The parathyroid glands and the thyroid gland are two completely different endocrine organs, despite the difference in word! In recent years, the understanding, awareness, and concern about thyroid disorders have become increasingly popular and strengthened, and people are even familiar with the physiological functions and clinical hazards of the thyroid gland to the extent that they can report several of them casually, but the physiological roles of the parathyroid glands and their clinical hazards may still be relatively unknown. Through timely study of international literature, I learned that in developed countries such as Europe and the United States, parathyroid disorders are a major concern because the risks are not only serious but also often insidious. In 2002, I received an orthopaedic patient who was admitted to our orthopaedic department because of a fracture of the left heel bone. During his medical history, he told me about the fracture: He was driving his child to school in the morning and stopped at a traffic light. Mr. D’s unusual “riding encounter” made me think more: could he be a pathological fracture? So I quickly accessed his heel x-ray and found that he had significant osteoporosis. Since I had read about parathyroid glands when I studied abroad, I couldn’t help but think that Mr. D might have a problem with his parathyroid glands. So I took the initiative to add a parathyroid ultrasound on the spot, and 5 minutes later I did uncover a parathyroid adenoma lurking in his neck. I promptly informed his attending orthopedic surgeon of this unexpected finding and the next day Mr. D’s blood test report indicated elevated calcium and parathyroid hormone. On the fourth day, Mr. D was transferred to general surgery for surgical exploration and treatment. The pathology confirmed my findings that it was indeed an insidious parathyroid adenoma that had caused the loss of calcium in Mr. D’s bones, and that a fracture that would not occur easily in a normal person had occurred in him. This fortuitous event further stimulated my interest in the study of parathyroid disorders. In addition to their anatomical location as neighbors, the parathyroid glands and thyroid glands not only have different “ancestors” but also have very different physiological functions and pathological hazards. From an anatomical point of view, the parathyroid glands are “small, numerous and diffuse”. Small – The parathyroid glands are only about 2mm to 5mm in size, and as independent endocrine glands, they are indeed small. There are usually 4 parathyroid glands, and in some cases there are even 8 to 10, which is a large population in the endocrine gland family. The four parathyroid glands in the neck live on both sides of the trachea, two on each side, and the two on the same side are divided into upper and lower, not close together. Even in the mediastinal cavity behind the sternum, the parathyroid glands are not uncommon. The four particles marked in yellow in the physical anatomy are the normal parathyroid glands in humans. As an endocrine organ, the parathyroid glands also use their own synthetic hormones to carry out their physiological functions in the corresponding effector organs or tissues through the bloodstream. The composition and structure of parathyroid hormone (PTH) is relatively homogeneous, being a short peptide chain consisting of only 84 amino acids, shaped like a straight chain with no branches. To date, scientific studies have found that PTH is the most important hormone regulating calcium and phosphorus metabolism in the human body. Calcium is an important ionic component of electrical signals in cardiomyocytes and nerve cells, as well as an extremely important signaling medium in the process of muscle cell contraction and hormone synthesis in endocrine cells, and is known as the “messenger”. In addition, calcium and phosphorus are also important components of human bones. Bone is composed of organic and inorganic materials, organic material is mainly protein, so that the bone has a certain degree of toughness, while inorganic material is mainly calcium and phosphorus so that the bone has a certain degree of hardness. The bone flexibility and plasticity of children and teenagers are relatively high, while the bone hardness of the elderly is relatively high and easy to break. Calcium and phosphorus metabolism in the human body are closely interrelated. Studies have found that the product of calcium and phosphorus concentration in human blood is a constant, and the relationship between the two is inversely proportional, i.e., high calcium levels result in low phosphorus levels, and vice versa for low calcium levels and high phosphorus levels. PTH enters the venous blood after leaving the maternal parathyroid glands and flows throughout the body with the blood circulation. The main effector organs of PTH throughout the body are bones, small intestine, kidneys, blood vessels, heart, joints, subcutaneous tissue, brain tissue and muscles. In normal individuals, PTH in the blood remains in a dynamic range of 13-65 ng/ml. Physiological concentrations of PTH promote intestinal absorption of calcium (which requires the assistance of active vitamin D3), reduce calcium excretion in urine, promote the exchange and balance between blood calcium and bone calcium, and maintain healthy and stable bones.PTH also has the effect of enhancing myocardial contractility, diastaging the aorta, reducing peripheral vascular resistance, lowering blood pressure, and increasing the pumping function of the heart. Recent studies have found that physiological concentrations of PTH are also important in maintaining the cognitive function of human brain tissue. When the parathyroid glands synthesize and secrete too much hormone, resulting in a blood PTH concentration of more than 65 ng/ml, it is called hyperparathyroidism; conversely, when the synthesis and secretion of hormone is reduced, resulting in a blood PTH concentration of less than 13 ng/ml, it is considered hypoparathyroidism. The most direct consequence of hyperparathyroidism is an increase in calcium concentration in the blood; conversely, hypoparathyroidism leads directly to a decrease in calcium concentration in the blood. In hyperparathyroidism, high levels of PTH may further reduce urinary calcium excretion and intestinal calcium absorption, but high blood calcium is more associated with the shedding of calcium from the bones into the blood. As the calcium in the bones decreases, the hardness of the bones decreases, the originally hard bones undergo cyst-like changes and the bones break, which is known