History

Fact Explanation
Renal colic Hypersecreted parathyroid hormone acts on kidney, and reduce the excretion of calcium via urine. Increased calcium can precipitate as stones[2,3] This nephrocalcinosis[4] causing loin to groin pain. Most of them are calcium oxalate and occasionally calcium phosphate.
Skeletal problems Bones are frequently affected by thgis problem[2]. Parathyroid hormone causes bone resorption, leading to bone pain and pathological fractures and osteoporosis[4].
Gout and pseudogout Due to chondrocalcinosis[5].
Peptic ulcer disease Peptic ulcer disease is one of the complications of hypercalcaemia[6]. This may be due to increased levels of gastrin and gastric acid secretion
Epigastric pain radiating to the back Pancreatitis is a known complication of hyperparathyroidism[7], which may be due to the blocking of the duct by stones occuring due to hypercalcaemia.
Neurological problems Neurological problems are a well defined manifestation of hyperparathyroidism[1]. There can be abnormalities in calcium transport across the cell membrane due to hypercalcaemia and hypophosphatemia[13]. Manifestations will be proximal muscle weakness, easy fatigubility, ansomnia, depression and poor memory.
Constipation Due to hypercalcaemia[8].
Polyuria, polydypsia Due to hypercalcaemia[9].
Skin pruritus This is due to calcium depositions in the skin. There can be itching of the skin, which sometimes can be a chronic problem[10].
Multiple Endocrine Neoplasia type 1 (MEN1) and MEN type 2a, Multiple Endocrine Neoplasia type 1 (MEN1) is an autosomal-dominant condition associated with parathyroid adenomas[2]. There are parathyroids, pancreas and pituitary tumours[11]. Multiple Endocrine Neoplasia type 2a include parathyroid hyperplasia, medullary thyroid carcinoma, pheachromocytoma and mucosal neuromas of the lips and tongue[12].
Weakness, malaise, fatigue These are non specific symptoms of hyperparathyroidism[4,5].
References
  1. PYRAM R, MAHAJAN G, GLIWA A. Primary hyperparathyroidism: Skeletal and non-skeletal effects, diagnosis and management. Maturitas [online] 2011 Nov, 70(3):246-55 [viewed 24 June 2014] Available from: doi:10.1016/j.maturitas.2011.07.021
  2. CARNEVALE V, ROMAGNOLI E, PIPINO M, SCILLITANI A, D'ERASMO E, MINISOLA S, MAZZUOLI G. [Primary hyperparathyroidism]. Clin Ter [online] 2005 Sep-Oct, 156(5):211-26 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16382970
  3. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  4. KHAN AA. Medical management of primary hyperparathyroidism. J Clin Densitom [online] 2013 Jan-Mar, 16(1):60-3 [viewed 24 June 2014] Available from: doi:10.1016/j.jocd.2012.11.010
  5. PRITCHARD MH, JESSOP JD. Chondrocalcinosis in primary hyperparathyroidism. Influence of age, metabolic bone disease, and parathyroidectomy. Ann Rheum Dis [online] 1977 Apr, 36(2):146-51 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/857741
  6. LINOS DA, VAN HEERDAN JA, ABBOUD CF, EDIS AJ. Primary hyperparathyroidism and peptic ulcer disease. Arch Surg [online] 1978 Apr, 113(4):384-6 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/637708
  7. EBERT EC. The parathyroids and the gut. J Clin Gastroenterol [online] 2010 Aug, 44(7):479-82 [viewed 24 June 2014] Available from: doi:10.1097/MCG.0b013e3181cd9d4c
  8. RAGNO A, PEPE J, BADIALI D, MINISOLA S, ROMAGNOLI E, SEVERI C, D'ERASMO E. Chronic constipation in hypercalcemic patients with primary hyperparathyroidism. Eur Rev Med Pharmacol Sci [online] 2012 Jul, 16(7):884-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22953636
  9. MISCHIS-TROUSSARD C, GOUDET P, VERGES B, COUGARD P, TAVERNIER C, MAILLEFERT JF. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM [online] 2000 Jun, 93(6):365-7 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10873186
  10. JABBOUR SA. Cutaneous manifestations of endocrine disorders: a guide for dermatologists. Am J Clin Dermatol [online] 2003, 4(5):315-31 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12688837
  11. THAKKER RV. Multiple endocrine neoplasia type 1 (MEN1). Best Pract Res Clin Endocrinol Metab [online] 2010 Jun, 24(3):355-70 [viewed 25 June 2014] Available from: doi:10.1016/j.beem.2010.07.003
  12. MOLINE J, ENG C. Multiple endocrine neoplasia type 2: an overview. Genet Med [online] 2011 Sep, 13(9):755-64 [viewed 25 June 2014] Available from: doi:10.1097/GIM.0b013e318216cc6d
  13. ZHU X, ZHAI H, TANG SF, CHENG Y. Intrathyroidal parathyroid adenoma presenting with neuromuscular manifestation. Neurol India [online] 2009 May-Jun, 57(3):340-3 [viewed 25 June 2014] Available from: doi:10.4103/0028-3886.53280

