The parathyroid glands, typically four small glands located in the neck behind the thyroid, produce parathyroid hormone (PTH). This hormone maintains calcium and phosphate levels in the blood. Maintaining these mineral levels is important for various bodily functions, including nerve and muscle activity, blood clotting, and bone health.
When blood calcium levels drop, the parathyroid glands release PTH to restore balance. PTH acts on bones to release stored calcium, signals the kidneys to reabsorb more calcium and excrete phosphate, and promotes the activation of vitamin D, which helps the intestines absorb calcium from food. An elevated level of PTH in the bloodstream indicates a disruption in this delicate regulatory system, pointing to an underlying issue affecting calcium balance.
Primary Hyperparathyroidism
Primary hyperparathyroidism occurs when one or more of the parathyroid glands become overactive, producing too much PTH independently. This overactivity occurs regardless of the body’s calcium levels, meaning the glands continue to secrete PTH even when calcium is already high. The most frequent cause of this condition is a benign tumor, known as an adenoma, which develops on one of the parathyroid glands.
Less commonly, primary hyperparathyroidism can result from the enlargement of all four parathyroid glands, a condition called hyperplasia. In rare instances, a cancerous tumor, or parathyroid carcinoma, can also lead to an overproduction of PTH. The excess PTH then causes calcium to be released from bones, increases calcium reabsorption in the kidneys, and boosts intestinal calcium absorption, leading to persistently high calcium levels in the blood, known as hypercalcemia.
Secondary Hyperparathyroidism
Secondary hyperparathyroidism develops as a compensatory response to another condition that causes persistently low calcium levels in the blood. The parathyroid glands, sensing this low calcium, continuously produce PTH in an attempt to raise blood calcium back to normal. This sustained stimulation leads to enlargement and overactivity of all four parathyroid glands.
Chronic kidney disease is the most common cause of secondary hyperparathyroidism. Damaged kidneys struggle to activate vitamin D, which is necessary for calcium absorption from the gut, and also fail to excrete phosphate effectively. The resulting low active vitamin D and high phosphate levels both contribute to lower blood calcium, triggering the parathyroid glands to produce more PTH. Other causes include severe vitamin D deficiency, which directly impairs calcium absorption, and malabsorption syndromes like Celiac disease or Crohn’s disease, which prevent the intestines from adequately absorbing calcium from food.
Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism arises as a progression from long-standing secondary hyperparathyroidism. After a prolonged period of continuous stimulation due to low blood calcium, the parathyroid glands can become autonomous. This means the glands no longer respond to normal feedback and continue to overproduce PTH, even after the underlying cause of secondary hyperparathyroidism (e.g., kidney disease or vitamin D deficiency) has been addressed.
The glands become unresponsive to normal regulation, leading to persistently high PTH and calcium levels. This autonomous overproduction of PTH often results in elevated calcium levels in the blood, similar to what is seen in primary hyperparathyroidism.
Symptoms and Diagnosis
Elevated parathyroid hormone levels often lead to hypercalcemia, which can manifest through a variety of symptoms. Individuals might experience fatigue, generalized weakness, and bone pain due to calcium being drawn from the bones. Other common indicators include kidney stones, increased thirst, and frequent urination as the kidneys work to excrete excess calcium. Muscle weakness, feelings of depression, and cognitive difficulties like brain fog or confusion can also occur.
Diagnosing high PTH involves specific blood tests that measure the levels of parathyroid hormone, calcium, and phosphate in the bloodstream. If PTH levels are high in conjunction with elevated calcium, further investigation is often warranted. Additional diagnostic steps may include urine tests to assess calcium excretion or imaging techniques, such as a sestamibi scan or ultrasound, to precisely locate an overactive parathyroid gland. Consulting a healthcare professional is important for accurate diagnosis and to determine the most appropriate management strategy.