as pathological fracture, and Mr. D mentioned at the beginning of the article belongs to pathological fracture of the heel bone. The high concentration of calcium ions in the blood is filtered from the glomerulus into the urine when passing through the kidney, and when it encounters an acidic environment, calcium salt crystals are easily formed and deposited in the renal tubules, calyces or ureter to form stones of different sizes, which further cause symptoms such as hydronephrosis and hematuria. Many patients are accidentally found to have parathyroid disease because of kidney stones. Shortly after the diagnosis of Mr. D’s parathyroid adenoma, our gastroenterology department admitted Ms. S., who had lost her appetite, dyspepsia, and was losing weight, and during my ultrasound examination, I found that her two kidneys were covered with stone crystals, as if they were covered with a white layer of salt frost. After continuous alkalinization of her urine, the stone crystals in her kidneys were significantly relieved after six months, and her gastrointestinal symptoms disappeared, as high blood calcium can cause nausea, vomiting, gastric distention, indigestion, dry mouth, thirst and other digestive symptoms. The patient’s gastrointestinal symptoms, such as nausea, vomiting, bloating, indigestion, dry mouth, and thirst, disappeared. However, not all patients are so lucky. The author has met several patients with persistent kidney stones who have undergone multiple surgical incisions to remove the stones. Ultimately, it was the author who took the initiative to perform parathyroid ultrasound examinations for them and discovered the parathyroid adenoma that had been hidden for years and gave them effective minimally invasive treatment. Whether lithotripsy or surgical extraction is performed, as long as parathyroid disease is not detected, high blood calcium will persist and kidney and ureteral stones can grow repeatedly and be very stubborn. High calcium levels (e.g., above 3.5) can also lead to psychiatric symptoms such as gaze and coma, as high calcium increases central nervous cell excitability. Hyperparathyroidism can be classified as primary, secondary, triphasic, or pseudoparathyroid. Primary hyperparathyroidism (PHPT) is caused by an adenoma or hyperplasia of the parathyroid glands, which not only increases the number of parathyroid cells, but also greatly enhances the secretion of parathyroid hormone. Secondary hyperparathyroidism (SHPT) is mainly due to a negative feedback stimulation of parathyroid cells by low blood calcium, which leads to hyperplasia of parathyroid cells. The causes of hypocalcemia can be a lack of intestinal absorption of calcium and a decrease in the excretion of phosphorus by the kidneys (an increase in blood phosphorus decreases blood calcium, the product of which is a constant). In our country, uremic hemodialysis is the main cause of secondary hyperparathyroidism. The risk of hyperparathyroidism in the maintenance hemodialysis population is quite high and often results in severe damage to the skin, eyes, form and joints of the patient due to hyperparathyroidism. In patients with secondary hyperparathyroidism, kidney transplantation is an ideal means of replacing renal function while the hyperplastic parathyroid glands are restored along with the renal function. However, in a small number of renal transplant patients, the hyperplastic parathyroid glands do not subside after normalization of renal function and continue to have a high PTH secretion capacity, and hyperparathyroidism persists, which is called tertiary hyperparathyroidism (THPT). In hyperparathyroidism, secondary hyperparathyroidism has the more typical underlying disease of renal failure with maintenance hemodialysis, which can easily alert both the doctor and the patient. The tertiary form may be overlooked due to paralysis of both the doctor and the patient, but after all, the number of incidences is small. The most insidious and easy to miss is primary hyperparathyroidism. Increased vigilance for primary hyperparathyroidism and timely blood PTH, blood calcium and neck ultrasound are effective ways to improve the diagnosis rate of accidental detection. Since 2001, the author has been studying the diagnosis of parathyroid gland by ultrasound imaging, and an important lesson has been learned: “I am not afraid of not finding it, but of not thinking about it. Over the years, the ultrasound department of Long March Hospital, which I lead, has developed a good habit of being highly alert to the presence of parathyroid adenomas or hyperplasia, and has taken the initiative to use ultrasound to extend the examination of patients’ parathyroid glands, which has led to the unexpected detection of dozens of parathyroid adenomas, exceeding the expected results. Even if no problematic parathyroid glands were found in the neck, he would persistently dig deeper for clues whenever signs existed and took the initiative to point patients to imaging methods other than ultrasound (mainly u-99 nuclear scan), which led to the discovery of 10 cases of ectopic parathyroid adenomas in the mediastinum. At present, she has developed systematic thinking, processes and original techniques and methods in the field of diagnosis, examination and minimally invasive treatment of parathyroid gland diseases. She has published more than 10 academic papers related to parathyroid gland and given many academic lectures at high-level academic conferences, and her diagnostic and treatment concepts, results and further in-depth thinking about parathyroid gland have been highly recognized by patients and colleagues at home and abroad. In hypoparathyroidism, a series of problems associated with low calcium can occur due to insufficient sources of PTH and reduced levels of calcium ions in the blood. The most obvious of these are reduced activity of transverse muscles, reduced electrical activity of neurons, and reduced excitability of the heart muscle. For example, reduced contraction of respiratory muscles leads to dyspnea, and reduced contraction of the limb muscles leads to peripheral weakness in patients. In addition, twitching of the limb muscles can occur, etc. Necrosis of the parathyroid glands and parathyroid glands being mistreated are the main causes of hypoparathyroidism. One of the major complications of thyroid surgery is intraoperative misinjury of the parathyroid glands, resulting in hypoparathyroidism in patients. Unfortunately, there are no drugs that can completely replace parathyroid hormone in clinical use to date, so it is important to protect normal parathyroid function.