Examination

Fact Explanation
Pallor Associated feature of hyperparathyroidism and also may be due to malignancy of parathyroid glands. There is very rare occasions where hyperparathyroidism is responsible for the pancytopenia[5].
Eye manifestations Subconjunctival,corneal and limbal deposits of calcium are seen[6].
Depressed mood One of the major manifestation of hypercalcaemia[3].
Dehydration Due to hypercalcaemia they can have polyuria, polydypsia[4].
Hypertension Hypertension is a complication of primary hyperparathyroidism[1]. May be due to hypercalcaemia, renal impairment or associated phaeachromocytoma in MEN 2a[2].
Localized swelling Accumulation of osteoclasts, osteoblasts will appear as localized swellings. [7]
Proximal muscle weakness,dysphasia Associated neurological manifestation of primary hyperparathyroidism[3].
Rare neurological manifestations Tongue atrophy[3], loss of vibratory sense, glove and stocking sensory loss
References
  1. MISCHIS-TROUSSARD C, GOUDET P, VERGES B, COUGARD P, TAVERNIER C, MAILLEFERT JF. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM [online] 2000 Jun, 93(6):365-7 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10873186
  2. MOLINE J, ENG C. Multiple endocrine neoplasia type 2: an overview. Genet Med [online] 2011 Sep, 13(9):755-64 [viewed 25 June 2014] Available from: doi:10.1097/GIM.0b013e318216cc6d
  3. ZHU X, ZHAI H, TANG SF, CHENG Y. Intrathyroidal parathyroid adenoma presenting with neuromuscular manifestation. Neurol India [online] 2009 May-Jun, 57(3):340-3 [viewed 25 June 2014] Available from: doi:10.4103/0028-3886.53280
  4. MISCHIS-TROUSSARD C, GOUDET P, VERGES B, COUGARD P, TAVERNIER C, MAILLEFERT JF. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM [online] 2000 Jun, 93(6):365-7 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10873186
  5. AKYAY A, CIHANGIROGLU G, ÖZKAN Y, DEVECI U, BAHCECI S, ÇETINKAYA Z. Primary hyperparathyroidism as an extremely rare cause of secondary myelofibrosis in childhood. J Pediatr Endocrinol Metab [online] 2013, 26(11-12):1185-8 [viewed 25 June 2014] Available from: doi:10.1515/jpem-2012-0421
  6. LEE DANNY K.. Ocular Calcifications in Primary Hyperparathyroidism. Arch Ophthalmol [online] 2006 January [viewed 25 June 2014] Available from: doi:10.1001/archopht.124.1.136
  7. CARNEVALE V, ROMAGNOLI E, PIPINO M, SCILLITANI A, D'ERASMO E, MINISOLA S, MAZZUOLI G. [Primary hyperparathyroidism]. Clin Ter [online] 2005 Sep-Oct, 156(5):211-26 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16382970

