ReviewLaboratory screening for hyperparathyroidism
Introduction
Since its first description in 1925, hyperparathyroidism (HPT) is being more diagnosed especially in developed countries. This might be explained, at least partially, by the newly discovered advanced diagnostic tools which allow early detection of hypercalcemia. Severe forms of HPT with bone disease and renal stones are rarely seen these days [1], [2]. Most patients with HPT present today with nonspecific general complaints associated with mild skeletal complications and mild to moderate degrees of hypercalcemia as the case with pHPT [3]. Moreover, the severity of sHPT and tHPT has dramatically declined because of the effective prophylactic measures taken by patients liable for these disorders such as patients with chronic renal failure or malabsorption syndromes [4], [5]. The shift from the classic presentation of HPT occurred during the 1970s when automated serum calcium measurements became liberally and widely utilized [6]. The changing face of hyperparathyroidism was coupled with a marked increase in its incidence [7], [8], [9]. Today, hyperparathyroidism in developed countries is usually associated with less dramatic laboratory changes and smaller parathyroid tumors, in developing countries, however, the old version of the disease is still being encountered [10], [11].
Section snippets
Pathophysiology and forms of HPT
The parathyroid glands are composed of two cellular components; the chief cells and oxyphil cells, and a stroma that is largely made up of fat cells. The chief cell produces most of the parathyroid hormone (PTH), which is an 84-amino-acid single-chain peptide [12]. Its molecular weight is about 9500 with a plasma half-life of 3–4 min. Smaller compounds with as few as 34 amino acids adjacent to the N-terminus of the molecule have also been isolated from the parathyroid gland exhibit full
Calcium–PTH–Vit D–calcitonin interaction
The skeleton, the largest calcium reservoir, contains more than 99% of the total body calcium. This reservoir is readily available for homeostatic needs [36]. Hypocalcemia and hypercalcemia are life-threatening conditions. Therefore, extracellular Ca concentration must be controlled in a narrow range (8.1–10.5 mg/dl). Three calciotropic hormones (PTH, calcitonin and vitamin D) targeting three organs (bone, kidney and intestine) work in coherence to achieve this goal. Acutely, slight changes
Clinical diagnosis
Primary hyperparathyroidism (pHPT) is the most common form of hyperparathyroidism. It is the third most common endocrine disorder, after diabetes mellitus and thyroid disease. In its classic form (which is becoming less common); symptomatic hyperparathyroidism patients have manifestations secondary to high serum calcium and PTH levels such as overt bone disease, kidney stones, and nonspecific gastrointestinal, cardiovascular, and neuromuscular dysfunction [3], [6], [42]. Currently, asymptomatic
Summary
Hyperparathyroidism is a common and potentially serious disorder. Primary hyperparathyroidism (pHPT) is the most common cause of hypercalcemia in outpatients' clinics and is usually mild, asymptomatic, and sustained for years. PTH measurement in the serum is the most direct and sensitive measure of parathyroid function. Diagnosis of pHPT has improved substantially since the introduction of sensitive and specific assays for intact 84-amino-acid peptide. The sensitivity for the diagnosis of
Acknowledgments
This work was supported by the Faculty of Medicine/University of Jordan. We thank Ms. Sana Al Tamemi for her help with the graphs.
References (106)
- et al.
Medical and surgical management of hyperparathyroidism
Mayo Clin. Proc.
(2002) - et al.
Secondary hyperparathyroidism in chronic renal failure: pathogenic and clinical aspects
Am. J. Kidney Dis.
(2001) Primary hyperparathyroidism: clinical presentation and factors influencing clinical management
Endocrinol. Metab. Clin. North Am.
(1989)- et al.
Primary hyperparathyroidism: changes in the pattern of clinical presentation
Lancet
(1980) Natural history of primary hyperparathyroidism
Endocrinol. Metab. Clin. North Am.
(2000)- et al.
Multiple endocrine neoplasia type 2. Clinical features and screening
Endocrinol. Metab. Clin. North Am.
(1994) - et al.
Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
Cell
(1993) - et al.
New directions in the treatment of patients with primary hyperparathyroidism
Curr. Probl. Surg.
(2003) Familial hypocalciuric hypercalcemia and other disorders with resistance to extracellular calcium
Endocrinol. Metab. Clin. North Am.
(2000)- et al.
The role of phosphorus in the development of secondary hyperparathyroidism and parathyroid cell proliferation in chronic renal failure
Am. J. Med. Sci.
(1999)
Total parathyroidectomy reduces elevated circulating fibroblast growth factor 23 in advanced secondary hyperparathyroidism
Am. J. Kidney Dis.
