Fact or Fiction? Psychiatric and Neurocognitive Dysfunction in Patients with Primary Hyperparathyroidism

Review Article

J Endocr Disord. 2015; 2(1): 1019.

Fact or Fiction? Psychiatric and Neurocognitive Dysfunction in Patients with Primary Hyperparathyroidism

Dean Libet BS¹ and Campbell MJ²*

¹Department of Endocrine Disorders, Boston University School of Medicine, USA

²Department of Endocrine Disorders, University of California, USA

*Corresponding author: Michael J Campbell, Department of Endocrine Disorders, University of California, USA

Received: November 09, 2015; Accepted: December 15, 2015; Published: December 18, 2015

Abstract

Primary Hyperparathyroidism (PHPT) is a disease characterized by elevated serum calcium in the setting of an inappropriately non-suppressed parathyroid hormone level. Classically, patients with PHPT presented with the repercussions of longstanding bone turnover such as osteoporosis, fractures, and nephrolithiasis. Today, many patients with PHPT are discovered incidentally on routine biochemical testing and many lack the classic sequelae of the disease. Instead patients describe psychiatric and neurocognitive dysfunction that may or may not be attributable to their PHPT. In this review we examine the current literature on the non-classical manifestations of PHPT, as well as the evidence for and against early surgical intervention.

Keywords: Primary hyperparathyroidism; Neurocognitive dysfunction; Hypocalcaemia

Introduction

Primary Hyperparathyroidism (PHPT) is a disorder effecting 0.2-3% of the population [1] and is characterized by elevated serum calcium in the setting of an inappropriately non-suppressed Parathyroid Hormone (PTH) level. Classically, patients with PHPT presented with the repercussions of longstanding bone turnover such as osteoporosis, fractures, and nephrolithiasis [2]. Today, patients with PHPT are usually discovered on routine biochemical screening and many are considered “asymptomatic” because they lack the common repercussions of calcium dysregulation. Many of these “asymptomatic” patients suffer from vague psychiatric and neurocognitive symptoms including: depression, anxiety, fatigue, weakness, problems with word finding and sleep disturbances [3,4]. Such symptoms have long been associated with PHPT, however the mechanisms such psychiatric and neurocognitive dysfunction exclusive and the appropriate treatment remains a topic of debate [5,6]. The purpose of this review is to describe the current thoughts on the evaluation and management of patients with psychiatric and neurocognitive manifestations of PHPT.

Background

The parathyroid glands are located in the neck and typically lye adjacent to the thyroid. They are the chief regulators of calcium homeostasis in the body and function through the secretion of PTH. PTH is probably the most important regulator of calcium metabolism and works predominately by stimulating osteoclasts to resort bone, therefore increasing serum calcium and phosphorus levels. PTH also activates 1-a -hydroxylase in the kidney, which catalyzes the conversion of non-active 25-Hydroxy (25-OH) vitamin D to activated 1,25 dihydroxy (1,25-OH) vitamin D. This leads to increased absorption of calcium and phosphorus in the gut. Finally, PTH increases reabsorption of calcium and decreases reabsorption of phosphorus in the kidney (Figure 1).