Elevated calcium levels in the bloodstream, known as hypercalcemia, indicate a disruption in the body’s calcium regulation system. While calcium is necessary for nerve function, muscle contraction, and bone strength, an excess negatively affects these systems, particularly the kidneys and heart. Hypercalcemia is often detected during routine blood tests and can range from mild elevation to a life-threatening medical emergency. Because high calcium levels frequently indicate a serious underlying health problem, anyone diagnosed with hypercalcemia should immediately consult a healthcare provider for a thorough medical evaluation.
Identifying the Underlying Cause
Successfully lowering calcium levels requires pinpointing the specific reason the body’s regulatory mechanisms have failed, as treatment depends entirely on the diagnosis. The majority of chronic hypercalcemia cases are linked to two primary conditions: an overactive parathyroid gland or certain types of cancer. The four small parathyroid glands, located in the neck, produce parathyroid hormone, which regulates calcium levels.
When one or more of these glands become overactive, known as primary hyperparathyroidism (PHPT), excess hormone is released, causing calcium to be drawn from the bones and absorbed from the gut. PHPT is the most common cause of hypercalcemia in non-hospitalized individuals. Malignancy-associated hypercalcemia often involves tumors releasing a substance similar to parathyroid hormone, which accelerates bone breakdown and calcium release into the blood. This non-parathyroid cause is frequently more severe and requires aggressive management.
Certain medications can also contribute to hypercalcemia by altering how the kidneys handle calcium or by affecting parathyroid function. Thiazide diuretics, prescribed for high blood pressure, decrease the amount of calcium excreted in the urine, leading to mild elevation. The mood stabilizer lithium can shift the set point at which the parathyroid glands respond to calcium, causing increased hormone secretion.
Less common causes include excessive intake of Vitamin D or high-dose Vitamin A supplements, which enhance calcium absorption from the intestines. Granulomatous diseases, such as sarcoidosis, can also cause immune cells to produce an active form of Vitamin D, leading to increased calcium absorption. A medical workup, including measurements of serum calcium, parathyroid hormone, and Vitamin D levels, helps the provider differentiate causes and establish a precise diagnosis.
Immediate Dietary and Hydration Strategies
While a medical investigation is underway, certain self-managed adjustments can offer an immediate, temporary reduction in blood calcium levels. Aggressive hydration is the most important initial step, as it helps the kidneys flush out excess calcium through the urine. Drinking significant amounts of plain water increases the volume of fluid passing through the kidneys, promoting calcium excretion.
Patients should immediately review all dietary intake and supplements with their healthcare provider. This includes limiting foods with high calcium content, such as certain dairy products, fortified juices, and cereals, to reduce the amount of calcium absorbed through the digestive tract.
All over-the-counter calcium supplements, including those taken for bone health, should be discontinued. High-dose Vitamin D supplements and calcium-containing antacids must also be paused, as they directly increase calcium absorption from the gut. A daily intake of Vitamin D above 4,000 international units is associated with the potential for calcium elevation.
Physical activity also plays a role in maintaining calcium balance. Extended periods of immobility, such as being bedridden after surgery or injury, increase bone resorption and lead to elevated blood calcium levels. Returning to or maintaining a moderate level of weight-bearing activity, as advised by a physician, helps stabilize the bone and mineral environment.
Pharmacological and Procedural Interventions
Medical treatment for hypercalcemia depends on the severity of the calcium elevation and the underlying cause. For severe or acutely symptomatic hypercalcemia, the first line of treatment in a hospital setting involves intravenous (IV) hydration using saline solution. This rapid infusion of fluids restores volume and promotes the renal excretion of calcium, often providing a quick reduction in blood levels.
For a more sustained therapeutic effect, medications that inhibit the breakdown of bone are frequently administered. Bisphosphonates, such as zoledronic acid or pamidronate, are typically given intravenously to block the activity of osteoclasts, the cells responsible for dissolving bone tissue. These agents reduce the release of calcium from the skeleton, though their full effect may take two to three days to appear. Denosumab, a monoclonal antibody, is another potent option often used for malignancy-related hypercalcemia that has not responded well to bisphosphonates.
For rapid, short-term reduction in severe cases, the hormone calcitonin can be given by injection. Calcitonin acts quickly to inhibit bone resorption and increase calcium excretion by the kidneys, but its effect is transient, and patients can develop tolerance after a few days. Steroids like prednisone may be used in specific cases, such as hypercalcemia caused by excess Vitamin D production from granulomatous diseases, as they reduce intestinal calcium absorption.
In cases of primary hyperparathyroidism, the definitive treatment is often a surgical procedure called parathyroidectomy. This intervention involves removing the overactive parathyroid gland or glands, curing the hypercalcemia by eliminating the source of excess parathyroid hormone. For patients with PHPT who are not surgical candidates, calcimimetics like cinacalcet can be prescribed to increase the sensitivity of the parathyroid gland’s calcium-sensing receptors, effectively lowering hormone and calcium levels.
Monitoring and Sustained Management
Once initial calcium levels are controlled, long-term monitoring is necessary to ensure stability and prevent recurrence. Sustained management involves regular blood tests, including serum calcium, parathyroid hormone, and Vitamin D levels, to track the body’s regulatory response. The frequency of these tests is determined by the healthcare provider based on the patient’s underlying condition and treatment plan.
The ultimate goal is the continuous treatment of the root cause identified during the diagnostic phase. Monitoring confirms that pharmacological agents are maintaining calcium within the normal reference range or, following a parathyroidectomy, that the procedure was successful. This ongoing surveillance is necessary to protect against the long-term complications of hypercalcemia, such as kidney damage and bone density loss.