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  • Abstract: Adrenal x
  • Abstract: Addisons x
  • Abstract: Androgens x
  • Abstract: Catecholamines x
  • Abstract: hyperplasia x
  • Abstract: Cortex x
  • Abstract: Cushings x
  • Abstract: Medulla x
  • Abstract: Noradrenaline x
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Bekir Cakir Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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F Neslihan Cuhaci Seyrek Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Oya Topaloglu Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Didem Ozdemir Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Ahmet Dirikoc Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Cevdet Aydin Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Sefika Burcak Polat Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Berna Evranos Ogmen Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Ali Abbas Tam Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Husniye Baser Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Aylin Kilic Yazgan Department of Pathology, Ankara Ataturk Education and Research Hospital, Ankara, Turkey

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Mehmet Kilic Department of General Surgery, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Afra Alkan Department of Biostatistics, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Reyhan Ersoy Department of Endocrinology and Metabolism, Faculty of Medicine, Ankara Yildirim Beyazit University, Ankara, Turkey

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Background

Despite significant improvement in imaging quality and advanced scientific knowledge, it may still sometimes be difficult to distinguish different parathyroid lesions. The aims of this prospective study were to evaluate parathyroid lesions with ultrasound elastography and to determine whether strain index can help to differentiate parathyroid lesions.

Methods

Patients with biochemically confirmed hyperparathyroidism and localised parathyroid lesions in ultrasonography were included. All patients underwent B-mode US and USE examination. Ultrasound elastography scores and strain index of lesions were determined. Strain index was defined as the ratio of strain of the thyroid parenchyma to the strain of the parathyroid lesion.

Results

Data of 245 lesions of 230 patients were analysed. Histopathologically, there were 202 (82.45%) parathyroid adenomas, 26 (10.61%) atypical parathyroid adenomas, and 17 (6.94%) cases of parathyroid hyperplasia. Median serum Ca was significantly higher in atypical parathyroid adenoma patients than parathyroid hyperplasia patients (P = 0.019) and median PTH was significantly higher in APA compared to PA patients (P < 0.001). In 221 (90.2%) of the parathyroid lesions, USE score was 1 or 2. The median SI of atypical parathyroid adenomas was significantly higher than parathyroid adenomas and hyperplasia lesions (1.5 (0.56–4.86), 1.01 (0.21–8.43) and 0.91 (0.26–2.02), respectively, P = 0.003).

Conclusion

Our study revealed that SI of parathyroid lesions as well as serum calcium, parathyroid hormone levels, and B-mode US features may help to predict the atypical parathyroid adenoma. Ultrasound elastography can be used to differentiate among parathyroid lesions and guide a surgical approach.

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Sofia Maria Lider Burciulescu University of Medicine and Pharmacy Carol Davila Bucharest, Bucharest, Romania
National Institute of Endocrinology CI Parhon, Bucharest, Romania

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Monica Livia Gheorghiu University of Medicine and Pharmacy Carol Davila Bucharest, Bucharest, Romania
National Institute of Endocrinology CI Parhon, Bucharest, Romania

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Andrei Muresan National Institute of Endocrinology CI Parhon, Bucharest, Romania

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Iuliana Gherlan University of Medicine and Pharmacy Carol Davila Bucharest, Bucharest, Romania
National Institute of Endocrinology CI Parhon, Bucharest, Romania

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Attila Patocs Department of Laboratory Medicine and Molecular Genetics, Clinical Genetics and Endocrinology Laboratory, Semmelweis University National Institute of Oncology, Budapest, Hungary

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Corin Badiu University of Medicine and Pharmacy Carol Davila Bucharest, Bucharest, Romania
National Institute of Endocrinology CI Parhon, Bucharest, Romania

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Background

Pheochromocytomas (PHEOs) are rare catecholamine-secreting adrenal tumors. Approximately 60–90% of bilateral PHEOs are hereditary. We retrospectively analyzed the clinical characteristics of patients with bilateral PHEOs and the morbidity rate (malignancy, tumor recurrence and adrenal insufficiency (AI) rate) related to surgery technique and genetic status of the patients.

