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Hyperparathyroidism Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]

Classification

Classification of hyperparathyridism
Features Primary hyperparathyroidism Secondary hyperparathyroidism Tertiary hyperparathyroidism
Pathology Hyperfunction of parathyroid cells due to hyperplasia, adenoma or carcinoma. Physiological stimulation of parathyroid in response to hypocalcaemia. Following long term physiological stimulation leading to hyperplasia.
Cause
Associations May be associated with multiple endocrine neoplasia. Usually due to chronic renal failure or other causes of Vitamin D deficiency. Seen in chronic renal failure.
Serum calcium High Low/Normal High
Serum phosphate Low/Normal High High
Management Usually surgery if symptomatic. Cincacalcet can be considered in those not fit for surgery. Treatment of underlying cause. Usually cinacalcet or surgery in those that don't respond.

Causes

Overview

Hyperparathyroidism is caused by an increase in concentration of parathyroid hormone in serum. There are three type of hyperparathyroidism including primary, secondary and tertiary hyperparathyroidism. The are an array of different causes for all types of hyperparathyroidism.

Causes of Primary hyperparathyroidism

Causes of primary hyperparathyroidism are as follows:

Common causes

  • Parathyroid adenoma
    • Usually single gland affected
    • Sometimes multiple gland affected

Less common causes

  • Parathyroid hyperplasia
  • Parathyroid carcinoma
  • Familial isloated hyperparathyroidism
  • Radiation exposure (due to development of parathyroid adenoma or parathyroid hyperplasia)[1][2][3]
  • Celiac disease[4][5]

Genetic causes

  • HRPT2 gene mutations:[6]
    • HRPT2 gene code for parafibromin protein.
    • HRPT2 gene mutations are found in a type of familial hyperparathyroidism, hyperparathyroidism-jaw tumor (HPT-JT) syndrome.
    • HRTP2 gene mutations increases risk of parathyroid carcinoma.
  • Cyclin D1 gene (CCND1)/PRAD1 gene:[7][8]
    • PRAD1 (parathyroid adenoma 1) is a protooncogene located on chromosome 11q13.
    • Cyclin D1 gene translocation and oncogene action observerd in 8% of adenomas
    • Cyclin D1 gene overexpression is pbserved in 20% to 40% of parathyroid adenomas
  • MEN1 gene:[7][9]
    • MEN1 is a tumor supressor gene on chronosome 11q13.
    • Somatic loss of single MEN1 allele is observed in 25% to 40% of sporadic parathyroid adenomas.

Causes of secondary hyperparathyroidism

Causes of secondary hyperparathyroidism are as follows:

Common causes

  • Chronic renal failure (leading to parathyroid hyperplasia)[10]
  • Vitamin D deficiency[11]

Less common causes

  • Severe calcium deficiency[12]
  • Gastric bypass surgery, particularly roux-en-Y gastric bypass (RYGBP)[13]
  • Malabsorption syndrome[14]

Causes of tertiary hyperparathyroidism

Causes of tertiary hyperparathyroidism are as follows:

Common causes

  • Chronic renal failure (leading to parathyroid hyperplasia)
  • Renal transplant patients[15]

Less common cause

  • Long standing celiac disease[4]


Pathogenesis

Associated conditions

  • Hypercalcemia
  • Chronic renal failure
  • Osteitis fibrous cystica
  • Osteoporosis
  • Osteomalacia
  • Osteoarthritis
  • Brown tumor
  • Multiple endocrine neoplasia type 1, type 2A, and type 4
  • Familial isolated hyperparathyroidism
  • Neonatal severe hyperparathyroidism
  • Familial hypocalciuric hypercalcemia
  • Hyperparathyroid-jaw tumor syndrome
  • Pancreatitis[16]

