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Review
. 2021 Apr 9;10(8):1604.
doi: 10.3390/jcm10081604.

Primary Hyperparathyroidism: A Narrative Review of Diagnosis and Medical Management

Karel Dandurand  1 , Dalal S Ali  1 , Aliya A Khan  1
Affiliations
Review

Primary Hyperparathyroidism: A Narrative Review of Diagnosis and Medical Management

Karel Dandurand et al. J Clin Med. .

Abstract

Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia in the outpatient setting. Symptomatic presentation includes non-specific signs and symptoms of hypercalcemia, skeletal fragility, nephrolithiasis and nephrocalcinosis. The majority of individuals present at an asymptomatic stage following routine biochemical screening, without any signs or symptoms of calcium or parathyroid hormone (PTH) excess or target organ damage. Indications for surgery have recently been revised as published in recent guidelines and consensus statements. Parathyroidectomy is advised in patients younger than 50 years old and in the presence of either significant hypercalcemia, impaired renal function, renal stones or osteoporosis. Surgery is always appropriate in suitable surgical candidates, however, medical management may be considered in those with mild asymptomatic disease, contraindications to surgery or failed previous surgical intervention. We summarized the optimal medical interventions available in the care of PHPT patients not undergoing parathyroidectomy. Calcium and vitamin D intake should be optimized. Antiresorptive therapy may be used for skeletal protection in patients with an increased fracture risk. Cinacalcet, a calcimimetic agent, has been shown to effectively lower serum calcium and PTH levels. The effect of medical treatment on the reduction in fracture risk is unknown and should be the focus of future research.

Keywords: bisphosphonates; cinacalcet; denosumab; estrogen; primary hyperparathyroidism; raloxifene.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
(Reproduced with permission from Khan et al., CMAJ 2000) Simplified representation of calcium homeostasis, with the regulation of serum calcium levels via feedback inhibition through the calcium receptor. ECF, extracellular; Ca, calcium; PTH, parathyroid hormone [8].
Figure 2
Figure 2
(Reproduced with permission from Lundstam et al., JCEM 2015) Biochemistry and bone mineral density (BMD). Serum calcium and PTH levels, and BMD Z-scores in lumbar spine (LS) and femoral neck (FN) at inclusion and after 5 years of follow-up in the two groups. P denotes a significant level for difference in change between groups. * p < 0.02 and ** p < 0.01 for within group change between inclusion and 5 years [30].
Figure 3
Figure 3
(Reproduced with permission from Khan et al. JCEM 2004) Effect of Alendronate on LS (A); TH (B); FN (C); and one third distal radius (D). * Significantly higher than baseline (p < 0.001), † significantly higher than baseline (p < 0.05) [80].
Figure 4
Figure 4
(Reproduced with permission from Khan et al., CMAJ 2000) Schematic illustration of calcium binding to the calcium receptor at the parathyroid cell and inhibiting PTH secretion. Ca, calcium; PTH, parathyroid hormone [8].
Figure 5
Figure 5
(Reproduced with permission from Khan et al. EJE 2015) Mean corrected serum calcium over time. OL: open label [87].
See this image and copyright information in PMC

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