| Low PTH (hypoparathyroidism) |
| Impaired synthesis or secretion of PTH |
| Genetic |
| |
- Genetic mutations interfering with the production of PTH (autosomal dominant, autosomal recessive)
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- HDR syndrome (hypoparathyroidism, deafness, renal anomaly)
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- Sanjad-Sakati or Kenny-Caffey syndromes
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- Mutations of the CaSR and related proteins (autosomal dominant hypocalcemia)
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- Mutations interfering with parathyroid gland development (X-linked)
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- Mitochondrial disorders (eg, MELAS syndrome, Kearns-Sayre syndrome, mitochondrial trifunctional protein deficiency)
|
| Autoimmune |
| |
| Other |
- Parathyroid or thyroid gland surgery
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- Infiltration of parathyroid gland (eg, iron overload)
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| High PTH |
| Deficient calcium intake or intestinal absorption |
| Deficient vitamin D intake, intestinal absorption and/or dermal synthesis |
| Defects in vitamin D metabolism |
| Hepatic dysfunction |
| |
- Drugs that increase cytochrome P450 activity, which accelerate catabolism of vitamin D to inactive metabolites (eg, antiseizure medications, isoniazid, and rifampin)
|
| Renal dysfunction |
| Genetic disorders |
- 25-hydroxylase deficiency
|
- 1-alpha-hydroxylase deficiency (previously known as vitamin D-dependent rickets type 1 or pseudovitamin D-deficient rickets)
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- Increased catabolism of vitamin D (gain-of-function variants in the CYP3A4 gene)
|
| Defects in vitamin D action |
| Hereditary resistance to vitamin D (previously known as vitamin D-dependent rickets type 2) |
| End-organ resistance to PTH (pseudohypoparathyroidism) |
| Type 1 (1a, 1b, and 1c) |
| Type 2 |
| Miscellaneous |
| Hungry bone syndrome |
| Osteopetrosis |
| Sepsis or acute severe illness |
| Hyperphosphatemia |
| Alkalosis |
| Intravenous products with citrate or lactate |
| Pancreatitis |
| Fluoride poisoning |
| Drugs – Bisphosphonates, denosumab, calcimimetics (cinacalcet), foscarnet, and some chemotherapeutic drugs |
| Hypomagnesemia |
