A disorder of calcium and phosphorus metabolism caused by excessive secretion of parathyroid hormone (PTH) by the parathyroid glands. This is referred to as hyperparathyroidism. The main manifestations are skeletal changes, urinary stones, high blood calcium and low blood phosphorus. There are four types of hyperparathyroidism: primary, secondary, triphasic and pseudohypoparathyroid. Primary hyperparathyroidism is the main cause of hyperparathyroidism. Secondary hyperparathyroidism is caused by long-term stimulation of the parathyroid glands due to various causes of hypocalcemia, such as chronic renal failure, vitamin D deficiency, malabsorption and impaired production of vitamin D due to intestinal, liver and kidney diseases. The cause is usually parathyroid adenoma, but parathyroid hyperplasia and parathyroid cancer are less common. Some patients have a family history of familial hyperparathyroidism, which is autosomal dominant and can develop in adults, children and newborns. It is mainly a hyperplasia of the main parathyroid cells. The autosomal recessive form is common in infants and can develop after birth and lead to death due to severe hypercalcemia. If the mother is chronically hypoparathyroid and has persistent hypocalcemia, temporary hyperparathyroidism may result in the newborn. The main pathophysiological change is the overproduction of PTH, which leads to bone lysis, release of bone calcium into the blood, and increased calcium absorption by the renal tubules and intestine. High blood calcium causes decreased neuromuscular excitability and gastrointestinal tract relaxation, resulting in neuromuscular and psychoneurological manifestations, such as easy fatigue, reduced muscle strength and tone, personality changes, reduced intelligence and memory, as well as irritability, allergy, insomnia and emotional instability, and occasionally obvious psychosis, and in severe cases, coma. There may also be symptoms of loss of appetite, nausea, vomiting and constipation. The incidence of ulcer disease is higher than the general population. Excessive PTH decreases phosphorus reabsorption by the renal tubules, so urinary phosphorus increases, blood phosphorus decreases, phosphorus is in negative equilibrium, and phosphorus deficit is also borne by skeletal tissue. excessive PTH increases osteoclast activity, which is accompanied by increased osteoblast activity and increased secretion of alkaline phosphatase by osteoblasts, resulting in elevated blood alkaline phosphatase. Diagnosis Blood PTH concentration is a direct and sensitive indicator for the diagnosis of hyperparathyroidism, and it is used to diagnose hyperparathyroidism and surgery in about 90% of cases. The degree of PTH elevation parallels the calcium concentration, tumor size, and severity of the disease. However, in secondary hyperparathyroidism, PTH may also be elevated. Combining blood PTH with blood calcium, urine calcium, x-ray and clinical manifestations can help in the differential diagnosis of the two. Urinary cyclic adenosine monophosphate (cAMP) may be elevated. Bone density is generally decreased. characteristic bone changes on X-ray are mostly seen in the skull, dental sclerosis, hands and pelvis. Urinary calculi and renal calcifications may be present on abdominal plain films. Most lesions of the parathyroid glands are located in the neck, and if the first exploratory neck surgery fails, the presence of other causes of hypercalcemia should be considered. If the diagnosis of hyperparathyroidism is still considered consistent, localization is best performed before reoperation. Non-invasive investigations include ultrasound tomography, CT, and MR. Patients with secondary and triple hyperparathyroidism often have concomitant renal failure, osteochondrosis, and other characteristic clinical manifestations of the primary lesion. Secondary hyperparathyroidism has normal or decreased blood and urine calcium values and is not associated with urinary stones. Patients with pseudohyperparathyroidism have concomitant presence of primary tumors. In identifying the cause of hypercalcemia, attention should be paid to the presence of multiple myeloma, acute leukemia, nodular disease, vitamin A and D overdose, hyperthyroidism, and benign familial hypercalcemia. Treatment Surgical treatment is appropriate for primary and triple hyperparathyroidism with symptoms or complications. All parathyroid glands should be explored, either for tumors or hyperplasia. If it is an adenoma, removal should be done. In case of hyperplasia, some of the glands can be removed or all 4 glands can be removed and then a small portion can be taken as an autologous parathyroid graft and buried in the muscle. In case of adenocarcinoma, radical surgery should be done. In cases where the diseased parathyroid glands are missed during surgery, ectopic diseased glands or hyperplastic parathyroid glands are not sufficiently removed, reoperation is required. Most of them are still surgically removed from the neck, while a few require dissection of the sternum to remove the ectopic parathyroid glands, the chance of the latter in the mediastinum varying from 2 to 20%, and occasionally in the thyroid gland or pericardium. Complications of surgery are rare, about 1%, such as injury to the recurrent laryngeal nerve and permanent hypoparathyroidism. The surgical mortality rate is almost zero. Asymptomatic cases with only mild hypercalcemia should be followed up and observed. Hypocalcemia can occur after parathyroid surgery, ranging from numbness of the hands, feet, lips and face in mild cases to hand and foot twitching in severe cases. Hypocalcemia symptoms may appear within 24 hours after surgery. Most patients can recover their blood calcium to more than 8 mg% within 1 to 2 months after surgery. Treatment of hypocalcemia should include calcium and vitamin D supplementation and, if necessary, intravenous or drip calcium gluconate. In case of persistent and refractory hypocalcemia, the possibility of combined hypomagnesemia should be considered, and magnesium can be supplemented at the same time.