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Heng Yeh Department of Emergency Medicine, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan
College of Medicine, Chang Gung University, Taoyuan, Taiwan

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Hsuan Yeh College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Chun-Cheng Chiang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ju-Ching Yen College of Medicine, China Medical University, Taichung, Taiwan

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I-Kuan Wang College of Medicine, China Medical University, Taichung, Taiwan
Department of Nephrology, China Medical University Hospital, Taichung, Taiwan

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Shou-Hsuan Liu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Chia Lee College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Cheng-Hao Weng College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Wen-Hung Huang College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Ching-Wei Hsu College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Tzung-Hai Yen College of Medicine, Chang Gung University, Taoyuan, Taiwan
Department of Nephrology, Clinical Poison Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan

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Secondary hyperparathyroidism (SHPT) is a common complication of end-stage kidney disease (ESKD). Hungry bone syndrome (HBS) occurs frequently in patients on maintenance dialysis receiving parathyroidectomy for refractory SHPT. However, there is scanty study investigating the clinical risk factors that predict postoperative HBS, and its outcome in peritoneal dialysis (PD) patients. We conducted a single-center retrospective study to analyze 66 PD patients who had undergone parathyroidectomy for secondary hyperparathyroidism at Chang Gung Memorial Hospital between 2009 and 2019. The patients were stratified into two groups based on the presence (n=47) or absence (n=19) of HBS after parathyroidectomy. Subtotal parathyroidectomy was the most common surgery performed (74.2%), followed by total parathyroidectomy with autoimplantation (25.8%). Pathological examination of all surgical specimens revealed parathyroid hyperplasia (100%). Patients with HBS had lower levels of postoperative nadir corrected calcium, higher alkaline phosphate (ALP), and higher potassium levels compared with patients without HBS (all P<0.05). A multivariate logistic regression model confirmed that lower preoperative serum calcium level (OR 0.354, 95% CI 0.133–0.940, P=0.037), higher ALP (OR 1.026, 95% CI 1.008–1.044, P=0.004), and higher potassium level (OR 6.894, 95% CI 1.806–26.317, P=0.005) were associated with HBS after parathyroidectomy. Patients were followed for 58.2±30.8 months after the surgery. There was no significant difference between HBS and non-HBS groups in persistence (P=0.496) or recurrence (P=1.000) of hyperparathyroidism. The overall mortality rate was 10.6% with no significant difference found between both groups (P=0.099). We concluded that HBS is a common complication (71.2%) of parathyroidectomy for SHPT and should be managed appropriately.

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Cheng Han Ng Yong Loo Lin School of Medicine, National University of Singapore, Singapore

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Yip Han Chin Yong Loo Lin School of Medicine, National University of Singapore, Singapore

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Marcus Hon Qin Tan Yong Loo Lin School of Medicine, National University of Singapore, Singapore

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Jun Xuan Ng Yong Loo Lin School of Medicine, National University of Singapore, Singapore

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Samantha Peiling Yang Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Department of Medicine, National University Hospital, Singapore

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Jolene Jiayu Kiew Department of Medicine, National University Hospital, Singapore

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Chin Meng Khoo Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Department of Medicine, National University Hospital, Singapore

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Purpose:

Primary hyperparathyroidism (PHPT) is a common condition affecting people of all ages and is mainly treated with parathyroidectomy. Cinacalcet has been widely used in secondary or tertiary hyperparathyroidism, but the use of cinacalcet in PHPT is less clear.

Methods:

Searches were conducted in Medline and Embase for cinacalcet use in PHPT from induction to 10 April 2020. Articles and conferences abstracts describing the use of cinacalcet for PHPT in prospective or retrospective cohorts and randomized controlled trials restricted to English language only. We initially identified 1301 abstracts. Each article went extraction by two blinded authors on a structured proforma. Continuous outcomes were pooled with weight mean difference (WMD). Quality of included articles was assessed with Newcastle Ottwa Scale and Cochrane Risk of Bias 2.0.

