Secondary hyperparathyroidism

Introduction to secondary hyperparathyroidism Secondary hyperparathyroidism (SHPT, referred to as secondary hyperparathyroidism) refers to chronic renal insufficiency, intestinal malabsorption syndrome, Fanconi syndrome and renal tubular acidosis, vitamin D deficiency or In the case of resistance, pregnancy, breastfeeding, etc., the parathyroid gland is stimulated by hypocalcemia, hypomagnesemia or hyperphosphatemia for a long time to secrete excess PTH to improve blood calcium, blood magnesium and reduce blood phosphorus. Sexual clinical syndrome. With varying degrees of parathyroid hyperplasia, but not caused by the disease of the parathyroid gland itself. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: fracture

The cause of secondary hyperparathyroidism

First, the cause of the disease

1, vitamin D with calcium deficiency caused by low blood calcium

(1) Insufficient calcium intake or pregnancy, increased calcium requirements during lactation.

(2) After gastric resection, steatorrhea, intestinal malabsorption syndrome and liver, gallbladder, pancreatic chronic diseases affecting the secretion of digestive juice can cause calcium malabsorption.

(3) Chronic liver disease or long-term use of anti-epileptic drugs cause insufficient intrahepatic 25-hydroxylase activity, leading to vitamin D activation disorder and reduced intestinal calcium absorption.

(4) long-term use of laxatives or cholestyramine causes intestinal calcium loss, phenobarbital can block the activation of vitamin D, can induce hypocalcemia.

2, chronic kidney disease, chronic renal insufficiency caused by 1,25 dihydroxyvitamin D3 deficiency

(1) Chronic renal insufficiency: reduced renal phosphorus excretion, leading to phosphate retention, hyperphosphatemia causes blood calcium reduction; at the same time due to lack of renal 1-hydroxylase, intestinal calcium absorption is insufficient, resulting in hypocalcemia; Insufficient calcium supplementation during dialysis also causes hypocalcemia.

(2) renal tubular acidosis (such as Fanconi syndrome): a large amount of phosphate is excreted in the urine, resulting in insufficient hydroxyapatite in the bone, loss of calcium in the bone, leading to hypocalcemia, indirectly stimulating the parathyroid gland, Lead to secondary hyperparathyroidism.

(3) autoimmune renal tubular damage: many autoimmune diseases can lead to renal tubular damage, lack of active vitamin D, leading to intestinal calcium absorption disorders and poor bone mineralization, induced secondary hyperparathyroidism.

3, pseudo-hyperparathyroidism: pseudo-hyperthyroidism is a kind of atopic endocrine syndrome, organs outside the parathyroid, especially the lung, kidney, liver and pancreas The tumor secretes one or several different ascending calcium active substances (such as PTHrP), which causes hypercalcemia, hypophosphatemia, and bone lesions.

4, three hyperparathyroidism: excessive response to pathological factors, secondary hyperparathyroidism for too long, parathyroid gland developed by compensatory hyperfunction into autonomous hyperfunction, the formation of adenoma Excessive secretion of PTH.

5, other endocrine diseases: cortisol caused by various causes, excessive secretion of calcitonin, can cause secondary hyperparathyroidism; vitamin D activation and intestinal calcium absorption in postmenopausal women with osteoporosis Decreased ability, or a slower rate of renal clearance of PTH, leads to elevated plasma PTH.

6, severe hypomagnesemia and lithium salt treatment, can induce secondary hyperparathyroidism.

(two) pathogenesis

1. Chronic renal failure: In patients with chronic renal failure and experimental renal failure, the carboxy-terminal fragment (iPTH) without biological activity PTH35-84 and the increase in bioactive intact PTH can be measured. Parathyroid gland Hyperplasia, its pathogenesis is due to:

(1) Hypocalcemia and hyperphosphatemia caused by chronic renal failure, causing compensatory hyperplasia and hypersecretion of parathyroid glands. When the glomerular filtration rate drops to 25 ml/min, the renal pelvis Phosphorus is reduced, blood phosphate is retained, and strontium causes a decrease in ionized calcium in the extracellular fluid, and a decrease in total calcium in the blood.

(2) Hyperphosphatemia can also directly inhibit renal 1-hydroxylase, combined with the destruction of renal tissue itself, causing the formation of 1,25-(OH)2D3 in the kidney, resulting in reduced intestinal calcium absorption and decreased blood calcium.

(3) 1,25-(0H)2D3 reduction can make the bones have different degrees of resistance to PTH, and the parathyroid glands are increased by compensatory secretion.

(4) In renal failure, not only the half-life of PTH and its degradation fragments (especially the carboxy terminal fragment of PTH35-84) is greatly prolonged, but also the clearance rate of catecholamines and vitamin A is also reduced; catecholamines and vitamin A all contribute to the release of PTH. .