Natural history, Prognosis and Complications

Natural history

  • Primary hyperparathyroidism usually develops in the fifth decade of life, in post-menopausal women and starts as asymptomatic hypercalcemia in presence of increased parathyroid hormone.
  • If left untreated, some of patients with primary hyperparathyroidism may commonly develop marked hypercalcemia, marked hypercalciuria, cortical bone demineralization and nephrolithiasis.[17][18]
  • Secondary hyperparathyroidism arise in the early course of chronic renal failure. As renal failure progress, secondary hyperparathyroidism becomes more notable.[19]
  • Secondary hyperparathyroidism leads to vascular calcification due to elevated calcium and phosphorus levels. This is strongly associated with increase in morbidity and mortality.[20]
  • If left untreated, secondary hyperparathyroidism carries an increased risk of vascular calcification with increasing age and duration of dialysis in patients.
  • Tertiary hyperparathyroidism usually develops in post renal transplant patients.[21]
  • If left untreated, tertiary hyperparathyroidism in post renal transplant patients may carry the risk of amyloid deposition, calciphylaxis, destructive or erosive spondyloarthropathy, osteonecrosis, and musculoskeletal infections.

Complications

Primary hyperparathyroidism

Majority of complications of primary hyperparathyroidism are due to hypercalcemia. Common complications of primary hyperparathyroidism include:

  • Bone related complication:[22][23]
    • Brown tumor
    • Osteitis fibrous cystica
    • Osteoporosis
  • Cardiac complications:[24]
    • Aortic and mitral valve calcification
    • Calcific deposits in the myocardium
    • Left ventricular hypertrophy
  • Endocrine complications:[16]
    • Pancreatitis
  • Gastrointestinal complications:[25]
    • Peptic ulcer disease
  • Metabolic complications:[26][27][25][11]
    • Hypercalcemic crisis
    • Osteomalacia
  • Neuromuscular complications:
    • Neuropathic muscle disease
  • Pregnancy related complications:[28]
    • Neonatal hypoparathyroidism
  • Psychiatric complications:[29][30][31]
    • Anxiety
    • Cognitive dysfunction including verbal memory and nonverbal abstraction
    • Depression
    • Irritability
    • Lack of concentration
    • Sleep disturbances
  • Renal complications:[17][32][33]
    • Hypercalciuria
    • Nephrolithiasis
    • Nephrocalcinosis
    • Renal insufficiency (impairement of GFR)
  • Rheumatologic complications:[34][35][36]
    • Gout
    • Osteoarthritis
    • Pseudogout

Secondary hyperparathyroidism

Complications of secondary hyperparathyroidism includes:

  • Cardiovascular complications:[37]
    • Impaired left ventricular diastolic function
    • Left ventricular hypertrophy
  • Hematologic complication:[38]
    • Platlet function inhibition
  • Metabolic complicattions:[39][40]
    • Metabolic syndrome
  • Musculoskeletal complications:[41][42][43]
    • Renal Osteodystrophy
      • Brown cysts
      • Osteitis fibrosa cystica
      • Osteoporosis
      • Osteosclerosis
  • Neurologic complications:[44][45]
    • Electroencephalogram abnormalities
    • Uremic neuropathy
  • Neuromuscular complications:[46]
    • Neuropathic muscle disease
  • System non-specific complications:[47]
    • Metastatic calcifications

Tertiary hyperparathyroidism

Complications of tertiary hyperparathyroidism post renal transplantation includes:[21]

  • Metabolic complications:[48]
    • Calciphylaxis
  • Musculoskeletal complications:
    • Musculoskeletal infections
    • Osteonecrosis
  • Neuromuscular complications:[49]
    • Neuropathic muscle disease
  • Renal complications:[50]
    • Nephrolithiasis
  • Rheumatologic complications:[51]
    • Destructive or erosive spondyloarthropathy
  • System non-specific complications:
    • Amyloid deposition
    • Metastatic calcifications

Prognosis

  • Prognosis of primary hyperparathyroidism is generally excellent after parathyroidectomy.
  • The complications of primary hyperparathyroidism resolves after the treatment.
  • Untreated complication of primary hyperparathyroidism may be fatal.[25]
  • Effective treatment can reduce morbidity and mortality associated with uncontrolled secondary hyperparathyroidism.[20]
  • Hyperphosphatemia and metastatic calcification results due elevated product of serum calcium and serum phosphorus. Both conditions are present in patients with secondary hyperparathyroidism in presence of end stage renal disease. This leads to a significant increase in morbidity and mortality. Aggressive control of hyperphosphatemia may improve prognosis[47].
  • Prognosis of tertiary hyperparathyroidism is generally good after resection of abnormal hyperplastic gland.[52]


