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Primary Hyperparathyroidism: a Narrative Review of Diagnosis and Medical Management

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Primary Hyperparathyroidism: a Narrative Review of Diagnosis and Medical Management Journal of Clinical Medicine Review Primary Hyperparathyroidism: A Narrative Review of Diagnosis and Medical Management Karel Dandurand , Dalal S. Ali and Aliya A. Khan * Division of Endocrinology and Metabolism, McMaster University, Hamilton, ON L8S 4L8, Canada; [email protected] (K.D.); [email protected] (D.S.A.) * Correspondence: [email protected] 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. Citation: Dandurand, K.; Ali, D.S.; Cinacalcet, a calcimimetic agent, has been shown to effectively lower serum calcium and PTH levels. Khan, A.A. Primary The effect of medical treatment on the reduction in fracture risk is unknown and should be the focus Hyperparathyroidism: A Narrative of future research. Review of Diagnosis and Medical Management. J. Clin. Med. 2021, 10, Keywords: primary hyperparathyroidism; cinacalcet; bisphosphonates; denosumab; estrogen; raloxifene 1604. https://doi.org/10.3390/ jcm10081604 Academic Editor: Marie-Lise Jaffrain-Rea 1. Introduction Primary hyperparathyroidism (PHPT) is a common endocrine disorder with an es- Received: 9 February 2021 timated prevalence of 0.86% in the United States [1,2] and represents the leading cause Accepted: 6 April 2021 of hypercalcemia in the outpatient setting [3]. It results from the abnormal regulation Published: 9 April 2021 and excessive release of parathyroid hormone (PTH) from one or more of the parathyroid glands. Increased levels of PTH lead to hypercalcemia through increased renal tubular Publisher’s Note: MDPI stays neutral calcium reabsorption, stimulation of osteoclast-mediated bone resorption and increased with regard to jurisdictional claims in renal synthesis of 1.25 (OH)2D3, which in turn promotes enhanced intestinal calcium and published maps and institutional affil- phosphate absorption (Figure1). Overt manifestations of PHPT have classically targeted iations. the skeletal and renal systems, with patients traditionally presenting with reduced bone mineral density (BMD) or fragility fractures, as well as kidney stones, nephrocalcinosis or renal insufficiency [4]. However, the inclusion of serum calcium measurement in baseline metabolic panels has led to a gradual shift in the clinical presentation of PHPT in recent Copyright: © 2021 by the authors. decades, from symptomatic disease to an asymptomatic presentation which is now the Licensee MDPI, Basel, Switzerland. dominant phenotype in the Western world [5]. Approximately 70–80% of patients now This article is an open access article present at an asymptomatic stage [6] and do not meet traditional criteria for surgery and distributed under the terms and may be followed with medical intervention if and as needed. Surgery is clearly the option conditions of the Creative Commons of choice for those with symptomatic disease and may also be suitable for those with Attribution (CC BY) license (https:// asymptomatic disease in the absence of comorbidities, as it is the only curative treatment creativecommons.org/licenses/by/ strategy [7]. A conservative approach may also be warranted in patients who are not 4.0/). J. Clin. Med. 2021, 10, 1604. https://doi.org/10.3390/jcm10081604 https://www.mdpi.com/journal/jcm J. Clin.J. Clin. Med. Med.2021 2021, 10, 10, 1604, 1604 2 of 152 of 15 strategy [7]. A conservative approach may also be warranted in patients who are not suit‐ suitable surgical candidates or who do not wish to proceed with surgery or who have able surgical candidates or who do not wish to proceed with surgery or who have failed failed previous surgical intervention. Recent guidelines [7] and consensus statements [1] previous surgical intervention. Recent guidelines [7] and consensus statements [1] have have provided recommendations on the evaluation, diagnosis and management of PHPT. provided recommendations on the evaluation, diagnosis and management of PHPT. This This article summarizes the optimal medical management of patients with PHPT not article summarizes the optimal medical management of patients with PHPT not undergo‐ undergoinging parathyroidectomy. parathyroidectomy. FigureFigure 1.1. (Reproduced(Reproduced with with permission permission from from Khan Khan et al., et al., CMAJ CMAJ 2000) 2000) Simplified Simplified representation representation of of calcium homeostasis, with the regulation of serum calcium levels via feedback inhibition through calcium homeostasis, with the regulation of serum calcium levels via feedback inhibition through the the calcium receptor. ECF, extracellular; Ca, calcium; PTH, parathyroid hormone [8]. calcium receptor. ECF, extracellular; Ca, calcium; PTH, parathyroid hormone [8]. 