@article{3086086,
    title = "Diagnosis, management, histology and genetics of sporadic primary hyperparathyroidism: Old knowledge with new tricks",
    author = "Mizamtsidi, M. and Nastos, C. and Mastorakos, G. and Dina, R. and Vassiliou, I. and Gazouli, M. and Palazzo, F.",
    journal = "Endocrine Connections",
    year = "2018",
    volume = "7",
    number = "2",
    pages = "R56-R68",
    publisher = "BioScientifica Ltd",
    issn = "2049-3614",
    doi = "10.1530/EC-17-0283",
    keywords = "beta catenin;  carbon 11;  methionine;  methoxy isobutyl isonitrile technetium tc 99m;  parathyroid hormone;  Wnt protein, adenoma;  apoptosis;  carcinogenesis;  clinical feature;  creatinine clearance;  echography;  gene mutation;  genetic predisposition;  genetics;  histopathology;  human;  hypercalcemia;  hyperplasia;  malabsorption;  nuclear magnetic resonance imaging;  parathyroid carcinoma;  phenotype;  positron emission tomography-computed tomography;  primary hyperparathyroidism;  priority journal;  protein expression;  Review;  scintigraphy;  signal transduction;  vitamin D deficiency;  x-ray computed tomography",
    abstract = "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. © 2018 The authors."
}