ECG

There are no CT scan findings associated with hyperparathyroidism. However, a CT scan may be helpful in the diagnosis of cardiac complications of hyperparathyroidism. Findings on ECG are due to hypercalcemia and includes:[53]

  • ST segment - ST segment is short in patients with hyperparathyroidism when compared to normocalcemic patients. This represents a decrease in systolic interval.
  • QRS complex - QRS complex has an increased amplitudein patients with hyperparathyroidism when compared to normocalcemic patients. This represents an increase in ventricular muscle mass.
  • T wave - T wave is prolonged in patients with hyperparathyroidism when compared to normocalcemic patients.

X-ray

Finding in primary hyperparathyroidism includes:[54]

  • Subperiosteal bone resorption
    • Classically affects the radial aspects of the proximal and middle phalanges of the 2nd and 3rd fingers
    • Medial aspect of tibia, femur, humerus
    • Phalyngeal tuft erosion (acro-osteolysis)
    • Lamina dura around teeth (floating teeth)
  • Endoosteal bone resorption
    • Widening of medullary cavity
    • Thinning of the inner cortex
  • Subchondral resorption
    • Lateral end of the clavicles
    • Symphysis pubis
    • Sacroiliac joints
  • Subligamentous resorption
    • Ischial tuberosity
    • Humeral tuberosity
    • Trochanters
    • Inferior surface of calcaneus
    • Inferior margin of lateral clavicle
  • Intracortical resorption: cigar/oval-shaped or tunnel-shaped radiolucency in the cortex
  • Osteopaenia
  • Brown tumours
  • Salt and pepper sign in the skull (pepper pot skull)
  • Chondrocalcinosis

X-ray is the preferred imaging for diagnosis of secondary hyperparathyroidism as majority of findings are radiological. [55] Findings in secondary and tertiary hyperparathyroidism are often associated with the osteosclerosis of renal osteodystrophy, and the osteomalacia of vitamin D deficiency:

  • Subperiosteal bone resorption
    • Radial aspect of middle phalanges of index and long fingers are involved.
  • Subchondral resorption
    • Hands, hips, shoulders, patellofemoral and sacroiliac joints are involved.
    • Hands are involves in the ulnar side.
    • Distal interphalangeal and metacarpophalangeal joints are involved.
    • Subchondral resorption is very severe. It may lead to bony collapse.
  • Subligamentous resorption
    • Retrocalcaneal bursa and insertion of planter aponeurosis may be involved.
  • Severe osteopenia, may be complicated by pathologic fractures
  • Osteosclerosis, e.g. rugger-jersey spine
  • Brown tumor
  • Amyloid deposition
    • May be manifested as lytic bone lesion on radiograph
  • Soft tissue and vascular calcification
  • Superior and inferior rib notching
  • Osteonecrosis may be often observed in patients in whom steroid is administered for prevention of renal transplant rejection.
Subperiosteal bone resorption - Source:Radiopedia
Brown tumors - Source:Case courtesy of A.Prof Frank Gaillard, Radiopedia
Normal skull compared to Salt & pepper appearance of skull - Source:Radiopedia
Acro-osteolytis, terminal tufts erosion - Source:Case courtesy of Dr Andrew Dixon, Radiopedia

