Parathyroid Hormone (PTH) is produced by four small glands in the neck and regulates the body’s mineral balance, primarily maintaining stable levels of calcium and phosphorus in the blood and bones. When calcium levels drop, PTH is released, triggering mechanisms that raise calcium by drawing it from bone, increasing kidney reabsorption, and stimulating Vitamin D activation. Abnormally elevated PTH levels, known as hyperparathyroidism, disrupt this balance and can negatively affect the bones and kidneys. A diagnosis of elevated PTH requires a thorough medical evaluation to determine the underlying cause and the correct intervention.
Identifying the Root Cause of Elevated PTH
Determining the specific origin of elevated PTH is the necessary first step because treatment strategies vary significantly based on the diagnosis. Hyperparathyroidism is classified into three main types, each with a distinct pathophysiology.
Primary Hyperparathyroidism
Primary hyperparathyroidism arises from an issue within the parathyroid glands themselves, causing them to overproduce PTH regardless of the body’s calcium needs. The most common cause is a single benign growth, called an adenoma, on one of the four glands, accounting for about 85% of cases. Less often, it is caused by the enlargement of multiple glands (hyperplasia) or, rarely, by parathyroid cancer. This form typically leads to elevated calcium levels in the blood.
Secondary Hyperparathyroidism
Secondary hyperparathyroidism occurs as a physiological response to a separate condition that causes chronically low calcium levels in the blood. The parathyroid glands continuously secrete PTH in an attempt to restore balance. Chronic Kidney Disease (CKD) is the most frequent cause, as impaired kidneys struggle to convert Vitamin D to its active form and regulate phosphorus, both contributing to low calcium. Low Vitamin D status or severe dietary calcium deficiency can also be a factor.
Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism is a rare progression that develops after long-term secondary hyperparathyroidism, typically in patients with CKD. The parathyroid glands become chronically overstimulated and enlarged, functioning autonomously. They continue to oversecrete PTH even after the underlying cause, such as kidney failure, has been corrected, resulting in high calcium levels similar to the primary form.
Dietary and Nutritional Adjustments
For many individuals, particularly those with secondary hyperparathyroidism or mild cases, lifestyle changes can help support PTH management. Controlling phosphorus intake is important, especially in the context of chronic kidney disease. High phosphorus levels in the blood stimulate PTH release, so limiting foods rich in this mineral is recommended.
This involves reducing consumption of processed foods, which often contain phosphate additives. Specific items like dark sodas, processed and hard cheeses, and certain whole grains are naturally high in phosphorus and should be limited. Maintaining a balanced calcium intake, generally between 1,000 and 1,200 milligrams daily, is important, as severely restricting calcium can inadvertently cause PTH levels to rise further.
Vitamin D requires management, as a deficiency is a known cause of high PTH. Addressing a low Vitamin D level through monitored supplementation can help suppress PTH secretion. However, excessive or unprescribed Vitamin D or calcium supplementation can be detrimental, potentially leading to high blood calcium levels, especially in primary hyperparathyroidism.
Maintaining proper hydration helps dilute the urine and reduces the risk of kidney stone formation, a common complication of elevated calcium levels. Regular, moderate exercise also supports bone health, which is often compromised when PTH is high, by encouraging the body to retain bone density.
Pharmacological Treatments
When PTH levels remain high and lifestyle adjustments are insufficient, specific prescription medications can be employed to suppress hormone production. One class of drugs is the calcimimetics, such as cinacalcet, which alter the parathyroid glands’ sensitivity to circulating calcium. These agents bind to the calcium-sensing receptors on the glands, signaling the parathyroid glands to reduce their output of PTH and subsequently lower blood calcium levels.
Active Vitamin D analogs are primarily used in secondary hyperparathyroidism associated with CKD. Because kidney impairment reduces the body’s ability to activate Vitamin D, prescription forms like calcitriol or paricalcitol are administered. These active forms suppress the overproduction of PTH and improve the body’s ability to absorb calcium from the diet. By normalizing the mineral balance, these analogs manage chronic PTH overproduction.
In patients with kidney disease, controlling phosphorus is a necessary step that indirectly helps to lower PTH. Phosphate binders are medications taken with meals that attach to phosphorus in the digestive tract, preventing its absorption into the bloodstream. By reducing the burden of high phosphorus, a stimulator of PTH release, these binders manage the overall mineral imbalance.
Parathyroid Gland Surgery
Parathyroidectomy, the surgical removal of the overactive gland or glands, is the definitive treatment for primary hyperparathyroidism. Surgery is indicated when high PTH and calcium levels cause complications, such as significant bone density loss, kidney stones, or impaired kidney function. It is also recommended for patients whose blood calcium levels are significantly elevated or who are under the age of 50.
The procedure involves locating and removing the abnormal parathyroid tissue, often a single adenoma. Minimally invasive techniques have made the operation highly targeted, frequently requiring only a small incision and a short hospital stay. The success rate for curing primary hyperparathyroidism through parathyroidectomy exceeds 95% when performed by experienced surgeons.
Following removal of the problematic gland, PTH and calcium levels typically return to a normal range. Surgery addresses the root cause of hormone overproduction. In some complex cases of tertiary hyperparathyroidism, where multiple glands are autonomously overactive, a partial parathyroidectomy may also be performed.