Differential Diagnoses

Fact Explanation
Secondary hyperparathyroidism This usually occurs in disease conditions such as chronic kidney disease and malabsorption. This usually develops in response to hypocalcaemia, Calcium will be low or normal and parathyroid hormone level will be high[3].
Tertiary hyperparathyroidism This usually occurs after long-term history of secondary hyperparathyroidism as in the case of, chronic kidney disease, due to the hyperplasia of glands[4]. Gland will autonomously secrete parathyroid hormone after continuous stimulation. Calcium and parathyroid hormone level, both will be high as in primary hyperparathyroidism.
Drugs Reduced renal calcium excretion by thiazide diuretics[1] and lithium can cause hypercalcaemia[3]. This will respond to discontinuation of medication.
Familial hypocalciuric hypercalciuria The problem is in the calcium sensing receptor in the parathyroid glands. There will be low urinary calcium in 24h urine, and calcium/creatinine clearance ratio is decreased[2,3].
Malignancy They can present with hypercalcaemia and parathyroid hormone level is usually low in these conditions[3].
References
  1. CORDELLAT IM. Hyperparathyroidism: primary or secondary disease? Reumatol Clin [online] 2012 Sep-Oct, 8(5):287-91 [viewed 25 June 2014] Available from: doi:10.1016/j.reuma.2011.06.001
  2. PASIEKA JL, ANDERSEN MA, HANLEY DA. Familial benign hypercalcaemia: hypercalciuria and hypocalciuria in affected members of a small kindred. Clin Endocrinol (Oxf) [online] 1990 Oct, 33(4):429-33 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/2225487
  3. MARTíNEZ CORDELLAT ISABEL. Hyperparathiroidism: Primary or Secondary Disease?. Reumatología Clínica (English Edition) [online] 2012 September, 8(5):287-291 [viewed 25 June 2014] Available from: doi:10.1016/j.reumae.2011.06.002
  4. PITT SUSAN C., PANNEERSELVAN RAJARAJAN, CHEN HERBERT, SIPPEL REBECCA S.. Secondary and Tertiary Hyperparathyroidism: The Utility of ioPTH Monitoring. World J Surg [online] December, 34(6):1343-1349 [viewed 25 June 2014] Available from: doi:10.1007/s00268-010-0575-4

Investigations - for Diagnosis

Fact Explanation
Serum parathyroid hormone level This is elevated or normal[1,2,5] Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. 3
Serum calcium Almost always high[5].
Serum phosphate This may be low[5].
Alkaline phosphate level May be high[5] due to bone resorption.
Vitamin D metabolites Serum 25-hydroxyvitamin D levels should be measured and correction should be done in a deficiency[1].
24 hour urinary calcium Increased due to hypercalcaemia[5].
Protein electrophoresis To exclude the other conditions presenting with hypercalcaemia such as multiple myeloma[6].
Cervical ultrasound, computer tomography and magnetic resonance imaging of the neck This is done to demonstrate the parathyroid adenoma[4]. This is also used to localize the adenoma prior to surgery[5,7].
X-ray On X-ray imaging, brown tumors will be appearing as lytic lesions[8]. Other changes would be osteopenia, 'salt-and-pepper' appearance on skull x-ray, subperiostal bone resorption and patchy diffuse areas of osteoclerosis.
References
  1. EASTELL R, ARNOLD A, BRANDI ML, BROWN EM, D'AMOUR P, HANLEY DA, RAO DS, RUBIN MR, GOLTZMAN D, SILVERBERG SJ, MARX SJ, PEACOCK M, MOSEKILDE L, BOUILLON R, LEWIECKI EM. Diagnosis of asymptomatic primary hyperparathyroidism: proceedings of the third international workshop. J Clin Endocrinol Metab [online] 2009 Feb, 94(2):340-50 [viewed 24 June 2014] Available from: doi:10.1210/jc.2008-1758
  2. CARNEVALE V, ROMAGNOLI E, PIPINO M, SCILLITANI A, D'ERASMO E, MINISOLA S, MAZZUOLI G. [Primary hyperparathyroidism]. Clin Ter [online] 2005 Sep-Oct, 156(5):211-26 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/16382970
  3. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  4. MISCHIS-TROUSSARD C, GOUDET P, VERGES B, COUGARD P, TAVERNIER C, MAILLEFERT JF. Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. QJM [online] 2000 Jun, 93(6):365-7 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/10873186
  5. ZHU X, ZHAI H, TANG SF, CHENG Y. Intrathyroidal parathyroid adenoma presenting with neuromuscular manifestation. Neurol India [online] 2009 May-Jun, 57(3):340-3 [viewed 25 June 2014] Available from: doi:10.4103/0028-3886.53280
  6. DOYLE A, SOUTAR R, GEDDES CC. Multiple myeloma in chronic kidney disease. Utility of discretionary screening using serum electrophoresis. Nephron Clin Pract [online] 2009, 111(1):c7-11 [viewed 25 June 2014] Available from: doi:10.1159/000175798
  7. TOMASELLA G. [Diagnostic imaging in primary hyperparathyroidism. Radiological techniques: US--CAT--MR]. Minerva Endocrinol [online] 2001 Mar, 26(1):3-12 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11323562
  8. VERA LARA, DOLCINO MARA, MORA MARCO, ODDO SILVIA, GUALCO MARINA, MINUTO FRANCESCO, GIUSTI MASSIMO. Primary hyperparathyroidism diagnosed after surgical ablation of a costal mass mistaken for giant-cell bone tumor: a case report. Array [online] 2011 December [viewed 25 June 2014] Available from: doi:10.1186/1752-1947-5-596