CT scan

  • Good quality preoperative evaluation favors post operative results.
  • 4-Dimentional CT scan is an investigation for preoperative localizing of hyperfunctioning pituitary gland.[56]
  • 4D-CT may be used for preoperative localization of hyper-functioning parathyroid glands in hyperparathyroidism. 4D-CT is significantly more sensitive than sestamibi imaging and ultrasound for precise (quadrant) localization of hyper-functioning parathyroid glands.[57]
  • The name 4D-CT refers to 3-dimensional CT scanning plus additional dimension of changes observed with respect to time as perfusion of contrast occurs. The principle is similar to CT angiography.
  • 4D-CT provides extremely detailed images of neck in multiple planes and enables the visualization of difference in hyper-functioning parathyroid gland compared with normal parathyroid glands and other structures in the neck on the basis on perfusion characteristics ( rapid uptake and washout).
  • 4D-CT has a sensitive of 88% in preoperative lateralizing hyper-functioning parathyroid glands to one side of neck.[58]
  • 4D-CT has a sensitive of 79-88% in preoperative localizing the hyper-functioning parathyroid gland to the correct quadrant of the neck (right inferior, right superior, left inferior, or left superior).[59]
  • 4D-CT has a specificity of 75-100% in preoperative localizing the hyper-functioning parathyroid gland.[60]
  • 4D-CT enables an improved planning preoperativively, particularly in case of reoperation.
  • A modified technique of 4D-CT/Ultrasound (Mod 4D-CT/US) has a sensitivity of 94% and specificity of 96% for lateralizing the hyperfunctioning parathyroid glands to one side of the neck. Mod 4D-CT/US has a sensitivity of 82% and specificity of 93% for localizing the hyper-functioning parathyroid gland to the correct quadrant of the neck (right inferior, right superior, left inferior, or left superior). Mod 4D-CT/US has a positive predictive vaue of 92% for single-gland disease and 75% for multi-gland disease.Mod 4D-CT/US has a negative predictive value of 73% for single-gland disease and 92% multi-gland disease.[61]
  • The major disadvantage of 4D-CT is significant radiation exposure associated with scanning the patient multiple times.

MRI

MRI may be helpful in the preoperative evaluation of hype-functioning parathyroid glands.

Ultrasound

  • Neck ultrasound is used for preoperative localization of hyper-functioning gland. Neck ultrasound alone is not a sensitive investigation for this purpose. Also it is an operator dependent method.[62]
  • Neck ultrasound is most commonly used along with TC-99m sestamibi scintigraphy for preoperative localization of hyper-functioning gland.[63]
  • Presence of thyroid nodule may lead to false positive results.[64]
  • Ultrasound is the most cost-effective method used for preoperative localization of hyper-functioning parathyroid gland followed by 4-dimentional CT.[65]
  • Surgeon performed ultrasound has a sensitivity of 69% to 92.5%.[66][67][68][69]

Sestamibi scintigraphy

  • Technetium-99m-methoxyisobutylisonitrile (99mTc-sestamibi or MIBI) scintigraphy is the most popular investigation for preoperative localization of hyper-functioning parathyroid glands.[70]
  • Most of the sestamibi is retained in mitochondria of thyroid and abnormal parathyroid tissue and is a function of mitochondrial activity.[71]
  • The basis of this "single-isotope, double-phase technique" is that sestamibi washes out of the thyroid more rapidly than from abnormal parathyroid tissue.[72]
  • Multiple planar images are obtained, typically one shortly after injection of 99mTc-sestamibi and another after two hours to identify the foci of retained sestamibi showing hyper-functioning parathyroid tissue.
  • As all parathyroid lesions does not retain sestamibi nor all thyroid tissue washes out quickly, subtraction imaging may be beneficial.[73][74]
  • Presence of solid thyroid nodule is the most common cause of false positive results. Other causes of false positive results may include thyroid carcinoma, lymphoma, and lymphadenopathy.
  • The sensitivity of sestamibi scintigraphy can be increased by using it concomitantly with neck ultrasound and/or SPECT. [75][62]
  • The sensitivity of sestamibi scintigraphy is 80% - 90%.[68][67][76]

