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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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Nancy Martini Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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Lucas Streckwall Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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Antonio Desmond McCarthy Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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In post-menopausal women, aged individuals, and patients with diabetes mellitus or chronic renal disease, bone mineral density (BMD) decreases while the vasculature accumulates arterial calcifications (ACs). AC can be found in the tunica intima and/or in the tunica media. Prospective studies have shown that patients with initially low BMD and/or the presence of fragility fractures have at follow-up a significantly increased risk for coronary and cerebrovascular events and for overall cardiovascular mortality. Similarly, patients presenting with abdominal aorta calcifications (an easily quantifiable marker of vascular pathology) show a significant decrease in the BMD (and an increase in the fragility) of bones irrigated by branches of the abdominal aorta, such as the hip and lumbar spine. AC induction is an ectopic tissue biomineralization process promoted by osteogenic transdifferentiation of vascular smooth muscle cells as well as by local and systemic secreted factors. In many cases, the same regulatory molecules modulate bone metabolism but in reverse. Investigation of animal and in vitro models has identified several potential mechanisms for this reciprocal bone–vascular regulation, such as vitamin K and D sufficiency, advanced glycation end-products–RAGE interaction, osteoprotegerin/RANKL/RANK, Fetuin A, oestrogen deficiency and phytooestrogen supplementation, microbiota and its relation to diet, among others. Complete elucidation of these potential mechanisms, as well as their clinical validation via controlled studies, will provide a basis for pharmacological intervention that could simultaneously promote bone and vascular health.

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Laurent Maïmoun Département de Médecine Nucléaire, Hôpital Lapeyronie, Centre Hospitalier Régional Universitaire (CHU) Montpellier, Montpellier, France
PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France

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Denis Mariano-Goulart Département de Médecine Nucléaire, Hôpital Lapeyronie, Centre Hospitalier Régional Universitaire (CHU) Montpellier, Montpellier, France
PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France

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Helena Huguet Unité de Recherche Clinique et Epidémiologie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France

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Eric Renard Departement d’Endocrinologie, Diabète, Nutrition, Hôpital Lapeyronie, CHRU Montpellier, Montpellier, France
CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France
Institut de Génomique Fonctionnelle, CNRS UMR 5203/INSERM U661/Université Montpellier, Montpellier, France

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Patrick Lefebvre Departement d’Endocrinologie, Diabète, Nutrition, Hôpital Lapeyronie, CHRU Montpellier, Montpellier, France

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Marie-Christine Picot Unité de Recherche Clinique et Epidémiologie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France

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Anne-Marie Dupuy Département de Biochimie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France

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Jean-Paul Cristol PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
Département de Biochimie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France

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Philippe Courtet Institut de Génomique Fonctionnelle, CNRS, INSERM Université Montpellier, Montpellier, France
Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France

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Vincent Boudousq Département de Médecine Nucléaire, Hôpital Carémeau, CHU Nîmes, Nîmes, France

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Antoine Avignon Département Endocrinologie, Nutrition, Diabète, Equipe Nutrition, Diabète, CHU Montpellier, Montpellier, France

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Sébastien Guillaume Institut de Génomique Fonctionnelle, CNRS, INSERM Université Montpellier, Montpellier, France
Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France

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Ariane Sultan PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
Département Endocrinologie, Nutrition, Diabète, Equipe Nutrition, Diabète, CHU Montpellier, Montpellier, France

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Objectives

The two-fold aim of this study was: (i) to determine the effects of undernutrition on the myokines in patients with restrictive anorexia nervosa (AN) and (ii) to examine the potential link between myokines and bone parameters.

Methods

In this study, 42 young women with restrictive AN and 42 age-matched controls (CON) (mean age, 18.5 ± 4.2 years and 18.6 ± 4.2 years, respectively) were enrolled. aBMD and body composition were determined with DXA. Resting energy expenditure (REEm), a marker of energy status, was indirectly assessed by calorimetry. Bone turnover markers and myokines (follistatin, myostatin and irisin) were concomitantly evaluated.

Results

AN patients presented low aBMD at all bone sites. REEm, bone formation markers, myostatin and IGF-1 were significantly lower, whereas the bone resorption marker and follistatin were higher in AN compared with controls. No difference was observed between groups for irisin levels. When the whole population was studied, among myokines, only myostatin was positively correlated with aBMD at all bone sites. However, multiple regression analyses showed that in the AN group, the independent variables for aBMD were principally amenorrhoea duration, lean tissue mass (LTM) and procollagen type I N-terminal propeptide (PINP). For CON, the independent variables for aBMD were principally LTM, age and PINP. Whatever the group analysed, none of the myokines appeared as explicative independent variables of aBMD.

Conclusion

This study demonstrated that despite the altered myokine levels in patients with AN, their direct effect on aBMD loss and bone turnover alteration seems limited in comparison with other well-known disease-related factors such as oestrogen deprivation.

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