Sandbox : anmol: Difference between revisions
No edit summary |
|||
Line 59: | Line 59: | ||
*Parathyroid carcinoma | *Parathyroid carcinoma | ||
*Familial isloated hyperparathyroidism | *Familial isloated hyperparathyroidism | ||
*Radiation exposure (due to development of parathyroid adenoma or parathyroid hyperplasia) | *Radiation exposure (due to development of parathyroid adenoma or parathyroid hyperplasia)<ref name="pmid21848480">{{cite journal| author=Boehm BO, Rosinger S, Belyi D, Dietrich JW| title=The parathyroid as a target for radiation damage. | journal=N Engl J Med | year= 2011 | volume= 365 | issue= 7 | pages= 676-8 | pmid=21848480 | doi=10.1056/NEJMc1104982 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21848480 }} </ref><ref name="pmid18774659">{{cite journal| author=McMullen T, Bodie G, Gill A, Ihre-Lundgren C, Shun A, Bergin M et al.| title=Hyperparathyroidism after irradiation for childhood malignancy. | journal=Int J Radiat Oncol Biol Phys | year= 2009 | volume= 73 | issue= 4 | pages= 1164-8 | pmid=18774659 | doi=10.1016/j.ijrobp.2008.06.1487 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18774659 }} </ref><ref name="pmid890665">{{cite journal| author=Tisell LE, Hansson G, Lindberg S, Ragnhult I| title=Hyperparathyroidism in persons treated with X-rays for tuberculous cervical adenitis. | journal=Cancer | year= 1977 | volume= 40 | issue= 2 | pages= 846-54 | pmid=890665 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=890665 }} </ref> | ||
*Celiac disease | *Celiac disease<ref name="pmid17148709">{{cite journal |vauthors=Maida MJ, Praveen E, Crimmins SR, Swift GL |title=Coeliac disease and primary hyperparathyroidism: an association? |journal=Postgrad Med J |volume=82 |issue=974 |pages=833–5 |year=2006 |pmid=17148709 |pmc=2653933 |doi=10.1136/pgmj.2006.045500 |url=}}</ref><ref name="pmid22238405">{{cite journal |vauthors=Ludvigsson JF, Kämpe O, Lebwohl B, Green PH, Silverberg SJ, Ekbom A |title=Primary hyperparathyroidism and celiac disease: a population-based cohort study |journal=J. Clin. Endocrinol. Metab. |volume=97 |issue=3 |pages=897–904 |year=2012 |pmid=22238405 |pmc=3319223 |doi=10.1210/jc.2011-2639 |url=}}</ref> | ||
===Genetic causes=== | ===Genetic causes=== | ||
*HRPT2 gene mutations: | *HRPT2 gene mutations:<ref name="pmid14585940">{{cite journal| author=Shattuck TM, Välimäki S, Obara T, Gaz RD, Clark OH, Shoback D et al.| title=Somatic and germ-line mutations of the HRPT2 gene in sporadic parathyroid carcinoma. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 18 | pages= 1722-9 | pmid=14585940 | doi=10.1056/NEJMoa031237 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14585940 }} </ref> | ||
**HRPT2 gene code for parafibromin protein. | **HRPT2 gene code for parafibromin protein. | ||
**HRPT2 gene mutations are found in a type of familial hyperparathyroidism, hyperparathyroidism-jaw tumor (HPT-JT) syndrome. | **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. | **HRTP2 gene mutations increases risk of parathyroid carcinoma. | ||
*Cyclin D1 gene (CCND1)/PRAD1 gene: | *Cyclin D1 gene (CCND1)/PRAD1 gene:<ref name="pmid19373510">{{cite journal| author=Westin G, Björklund P, Akerström G| title=Molecular genetics of parathyroid disease. | journal=World J Surg | year= 2009 | volume= 33 | issue= 11 | pages= 2224-33 | pmid=19373510 | doi=10.1007/s00268-009-0022-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19373510 }} </ref><ref name="pmid8626826">{{cite journal| author=Hsi ED, Zukerberg LR, Yang WI, Arnold A| title=Cyclin D1/PRAD1 expression in parathyroid adenomas: an immunohistochemical study. | journal=J Clin Endocrinol Metab | year= 1996 | volume= 81 | issue= 5 | pages= 1736-9 | pmid=8626826 | doi=10.1210/jcem.81.5.8626826 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8626826 }} </ref> | ||