Results

Fourteen patients (12.5%, nine women, five men) had synchronous or metachronous bilateral PHEOs (out of 112 PHEO patients who underwent surgery between 1976 and 2021). The median age at diagnosis was 32 years (9–76) (three were children). Nine patients (64.2%) presented synchronous bilateral tumors, five (35.7%) contralateral metachronous tumors, 2–12 years after the first surgical intervention; three (21.4%) were metastatic. Median follow-up: 5 years (1–41), IQR 19 months. A total of 78.5% had a germline mutation (eight RET gene with MEN2A syndrome, three VHL syndrome, three not tested). Post-surgery recurrence was noted in 16.6% of patients (one with MEN2A syndrome and metastatic PHEOs, one with VHL syndrome), with similar rates after total adrenalectomy or cortical-sparing adrenal surgery. AI was avoided in 40% after cortical-sparing surgery.

Conclusion

Bilateral PHEOs are usually associated with genetic syndromes. The surgical technique for patients with hereditary bilateral PHEOs should be chosen based on a personalized approach, as they are at higher risk for developing new adrenal tumors requiring additional surgeries.

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Paal Methlie Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Steinar Hustad Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Ralf Kellman Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Bjørg Almås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Martina M Erichsen Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Eystein S Husebye Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Kristian Løvås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Objective

Liquid chromatography–tandem mass spectrometry (LC–MS/MS) offers superior analytical specificity compared with immunoassays, but it is not available in many regions and hospitals due to expensive instrumentation and tedious sample preparation. Thus, we developed an automated, high-throughput LC–MS/MS assay for simultaneous quantification of ten endogenous and synthetic steroids targeting diseases of the hypothalamic–pituitary–adrenal axis and gonads.

Methods

Deuterated internal standards were added to 85 μl serum and processed by liquid–liquid extraction. Cortisol, cortisone, prednisolone, prednisone, 11-deoxycortisol, dexamethasone, testosterone, androstenedione and progesterone were resolved by ultra-high-pressure chromatography on a reversed-phase column in 6.1 min and detected by triple-quadrupole mass spectrometry. The method was used to assess steroid profiles in women with Addison's disease (AD, n=156) and blood donors (BDs, n=102).

Results

Precisions ranged from 4.5 to 10.1% relative standard deviations (RSD), accuracies from 95 to 108% and extraction recoveries from 60 to 84%. The method was practically free of matrix effects and robust to individual differences in serum composition. Most postmenopausal AD women had extremely low androstenedione concentrations, below 0.14 nmol/l, and median testosterone concentrations of 0.15 nmol/l (interquartile range 0.00–0.41), considerably lower than those of postmenopausal BDs (1.28 nmol/l (0.96–1.64) and 0.65 nmol/l (0.56–1.10) respectively). AD women in fertile years had androstenedione concentrations of 1.18 nmol/l (0.71–1.76) and testosterone concentrations of 0.44 nmol/l (0.22–0.63), approximately half of those found in BDs of corresponding age.

Conclusion

This LC–MS/MS assay provides highly sensitive and specific assessments of glucocorticoids and androgens with low sample volumes and is suitable for endocrine laboratories and research. Its utility has been demonstrated in a large cohort of women with AD, and the data suggest that women with AD are particularly androgen deficient after menopause.