Results:

Twenty-eight articles were included. Normalization rate of serum Ca levels was reported at 90% (CI: 0.82 to 0.96). Serum levels of Ca and PTH levels were significantly reduced (Ca, WMD: 1.647, CI: −1.922 to −1.371; PTH, WMD: −31.218, CI: −41.671 to −20.765) and phosphate levels significantly increased (WMD: 0.498, CI: 0.400 to 0.596) after cinacalcet therapy. The higher the baseline Ca levels, the greater Ca reduction with cinacalcet treatment. Age and gender did not modify the effect of cinacalcet on serum Ca levels.

Conclusion:

The results from the meta-analysis support the use of cinacalcet as an alternative or bridging therapy to treat hypercalcemia in people with PHPT.

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Sara Storvall Department of Endocrinology, Abdominal Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Helena Leijon Department of Pathology and Huslab, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Eeva Ryhänen Department of Endocrinology, Abdominal Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Johanna Louhimo Department of Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Caj Haglund Department of Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Camilla Schalin-Jäntti Department of Endocrinology, Abdominal Center, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Johanna Arola Department of Pathology and Huslab, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

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Introduction

Parathyroid carcinoma represents a rare cause of primary hyperparathyroidism. Distinguishing carcinoma from the benign tumors underlying primary hyperparathyroidism remains challenging. The diagnostic criteria for parathyroid carcinoma are local and/or metastatic spreading. Atypical parathyroid adenomas share other histological features with carcinomas but lack invasive growth. Somatostatin receptors are commonly expressed in different neuroendocrine tumors, but whether this also holds for parathyroid tumors remains unknown.

Aim

Our aim is to examine the immunohistochemical expression of somatostatin receptor 1–5 in parathyroid typical adenomas, atypical adenomas and carcinomas.

Methods

We used a tissue microarray construct from a nationwide cohort of parathyroid carcinomas (n = 32), age- and gender-matched typical parathyroid adenomas (n = 72) and atypical parathyroid adenomas (n = 27) for immunohistochemistry of somatostatin receptor subtypes 1–5. We separately assessed cytoplasmic, membrane and nuclear expression and also investigated the associations with histological, biochemical and clinical characteristics.

Results

All parathyroid tumor subgroups expressed somatostatin receptors, although membrane expression appeared negligible. Except for somatostatin receptor 1, expression patterns differed between the three tumor types. Adenomas exhibited the weakest and carcinomas the strongest expression of somatostatin receptor 2, 3, 4 and 5. We observed the largest difference for cytoplasmic somatostatin receptor 5 expression.

Conclusions

Parathyroid adenomas, atypical adenomas and carcinomas all express somatostatin receptor subtypes 1–5. Somatostatin receptor 5 may serve as a potential tumor marker for malignancy. Studies exploring the role of somatostatin receptor imaging and receptor-specific therapies in patients with parathyroid carcinomas are needed.

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Veronica Kieffer
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Kate Davies University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Christine Gibson University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Morag Middleton University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Jean Munday University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Shashana Shalet University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Lisa Shepherd University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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Phillip Yeoh University Hospitals of Leicester NHS Trust, Great Ormond Street Hospital for Children NHS Trust, Central Manchester University Hospitals NHS Foundation Trust, NHS Grampian, Portsmouth Hospitals NHS Trust, Salford Royal Hospitals Foundation Trust, Heart of England NHS Foundation Trust, The London Clinic, Department of Diabetes and Endocrinology, Leicester Royal Infirmary, Leicester, LE1 5WW, UK

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This competency framework was developed by a working group of endocrine specialist nurses with the support of the Society for Endocrinology to enhance the clinical care that adults with an endocrine disorder receive. Nurses should be able to demonstrate that they are functioning at an optimal level in order for patients to receive appropriate care. By formulating a competency framework from which an adult endocrine nurse specialist can work, it is envisaged that their development as professional practitioners can be enhanced. This is the second edition of the Competency Framework for Adult Endocrine Nursing. It introduces four new competencies on benign adrenal tumours, hypo- and hyperparathyroidism, osteoporosis and polycystic ovary syndrome. The authors and the Society for Endocrinology welcome constructive feedback on the document, both nationally and internationally, in anticipation that further developments and ideas can be incorporated into future versions.