**PRAD1 (parathyroid adenoma 1) is a protooncogene located on chromosome 11q13. | **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 translocation and oncogene action observerd in 8% of adenomas | ||
**Cyclin D1 gene overexpression is pbserved in 20% to 40% of parathyroid adenomas | **Cyclin D1 gene overexpression is pbserved in 20% to 40% of parathyroid adenomas | ||
*MEN1 gene: | *MEN1 gene:<ref name="pmid19373510">{{cite journal| author=Westin G, Björklund P, Akerström G| title=Molecular genetics of parathyroid disease. | journal=World J Surg | year= 2009 | volume= 33 | issue= 11 | pages= 2224-33 | pmid=19373510 | doi=10.1007/s00268-009-0022-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19373510 }} </ref><ref name="pmid9215689">{{cite journal| author=Agarwal SK, Kester MB, Debelenko LV, Heppner C, Emmert-Buck MR, Skarulis MC et al.| title=Germline mutations of the MEN1 gene in familial multiple endocrine neoplasia type 1 and related states. | journal=Hum Mol Genet | year= 1997 | volume= 6 | issue= 7 | pages= 1169-75 | pmid=9215689 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9215689 }} </ref> | ||
**MEN1 is a tumor supressor gene on chronosome 11q13. | **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. | **Somatic loss of single MEN1 allele is observed in 25% to 40% of sporadic parathyroid adenomas. | ||
Line 78: | Line 78: | ||
Causes of secondary hyperparathyroidism are as follows: | Causes of secondary hyperparathyroidism are as follows: | ||
===Common causes=== | ===Common causes=== | ||
*Chronic renal failure (leading to parathyroid hyperplasia) | *Chronic renal failure (leading to parathyroid hyperplasia)<ref name="pmid15507543">{{cite journal| author=Rodriguez M, Nemeth E, Martin D| title=The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism. | journal=Am J Physiol Renal Physiol | year= 2005 | volume= 288 | issue= 2 | pages= F253-64 | pmid=15507543 | doi=10.1152/ajprenal.00302.2004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15507543 }} </ref> | ||
*Vitamin D deficiency | *Vitamin D deficiency<ref name="pmid11493580">{{cite journal| author=Lips P| title=Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications. | journal=Endocr Rev | year= 2001 | volume= 22 | issue= 4 | pages= 477-501 | pmid=11493580 | doi=10.1210/edrv.22.4.0437 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11493580 }} </ref> | ||
===Less common causes=== | ===Less common causes=== | ||
*Severe calcium deficiency | *Severe calcium deficiency<ref name="pmid16512945">{{cite journal| author=Mehrotra M, Gupta SK, Kumar K, Awasthi PK, Dubey M, Pandey CM et al.| title=Calcium deficiency-induced secondary hyperparathyroidism and osteopenia are rapidly reversible with calcium supplementation in growing rabbit pups. | journal=Br J Nutr | year= 2006 | volume= 95 | issue= 3 | pages= 582-90 | pmid=16512945 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16512945 }} </ref> | ||
*Gastric bypass surgery, particularly roux-en-Y gastric bypass (RYGBP) | *Gastric bypass surgery, particularly roux-en-Y gastric bypass (RYGBP)<ref name="pmid16633006">{{cite journal |vauthors=Johnson JM, Maher JW, DeMaria EJ, Downs RW, Wolfe LG, Kellum JM |title=The long-term effects of gastric bypass on vitamin D metabolism |journal=Ann. Surg. |volume=243 |issue=5 |pages=701–4; discussion 704–5 |year=2006 |pmid=16633006 |pmc=1570540 |doi=10.1097/01.sla.0000216773.47825.c1 |url=}}</ref> | ||
*Malabsorption syndrome | *Malabsorption syndrome<ref name="pmid19836494">{{cite journal |vauthors=Pitt SC, Sippel RS, Chen H |title=Secondary and tertiary hyperparathyroidism, state of the art surgical management |journal=Surg. Clin. North Am. |volume=89 |issue=5 |pages=1227–39 |year=2009 |pmid=19836494 |pmc=2905047 |doi=10.1016/j.suc.2009.06.011 |url=}}</ref> | ||
==Causes of tertiary hyperparathyroidism== | ==Causes of tertiary hyperparathyroidism== | ||
Line 90: | Line 90: | ||
===Common causes=== | ===Common causes=== | ||
*Chronic renal failure (leading to parathyroid hyperplasia) | *Chronic renal failure (leading to parathyroid hyperplasia) | ||