Investigations - Fitness for Management

Fact Explanation
Arterial blood gas Hyperchloremic metabolic acidosis occur in hyperparathyroidism[1].
References
  1. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781

Investigations - Followup

Fact Explanation
Post op Calcium level an parathyroid hormone level is important in follow up after surgery[1].
Disease activity Serum calcium, phosphate and parathyroid hormone levels are important to assess disease activity[1].
DEXA scan Useful in patients who are known to have osteoporosis as a complication[2].
References
  1. HEDBäCK G, ODéN A. Recurrence of hyperparathyroidism; a long-term follow-up after surgery for primary hyperparathyroidism. Eur J Endocrinol [online] 2003 Apr, 148(4):413-21 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/12656661
  2. PYRAM R, MAHAJAN G, GLIWA A. Primary hyperparathyroidism: Skeletal and non-skeletal effects, diagnosis and management. Maturitas [online] 2011 Nov, 70(3):246-55 [viewed 24 June 2014] Available from: doi:10.1016/j.maturitas.2011.07.021

Investigations - Screening/Staging

Fact Explanation
Renal function tests(blood urea, serum creatinine[1], serum electrolytes) Loss of renal function[5] is a can be a complication of hypercalcaemia, and phosphate retention.
Electrocardiogram Hypercalcaemia can cause shortening of QT interval[4] and elevation of ST segment[3] which can mimics acute myocardial infarction.
Echocardiogram There can be left ventricular hypertrophy and myocardial calcific deposits[2].
DEXA scan (Dual-emission X-ray absorptiometry) This is to detect osteoporosis and Z -score <-2.0 forearm is suggestive of osteoporosis[5,7].
References
  1. WALSER M. Assessing renal function from creatinine measurements in adults with chronic renal failure. Am J Kidney Dis [online] 1998 Jul, 32(1):23-31 [viewed 24 June 2014] Available from: doi:10.1053/ajkd.1998.v32.pm9669420
  2. STEFENELLI T, GLOBITS S, BERGLER-KLEIN J, WOLOSZCZUK W, LäNGLE F, NIEDERLE B. [Cardiac changes in patients with hypercalcemia]. Wien Klin Wochenschr [online] 1993, 105(12):339-41 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8333202
  3. NISHI SP, BARBAGELATA NA, ATAR S, BIRNBAUM Y, TUERO E. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. J Electrocardiol [online] 2006 Jul, 39(3):298-300 [viewed 24 June 2014] Available from: doi:10.1016/j.jelectrocard.2005.10.015
  4. AHMED R, HASHIBA K. Reliability of QT intervals as indicators of clinical hypercalcemia. Clin Cardiol [online] 1988 Jun, 11(6):395-400 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/2899466
  5. PYRAM R, MAHAJAN G, GLIWA A. Primary hyperparathyroidism: Skeletal and non-skeletal effects, diagnosis and management. Maturitas [online] 2011 Nov, 70(3):246-55 [viewed 24 June 2014] Available from: doi:10.1016/j.maturitas.2011.07.021
  6. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  7. VERA LARA, DOLCINO MARA, MORA MARCO, ODDO SILVIA, GUALCO MARINA, MINUTO FRANCESCO, GIUSTI MASSIMO. Primary hyperparathyroidism diagnosed after surgical ablation of a costal mass mistaken for giant-cell bone tumor: a case report. Array [online] 2011 December [viewed 25 June 2014] Available from: doi:10.1186/1752-1947-5-596

Management - General Measures

Fact Explanation
Rehydration Management of emergency hypercalcaemic conditions, usually started with hydration[1].
Loop diuretics If the patients is having heart failure, diuretics are used to prevent fluid overload[1].
Dialysis This is used for the patients with severe hypercalcemia presenting with kidney failure[2].
Prevention of falls As the people with primary hyperparathyroidism ishaving osteoporosis[3], they are vulnerable to fractures, therefore measures shoul be taken to prevent falls and fractures.
References
  1. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  2. ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  3. KHAN AA. Medical management of primary hyperparathyroidism. J Clin Densitom [online] 2013 Jan-Mar, 16(1):60-3 [viewed 24 June 2014] Available from: doi:10.1016/j.jocd.2012.11.010

