How is parathyroid hyperplasia treated?

summary

Primary parathyroid hyperplasia is often caused by fire. Almost all the four parathyroids proliferate, and the weight can reach hundreds of times of normal. However, the proliferation is not evenly distributed. Generally, the proliferation of the upper parathyroid is more significant. So, how do some patients treat parathyroid hyperplasia?, Today I'd like to share this with you.

How is parathyroid hyperplasia treated?

First: general treatment: diet should be high calcium, low phosphorus diet, limit milk and other dairy products, egg yolk, cauliflower and other high phosphorus food intake. Try to avoid the use of drugs that can aggravate hypocalcemia, such as contraceptives, glucocorticoids, diazepam, phenytoin sodium, phenobarbital and other preparations.

Second: tetany or convulsion: must be treated with intravenous calcium, usually 10% calcium gluconate. It should be noted that the concentrated calcium solution can stimulate the vein. If it overflows out of the vein, it can cause severe inflammation of soft tissue. Therefore, the calcium injection should be diluted with glucose and slowly injected intravenously for 5-10 minutes. Direct injection should be avoided. If necessary, it can be reused after 1-2 hours.

Third, if the blood calcium level of PA patients is as low as 2.0 mmol / L, but there is no tetany or only slight neuromuscular symptoms, they can only take calcium orally. The daily intake of calcium is 3-6 g (1-2 g elemental calcium), and the blood calcium should be controlled at 2.13-2.25 mmol / L; When the blood calcium rises to 2.25-2.5 mmol / L, the urinary calcium excretion is three times of that of normal people. Urinary calculi are easy to occur, and renal failure may occur in severe cases.

matters needing attention

Patients with parathyroid hypothyroidism have the following conditions, suggesting that the condition is serious: long-term and severe hypocalcemia, disappearance of reflex, repeated convulsions, optic disc edema and intracranial pressure increase, cataract formation and multiple intracranial calcification. Q-T interval was significantly prolonged. If the parathyroid hypothyroidism of pregnant women is not well controlled, the fetus may suffer from long-term hypocalcemia, resulting in secondary hyperparathyroidism and severe neonatal decalcification. Although the neonatal secondary hyperparathyroidism is transient, it may be complicated with fracture and die. The prognosis is generally good. However, it is necessary to prevent the formation of hypercalcemia, hypercalcemia, arrhythmia and kidney stones.