Understanding Hypercalcemia: Causes, Treatments, and Considerations

Hypercalcemia, a condition characterized by elevated levels of calcium in the blood, can stem from several medical issues, most notably primary hyperparathyroidism and malignancy. In primary hyperparathyroidism, the body’s regulation of calcium is disrupted due to an overproduction of parathyroid hormone (PTH). This scenario often arises in middle-aged individuals, particularly women, and has an incidence of approximately 1 in 1000 people. The condition can lead to significant health concerns if not addressed.

Effective treatment for hypercalcemia typically involves oral calcium and calcitriol supplementation. In cases where PTH is absent, the renal conversion of vitamin D into its active form is inadequate, leading to difficulties in maintaining proper calcium levels. The primary aim of treatment is to restore serum calcium to the lower end of the normal range, as complete normalization may sometimes not be achievable. However, a persistent elevation in PTH can result in hypercalcemia, leading to what is known as tertiary hyperparathyroidism.

Malignancy is another frequent cause of hypercalcemia, particularly in later stages of cancer. Eroding bony metastases, which release calcium from bones, and the secretion of paracrine factors that activate osteoclasts contribute to this condition. Additionally, humoral hypercalcemia of malignancy, which involves the secretion of parathyroid hormone-related peptide (PTHrP), can further elevate calcium levels in affected patients.

Beyond these primary causes, hypercalcemia can also result from certain medications and dietary factors. For instance, thiazide diuretics are known to increase calcium resorption in the kidneys, consequently raising blood calcium levels. An overdose of vitamin D, often from over-the-counter multivitamins, can also lead to hypercalcemia. While less common today due to the availability of certain medications for treating peptic ulcers, excessive intake of calcium-rich foods or antacids can sometimes result in elevated calcium levels.

Another important aspect to recognize is familial benign hypercalcemia, a hereditary condition that can mimic primary hyperparathyroidism. This autosomal dominant disorder is characterized by inactivating mutations in the calcium-sensing receptor (CaSR), leading to increased PTH and mild hypercalcemia without the need for treatment. A critical distinction between these conditions is the urinary excretion of calcium, which tends to be diminished in familial benign hypercalcemia, contrasting with the elevated excretion seen in primary hyperparathyroidism.

Overall, understanding the various causes and treatments of hypercalcemia is essential for effective management and prevention of potential complications associated with this condition. Regular monitoring and a thorough medical history can aid in identifying the underlying causes and tailoring appropriate therapeutic strategies.