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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.

Differential Diagnosis

Differential diagnosis of hyperparathyroidism on the basis of hypocalcemia
Disorders		Mechanism of hypocalcemia	Laboratory findings
			Serum PTH	Serum Calcium	Serum Phosphate	Other findings
Hypoparathyroidism		There is deficiency of parathyroid hormone in hypoparathyroidism. Deficiency of parathyroid hormone causes body to decrease: Reabsorption of calcium from bone. Excretion of phosphate. Reabsorbtion of calcium from distal tubules. Vitamin D mediated absorption of calcium from intestine.	↓	↓	↑	↓ 1,25 Dihydroxy vitamin D Normal urinary cAMP Normal urinary phosphate
Pseudohypoparathyroidism	Type 1a	Genetic defect causing end organ resistance to the action of parathyroid hormone (PTH). Heterozygous GNAS inactivating mutations that reduce expression or function of Gαs	↑	↓	↑	↓ 1,25 Dihydroxy vitamin D ↓ Urinary cAMP ↓ Urinary phosphate
	Type 1b	Genetic defect causing end organ resistance to the action of parathyroid hormone (PTH). Familial- heterozygous deletions in STX16, NESP55, and/or AS exons or loss of methylation at GNAS	↑	↓	↑	↓ 1,25 Dihydroxy vitamin D ↓ Urinary cAMP ↓ Urinary phosphate
	Type 1c	Genetic defect causing end organ resistance to the action of parathyroid hormone (PTH). Heterozygous GNAS inactivating mutations that reduce expression or function of Gαs	↑	↓	↑	↓ 1,25 Dihydroxy vitamin D ↓ Urinary cAMP ↓ Urinary phosphate
	Type 2	Genetic defect causing end organ resistance to the action of parathyroid hormone (PTH).	↑	↓	↑	↓ 1,25 Dihydroxy vitamin D Normal urinary cAMP ↓ Urinary phosphate
	Pseudopseudohypoparathyroidism	Genetic defect causing end organ resistance to the action of parathyroid hormone (PTH). Combination of inactivating mutations of GNAS1 and Albright's osteodystrophy	Normal	Normal	Normal	--
Hypomagnesemia		Decreased parathyroid hormone (PTH) secretion Skeletal resistance to PTH	Inappropriately ↓	Normal/↓	--	↓ serum magnesium ↓/Normal serum potassium
Hypoalbuminemia		Majority of calcium in blood is bound to albumin. So when there is a decrease in concentration of albumin due to any condition, there is a relative hypocalcemia as well.	--	↓	--	↓ serum albumin Normal albumin-corrected serum total calcium Normal ionised calcium
Hypovitaminosis D		Decrease in vitamin D meediated calcium absorption from gut.	↑	↓	↓/Low-normal	↓ 25 Hydroxy vitamin D
Chronic kidney disease		Chronic renal failure leads to high serum inorganic phosphate and low serum calcium and deficiency of active form of vitamin D (1,25-dihydroxy vitamin D/calcitriol)	↑	↓/Normal	↑	↓ Glomerular flitration rate