*Renal transplant patients | *Renal transplant patients<ref name="pmid9780988">{{cite journal |vauthors=Kilgo MS, Pirsch JD, Warner TF, Starling JR |title=Tertiary hyperparathyroidism after renal transplantation: surgical strategy |journal=Surgery |volume=124 |issue=4 |pages=677–83; discussion 683–4 |year=1998 |pmid=9780988 |doi=10.1067/msy.1998.91483 |url=}}</ref> | ||
===Less common cause=== | ===Less common cause=== | ||
*Long standing celiac disease | *Long standing celiac disease<ref name="pmid17148709">{{cite journal |vauthors=Maida MJ, Praveen E, Crimmins SR, Swift GL |title=Coeliac disease and primary hyperparathyroidism: an association? |journal=Postgrad Med J |volume=82 |issue=974 |pages=833–5 |year=2006 |pmid=17148709 |pmc=2653933 |doi=10.1136/pgmj.2006.045500 |url=}}</ref> | ||
Line 110: | Line 110: | ||
*Familial hypocalciuric hypercalcemia | *Familial hypocalciuric hypercalcemia | ||
*Hyperparathyroid-jaw tumor syndrome | *Hyperparathyroid-jaw tumor syndrome | ||
*Pancreatitis | *Pancreatitis<ref name="pmid22874807">{{cite journal |vauthors=Bai HX, Giefer M, Patel M, Orabi AI, Husain SZ |title=The association of primary hyperparathyroidism with pancreatitis |journal=J. Clin. Gastroenterol. |volume=46 |issue=8 |pages=656–61 |year=2012 |pmid=22874807 |pmc=4428665 |doi=10.1097/MCG.0b013e31825c446c |url=}}</ref> | ||
=Natural history, Prognosis and Complications= | =Natural history, Prognosis and Complications= | ||
Line 117: | Line 117: | ||
*If left untreated, some of patients with hyperparathyroidism may develop marked hypercalcemia, marked hypercalciuria, cortical bone demineralization and nephrolithiasis. | *If left untreated, some of patients with hyperparathyroidism may develop marked hypercalcemia, marked hypercalciuria, cortical bone demineralization and nephrolithiasis. | ||
*These complications resolves after the treatment. | *These complications resolves after the treatment. | ||
==Complications== | ==Complications== | ||
Complications of primary hyperparathyroidism are due to hypercalcemia. Common complications of primary hyperparathyroidism include: | Complications of primary hyperparathyroidism are due to hypercalcemia. Common complications of primary hyperparathyroidism include: | ||
*Bone related complication: | *Bone related complication: | ||
**Brown tumor | **Brown tumor | ||
**Osteitis fibrous cystica | **Osteitis fibrous cystica | ||
Line 126: | Line 127: | ||
**Osteomalacia | **Osteomalacia | ||
**Osteoporosis | **Osteoporosis | ||
*Cardiac complications: | *Cardiac complications:<ref name="pmid8989242">{{cite journal |vauthors=Stefenelli T, Abela C, Frank H, Koller-Strametz J, Globits S, Bergler-Klein J, Niederle B |title=Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up |journal=J. Clin. Endocrinol. Metab. |volume=82 |issue=1 |pages=106–12 |year=1997 |pmid=8989242 |doi=10.1210/jcem.82.1.3666 |url=}}</ref> | ||
**Left ventricular hypertrophy | **Left ventricular hypertrophy | ||
**Cardiac calcific deposits in the myocardium | **Cardiac calcific deposits in the myocardium | ||
Line 133: | Line 134: | ||
**Pancreatitis | **Pancreatitis | ||
**Parathyroid crisis | **Parathyroid crisis | ||
* | **Neuromuscular complications: | ||
*Neuromuscular complications: | |||
*Pregnancy related complications: | *Pregnancy related complications: | ||
**Neonatal hypoparathyroidism | **Neonatal hypoparathyroidism | ||
*Psychiatric complications: | **Psychiatric complications: | ||
*Renal complications: | *Renal complications: | ||
**Nephrolithiasis | **Nephrolithiasis | ||
Line 145: | Line 143: | ||
==References== | ==References== | ||
Revision as of 20:46, 21 August 2017
Hyperparathyroidism Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Sandbox : anmol On the Web |
American Roentgen Ray Society Images of Sandbox : anmol |
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
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 hyperparathyroidism may develop marked hypercalcemia, marked hypercalciuria, cortical bone demineralization and nephrolithiasis.