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Masatada Watanabe Laboratory of Tissue Regeneration, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Shinagawa, Tokyo, Japan

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Shuji Ohno Division of Research for Pharmacy Students Education, Hoshi University, Shinagawa, Tokyo, Japan

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Hiroshi Wachi Laboratory of Tissue Regeneration, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Shinagawa, Tokyo, Japan

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Emerging evidence suggests that sex steroids are important for human skin health. In particular, estrogen improves skin thickness, elasticity and moisture of older women. The major source of circulating estrogen is the ovary; however, local estrogen synthesis and secretion have important roles in, for example, bone metabolism and breast cancer development. We hypothesized that infiltrated peripheral monocytes are one of the sources of estrogen in skin tissues. We also hypothesized that, during atopic dermatitis under stress, a decline in the hypothalamus–pituitary–adrenal axis (HPA) and facilitation of the (hypothalamus)–sympathetic–adrenomedullary system (SAM) attenuates estrogen secretion from monocytes. Based on this hypothesis, we tested aromatase expression in the human peripheral monocyte-derived cell line THP-1 in response to the synthetic glucocorticoid dexamethasone (Dex), the synthetic β-agonist isoproterenol (Iso) and the β-antagonist propranolol (Pro). Dex mimics glucocorticoid secreted during excitation of the HPA, and Iso mimics catecholamine secreted during excitation of the SAM. We found that aromatase activity and the CYP19A1 gene transcript were both upregulated in THP-1 cells in the presence of Dex. Addition of Iso induced their downregulation and further addition of Pro rescued aromatase expression. These results may suggest that attenuation of estrogen secretion from peripheral monocytes could be a part of the pathology of stress-caused deterioration of atopic dermatitis. Further examination using an in vitro human skin model including THP-1 cells might be a valuable tool for investigating the therapeutic efficacy and mechanism of estrogen treatment for skin health.

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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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Milène Tetsi Nomigni INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Sophie Ouzounian INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Alice Benoit INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Jacqueline Vadrot INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Frédérique Tissier INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Sylvie Renouf INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Hervé Lefebvre INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Sophie Christin-Maitre INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Estelle Louiset INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France
INSERM, University of Rouen, Department of Endocrinology, Departments of Endocrinology, Pathology, Department of Pathology, Department of Endocrinology, INSERM, U982, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Institute for Research and Innovation in Biomedicine, Mont‐Saint‐Aignan, France

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Hirsutism induced by hyperandrogenism can be associated with polycystic ovary syndrome, 21-hydroxylase (OH) deficiency or androgen-secreting tumors, including ovarian and adrenal tumors. Adrenal androgen-secreting tumors are frequently malignant. Adrenal oncocytomas represent rare causes of hyperandrogenism. The aim of the study was to investigate steroidogenic enzyme expression and steroid secretion in an androgen-secreting adrenal oncocytoma in a young woman presenting with hirsutism. Hyperandrogenism was diagnosed on the basis of elevated plasma Δ4-androstenedione and testosterone levels. Pelvic ultrasound was normal, CT scanning revealed a right adrenal mass. Androgens were assessed in adrenal and ovarian vein samples and proved a right adrenal origin. Adrenalectomy normalized androgen levels and the adrenal tumor was diagnosed as an oncocytoma. Real time-PCR, immunohistochemistry and cell culture studies were performed on tumor explants to investigate the steroid secretion profile. Among enzymes required for cortisol synthesis, 17α-OH and 3β-hydroxysteroid dehydrogenase 2 (3β-HSD2) were highly expressed whereas 21-OH and 11β-OH were weakly produced at the mRNA and/or protein levels. Enzymes involved in testosterone production, 17β-HSD5 and 17β-HSD3, were also detected. ACTH receptor was present in the tissue. Cortisol, Δ4-androstenedione and testosterone secretions by cultured cells were increased by ACTH. These results provide the first demonstration, to our knowledge, of abnormal expression profile of steroidogenic enzymes in an adrenocortical oncocytoma. Our results also indicate that Δ4-androstenedione hypersecretion resulted from high 17α-OH and 3β-HSD2 expression in combination with low expression of 21-OH and 11β-OH. Testosterone production was ascribed to occurrence of 17β-HSD5 and 17β-HSD3. Finally, our results indicate that androgen secretion was stimulated by ACTH.

