Calcitonin is a hormone that helps regulate calcium levels in the blood. Calcium is necessary for nerve signaling, muscle function, and bone health. Calcitonin’s primary action is to prevent blood calcium from rising too high. Understanding its function clarifies why a deficiency may occur and what potential, often indirect, effects it may have on health.
Calcitonin’s Primary Role in the Body
Calcitonin is a peptide hormone produced by specialized C-cells, or parafollicular cells, located within the thyroid gland. Secretion is directly stimulated when blood calcium levels exceed their normal threshold. Calcitonin acts as a regulatory mechanism to help bring elevated calcium concentrations back down to a balanced state.
The hormone achieves its effect by targeting specific cells in the bones and kidneys. In bone tissue, calcitonin inhibits the activity of osteoclasts, the cells responsible for breaking down bone material and releasing stored calcium into the bloodstream. By temporarily suppressing osteoclast function, calcitonin slows the rate at which calcium enters the circulation.
Calcitonin also acts on the kidneys to promote the excretion of calcium through the urine. This dual action—reducing the release of calcium from bone and increasing its removal by the kidneys—effectively lowers circulating calcium. Calcitonin functions in opposition to parathyroid hormone (PTH), which acts to raise blood calcium levels when they are low. PTH is the primary regulator maintaining long-term calcium stability.
Clinical Situations Leading to Low Calcitonin Levels
The most common clinical scenario resulting in calcitonin deficiency is the surgical removal of the thyroid gland, known as a total thyroidectomy. Since the hormone-producing C-cells are located exclusively within the thyroid, their removal eliminates the body’s ability to secrete calcitonin. Low or undetectable levels of the hormone are an expected laboratory finding following this procedure.
Less common causes for low calcitonin levels include rare autoimmune disorders that destroy the C-cells, or certain genetic syndromes that impair cell function. However, these secondary causes are infrequent compared to the direct effect of thyroid surgery.
It is important to distinguish between a low calcitonin level, which is a measurable lab result, and a true symptomatic deficiency, which is a clinical state. Because parathyroid hormone effectively manages the day-to-day regulation of calcium, the absence of calcitonin is often well-compensated. Many individuals with undetectable calcitonin levels after a thyroidectomy remain completely asymptomatic regarding calcium balance.
The loss of calcitonin means the body is missing its natural brake on sudden increases in blood calcium. This leaves the PTH system as the sole hormonal control for calcium homeostasis.
Symptoms and Diagnostic Testing
A deficiency of calcitonin does not directly cause a distinct set of symptoms in most people. When symptoms do emerge, they are a manifestation of an associated complication: hypocalcemia, or low blood calcium. This occurs when the body’s regulatory systems fail to compensate adequately for the mineral imbalance.
The symptoms of hypocalcemia arise because calcium is necessary for normal nerve and muscle function. Mild hypocalcemia can cause paresthesias, which are sensations of tingling or numbness, often felt around the mouth, fingers, and toes. Individuals may also experience muscle cramps or spasms in the extremities.
In more severe instances, symptoms can affect the entire body. These manifestations include tetany, characterized by sustained, painful muscle contractions. Untreated, a severe drop in blood calcium can progress to life-threatening complications such as seizures or cardiac rhythm abnormalities.
The diagnosis of calcitonin deficiency primarily involves a blood test to measure serum calcitonin levels. This test is most commonly ordered following thyroid surgery to confirm the complete removal of C-cells or as part of the follow-up for medullary thyroid cancer. A very low or undetectable level confirms the deficiency.
The more clinically relevant diagnostic tests focus on the downstream effects. Clinicians regularly monitor serum calcium levels, both total and ionized, to detect hypocalcemia. Vitamin D levels are also measured, as this vitamin is involved in calcium absorption and bone health, providing a more complete picture of the patient’s overall mineral status.
Managing Calcitonin-Related Imbalances
Direct replacement therapy for calcitonin deficiency is not standard medical practice. This is because the body’s other regulatory hormones, particularly parathyroid hormone, are effective at maintaining calcium balance. Management focuses instead on preventing or treating the resulting hypocalcemia that can occasionally arise.
The primary strategy for managing potential calcium imbalance involves the use of nutritional supplements. Patients are often prescribed oral calcium supplements to ensure adequate dietary intake of the mineral. Supplementation supports bone health and proper physiological function when regulatory control is limited.
Vitamin D supplementation is also frequently administered, as it is necessary for the gut to absorb calcium efficiently. Often, a form of active Vitamin D, such as calcitriol, is used. Calcitriol bypasses the need for kidney-based activation, which ensures maximum calcium absorption from the diet.
Long-term management requires monitoring serum calcium levels to catch any developing hypocalcemia early. This vigilance is important following a total thyroidectomy, as patient needs can change over time. Adjustments to calcium and Vitamin D dosages are made based on blood test results to maintain blood calcium concentration within the healthy range.