2.2. MaterialsMaterials and Methods Methods InIn orderorder to produce produce this this narrative narrative review, review, we we carried carried out out a literature a literature search search on MED on MED-‐ LINE, EMBASE and PubMed databases, including terms for PHPT in association with LINE, EMBASE and PubMed databases, including terms for PHPT in association with calcium, vitamin D and all included drugs discussed. All relevant articles published be‐ calcium, vitamin D and all included drugs discussed. All relevant articles published be- tween 1 January 2000 and 31 December 2020 were reviewed in detail. Key articles pub‐ tween 1 January 2000 and 31 December 2020 were reviewed in detail. Key articles published lished before 2000 were also included in the synthesis. Recovered entries were limited to before 2000 were also included in the synthesis. Recovered entries were limited to data data pertaining to human patients written in English. pertaining to human patients written in English. 3. Diagnosis 3. Diagnosis Primary hyperparathyroidism is diagnosed in the presence of hypercalcemia and an Primary hyperparathyroidism is diagnosed in the presence of hypercalcemia and elevated or inappropriately normal PTH level [6]. It is essential to ensure that serum cal‐ ancium elevated is not fictitiously or inappropriately elevated, normaland as such, PTH serum level [calcium6]. It is corrected essential for to ensure albumin that or an serum calciumionized iscalcium not fictitiously should be elevated, obtained. and as such, serum calcium corrected for albumin or an ionizedThe calcium use of lithium should and be obtained.hydrochlorothiazide may lead to elevated serum calcium and PTHThe levels use and of lithiumshould be and discontinued hydrochlorothiazide 3 months mayprior lead to repeating to elevated the serumlab profile calcium and and PTHconfirming levels anda diagnosis should beof discontinuedPHPT. It is essential 3 months to priorexclude to repeatingfamilial hypocalciuric the lab profile hyper and‐ con- firmingcalcemia a (FHH), diagnosis a rare of PHPT. autosomal It is essentialdominant to disorder exclude with familial three hypocalciuric identified variants hypercalcemia lead‐ (FHH),ing to the a rare abnormal autosomal function dominant of the CaSR, disorder as surgery with three is not identified indicated variants in the presence leading of to the abnormalFHH. FHH1 function is caused of theby an CaSR, inactivating as surgery mutation is not in indicated the CaSR in gene the presenceitself and ofis the FHH. most FHH1 iscommon caused form by an as inactivating it comprises approximately mutation in the 65%CaSR of FHHgene patients itself [9]. and FHH2 is the accounts most common for form< 5% asof itFHH comprises cases and approximately is due to loss‐of 65%‐function of FHH mutations patients in [ 9the]. FHH2GNA11 accounts gene that for en‐ <5% ofcodes FHH the cases G‐alpha and subunit is due to11 loss-of-function (G11) protein, responsible mutations for in the CaSRGNA11 downstreamgene that acti encodes‐ thevation G-alpha of phospholipase subunit 11 (GC [9].α11) FHH3 protein, results responsible from the inactivating for the CaSR mutation downstream of the AP2S1 activation ofgene phospholipase that encodes the C [ 9adaptor]. FHH3‐protein results 2 sigma from the subunit, inactivating a scaffolding mutation protein of that the isAP2S1 essen‐gene thattial in encodes CaSR endocytosis, the adaptor-protein and this mutation 2 sigma subunit,is found ain scaffolding approximately protein 20% thatof FHH is essential pa‐ intients CaSR without endocytosis, CaSR mutations and this mutation[9]. Calculating is found the incalcium approximately to creatinine 20% clearance of FHH ratio patients without(CCCR)
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