(5) When using low-calcium and low-magnesium dialysate for dialysis treatment of renal failure, it is more likely to aggravate hypocalcemia and resistance to PTH and thus secondary hyperparathyroidism.

2, tertiary hyperthyroidism (tertiary hyperthyroidism): long-term hypocalcemia (most common in chronic renal insufficiency, occasionally seen in rickets) can cause secondary hyperparathyroidism, normal or higher than normal blood calcium When it is not able to feedback the inhibition of autonomic secretion of the parathyroid glands, it is called three-parathyroidism, and patients often have severe renal osteodystrophy.

3, vitamin D deficiency or resistance: vitamin D deficiency or its formation of hydroxylation active products (the latter such as liver disease or the use of anticonvulsants), pseudo-D deficiency (also known as hereditary 1-hydroxylation) Enzyme deficiency or hereditary vitamin D-dependent rickets), renal osteodystrophy, etc., can cause secondary hyperparathyroidism due to hypocalcemia caused by intestinal calcium absorption disorder.

Familial anti-vitamin D rickets (also known as phosphate polyuria), most patients because of lack of phosphorus rather than calcium deficiency, although it can cause rickets, but rare hypocalcemia and secondary hyperparathyroidism, only phosphoric acid After the salt treatment, hypocalcemia may occur secondary to parathyroidism; however, some patients with this disease may have secondary hyperparathyroidism due to the formation of 1,25-(OH)2D3.

Fanconi syndrome is another type of rickets caused by renal reabsorption of phosphorus disorders, but this disease also has sugar, "all" amino acid reabsorption disorder and high urinary calcium. A few critically ill patients can cause hypocalcemia and Secondary hyperparathyroidism; there is also a Lignac-Fanconi syndrome with cystineosis. Because cystine is accumulated in many organs, especially the kidneys, it is easy to cause renal failure. Hey.

4, renal tubular acidosis: the disease has alkali loss, accompanied by increased calcium and caused by low blood calcium, and secondary hyperparathyroidism, blood calcium can return to normal.

5, malabsorption syndrome: the disease has vitamin D, calcium, magnesium and other comprehensive absorption disorders, may be secondary to hyperparathyroidism due to lower blood calcium and magnesium.

Secondary hyperparathyroidism prevention

Active treatment of primary disease:

1, elderly patients with vitamin deficiency for sunbathing treatment, the most suitable for bedridden patients.

2. Patients caused by dietary factors increase the intake of vitamins and calcium in food.

3, pregnant and lactating women to increase calcium intake, as much as possible in the food supplement.

4, the epileptic drug caused by the drug can be discontinued, if not can be stopped, only the use of small doses of vitamins and calcium can be effective.

5, most of the patients with gastric resection need only one intramuscular injection of 300,000 units of vitamins.

6, the digestive tract vitamin malabsorption in addition to the cause of treatment, every 2-3 days use vitamins.

7, when renal tubular acidosis, use calcium citrate or sodium bicarbonate to correct acidosis, if necessary, add potassium and use potassium-sparing diuretics.

Secondary complications of hyperparathyroidism Complications

There are mainly pathological fractures and bone deformities, proximal muscle weakness and muscle atrophy, skin ischemic ulcers and muscle necrosis.

Symptoms of secondary hyperparathyroidism Common symptoms Hyperparathyroidism Metabolic acidosis Renal failure Hypocalcemia Blood calcium hyperactivity Joint deformity Bone pain

The main clinical manifestations of secondary hyperparathyroidism caused by CRF are:

1. Skeletal symptoms: Skeletal pain is spontaneous or promotes after compression. Bone pain is more common in the weight-bearing joints such as the spine, hips, knees, etc., and is aggravated during activity. The pain is episodic or persistent, and may also be pathological. Fractures and bone deformities, this and PTH promote osteolysis, osteoclasts, bone cell bone hyperplasia, bone cortex thinning, general decalcification of the whole body bone, fractures are more common in the ribs, spine and other parts, fractures are spontaneous Or slight external force; joint deformity can be seen scoliosis, thoracic deformation, children can have delayed bone growth, osteophyte detachment and femoral deformation; PTH is an important determinant of parathyroid bone disease, the degree of elevation and parathyroid bone The severity of the disease is consistent.

2, neurotoxicity and neuromuscular symptoms: the neurotoxic effects of PTH, can cause mental disorders, EEG disorders and peripheral neuropathy, but also proximal muscle loss and muscle atrophy, limb proximal muscle strength progressive decline, Affects upper limb lifts and walks.

