What Is Secondary Hyperparathyroidism?

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Secondary hyperparathyroidism

This disease (secondary hyperparathyroidism) is due to the presence of factors that stimulate the parathyroid glands in the body, especially blood calcium, magnesium is too low and blood phosphorus is too high. After the glands are stimulated to proliferate, hypertrophy, secrete excessive parathyroid hormone, Compensate to maintain normal blood calcium and phosphorus. This disease is more common in vitamin D deficiency, severe renal insufficiency, osteomalacia, pregnant or nursing women.

Treatment measures for secondary hyperparathyroidism

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1. In simple vitamin D deficiency and pseudoparathyroidism, generally only the appropriate amount of vitamin D needs to be added to correct blood calcium and phosphorus abnormalities.

2. In the case of hypophosphatemia caused by renal tubular lesions and vitamin D metabolic phosphorus disorders, neutral phosphate should be supplemented, 2 to 4 g daily, and combined application of vitamin D ranging from 50,000 to 400,000 units per day, or with 1a (OH) D, 0.5 2.0g daily.

3. Chronic renal insufficiency or failure: oral aluminum hydroxide or aluminum carbonate can be combined with a large amount of inorganic phosphorus, which can effectively reduce phosphorus absorption, such as those with mild bone disease, sometimes visible; oral calcium salt or increase dialysate content The amount of calcium to supplement calcium deficiency and inhibit parathyroid secretion. Renal osteodystrophy is only seen in patients whose dialysate contains less than 5.6% mg of calcium; then use vitamin D carefully, which can be taken orally from daily to 50000 Starting from 60,000 units, after 3 to 4 weeks, if necessary, the dose can be gradually increased, about 400,000 units per day, or its activated preparations are used; If the patient intends to be a kidney transplant, perform a subtotal parathyroidectomy, because Hyperfunction can persist for months or even years after kidney transplantation. Excessive blood calcium is not good for the transplanted kidney and the body.

Etiology of secondary hyperparathyroidism

(I) Osteomalacia caused by various reasons

1. Vitamin D deficiency reduces blood calcium due to reduced intestinal calcium absorption, stimulates hyperparathyroidism and secretes excessive hormones.

2. Gastric, intestinal, hepatobiliary, and pancreatic diseases cause malabsorption of fat-soluble vitamin D. The result is the same as insufficient intake of vitamin D, causing hypocalcemia.

3. Chronic kidney disease, renal insufficiency, loss of nephron units, decreased glomerular filtration rate, increased blood phosphorus, decreased blood calcium ions, thereby stimulating the secretion of parathyroid hormone, reduced phosphorus reabsorption in renal tubule Reduce blood phosphorus. However, in the early stages of renal insufficiency, the serum immunoactive parathyroid hormone has already increased. For example, when the filtration rate drops to 40ml / min, the increase in serum hormone concentration is even more pronounced. If renal insufficiency worsens, blood phosphorus continues to be apparent Increased, parathyroid hormone is correspondingly higher. In addition, in renal insufficiency, there are metabolic disorders activated by vitamin D, and the formation of 1,25- (OH) 2D3 is reduced, which affects intestinal calcium absorption and aggravates the tendency of hypocalcemia.

4. Long-term phosphate deficiency and hypophosphatemia are mostly renal tubular acidosis, such as Fanconi syndrome, genetically-associated hypophosphatemia, or long-term use of aluminum hydroxide. Both vitamin D activation and metabolic disorders and hypophosphatemia can cause osteomalacia and hypocalcemia to stimulate the parathyroid glands.

(2) Pseudohypoparathyroidism due to the lack of response of parathyroid hormone effector cells, blood calcium is too low, blood phosphorus is too high, which stimulates the parathyroid glands.

(3) Too much calcitonin, such as in medullary thyroid cancer, too much calcitonin, can also stimulate the parathyroid glands.

(4) Others such as pregnancy, breastfeeding, and hypercortisolism.

As hypocalcemia and hyperphosphatemia stimulate hyperplasia and hypertrophy of parathyroid glands, excessive parathyroid hormones act on the bones, bone absorption occurs, and they act on the kidneys to promote phosphorus excretion. Therefore, in primary diseases such as osteomalacia Fibroosteitis can still occur on the basis. Blood phosphorus is different depending on the disease. In general vitamin D deficiency and renal tubular lesions are too low, and in glomerular lesions, the blood phosphorus is too high, while alkaline phosphatase is increased. Pathologically, it is not easy to distinguish between secondary and primary hypertrophy, such as long-term excessive activity or stimulation, can form adenomas, such as adenomas on the basis of secondary hyperplasia, known as the third parathyroid Hyperthyroidism.