**Vitamin D3, parathyroid, calcium level, albumin checked?High blood calcium is called hypercalcemia. The two leading causes are overactive parathyroid glands and cancer. Many other causes are possible, including medicines, excess supplements, and certain inflammatory diseases.
A high total calcium result should be interpreted with albumin and, when appropriate, ionized calcium, which measures the active calcium directly. Dehydration or abnormal blood proteins can raise total calcium without raising ionized calcium. [1]
Calcium around 14 mg/dL (3.5 mmol/L) or higher generally requires emergency evaluation. Lower levels can also be urgent when accompanied by confusion, marked weakness, vomiting, dehydration, or heart symptoms. [1,3] NCBI Bookshelf (opens in new tab)
Below are 30 causes of true hypercalcemia. They are grouped by mechanism, not ranked by likelihood.
| No. | Cause | How it raises calcium |
|---|---|---|
| 1 | Primary hyperparathyroidism from a parathyroid adenoma | A usually benign gland tumor releases too much parathyroid hormone—PTH. A common cause of persistent mild hypercalcemia. [1,2] |
| 2 | Multigland parathyroid hyperplasia | Several parathyroid glands become overactive; sometimes associated with inherited syndromes such as MEN1. [2] |
| 3 | Parathyroid carcinoma | Rare cancer that can produce very high PTH and calcium. [2,3] |
| 4 | Tertiary hyperparathyroidism | After prolonged stimulation, usually from advanced kidney disease, parathyroid glands become independently overactive. [2] |
| 5 | Familial hypocalciuric hypercalcemia—FHH | An inherited calcium-sensing problem causes usually lifelong mild hypercalcemia with relatively low urinary calcium. [2] |
| 6 | PTH-related protein–producing cancer | Some cancers release PTHrP, which raises calcium. Examples include certain squamous-cell, kidney, and other cancers. [3] |
| 7 | Bone metastases | Cancer-related bone destruction releases calcium into blood. [3] |
| 8 | Multiple myeloma | Malignant plasma cells stimulate bone breakdown. [3] |
| 9 | Lymphoma producing excess active vitamin D | Increased calcitriol raises intestinal calcium absorption. [3,4] |
| 10 | Adult T-cell leukemia/lymphoma | This HTLV-1-associated malignancy can cause marked bone resorption and hypercalcemia. [1,3] |
Parathyroid disorders usually produce an elevated—or inappropriately normal—PTH despite high calcium. Most cancer-related causes suppress PTH. Wiley Online Library (opens in new tab)
| No. | Cause | How it raises calcium |
|---|---|---|
| 11 | Vitamin D supplement overdose | Excess vitamin D increases calcium absorption. Ordinary sunlight exposure does not cause vitamin D toxicity. [4] |
| 12 | Excess prescription active vitamin D or related drugs | Calcitriol and related preparations can cause excessive calcium absorption. [4] |
| 13 | Calcium-alkali syndrome | Excess calcium, commonly calcium-carbonate supplements or antacids, causes hypercalcemia, alkalosis, and kidney dysfunction. [5] |
| 14 | Vitamin A toxicity or retinoid medicines | Excess preformed vitamin A or certain retinoids can increase bone breakdown. [1] |
| 15 | Thiazide diuretics | Hydrochlorothiazide and chlorthalidone reduce urinary calcium loss and may uncover underlying hyperparathyroidism. [1] |
| 16 | Lithium | Alters calcium sensing and may cause parathyroid overactivity. [1,2] |
| 17 | Teriparatide or abaloparatide | These osteoporosis medicines can cause transient hypercalcemia. [1] |
| 18 | Rebound after stopping denosumab | Increased bone resorption can raise calcium, especially in children or high bone-turnover conditions; uncommon in adults. [1] |
Correct doses of calcium or vitamin D do not usually cause hypercalcemia in otherwise healthy people. Risk changes with kidney function, underlying disease, dose, and combinations of products. PMC (opens in new tab)
| No. | Cause | How it raises calcium |
|---|---|---|
| 19 | Sarcoidosis | Activated cells in granulomas make excess calcitriol. [4] |
| 20 | Tuberculosis | Granulomatous inflammation can increase calcitriol production. [4] |
| 21 | Certain fungal infections | Histoplasmosis and coccidioidomycosis are examples of infections that occasionally cause calcitriol-mediated hypercalcemia. [4] |
| 22 | Foreign-body granulomas | Reactions to silicone injections, paraffin, or other materials can produce excess calcitriol. [4] |
| 23 | Hyperthyroidism | Excess thyroid hormone accelerates bone turnover; the calcium elevation is usually mild. [1] |
| 24 | Adrenal insufficiency | Cortisol deficiency and associated volume depletion can occasionally cause hypercalcemia. [1] |
| 25 | Prolonged immobilization | Reduced weight-bearing increases calcium release from bone, particularly when bone turnover is already high. [1] |
| 26 | Recovery phase of rhabdomyolysis | Calcium deposited in injured muscle can return to blood during recovery. [1] |
| 27 | CYP24A1-related disease | Impaired breakdown of active vitamin D causes hypercalcemia or excess urinary calcium; it may present in adulthood with kidney stones. [4] |
| 28 | SLC34A1-related disease | Inherited renal phosphate wasting can increase active vitamin D and calcium absorption, often presenting in infancy. [1] |
| 29 | Williams syndrome | This genetic syndrome can cause hypercalcemia, particularly in young children. [1] |
| 30 | Subcutaneous fat necrosis of the newborn | Inflammation in damaged fatty tissue can increase calcitriol and cause significant infant hypercalcemia. [4] |
The infection-related causes above are uncommon complications, not expected findings in every person with those infections. PMC (opens in new tab)
The most useful first steps
Confirm the result with repeat calcium, albumin, and sometimes ionized calcium. Then measure intact PTH, review all medicines and supplements, and check kidney function. Depending on PTH and the clinical picture, additional testing may include vitamin D metabolites, PTHrP, urine calcium, or testing for myeloma. A parathyroid scan does not establish the initial diagnosis; blood testing comes first. [1,2] Wiley Online Library (opens in new tab)
Full references
- Goltzman D. Approach to hypercalcemia. In: Feingold KR, et al., editors. Endotext. South Dartmouth, MA: MDText.com, Inc.; 2000–. Updated March 19, 2026. Available at: NCBI Bookshelf (opens in new tab).
- Bilezikian JP, Khan AA, Silverberg SJ, et al.; International Workshop on Primary Hyperparathyroidism. Evaluation and management of primary hyperparathyroidism: Summary statement and guidelines from the Fifth International Workshop. Journal of Bone and Mineral Research. 2022;37(11):2293–2314. doi: 10.1002/jbmr.4677 (opens in new tab).
- El-Hajj Fuleihan G, Clines GA, Hu MI, et al. Treatment of hypercalcemia of malignancy in adults: An Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism. 2023;108(3):507–528. doi: 10.1210/clinem/dgac621 (opens in new tab).
- Tebben PJ, Singh RJ, Kumar R. Vitamin D-mediated hypercalcemia: Mechanisms, diagnosis, and treatment. Endocrine Reviews. 2016;37(5):521–547. doi: 10.1210/er.2016-1070 (opens in new tab).