosis nigricans (P = 0.047), keratosis pilaris (P = 0.019) and acne vulgaris (P < 0.001). The general mean QoL(QoL) score, as assessed by the WHO-5, was 70 out of 100. A total of 38.9% of participants reported impaired dermatological QoL.

Conclusions

This study shows the high prevalence of skin lesions in children and adolescents with obesity. The association between skin lesions and the HOMA score indicates that skin manifestations are a marker of insulin resistance. To prevent secondary diseases and improve QoL, thorough skin examinations and interdisciplinary cooperation are necessary.

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Ying-Lien Cheng Division of Endocrinology and Metabolism, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

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Ting-I Lee Division of Endocrinology and Metabolism, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
Division of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

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Yu-Mei Chien Division of Endocrinology and Metabolism, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

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Ting-Wei Lee Division of Endocrinology and Metabolism, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
Division of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

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Yi-Jen Chen Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Cardiovascular Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
Taipei Heart Institute, Taipei Medical University, Taipei, Taiwan

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Vitamin D deficiency is associated with hyperlipidemia, but it remains unclear whether vitamin D supplementation reduces serum lipid levels. The aims of this study were to investigate the associations between increased serum 25-hydroxyvitamin D (25(OH)D) concentrations and lipid levels and identify the characteristics of people with or without lipid reduction associated with increased 25(OH)D levels. The medical records of 118 individuals (53 men; mean age, 54.4 ± 10.6 years) whose serum 25(OH)D levels increased between 2 consecutive measurements were retrospectively reviewed. People with increased 25(OH)D levels (from 22.7 (17.6–29.2) to 32.1 (25.6–36.8) mg/dL; P < 0.01) had a significant reduction in serum levels of triglycerides (TGs) (from 111.0 (80–164) to 104.5 (73–142) mg/dL; P < 0.01) and total cholesterol (TC) (from 187.5 (155–213) to 181.0 (150–210) mg/dL; P < 0.05). The individuals who responded to vitamin D (≥10% reduction in TG or TC levels) exhibited significantly higher baseline TG and TC levels than those who did not. Only patients with hyperlipidemia (not those without hyperlipidemia) at baseline exhibited significantly reduced TG and TC levels at follow-up. However, increasing serum 25(OH)D concentrations were significantly correlated with decreasing lipid levels in individuals with baseline 25(OH)D levels less than 30 ng/mL and in individuals aged 50–65 years (not in patients younger than 50 years or older than 65 years). In conclusion, increasing serum 25(OH)D concentrations may be potentially helpful for the treatment of hyperlipidemia in people with vitamin D deficiency.

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Caihong Xin Department of Endocrinology and Metabolism, The Fourth People’s Hospital of Shenyang, Shenyang, P.R. China

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Lijuan Niu Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

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Huaying Fan Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

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Jing Xie Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

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Xin Sun Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

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Background

Sarcoidosis is a multiple systemic granulomatous disease, and its main pathological feature is non-caseous necrotic epithelial granuloma. The pathogenesis is not fully understood. The prevalence of thyroid disease is likely higher among individuals with sarcoidosis. However, this association still lacks clinical evidence.

Objective

The aim of this study was to estimate the incidence of thyroid disease in patients with sarcoidosis.

Methods

A literature search was conducted using PubMed, Web of Science, Embase, and China National Knowledge Infrastructure literature databases. Fixed- or random-effects models were used for analysis according to heterogeneity. The results were subjected to meta-analysis with odds ratios (ORs) and corresponding 95% confidence intervals (CIs).

Results

In total, six articles were included in this meta-analysis, which involved 2044 sarcoidosis cases and 5652 controls. The studies found that the incidence of thyroid disease in patients with sarcoidosis was significantly increased compared to the controls (OR 3.28, 95% CI 1.83–5.88).

Conclusions

This systematic review is the first to evaluate the incidence of thyroid disease in sarcoidosis patients, which was increased compared with the controls, suggesting that sarcoidosis patients should be screened for thyroid disease.

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Helene Bandsholm Leere Tallaksen Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark

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Emma B Johannsen Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark

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Jesper Just Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark

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Mette Hansen Viuff Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Gynaecology and Obstetrics, Aarhus University Hospital, Aarhus, Denmark

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Claus H Gravholt Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Endocrinology, Aarhus University Hospital, Aarhus, Denmark

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Anne Skakkebæk Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Genetics, Aarhus University Hospital, Aarhus, Denmark

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Sex chromosome abnormalities (SCAs) are chromosomal disorders with either a complete or partial loss or gain of sex chromosomes. The most frequent SCAs include Turner syndrome (45,X), Klinefelter syndrome (47,XXY), Trisomy X syndrome (47,XXX), and Double Y syndrome (47,XYY). The phenotype seen in SCAs is highly variable and may not merely be due to the direct genomic imbalance from altered sex chromosome gene dosage but also due to additive alterations in gene networks and regulatory pathways across the genome as well as individual genetic modifiers. This review summarizes the current insight into the genomics of SCAs. In addition, future directions of research that can contribute to decipher the genomics of SCA are discussed such as single-cell omics, spatial transcriptomics, system biology thinking, human-induced pluripotent stem cells, and animal models, and how these data may be combined to bridge the gap between genomics and the clinical phenotype.