Hyperparathyroidism associated with renal disease. Pathogenesis, natural history, and surgical treatment
Surg. Clin. North Am.
Results of surgical treatment for hyperparathyroidism associated with renal disease
Am. J. Surg.
The skeletal effects of primaryhyperparathyroidism
Bailliere's Clin. Endocrinol. Metab.
Hyperparathyroidism
Radiol. Clin. North Am.
Acute hypercalcemia causes acute pancreatitis and ectopic trypsinogen activation in the rat
Gastroenterology
Hypercalcemia causes acute pancreatic secretory block intracellular zymogen accumulation, and acinar cell injury
Am. J. Surg.
Electrolyte quintet: calcium
Lancet
The effects of stasis with and without exercise on free calcium, various cations, and related parameters
Clin. Chim. Acta
Magnesium and phosphorus
Lancet
Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: recommendations for a change in management
Am. J. Kidney Dis.
Screening for primary hyperparathyroidism (PHPT) in clinic patients: differential diagnosis between PHPT and malignancy-associated hypercalcemia by routine blood tests
Clin. Chim. Acta
Fracture incidence in postmenopausal women with primary hyperparathyroidism
Surgery
The history of hyperparathyroidism
Acta Chir. Scand.
Surgery for primary hyperparathyroidism 1962–1996: indications and outcomes
Med. J. Aust.
1,25 dihydroxycholecalciferol and parathyroid hormone in advanced chronic renal failure: effects of simultaneous protein and phosphorus restriction
Clin. Nephrol.
Primary hyperparathyroidism: incidence, morbidity and potential economic impact on the community
N. Engl. J. Med.
Clinical spectrum of primary hyperparathyroidism: evolution with changes in medical practice and technology
J. Bone Miner. Res.
Clinical spectrum of primary hyperparathyroidism
Saudi Med. J.
Unique clinical characteristics of primary hyperparathyroidism in India
Br. J. Surg.
An ultrastructural study of acid phosphatase activity in normal, adenomatous and hyperplastic (chief cell type) human parathyroid glands
Am. J. Pathol.
Cellular physiology and pathophysiology of the parathyroid glands
World J. Surg.
“Asymptomatic” primary hyperparathyroidism: is parathyroidectomy indicated?
Surgery
Role of vitamin D and calcium nutrition in disease expression and parathyroid tumor growth in primary hyperparathyroidism: a global perspective
J. Bone Miner. Res.
Dose–response relationships for radiation-induced hyperparathyroidism
J. Clin. Endocrinol. Metab.
Pathology and outcome of surgical treatment for lithium-associated hyperparathyroidism
Br. J. Surg.
Hyperparathyroidism in multiple endocrine neoplasia syndrome
Surgery
Hyperparathyroid and hypoparathyroid disorders
N. Engl. J. Med.
Familial hyperparathyroidism without multiple endocrine neoplasia
World J. Surg.
Genetic screening for MEN1 mutations in families presenting with familial primary hyperparathyroidism
World J. Surg.
Mechanisms of secondary hyperparathyroidism
Am. J. Physiol. Renal. Physiol.
Molecular mechanisms of secondary hyperparathyroidism
Pediatr. Nephrol.
Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol
Am. J. Physiol.
Fibroblast growth factor (FGF)-23 in patients with primary hyperparathyroidism
Eur. J. Endocrinol.
Serum calcium as an early indicator for surgical treatment of hyperparathyroidism after renal transplantation
World J. Surg.
Hypercalcemia
Curr. Probl. Surg.
Homeostatic mechanisms regulating extracellular and intracellular calcium metabolism
Osteoprotegerin: a physiological and pharmacological inhibitor of bone resorption
Curr. Pharm. Des.
Vitamin D intoxication causes hypercalcaemia by increased bone resorption which responds to pamidronate
Clin. Endocrinol. (Oxf)
Reduced bone mineral content in totally thyroidectomized patients: possible effect of calcitonin deficiency
J. Clin. Endocrinol. Metab.
Cited by (47)
COMMD5 is involved in the mechanisms of hypotension after parathyroidectomy in patients receiving hemodialysis
2023, European Journal of PharmacologyDisorders of calcium metabolism
2020, Handbook of Diagnostic EndocrinologyBrown tumors of hyperparathyroidism revealed by bone pain
2016, Presse MedicalePrimary hyperparathyroidism associated with a giant cell tumor: One case in the distal radius
2015, Chirurgie de la MainCitation Excerpt :Primary hyperparathyroidism is a common disease [1] that mainly affects woman after menopause.
A control engineering model of calcium regulation
2014, IFAC Proceedings Volumes (IFAC-PapersOnline)Disseminated brown tumors revealing primary hyperparathyroidism
2013, Medecine Nucleaire