- These complications resolves after the treatment.
Complications
Complications of primary hyperparathyroidism are due to hypercalcemia. Common complications of primary hyperparathyroidism include:
- Bone related complication:
- Brown tumor
- Osteitis fibrous cystica
- Osteoarthritis
- Osteomalacia
- Osteoporosis
- Cardiac complications:[17]
- Left ventricular hypertrophy
- Cardiac calcific deposits in the myocardium
- Aortic and mitral valve calcification
- Endocrine complications:
- Pancreatitis
- Parathyroid crisis
- Neuromuscular complications:
- Pregnancy related complications:
- Neonatal hypoparathyroidism
- Psychiatric complications:
- Renal complications:
- Nephrolithiasis
- Nephrocalcinosis
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 4.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 7.0 7.1 Westin G, Björklund P, Akerström G (2009). "Molecular genetics of parathyroid disease". World J Surg. 33 (11): 2224–33. doi:10.1007/s00268-009-0022-6. PMID 19373510.
- ↑ Hsi ED, Zukerberg LR, Yang WI, Arnold A (1996). "Cyclin D1/PRAD1 expression in parathyroid adenomas: an immunohistochemical study". J Clin Endocrinol Metab. 81 (5): 1736–9. doi:10.1210/jcem.81.5.8626826. PMID 8626826.
- ↑ Agarwal SK, Kester MB, Debelenko LV, Heppner C, Emmert-Buck MR, Skarulis MC; et al. (1997). "Germline mutations of the MEN1 gene in familial multiple endocrine neoplasia type 1 and related states". Hum Mol Genet. 6 (7): 1169–75. PMID 9215689.
- ↑ Rodriguez M, Nemeth E, Martin D (2005). "The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism". Am J Physiol Renal Physiol. 288 (2): F253–64. doi:10.1152/ajprenal.00302.2004. PMID 15507543.
- ↑ Lips P (2001). "Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications". Endocr Rev. 22 (4): 477–501. doi:10.1210/edrv.22.4.0437. PMID 11493580.
- ↑ Mehrotra M, Gupta SK, Kumar K, Awasthi PK, Dubey M, Pandey CM; et al. (2006). "Calcium deficiency-induced secondary hyperparathyroidism and osteopenia are rapidly reversible with calcium supplementation in growing rabbit pups". Br J Nutr. 95 (3): 582–90. PMID 16512945.
- ↑ Johnson JM, Maher JW, DeMaria EJ, Downs RW, Wolfe LG, Kellum JM (2006). "The long-term effects of gastric bypass on vitamin D metabolism". Ann. Surg. 243 (5): 701–4, discussion 704–5. doi:10.1097/01.sla.0000216773.47825.c1. PMC 1570540. PMID 16633006.
- ↑ Pitt SC, Sippel RS, Chen H (2009). "Secondary and tertiary hyperparathyroidism, state of the art surgical management". Surg. Clin. North Am. 89 (5): 1227–39. doi:10.1016/j.suc.2009.06.011. PMC 2905047. PMID 19836494.
- ↑ Kilgo MS, Pirsch JD, Warner TF, Starling JR (1998). "Tertiary hyperparathyroidism after renal transplantation: surgical strategy". Surgery. 124 (4): 677–83, discussion 683–4. doi:10.1067/msy.1998.91483. PMID 9780988.
- ↑ Bai HX, Giefer M, Patel M, Orabi AI, Husain SZ (2012). "The association of primary hyperparathyroidism with pancreatitis". J. Clin. Gastroenterol. 46 (8): 656–61. doi:10.1097/MCG.0b013e31825c446c. PMC 4428665. PMID 22874807.
- ↑ 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.