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Ruth Therese Casey Department of Endocrinology, University of Cambridge, Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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Deborah Saunders East Anglian Regional Radiation Protection Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Benjamin George Challis Department of Endocrinology, University of Cambridge, Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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Deborah Pitfield Department of Endocrinology, University of Cambridge, Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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Heok Cheow Department of Radiology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Ashley Shaw Department of Radiology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Helen Lisa Simpson Wolfson Diabetes and Endocrine Clinic, Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Context

Multiple endocrine neoplasia type 1 (MEN1) is a hereditary condition characterised by the predisposition to hyperplasia/tumours of endocrine glands. MEN1-related disease, moreover, malignancy related to MEN1, is increasingly responsible for death in up to two-thirds of patients. Although patients undergo radiological and biochemical surveillance, current recommendations for radiological monitoring are based on non-prospective data with little consensus or evidence demonstrating improved outcome from this approach. Here, we sought to determine whether cumulative radiation exposure as part of the recommended radiological screening programme posed a distinct risk in a cohort of patients with MEN1.

Patients and study design

A retrospective review of 43 patients with MEN1 attending our institution between 2007 and 2015 was performed. Demographic and clinical information including phenotype was obtained for all patients. We also obtained details regarding all radiological procedures performed as part of MEN1 surveillance or disease localisation. An estimated effective radiation dose (ED) for each individual patient was calculated.

Results

The mean ED for the total patient cohort was 121 mSv, and the estimated mean lifetime risk of cancer secondary to radiation exposure was 0.49%. Patients with malignant neuroendocrine tumours (NETS) had significantly higher ED levels compared to patients without metastatic disease (P < 0.0022).

Conclusions

In MEN1, radiological surveillance is associated with clinically significant exposure to ionising radiation. In patients with MEN1, multi-modality imaging strategies designed to minimise this exposure should be considered.

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Yali Cheng Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Qiaoying Lv Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Bingying Xie Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Bingyi Yang Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Weiwei Shan Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Chengcheng Ning Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Bing Li Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Liying Xie Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Chao Gu Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Xuezhen Luo Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Xiaojun Chen Department of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China

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Qin Zhu Department of Pathology, Obstetrics and Gynecology, Hospital of Fudan University, Shanghai, China

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Unopposed estrogen stimulation and insulin resistance are known to play important roles in endometrial cancer (EC), but the interaction between these two factors and how they contribute to endometrial lesions are not completely elucidated. To investigate the endometrial transcriptome profile and the associated molecular pathway alterations, we established an ovariectomized C57BL/6 mouse model treated with subcutaneous implantation of 17-β estradiol (E2) pellet and/or high-fat diet (HFD) for 12 weeks to mimic sustained estrogen stimulation and insulin resistance. Histomorphologically, we found that both E2 and E2 + HFD groups showed markedly enlarged uterus and increased number of endometrial glands. The endometrium samples were collected for microarray assay. GO and KEGG analysis showed that genes regulated by E2 and/or HFD are mainly responsible for immune response, inflammatory response and metabolic pathways. Further IPA analysis demonstrated that the acute phase response signaling, NF-κB signaling, leukocyte extravasation signaling, PPAR signaling and LXR/RXR activation pathways are mainly involved in the pathways above. In addition, the genes modulated reciprocally by E2 and/or HFD were also analyzed, and their crosstalk mainly focuses on enhancing one another’s activity. The combination analysis of microarray data and TCGA database provided potential diagnostic or therapeutic targets for EC. Further validation was performed in mice endometrium and human EC cell lines. In conclusion, this study unraveled the endometrial transcriptome profile alterations affected by E2 and/or HFD that may disturb endometrial homeostasis and contribute to the development of endometrial hyperplasia.

