Study highlights need to protect heart, kidney in hypoparathyroidism patients
Potential link between rare hormone disorder and cardiovascular problems
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People living with hypoparathyroidism have blood levels of a key phosphate-regulating hormone more than four times higher than healthy individuals and show signs of stiffer arteries, a new study from Spain suggests. The findings highlight a potential link between the rare hormone disorder and an increased risk of cardiovascular complications, though the exact biological mechanism remains unclear.
The hormone in question, fibroblast growth factor 23 (FGF23), is known to increase in patients with chronic kidney disease, where it is often associated with arterial stiffness and heart disease. Researchers sought to determine if the same connection existed in hypoparathyroidism, a condition characterized by the body’s lack of parathyroid hormone, resulting in severe imbalances in calcium and phosphate levels.
While the study confirmed that both FGF23 levels and arterial stiffness were elevated in patients, the researchers did not find a direct statistical link between the two. “A causal relationship could not be established,” the team wrote, suggesting that while both factors are present, the heart risks associated with hypoparathyroidism may be driven by more complex mechanisms than previously thought.
The study, “Assessment of arterial stiffness and plasma FGF23 levels in patients with hypoparathyroidism,” was published in the journal Endocrinología, Diabetes y Nutrición.
The link between hormone deficiency and heart health
Hypoparathyroidism is a condition marked by abnormally low levels of parathyroid hormone, which is produced by the parathyroid glands located in the neck near the thyroid. This hormone is involved in the metabolism of calcium and phosphate; when it is lacking, blood calcium levels fall, while phosphate levels rise. Often, the condition arises following a surgery that damages the parathyroid glands.
Standard treatment for hypoparathyroidism involves calcium supplements to prevent low calcium levels and help control excess phosphate, along with calcitriol or other forms of vitamin D, such as cholecalciferol or calcifediol, to enhance calcium absorption.
While this approach helps manage symptoms, both the disease itself and its long-term treatment can lead to complications, including kidney stones, impaired kidney function, and abnormal calcium buildup in tissues such as blood vessels. Calcium deposits in blood vessels, a process known as vascular calcification, can cause arterial stiffness.
In chronic kidney disease, elevated levels of FGF23 have been linked to vascular calcification and arterial stiffness, leading to higher cardiovascular disease risk. Since people with hypoparathyroidism are known to have a higher risk of cardiovascular disease, a team of researchers in Spain set out to examine whether FGF23 and arterial stiffness might also play a role in this condition.
The team conducted a study recruiting 20 adults with chronic hypoparathyroidism and 16 healthy controls matched for age and sex.
The patient group included 12 women and eight men, with a mean age of 58.6 years. Most (85%) had developed the condition following surgery, with a mean disease duration of 16.3 years.
All patients were treated with oral calcium, mainly calcium carbonate. Nearly all (90%) were also receiving calcitriol, while 50% were treated with cholecalciferol or calcifediol.
Compared with healthy controls, people with hypoparathyroidism had lower blood calcium levels and higher phosphate levels, consistent with the underlying disorder. They also had a significantly higher body mass index, a measure of body fat based on weight and height, and significantly poorer kidney function than individuals without hypoparathyroidism.
Blood tests showed that FGF23 levels were more than four times higher in patients with hypoparathyroidism than in healthy controls. Those with hypoparathyroidism also tended to have higher aortic pulse wave velocity values — a measure of arterial stiffness — although this difference did not reach statistical significance.
Investigating the role of kidney function
Among participants with hypoparathyroidism, arterial stiffness increased with longer disease duration and was greater in those with poorer kidney function.
“However, our study did not reveal a significant correlation between FGF23 and [arterial stiffness] that would have suggested a role for this hormone” in the disease processes of arterial stiffness and therefore of cardiovascular disease risk, the researchers wrote.
Because kidney function affects both phosphate regulation and blood vessel health, the researchers noted that impaired kidney function may have influenced both FGF23 levels and arterial stiffness measures.
“Further studies, probably longitudinal ones, are needed to better characterize the impact of hypoparathyroidism on cardiovascular health,” the researchers concluded. (Longitudinal studies track participants over prolonged periods of time.)
“In any case,” they added, “it is evident that patients with this disease must be managed carefully to minimize [cardiovascular risk] factors and kidney damage, and that we need the availability of more physiological replacement therapies for this hormone deficiency.”