SPECT

  • Single positron emission computed tomography may be used along with Tc-99m sestamibi scintigraphy for preoperative evaluation of hyper-functioning parathyroid gland.[77][78]
  • Sestamibi-SPECT is also called pinhone-SPECT (P-SPECT). P-SPECT uses cone beam collimator in contrast to parallel-hole collimator used in SPECT. cone bean collimator possess more suitable geometric properties leading to high spatial resolution.[79][80]
  • Using SPECT with sestamibi scintigraphy improves detection and localization of hyper-functioning parathyroid gland.[81][82]
  • SPECT provides more precise result of sestamibi scitigraphy allowing surgeon to choose best route for surgical intervention.
  • P-SPECT may detect glands not visible on planer images leading to increased sensitivity. It is very useful in case of uncertain result from conventional sestamibi scitigraphy.[83][84]
  • P-SPECT also enables accurate interpretation sestamibi uptake in upper mediastinum leading to a higher specificity.
  • In difficult cases, P-SPECT may also be adjuncted with subtraction Tc-99m sestamibi and I-123 scintigraphy or positron emission tomography.[85]
  • P-SPECT is approximately 84% sensitive, 91% specific with positive predictive value of around 91% and negative predictive value of around 84%.[86]
  • Fusion images of CT-MIBI-SPECT is superior to CT or MIBI-SPECT alone in preoperative localization of hyper-functioning parathyroid gland.[87]