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Alan D Rogol Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA

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The overall incidence of sex chromosome aneuploidies is approximately 1 per 500 live-born infants, but far more common at conception. I shall review the fertility aspects of the sex chromosome trisomies, XXY, XYY, and XXX, with special reference to the karyotype 45,X/47,XXX. Each has a ‘specific’ (but variable) phenotype but may be modified by mosaicism. Although the alterations in the hypothalamic–pituitary–gonadal axis are important (and discussed), the emphasis here is on potential fertility and if one might predict that at various epochs within an individual’s life span: fetal, ‘mini’-puberty, childhood, puberty, and adulthood. The reproductive axis is often affected in females with the 47,XXX karyotype with diminished ovarian reserve and accelerated loss of ovarian function. Fewer than 5% of females with Turner syndrome have the 45,X/47,XXX karyotype. They have taller stature and less severe fertility issues compared to females with the 45,X or other forms of Turner syndrome mosaicism. For the 47,XXY karyotype, non-obstructive azoospermia is almost universal with sperm retrieval by micro-testicular sperm extraction possible in slightly fewer than half of the men. Men with the 47,XYY karyotype have normal to large testes and much less testicular dysfunction than those with the 47,XXY karyotype. They do have a slight increase in infertility compared to the reference population but not nearly as severe as those with the 47,XXY karyotype. Assisted reproductive technology, especially micro-testicular sperm extraction, has an important role, especially for those with 47,XXY; however, more recent data show promising techniques for the in vitro maturation of spermatogonial stem cells and 3D organoids in culture. Assisted reproductive technology is more complex for the female, but vitrification of oocytes has shown promising advances.

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Rama Lakshman Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK

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Charlotte Boughton Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK
Cambridge University Hospitals NHS Foundation Trust, Wolfson Diabetes and Endocrine Clinic, Cambridge, UK

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Roman Hovorka Wellcome-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK

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Automated insulin delivery systems, also known as closed-loop or ‘artificial pancreas’ systems, are transforming the management of type 1 diabetes. These systems consist of an algorithm which responds to real-time glucose sensor levels by automatically modulating insulin delivery through an insulin pump. We review the rapidly changing landscape of automated insulin-delivery systems over recent decades, from initial prototypes to the different hybrid closed-loop systems commercially available today. We discuss the growing body of clinical trials and real-world evidence demonstrating their glycaemic and psychosocial benefits. We also address future directions in automated insulin delivery such as dual-hormone systems and adjunct therapy as well as the challenges around ensuring equitable access to closed-loop technology.

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Dongyan Han Department of Pathology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

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Min Ding Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Rongli Xie Department of General Surgery, RuiJin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, China

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Zhengshi Wang Thyroid Center, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China
Shanghai Center of Thyroid Diseases, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

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Guohui Xiao Department of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Xiaohong Wang Shanghai Rigen Biotechnology Co., Ltd. Shanghai, China

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Lei Dong Department of Pathology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Zhiqiang Yin Thyroid Center, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China
Shanghai Center of Thyroid Diseases, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

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Jian Fei Department of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Research Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China
State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai Jiao Tong University, Shanghai, China
Institute of Translational Medicine, Shanghai Jiao Tong University, Shanghai, China

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Thyroid fine needle aspiration biopsy (FNAB) remains indeterminate in 16–24% of the cases. Molecular testing could improve the diagnostic accuracy of FNAB. This study examined the gene mutation profile of patients with thyroid nodules and analyzed the diagnostic ability of molecular testing for thyroid nodules using a self-developed 18-gene test. Between January 2019 and August 2021, 513 samples (414 FNABs and 99 formalin-fixed paraffin-embedded (FFPE) specimens) underwent molecular testing at Ruijin Hospital. Sensitivity (Sen), specificity (Spe), positive predictive value (PPV), negative predictive value (NPV), and accuracy were calculated. There were 457 mutations in 428 samples. The rates of BRAF, RAS, TERT promoter, RET/PTC, and NTRK3 fusion mutations were 73.3% (n = 335), 9.6% (n = 44), 2.8% (n = 13), 4.8% (n = 22), and 0.4% (n = 2), respectively. The diagnostic ability of cytology and molecular testing were evaluated in Bethesda II and V–VI samples. For cytology alone, Sen, Spe, PPV, NPV, and accuracy were 100%, 25.0%, 97.4%, 100%, and 97.4%; these numbers were 87.5%, 50.0%, 98.0%, 12.5%, and 86.2% when considering positive mutation, and 87.5%, 75.0%, 99.0%, 17.6%, and 87.1% when considering positive cytology or and positive mutation. In Bethesda III–IV nodules, when relying solely on the presence of pathogenic mutations for diagnosis, Sen, Spe, PPV, NPV, and AC were 76.2%, 66.7%, 94.1%, 26.8%, and 75.0%, respectively. It might be necessary to analyze the molecular mechanisms of disease development at the genetic level to predict patients with malignant nodules more accurately in different risk strata and develop rational treatment strategies and definite management plans.