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Maria Mizamtsidi Department of Endocrinology, Diabetes and Metabolism, Hellenic Red Cross Hospital, Athens, Greece

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Constantinos Nastos Second Department of Surgery, Endocrine Surgery Unit, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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George Mastorakos Unit of Endocrinology, Diabetes and Metabolism, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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Roberto Dina Department of Pathology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK

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Ioannis Vassiliou Second Department of Surgery, Endocrine Surgery Unit, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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Maria Gazouli Department of Basic Medical Sciences, Laboratory of Biology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece

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Fausto Palazzo Department of Thyroid and Endocrine Surgery, Imperial College London, London, UK

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Primary hyperparathyroidism (pHPT) is a common endocrinopathy resulting from inappropriately high PTH secretion. It usually results from the presence of a single gland adenoma, multiple gland hyperplasia or rarely parathyroid carcinoma. All these conditions require different management, and it is important to be able to differentiate the underlined pathology, in order for the clinicians to provide the best therapeutic approach. Elucidation of the genetic background of each of these clinical entities would be of great interest. However, the molecular factors that control parathyroid tumorigenesis are poorly understood. There are data implicating the existence of specific genetic pathways involved in the emergence of parathyroid tumorigenesis. The main focus of the present study is to present the current optimal diagnostic and management protocols for pHPT as well as to review the literature regarding all molecular and genetic pathways that are to be involved in the pathophysiology of sporadic pHPT.

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Anna Gorbacheva Endocrinology Research Center, Moscow, Russian Federation

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Anna Eremkina Endocrinology Research Center, Moscow, Russian Federation

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Daria Goliusova Endocrinology Research Center, Moscow, Russian Federation

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Julia Krupinova Endocrinology Research Center, Moscow, Russian Federation

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Natalia Mokrysheva Endocrinology Research Center, Moscow, Russian Federation

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Multiple endocrine neoplasia type 1 (MEN1) is the most common cause of hereditary primary hyperparathyroidism (PHPT). Bone disorders are considered one of the key symptoms in PHPT present with the significant reduction in bone mineral density and low-energy fractures. Previously, these bone disorders were believed to be caused solely by the increase in the level of parathyroid hormone and its subsequent effect on bone resorption. The current paradigm, however, states that the mutations in the menin gene, which cause the development of MEN1, can also affect the metabolism of the cells of the osteoid lineage. This review analyzes both the proven and the potential intracellular mechanisms through which menin can affect bone metabolism.

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Rong Xu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Difei Lian Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Yan Xie Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Lin Mu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Yali Wu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Zhilei Chen Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Baoyu Zhang Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Osteoporosis (OP) is a systemic bone disease in which bone density and quality decrease and bone fragility increases due to a variety of causes, making it prone to fractures. The development of OP is closely related to oxidative stress. Uric acid (UA) is the end product of purine metabolism in the human body. Extracellular UA has antioxidant properties and is thought to have a protective effect on bone metabolism. However, the process of UA degradation can lead to intracellular oxidative stress, which together with UA-induced inflammatory factors, leads to increased bone destruction. In addition, UA can inhibit vitamin D production, resulting in secondary hyperparathyroidism and further exacerbating UA-associated bone loss. This review summarizes the relationship between serum UA levels and bone mineral density, bone turnover markers, and so on, in the hope of providing new insights into the pathogenesis and treatment of OP.

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Lu Yang Department of Nuclear Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China

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Xingguo Jing Department of Nuclear Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China

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Hua Pang Department of Nuclear Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China

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Lili Guan Department of Nuclear Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China

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Mengdan Li Department of Nuclear Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China

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In this review, we discuss the definition, prevalence, and etiology of sporadic multiglandular disease (MGD), with an emphasis on its preoperative and intraoperative predictors. Primary hyperparathyroidism (PHPT) is the third-most common endocrine disorder, and multiglandular parathyroid disease (MGD) is a cause of PHPT. Hereditary MGD can be definitively diagnosed with detailed family history and genetic testing, whereas sporadic MGD presents a greater challenge in clinical practice, and parathyroidectomy for MGD is associated with a higher risk of surgical failure than single gland disease (SGD). Therefore, it is crucial to be able to predict the presence of sporadic MGD in a timely manner, either preoperatively or intraoperatively. Various predictive methods cannot accurately identify all cases of sporadic MGD, but they can greatly optimize the management of MGD diagnosis and treatment and optimize the cure rate. Future research will urge us to investigate more integrative predictive models as well as increase our understanding of MGD pathogenesis.