References

  1. ↑ Boehm BO, Rosinger S, Belyi D, Dietrich JW (2011). "The parathyroid as a target for radiation damage". N Engl J Med. 365 (7): 676–8. doi:10.1056/NEJMc1104982. PMID 21848480.
  2. ↑ McMullen T, Bodie G, Gill A, Ihre-Lundgren C, Shun A, Bergin M; et al. (2009). "Hyperparathyroidism after irradiation for childhood malignancy". Int J Radiat Oncol Biol Phys. 73 (4): 1164–8. doi:10.1016/j.ijrobp.2008.06.1487. PMID 18774659.
  3. ↑ Tisell LE, Hansson G, Lindberg S, Ragnhult I (1977). "Hyperparathyroidism in persons treated with X-rays for tuberculous cervical adenitis". Cancer. 40 (2): 846–54. PMID 890665.
  4. ↑ 4.0 4.1 Maida MJ, Praveen E, Crimmins SR, Swift GL (2006). "Coeliac disease and primary hyperparathyroidism: an association?". Postgrad Med J. 82 (974): 833–5. doi:10.1136/pgmj.2006.045500. PMC 2653933. PMID 17148709.
  5. ↑ Ludvigsson JF, Kämpe O, Lebwohl B, Green PH, Silverberg SJ, Ekbom A (2012). "Primary hyperparathyroidism and celiac disease: a population-based cohort study". J. Clin. Endocrinol. Metab. 97 (3): 897–904. doi:10.1210/jc.2011-2639. PMC 3319223. PMID 22238405.
  6. ↑ Shattuck TM, Välimäki S, Obara T, Gaz RD, Clark OH, Shoback D; et al. (2003). "Somatic and germ-line mutations of the HRPT2 gene in sporadic parathyroid carcinoma". N Engl J Med. 349 (18): 1722–9. doi:10.1056/NEJMoa031237. PMID 14585940.
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  17. ↑ 17.0 17.1 Peacock M (2002). "Primary hyperparathyroidism and the kidney: biochemical and clinical spectrum". J. Bone Miner. Res. 17 Suppl 2: N87–94. PMID 12412783.
  18. ↑ Silverberg SJ, Shane E, de la Cruz L, Dempster DW, Feldman F, Seldin D, Jacobs TP, Siris ES, Cafferty M, Parisien MV (1989). "Skeletal disease in primary hyperparathyroidism". J. Bone Miner. Res. 4 (3): 283–91. doi:10.1002/jbmr.5650040302. PMID 2763869.
  19. ↑ Nikodimopoulou M, Liakos S (2011). "Secondary hyperparathyroidism and target organs in chronic kidney disease". Hippokratia. 15 (Suppl 1): 33–8. PMC 3139677. PMID 21897756.
  20. ↑ 20.0 20.1 Cunningham J, Locatelli F, Rodriguez M (2011). "Secondary hyperparathyroidism: pathogenesis, disease progression, and therapeutic options". Clin J Am Soc Nephrol. 6 (4): 913–21. doi:10.2215/CJN.06040710. PMID 21454719.
  21. ↑ 21.0 21.1 Jevtic V (2003). "Imaging of renal osteodystrophy". Eur J Radiol. 46 (2): 85–95. doi:10.1016/S0720-048X(03)00072-X. PMID 12714225.
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  24. ↑ Stefenelli T, Abela C, Frank H, Koller-Strametz J, Globits S, Bergler-Klein J, Niederle B (1997). "Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up". J. Clin. Endocrinol. Metab. 82 (1): 106–12. doi:10.1210/jcem.82.1.3666. PMID 8989242.
  25. ↑ 25.0 25.1 25.2 Corlew DS, Bryda SL, Bradley EL, DiGirolamo M (1985). "Observations on the course of untreated primary hyperparathyroidism". Surgery. 98 (6): 1064–71. PMID 3878002.
  26. ↑ Fitzpatrick LA, Bilezikian JP (1987). "Acute primary hyperparathyroidism". Am. J. Med. 82 (2): 275–82. PMID 3812520.
  27. ↑ Ahmad S, Kuraganti G, Steenkamp D (2015). "Hypercalcemic crisis: a clinical review". Am. J. Med. 128 (3): 239–45. doi:10.1016/j.amjmed.2014.09.030. PMID 25447624.
  28. ↑ Poomthavorn P, Ongphiphadhanakul B, Mahachoklertwattana P (2008). "Transient neonatal hypoparathyroidism in two siblings unmasking maternal normocalcemic hyperparathyroidism". Eur. J. Pediatr. 167 (4): 431–4. doi:10.1007/s00431-007-0528-6. PMID 17569990.
  29. ↑ Walker MD, McMahon DJ, Inabnet WB, Lazar RM, Brown I, Vardy S, Cosman F, Silverberg SJ (2009). "Neuropsychological features in primary hyperparathyroidism: a prospective study". J. Clin. Endocrinol. Metab. 94 (6): 1951–8. doi:10.1210/jc.2008-2574. PMC 2690425. PMID 19336505.
  30. ↑ Espiritu RP, Kearns AE, Vickers KS, Grant C, Ryu E, Wermers RA (2011). "Depression in primary hyperparathyroidism: prevalence and benefit of surgery". J. Clin. Endocrinol. Metab. 96 (11): E1737–45. doi:10.1210/jc.2011-1486. PMID 21917870.
  31. ↑ McAllion SJ, Paterson CR (1989). "Psychiatric morbidity in primary hyperparathyroidism". Postgrad Med J. 65 (767): 628–31. PMC 2429194. PMID 2608590.
  32. ↑ Lila AR, Sarathi V, Jagtap V, Bandgar T, Menon PS, Shah NS (2012). "Renal manifestations of primary hyperparathyroidism". Indian J Endocrinol Metab. 16 (2): 258–62. doi:10.4103/2230-8210.93745. PMC 3313745. PMID 22470864.
  33. ↑ Tassone F, Gianotti L, Emmolo I, Ghio M, Borretta G (2009). "Glomerular filtration rate and parathyroid hormone secretion in primary hyperparathyroidism". J. Clin. Endocrinol. Metab. 94 (11): 4458–61. doi:10.1210/jc.2009-0587. PMID 19808852.
  34. ↑ Michael JW, Schlüter-Brust KU, Eysel P (2010). "The epidemiology, etiology, diagnosis, and treatment of osteoarthritis of the knee". Dtsch Arztebl Int. 107 (9): 152–62. doi:10.3238/arztebl.2010.0152. PMC 2841860. PMID 20305774.
  35. ↑ Hochberg, Marc (2015). "204. Primary hyperparathyroidism: rheumatologic manifestations and bone disease". Rheumatology. Philadelphia, PA: Mosby/Elsevier. p. 1668. ISBN 9780323091381.
  36. ↑ Rubin MR, Silverberg SJ (2002). "Rheumatic manifestations of primary hyperparathyroidism and parathyroid hormone therapy". Curr Rheumatol Rep. 4 (2): 179–85. PMID 11890884.
  37. ↑ Strózecki P, Adamowicz A, Nartowicz E, Odrowaz-Sypniewska G, Włodarczyk Z, Manitius J (2001). "Parathormon, calcium, phosphorus, and left ventricular structure and function in normotensive hemodialysis patients". Ren Fail. 23 (1): 115–26. PMID 11256521.
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