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Satoshi Higuchi Department of Diagnostic Radiology, Tohoku University Hospital, Sendai, Miyagi, Japan

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Hideki Ota Department of Diagnostic Radiology, Tohoku University Hospital, Sendai, Miyagi, Japan

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Takuya Ueda Department of Diagnostic Radiology, Tohoku University Hospital, Sendai, Miyagi, Japan

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Yuta Tezuka Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan

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Kei Omata Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan

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Yoshikiyo Ono Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan

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Ryo Morimoto Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan

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Masataka Kudo Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan

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Fumitoshi Satoh Division of Nephrology, Endocrinology and Vascular Medicine, Department of Medicine, Tohoku University Hospital, Sendai, Miyagi, Japan
Division of Clinical Hypertension, Endocrinology and Metabolism, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan

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Kei Takase Department of Diagnostic Radiology, Tohoku University Hospital, Sendai, Miyagi, Japan

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Objective

Regional differences in cardiac magnetic resonance, which can reveal catecholamine-induced myocardial injury in patients with pheochromocytoma, have not yet been assessed using 3T magnetic resonance imaging. We evaluated these differences using myocardial T1-mapping and strain analysis.

Design and Methods

We retrospectively reviewed 16 patients newly diagnosed with catecholamine-producing tumors (CPT group) and 16 patients with essential hypertension (EH group), who underwent cardiac magnetic resonance imaging between May 2016 and March 2018. We acquired 3T magnetic resonance cine and native T1-mapping images and performed feature-tracking-based strain analysis in the former.

Results

Global cardiac function, morphology, global strain and peak strain rate were similar, but end-diastolic wall thickness differed between groups (CPT vs EH: 10.5 ± 1.7 vs 12.6 ± 2.8 mm; P < 0.05). Basal, but not apical, circumferential strain was significantly higher in the CPT than the EH group (19.4 ± 3.2 vs 16.8 ± 3.6 %; P < 0.05). Native T1 values were significantly higher in CPT than in EH patients, in both the basal septum (1307 ± 48 vs 1241 ± 45 ms; P < 0.01) and the apical septum (1377 ± 59 vs 1265 ± 58 ms; P < 0.01) mid-walls. In the CPT, but not in the EH group, native T1 values in the apical wall were significantly higher than those in the basal wall (P < 0.01).

Conclusion

3T magnetic resonance-based T1-mapping can sensitively detect subclinical catecholamine-induced myocardial injury; the influence of catecholamines may be greater in the apical than in the basal wall.

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Jan Kvasnička 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Ondřej Petrák 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Tomáš Zelinka 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Judita Klímová 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Barbora Kološová 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Květoslav Novák Department of Urology, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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David Michalský 1st Department of Surgery, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Jiří Widimský Jr 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Robert Holaj 3rd Department of Medicine, General University Hospital and 1st Faculty of Medicine, Charles University in Prague, Praha, Czech Republic

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Background

Pheochromocytomas (PHEO) are tumours with the ability to produce, metabolize and secrete catecholamines. Catecholamines overproduction leads to the decrease of longitudinal function of the left ventricle (LV) measured by speckle-tracking echocardiography. Patients with PHEO have a lower magnitude of global longitudinal strain (GLS) than patients with essential hypertension. GLS normalization is expected after resolution of catecholamine overproduction.

Methods

Twenty-four patients (14 females and 10 males) with a recent diagnosis of PHEO have been examined before and 1 year after adrenalectomy. An echocardiographic examination including speckle-tracking analysis with the evaluation of GLS and regional longitudinal strain (LS) in defined groups of LV segments (basal, mid-ventricular and apical) was performed.

Results

One year after adrenalectomy, the magnitude of GLS increased (−14.3 ± 1.8 to −17.7 ± 1.6%; P < 0.001). When evaluating the regional LS, the most significant increase in the differences was evident in the apical segment compared to mid-ventricular and basal segments of LV (−5.4 ± 5.0 vs −1.9 ± 2.7 vs −1.6 ± 3.8; P < 0.01).

Conclusions

In patients with PHEO, adrenalectomy leads to an improvement of subclinical LV dysfunction represented by the increasing magnitude of GLS, which is the most noticeable in apical segments of LV.

Open access