What is secondary hyperparathyroidism? How is it**? Punbifu--- new helper is here!
For dialysis patients, there is a complication that is both familiar and unfamiliar, familiar because doctors often mention it in their ears, strange because patients often do not understand, what is secondary "hyperparathyroidism"? What pth? I don't understand, I don't know! Okay, let's talk about it today!
What is secondary hyperparathyroidism?
Secondary hyperparathyroidism is a simplified idiom term, the full name is secondary hyperparathyroidism, which is a disease that causes excessive production of parathyroid hormone (PTH) due to chronic renal insufficiency, active vitamin D deficiency, hypocalcemia, high blood phosphorus and other reasons [1], which will bring a lot of trouble to patients, such as bone pain, fractures, cardiovascular lesions, itching, etc.
According to statistics, there are nearly 1 million hemodialysis patients in China, of which more than 60% suffer from secondary hyperparathyroidism. So, what exactly is secondary "hyperparathyroidism"? And how do we ** it? Don't worry, I'll answer them one by one.
How does secondary hyperparathyroidism occur?
To understand the causes of secondary hyperparathyroidism, we first need to know what parathyroid glands are. The parathyroid gland is a small gland located in the neck, and its main function is to secrete a hormone called PTH. The role of PTH is to regulate the balance of calcium and phosphorus in the blood and maintain the health of bones and teeth.
For example, under normal circumstances, when the calcium in the blood is too low, the parathyroid glands will secrete more PTH, which promotes the absorption of calcium by the kidneys and intestines, inhibits the excretion of phosphorus by the kidneys, and stimulates the bones to release calcium and phosphorus, thereby increasing the level of calcium and phosphorus in the blood to maintain the balance of calcium and phosphorus in the blood.
When a disease occurs, such as due to a decrease or loss of kidney function, the phosphorus in the blood rises and calcium decreases, causing the parathyroid glands to secrete more PTH in an attempt to restore balance. However, in the disease state, PTH secreted by the parathyroid glands is not effective in reducing phosphorus in the blood, nor can it effectively increase the calcium in the blood, but will cause the bones to be overbroken down, releasing more calcium and phosphorus, further aggravating the imbalance of calcium and phosphorus in the blood. As a result, the parathyroid glands fall into a vicious cycle and continue to secrete more PTH, causing hypertrophy and hyperfunction of the parathyroid glands.
What are the dangers of secondary hyperparathyroidism?
Secondary hyperparathyroidism is very serious and can affect multiple systems in patients, such as:
Skeletal lesions: Secondary hyperparathyroidism can cause excessive breakdown of bones, releasing large amounts of calcium and phosphorus, resulting in osteoporosis, skeletal deformities, fractures, etc. Skeletal lesions can cause severe bone pain, interfere with daily activities, and even lead to disability. Cardiovascular disease: secondary "hyperparathyroidism" will lead to an increase in the level of calcium and phosphorus in the blood, which will be deposited on the blood vessel wall, causing vascular calcification, increased arteriosclerosis, increased blood pressure, increased heart burden, myocardial ischemia, arrhythmia, etc., and cardiovascular disease is the most common cause of death in dialysis patients. Itching: Secondary hyperparathyroidism causes increased levels of calcium and phosphorus in the blood, which are deposited on the nerve endings and cause itching. Itching can seriously affect the patient's sleep quality, and even lead to scratching, infection with bacteria, and inflammation. The above is the main harm of secondary "hyperparathyroidism", it can be seen that secondary "hyperparathyroidism" is a very serious complication of kidney disease, if not timely, it will bring a lot of trouble to patients, and even life-threatening. So, how do we develop secondary hyperparathyroidism?
How to ** secondary "hyperparathyroidism"?
* The purpose of secondary hyperparathyroidism is to restore the balance of calcium and phosphorus in the blood and reduce PTH levels to reduce bone and cardiovascular damage. At present, there are two main methods of secondary "hyperparathyroidism":
Surgery**: Surgery is mainly indicated for patients who are ineffective or intolerant of medications, or who have serious skeletal or cardiovascular complications. Surgery** involves removing some or all of the parathyroid glands, thereby reducing the level of PTH.
Drugs: Drugs are the first-line option for secondary hyperparathyroidism and mainly include calcimimetics and active vitamin D and its analogues.
A calcimimetic agent is a calcimimetic agent that mimics the action of calcium, binds to calcium-sensitive receptors on the parathyroid glands, inhibits the secretion of PTH, and also reduces the level of phosphorus in the blood.
Active vitamin D and its analogues are hormones that promote intestinal absorption of calcium, increase the level of calcium in the blood, and also inhibit the secretion of PTH.
According to the 2017 KDIGO Clinical Practice Guidelines: Diagnosis, Evaluation, Prevention and ** of Mineral and Bone Abnormalities in Chronic Kidney Disease and the 2019 Guidelines for the Diagnosis and Treatment of Mineral and Bone Abnormalities in Chronic Kidney Disease in China, calcimimetry, calcitriol or vitamin D analogues are recommended for lowering PTH in hemodialysis patients**.
At present, in clinical practice, the commonly used calcimimetic agent is cinacalcet, and calcitriol or vitamin D analogues include alfacalciferol tablets, calcitriol capsules and other drugs. But today, we are talking about a new generation of calcimimetic agents - etcatide.
Epcatide hydrochloride is an 8-amino acid polypeptide calcimimetic agent that also shows activity in the setting of extracellular calcium deficiency.
It has a significant effect on reducing PTH: Chinese data show that the new calcimimetic agent etecatide can be reduced by 35 in 4 weeks13%；A prospective study in Japan showed a decrease in PTH of about 62% at 52 weeks (range of 60-240 pg ml), with a rate of 19 from baseline5% rose steadily and then remained at 641%。[2]
A network meta-analysis showed that eticatide was the drug with the highest likelihood of achieving PTH targets, superior to cinacalcet178 times (OR, 2.)78;95% ci, 1.19-6.67) [3], a further 50% reduction in PTH levels can be achieved with switching to eticatide in patients originally treated with cinacalcet [4].
In terms of improving patient benefits: calcimimetic eticatide can significantly reduce FGF23 levels, delay the progression of left ventricular hypertrophy, and achieve both cardiovascular and bone benefits, reducing the risk of all-cause mortality by 17%, cardiovascular mortality by 8%, and fracture by 16% and 29% [5]-[6].
In addition, intravenous etecatide after dialysis is safe and well tolerated by patients; It can significantly reduce the burden of pills and long-term drug costs, and further improve patients' drug compliance [7]-[8].
In general, the new calcimimetic agent Pempira, as a newly marketed drug for secondary hyperparathyroidism, is a long-acting calcimimetic agent, which can more effectively reduce the level of PTH and become a new helper for secondary hyperparathyroidism, bringing new hope to patients. At the same time, the drug has relevant patient commercial insurance benefits, and patients can consult the doctor in the hemodialysis room or scan the Ilway escort sun code at the end of the article to understand.