3, with PTH too high, hypercalcemia or metastatic calcification related to other symptoms: varying degrees of skin itching and calcium deposition in the skin, PTH excess caused by soft tissue, vascular calcification, leading to ischemic necrosis, skin ischemic Ulcer and muscle necrosis occur mostly at the tip of the finger. The site of calcification of atopic calcification is cornea, around the joint, blood vessels, etc. Some may present as joint pain, pseudogout syndrome, occasionally ischemic muscle. pain.

Examination of secondary hyperparathyroidism

1, laboratory inspection

(1) Serum calcium: mostly normal or normal low and below normal.

(2) 24-hour urinary calcium: Vitamin D deficiency and renal uremia are reduced, renal tubular acidosis is close to normal, and its significance is not as great as primary hyperparathyroidism.

(3) Serum phosphorus: decreased in the absence of vitamin D, increased in renal insufficiency, and mostly normal in tubular lesions.

(4) 24-hour urinary phosphorus is of little significance.

(5) Renal function test: creatinine is often increased in renal osteodystrophy, and parathyroid bone disease is parallel after creatinine is increased.

(6) Serum electrolytes: When renal tubular acidosis occurs, blood chlorine increases and blood potassium decreases.

(7) Urine electrolyte: When renal tubular acidosis occurs, blood potassium is reduced and urinary potassium is increased.

(8) Uric acidification function: In type I RTA, the urine pH is increased, the titratable acid discharge is reduced; the type II RTA is increased in the urine carbon dioxide partial pressure.

(9) Determination of vitamin D: deficiency of vitamin D, decreased renal dystrophy, renal tubular acidosis is mostly normal.

(10) Blood gas analysis: Metabolic acidosis changes in renal tubular acidosis and renal osteodystrophy.

2, imaging examination

X-ray and radionuclide bone scan are helpful for the diagnosis and classification of renal osteodystrophy. Imaging examination of parathyroid glands can not only find enlarged parathyroid glands, but also identify the sites of 4 parathyroid glands. The position of the parathyroid gland, this examination can help determine the diagnosis of SHPT, repeated examination can also assess the effect of non-surgical treatment.

3, other

Routine electromyography, EEG, electrocardiogram, bone X-ray, etc., if necessary, renal biopsy can help rule out other kidney diseases.

Diagnosis and diagnosis of secondary hyperparathyroidism

diagnosis

Secondary hyperparathyroidism caused by common CRF can be diagnosed by relying on the corresponding symptoms and signs and laboratory results.

1. Symptoms caused by primary diseases that cause hypocalcemia, such as chronic renal failure, renal osteodystrophy or rickets syndrome and laboratory abnormalities.

2, there are symptoms and signs of hypocalcemia, such as limb numbness, paralysis, proximal limb muscle strength progressive decline.

3, severe patients may have symptoms of primary hyperparathyroidism, such as proximal muscle weakness, bone pain, bone disease (may have fibrous osteitis, osteomalacia, osteosclerosis and osteoporosis), only bone cysts are rare According to the study, the early bone disease of renal osteodystrophy is mainly caused by osteoporosis and osteoporosis caused by excessive PTH. Later, due to the formation of 1,25-(OH)2D3, chondrosis is more See also, osteosclerosis is also seen. In recent years, patients with chronic renal failure have prolonged their life with dialysis therapy. The incidence of renal osteodystrophy is greatly increased and progressively increased. It may also be removed with heparin and arteriovenous shunt. In addition to bone growth factors in the blood, in addition, secondary hyperparathyroidism, there may be subtype urinary tract stones associated with renal calcium leakage, such patients often accompanied by mild hypophosphatemia and increased urinary cAMP Some secondary hyperparathyroidism may also have mild metabolic acidosis.

4, blood biochemical examination blood calcium concentration decreased, blood phosphorus increased, blood alkaline phosphatase abnormal changes, blood 1,25-(OH)2D3 decreased, blood three forms of PTH were elevated, imaging examination if The diagnosis of 2-HPT can be determined by finding a swollen parathyroid gland.

Differential diagnosis

The disease is mainly primary, secondary and triad hyperparathyroidism differentiation, primary and secondary hyperparathyroidism can cause renal tubular acidosis, which may be PTH directly Acting on the renal tubules, reducing the reabsorption of bicarbonate, phosphate deficiency also inhibits the reabsorption of bicarbonate, hypercalciuria in the hyperparathyroidism, damage to the renal tubules, distal and proximal tubules can occur Acidosis, and untreated renal tubular acidosis due to excessive urinary calcium excretion, low calcium often increases PTH, although there is renal tubular acidosis and elevated PTH, but early hypocalcemia can be identified The function of reabsorption of amino acids in proximal tubules is regulated by PTH. When PTH is increased, amino acid reabsorption is reduced. Therefore, hyperparathyroidism often has amino aciduria, primary, secondary and tertiary parathyroid function. Into the identification.

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