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Chiara Jongerius Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands
Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands

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Marij A Hillen Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands
Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands

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Ellen M A Smets Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands
Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands

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Mathijs J Mol Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands

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Eefje S Kooij Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands

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Maria A de Nood Amsterdam UMC, Location AMC, Medical Psychology, Amsterdam, The Netherlands

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Edwin S Dalmaijer MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, United Kingdom

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Eric Fliers Department of Endocrinology & Metabolism, Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands

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Johannes A Romijn Department of Medicine, Amsterdam Gastroenterology, Endocrinology & Metabolism, Amsterdam UMC, Location AMC, Amsterdam, The Netherlands

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Daniel S Quintana University of Oslo, Department of Psychology, Oslo, Norway
Department of Rare Disorders and Disabilities, Oslo University Hospital, NevSom, Oslo, Norway
University of Oslo, Norwegian Centre for Mental Disorders Research (NORMENT) and KG Jebsen Centre for Neurodevelopmental Disorders, Oslo, Norway

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The patient–physician relationship is a critical determinant of patient health outcomes. Verbal and non-verbal communication, such as eye gaze, are vital aspects of this bond. Neurobiological studies indicate that oxytocin may serve as a link between increased eye gaze and social bonding. Therefore, oxytocin signaling could serve as a key factor influencing eye gaze as well as the patient–physician relationship. We aimed to test the effects of oxytocin on gaze to the eyes of the physician and the patient–physician relationship by conducting a randomized placebo-controlled crossover trial in healthy volunteers with intranasally administered oxytocin (with a previously effective single dose of 24 IU, EudraCT number 2018-004081-34). The eye gaze of 68 male volunteers was studied using eye tracking during a simulated video call consultation with a physician, who provided information about vaccination against the human papillomavirus. Relationship outcomes, including trust, satisfaction, and perceived physician communication style, were measured using questionnaires and corrected for possible confounds (social anxiety and attachment orientation). Additional secondary outcome measures for the effect of oxytocin were recall of information and pupil diameter and exploratory outcomes included mood and anxiety measures. Oxytocin did not affect the eye-tracking parameters of volunteers’ gaze toward the eyes of the physician. Moreover, oxytocin did not affect the parameters of bonding between volunteers and the physician nor other secondary and exploratory outcomes in this setting. Bayesian hypothesis testing provided evidence for the absence of effects. These results contradict the notion that oxytocin affects eye gaze patterns or bonding.

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Merlin C Thomas Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia

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Brendon L Neuen The George Institute for Global Health, Sydney, NSW, Australia

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Stephen M Twigg The University of Sydney School of Medicine, Sydney, NSW, Australia
Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, NSW, Australia

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Mark E Cooper Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC, Australia

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Sunil V Badve The George Institute for Global Health, Sydney, NSW, Australia
Department of Renal Medicine, St George Hospital, Sydney, NSW, Australia
Faculty of Medicine and Health, University of New South Wales, Sydney, NSW, Australia

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Sodium‐glucose co-transporter 2 (SGLT2) inhibitors have recently emerged as an effective means to protect kidney function in people with type 2 diabetes and chronic kidney disease (CKD). In this review, we explore the role of SGLT2 inhibition in these individuals. SGLT2 inhibitors specifically act to inhibit sodium and glucose reabsorption in the early proximal tubule of the renal nephron. Although originally developed as glucose-lowering agents through their ability to induce glycosuria, it became apparent in cardiovascular outcome trials that the trajectory of kidney function decline was significantly slowed and the incidence of serious falls in kidney function was reduced in participants receiving an SGLT2 inhibitor. These observations have recently led to specific outcome trials in participants with CKD, including DAPA-CKD, CREDENCE and EMPA-KIDNEY, and real-world studies, like CVD-REAL-3, that have confirmed the observation of kidney benefits in this setting. In response, recent KDIGO Guidelines have recommended the use of SGLT2 inhibitors as first-line therapy in patients with CKD, alongside statins, renin–angiotensin–aldosterone system inhibitors and multifactorial risk factor management as indicated. However, SGLT2 inhibitors remain significantly underutilized in the setting of CKD. Indeed, an inertia paradox exists, with patients with more severe disease less likely to receive an SGLT2 inhibitor. Concerns regarding safety appear unfounded, as acute kidney injury, hyperkalaemia, major acute cardiovascular events and cardiac death in patients with CKD appear to be lower following SGLT2 inhibition. The first-in-class indication of dapagliflozin for CKD may begin a new approach to managing kidney disease in type 2 diabetes.

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