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Maria Stelmachowska-Banaś Department of Endocrinology, The Centre of Postgraduate Medical Education, Warsaw, Polska, Poland

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Izabella Czajka-Oraniec Department of Endocrinology, The Centre of Postgraduate Medical Education, Warsaw, Polska, Poland

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Immune checkpoint inhibitors (ICIs) belong to a new group of anticancer drugs targeting T-cell proteins involved in the activation of immune response toward malignancies. Their introduction into clinical practice was a milestone in modern cancer treatment. However, the significant advantage of ICIs over conventional chemotherapy in terms of therapeutic efficacy is accompanied by new challenges related to specific side effects. ICI-induced immune system activation could lead to the loss of self-tolerance, presenting as autoimmune inflammation and dysfunction of various tissues and organs. Thus, the typical side effects of ICIs include immune-related adverse events (irAEs), among which endocrine irAEs, affecting numerous endocrine glands, have been commonly recognized. This review aimed to outline the current knowledge regarding ICI-induced endocrine disorders from a clinical perspective. We present updated information on the incidence and clinical development of ICI-induced endocrinopathies, including the most frequent thyroiditis and hypophysitis, the rarely observed insulin-dependent diabetes mellitus and primary adrenal insufficiency, and the recently described cases of hypoparathyroidism and lipodystrophy. Practical guidelines for monitoring, diagnosis, and treatment of ICI-related endocrine toxicities are also offered. Rising awareness of endocrine irAEs among oncologists, endocrinologists, and other health professionals caring for patients receiving ICIs could contribute to better safety and efficacy. As immunotherapy becomes widespread and approved for new types of malignancies, increased incidences of endocrine irAEs are expected in the future.

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E Vignali Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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F Cetani Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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S Chiavistelli Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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A Meola Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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F Saponaro Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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R Centoni Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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L Cianferotti Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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C Marcocci Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy
Endocrine Unit 2, Department of Clinical and Experimental Medicine, Laboratory of Chemistry and Endocrinology, University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy

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We investigated the prevalence of normocalcemic primary hyperparathyroidism (NPHPT) in the adult population living in a village in Southern Italy. All residents in 2010 (n=2045) were invited by calls and 1046 individuals accepted to participate. Medical history, calcium intake, calcium, albumin, creatinine, parathyroid hormone (PTH) and 25OHD were evaluated. NPHPT was defined by normal albumin-adjusted serum calcium, elevated plasma PTH, and exclusion of common causes of secondary hyperparathyroidism (SHPT) (serum 25OHD <30 ng/ml, estimated glomerular filtration rate (eGFR) <60 ml/min per 1.73 m2 and thiazide diuretics use), overt gastrointestinal and metabolic bone diseases. Complete data were available for 685 of 1046 subjects. Twenty subjects did not meet the inclusion criteria and 341 could not be evaluated because of thawing of plasma samples. Classical PHPT was diagnosed in four women (0.58%). For diagnosing NPHPT the upper normal limit of PTH was established in the sample of the population (n=100) who had 25OHD ≥30 ng/ml and eGFR ≥60 ml/min per 1.73 m2 and was set at the mean+3s.d. Three males (0.44%) met the diagnostic criteria of NPHPT. These subjects were younger and with lower BMI than those with classical PHPT. Our data suggest, in line with previous studies, that NPHPT might be a distinct clinical entity, being either an early phenotype of asymptomatic PHPT or a distinct variant of it. However, we cannot exclude that NPHPT might also represent an early phase of non-classical SHPT, since other variables, in addition to those currently taken into account for the diagnosis of NPHPT, might cumulate in a normocalcemic subject to increase PTH secretion.

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