Management - Specific Treatments

Fact Explanation
Management of hypercalcemic emergency Adequate rehydration is the first step in the management of hypercalcaemia. Then calcium excretion is achieved by furosemide combined with calcitionin. Bisphosphonates are also given as a slo.w infusion[3]
Surgical management-Parathyroidectomy Parathyroidectomy is a major mode of treatment for primary hyperparathyroidism[1]. Studies have shown that the indications for the surgery would be significant hypercalcemia, impaired renal function, osteoporosis and age less than 50 years[4].
Medical management of primary hyperparathyroidism If the patient is not suitable for surgery, medical management is warranted. Methods used are bisphosphonates, calcitonin and calcimimetics[1].
Bisphosphonates Patients with severe or symptomatic hypercalcemia, need biphosphonate to acheive the long term control. Zoledronic acid and pamidronate are examples of such bisphosphonates. [1,2]. These are inhibitors of osteoclast-mediated bone resorption[6]. Side effects include avascular mandibular osteonecrosis[7], gastrointestinal discomfort, acute influenza-like illness and occasionaly renal complications[8]
Calcitonin CalcitoninCalcitonin is given for the immediate management of hypercalcemia[2]. It reduces both calcium and phosphate levels in the blood[12]. Usually there are no serious adverse effects[11].
Calcimimetics Calcimimetics are useful agents in reversing the cortical bone loss by enhancing the sensitivity of calcium sensing receptors[10]. Cinacalcet is one such examples calcimimetics. Side effects are nausea, vomiting and hypocalcemia[9].
References
  1. PYRAM R, MAHAJAN G, GLIWA A. Primary hyperparathyroidism: Skeletal and non-skeletal effects, diagnosis and management. Maturitas [online] 2011 Nov, 70(3):246-55 [viewed 24 June 2014] Available from: doi:10.1016/j.maturitas.2011.07.021
  2. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.2ASSADI F. Hypercalcemia: an evidence-based approach to clinical cases. Iran J Kidney Dis [online] 2009 Apr, 3(2):71-9 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19395781
  3. ROSENMUND A. [Hypercalcemia as an emergency]. Schweiz Med Wochenschr [online] 1993 Apr 17, 123(15):735-8 [viewed 24 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/8488377
  4. KHAN AA. Medical management of primary hyperparathyroidism. J Clin Densitom [online] 2013 Jan-Mar, 16(1):60-3 [viewed 24 June 2014] Available from: doi:10.1016/j.jocd.2012.11.010
  5. KHAN AA. Medical management of primary hyperparathyroidism. J Clin Densitom [online] 2013 Jan-Mar, 16(1):60-3 [viewed 24 June 2014] Available from: doi:10.1016/j.jocd.2012.11.010
  6. VASIKARAN SD. Bisphosphonates: an overview with special reference to alendronate. Ann Clin Biochem [online] 2001 Nov, 38(Pt 6):608-23 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/11732644
  7. FRIEDRICH RE, BLAKE FA. Avascular mandibular osteonecrosis in association with bisphosphonate therapy: a report on four patients. Anticancer Res [online] 2007 Jul-Aug, 27(4A):1841-5 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/17649782
  8. ABRAHAMSEN B. Adverse effects of bisphosphonates. Calcif Tissue Int [online] 2010 Jun, 86(6):421-35 [viewed 25 June 2014] Available from: doi:10.1007/s00223-010-9364-1
  9. DONG BJ. Cinacalcet: An oral calcimimetic agent for the management of hyperparathyroidism. Clin Ther [online] 2005 Nov, 27(11):1725-51 [viewed 25 June 2014] Available from: doi:10.1016/j.clinthera.2005.11.015
  10. HARRINGTON PE, FOTSCH C. Calcium sensing receptor activators: calcimimetics. Curr Med Chem [online] 2007, 14(28):3027-34 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/18220738
  11. SJöBERG HE, HJERN B. Acute treatment with calcitonin in primary hyperparathyroidism and severe hypercalcaemia of other origin. Acta Chir Scand [online] 1975, 141(2):90-5 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/1171565
  12. TøRRING O, BUCHT E, SJöSTEDT U, SJöBERG HE. Salmon calcitonin treatment by nasal spray in primary hyperparathyroidism. Bone [online] 1991, 12(5):311-6 [viewed 25 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/1782100