scholarly journals Phosphate Metabolism and Pathophysiology in Parathyroid Disorders and Endocrine Tumors

2021 ◽  
Vol 22 (23) ◽  
pp. 12975
Author(s):  
Guido Zavatta ◽  
Paola Altieri ◽  
Giulia Vandi ◽  
Valentina Vicennati ◽  
Uberto Pagotto ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Renal Tubule ◽  
Mineral Metabolism ◽  
Bone Diseases ◽  
Serum Phosphate ◽  
Endocrine Tumors ◽  
Phosphate Metabolism ◽  
Metabolic Bone Diseases ◽  
New Information ◽  
Metabolic Bone

The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, and also of rarer endocrine metabolic bone diseases, such as hypoparathyroidism and tumor-induced hypophosphatemia. These rare diseases of mineral metabolism have been and will be a precious source of new information about phosphate and other minerals in the coming years. The parathyroid glands, the kidneys, and the intestine are the main organs affecting phosphate levels in the blood and urine. Parathyroid disorders, renal tubule defects, or phosphatonin-producing tumors might be unveiled from alterations of such a simple and inexpensive mineral as serum phosphate. This review will present all these disorders from a ‘phosphate perspective’.

scholarly journals Normocalcemic primary hyperparathyroidism: a survey in a small village of Southern Italy

2015 ◽  
Vol 4 (3) ◽  
pp. 172-178 ◽  
Author(s):  
E Vignali ◽  
F Cetani ◽  
S Chiavistelli ◽  
A Meola ◽  
F Saponaro ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Southern Italy ◽  
Adult Population ◽  
Bone Diseases ◽  
Inclusion Criteria ◽  
Metabolic Bone Diseases ◽  
Metabolic Bone ◽  
Common Causes ◽  
The Mean ◽  
Normal Albumin

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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