Primary Hyperparathyroidism: Mechanisms and Treatment

Dear Colleagues,

Primary hyperparathyroidism (PHPT) is one of the most common endocrine disorders, characterized by hypercalcemia and elevated or unsuppressed levels of parathyroid hormone (PTH) due to dysfunction in one or more parathyroid glands. Historically, PHPT has often been associated with severe skeletal and renal complications, but milder forms of the disease, including asymptomatic and normocalcemic PHPT, have become more prevalent in recent years.

In patients with classic symptomatic PHPT, diagnosis is straightforward, and the primary treatment is surgical parathyroidectomy, which restores calcium and PTH levels and often improves bone mineral density (BMD) while reducing the risk of nephrolithiasis. However, in milder forms of the disease, such as normocalcemic PHPT, diagnosis is more challenging and treatment decisions are more complex. Recent studies suggest a trend toward earlier intervention, even in cases with less severe biochemical abnormalities, given the long-term metabolic consequences of untreated disease.

Parathyroidectomy has been shown to lead to significant metabolic improvements, including increased BMD and a reduction in kidney stone formation. While medical therapies can also improve BMD or lower serum calcium, no single agent has been found to address both issues simultaneously.

The metabolic impact of PHPT extends beyond calcium and phosphate homeostasis, affecting bone remodeling, renal function, and potentially other metabolic pathways. Understanding the biochemical markers associated with disease progression and treatment response is critical in optimizing management. Furthermore, the localization of hyperfunctioning parathyroid tissue, particularly in cases of multiglandular disease or ectopic adenomas, presents additional challenges that can complicate both diagnosis and treatment.

This Special Issue will explore the metabolic mechanisms underlying PHPT, from calcium and bone metabolism to the clinical effects of surgical and medical interventions. By examining the metabolic pathways involved in PHPT and the metabolic outcomes of treatment strategies, we aim to provide insights into more personalized and effective management of this common endocrine disorder.

Dr. Elena Castellano
Dr. Federica Saponaro
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• primary pyperparathyroidism
• mechanism
• metabolism