Secondary hyperparathyroidism

Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on the blood, immune system, and neurological system.{{citation needed|date=August 2020}}

Chronic kidney failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active form, and they do not adequately excrete phosphate. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes lead to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from malabsorption (chronic pancreatitis, small bowel disease, malabsorption-dependent bariatric surgery) in that the fat-soluble vitamin D can not get reabsorbed. This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum calcium levels. A few other causes can stem from inadequate dietary intake of calcium, a vitamin D deficiency, or steatorrhea.{{Cite book|title=Robbins and Cotran pathologic basis of disease|others=Kumar, Vinay, 1944-, Abbas, Abul K.,, Aster, Jon C.,, Perkins, James A.|year=2014|isbn=9781455726134|edition= Ninth |location=Philadelphia, PA|pages=1103|oclc=879416939}}

The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D₃. It is usually seen in cases of chronic kidney disease{{cite journal |last1=Slatopolsky |first1=Eduardo |last2=Brown |first2=Alex |last3=Dusso |first3=Adriana |title=Pathogenesis of secondary hyperparathyroidism |journal=Kidney International |date=December 1999 |volume=56 |pages=S14–S19 |doi=10.1046/j.1523-1755.1999.07304.x|pmid=10633458 |doi-access=free }} or defective calcium receptors on the surface of parathyroid glands.{{cite journal |last1=Rodriguez |first1=Mariano |last2=Nemeth |first2=Edward |last3=Martin |first3=David |title=The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism |journal=American Journal of Physiology. Renal Physiology |date=1 February 2005 |volume=288 |issue=2 |pages=F253–F264 |doi=10.1152/ajprenal.00302.2004 |pmid=15507543 |url=https://journals.physiology.org/doi/full/10.1152/ajprenal.00302.2004 |access-date=19 January 2023 |issn=1931-857X|url-access=subscription }}

If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In people with chronic kidney failure, treatment consists of dietary restriction of phosphorus; supplements containing an active form of vitamin D, such as calcitriol, doxercalciferol, paricalcitol; and phosphate binders, which are either calcium-based and non-calcium based.{{cite journal |last1=Tomasello |first1=Sarah |title=Secondary Hyperparathyroidism and Chronic Kidney Disease |journal=Diabetes Spectrum |date=1 January 2008 |volume=21 |issue=1 |pages=19–25 |doi=10.2337/diaspect.21.1.19|doi-access=free }}

Extended Release Calcifediol was recently approved by the FDA as a treatment for secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic kidney disease (CKD) and low vitamin D blood levels (25-hydroxyvitamin D less than 30 ng/mL). It can help treat SHPT by increasing Vitamin D levels and lowering parathyroid hormone or PTH. It is not indicated for people with stage 5 CKD or on dialysis.{{citation needed|date=August 2020}}

In the treatment of secondary hyperparathyroidism due to chronic kidney disease on dialysis calcimimetics do not appear to affect the risk of early death. It does decrease the need for a parathyroidectomy but caused more issues with low blood calcium levels and vomiting.{{cite journal|last1=Ballinger|first1=AE|last2=Palmer|first2=SC|last3=Nistor|first3=I|last4=Craig|first4=JC|last5=Strippoli|first5=GF|title=Calcimimetics for secondary hyperparathyroidism in chronic kidney disease patients.|journal=The Cochrane Database of Systematic Reviews|date=9 December 2014|volume=12|issue=12|pages=CD006254|pmid=25490118|doi=10.1002/14651858.CD006254.pub2|doi-access=free|pmc=10614033}}

Most people with hyperparathyroidism secondary to chronic kidney disease will improve after renal transplantation, but many will continue to have a degree of residual hyperparathyroidism (tertiary hyperparathyroidism) post-transplant with associated risk of bone loss.{{cite journal |last1=Sutton |first1=Whitney |last2=Chen |first2=Xiaomeng |last3=Patel |first3=Palak |last4=Karzai |first4=Shkala |last5=Prescott |first5=Jason D. |last6=Segev |first6=Dorry L. |last7=McAdams-DeMarco |first7=Mara |last8=Mathur |first8=Aarti |title=Prevalence and risk factors for tertiary hyperparathyroidism in kidney transplant recipients |journal=Surgery |date=January 2022 |volume=171 |issue=1 |pages=69–76 |doi=10.1016/j.surg.2021.03.067|pmid=34266650 |pmc=8688275 }}

If left untreated, the disease will progress to tertiary hyperparathyroidism, where correction of the underlying cause will not stop excess PTH secretion, i.e. parathyroid gland hypertrophy becomes irreversible. In contrast with secondary hyperparathyroidism, tertiary hyperparathyroidism is associated with hypercalcemia rather than hypocalcemia.{{citation needed|date=August 2020}}

• Primary hyperparathyroidism
• Tertiary hyperparathyroidism

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{{Medical resources

| DiseasesDB = 6301 |

| ICD10 = {{ICD10|E|21|1|e|20}} |

| ICD9 = {{ICD9|252.02}}, {{ICD9|588.81}} |

| ICDO = |

| OMIM = |

| MedlinePlus = 000318 |

| eMedicineSubj = |

| eMedicineTopic = |

| MeshID = D006962 |

}}

{{Parathyroid disease}}

Category:Parathyroid disorders