Hypercalcemia

Introduction Hypercalcemia is a phenomenon of hypercalcemia, which is a disorder of calcium metabolism. When adult blood calcium is greater than 2.75 mmol / L (11 mg / dl) is high blood calcium, the normal value of 2.2 ~ 2.75 mmol / L, different hospital blood calcium test reference values have small differences, there are blood calcium more than 2.6mmol / l ( 10.5 mg / l), normal value of 2.0 ~ 2.55 mmol / L, identified as hypercalcemia. The clinical manifestations of hypercalcemia vary widely. Some people accidentally find it only during blood tests. Some can have serious complications such as disturbance of consciousness, muscle weakness, headache, high blood pressure, vomiting, etc. High calcium crisis is critically ill. , refers to serum calcium greater than 4.5mmol / L.

Cause

Classification of causes:

(1) Primary hyperparathyroidism:

The main cause of hypercalcemia is common in parathyroid adenoma and parathyroid hyperplasia, and a small number of parathyroid carcinoma. Due to the abnormal secretion of PTH, blood calcium is elevated.

(B) secondary hyperparathyroidism:

Chronic nephritis, vitamin D deficiency, hypophosphatemia and renal failure repeated hemodialysis and other causes of long-term hypocalcemia, can stimulate parathyroid hyperplasia, increased PTH secretion, leading to high blood calcium.

(three) hyperthyroidism:

Thyroxine and triiodothyronine (T3) can promote bone resorption, increase blood calcium, and increase urinary calcium. 15%-20% of patients with moderate hyperthyroidism are associated with hypercalcemia.

(4) Malignant tumors:

The incidence of high blood calcium is second only to primary hyperparathyroidism. In malignant tumors, bone metastases account for about 70%, leukemias for 20%, and metastasis-free tumors for only 10%. Bone metastasis causes increased blood calcium, on the one hand due to bone destruction, bone calcium release; on the other hand, bone metastasis can also produce some cytokines, such as metastatic growth factor, epidermal growth factor, tumor necrosis factor, etc. Locally, it can exhibit activity of promoting bone resorption and release of bone calcium. Systemic osteoclastic osteolysis without metastatic tumors is mainly due to the production of factors such as PTH or PTH-like substances, prostaglandins, and osteoclast activating factor.

mechanism:

PTH, calcitonin (CT) and cholecalciferol [1,25(OH2)D3] play important regulatory roles in calcium and phosphorus metabolism. PllH activates various cells in bone tissue, including bone cells, osteoclasts, osteoblasts, and the like. After activation of bone cells, bone calcium can be quickly released into the blood and rapidly increase blood calcium. The effect of osteoclasts releasing bone calcium begins after 12-14 hours of PTH action, but the effect is strong and long lasting. PTH enhances the reabsorption of calcium by the distal convoluted tubules and inhibits the reabsorption of phosphorus by the proximal convoluted tubules. PTH also promotes the hydroxylation of 25(OH)D3 in the renal tubules, which is converted to 1,25(OH)D3, which is activated vitamin D3, which promotes the absorption of calcium and phosphorus in the intestines and kidneys. PTH also promotes the absorption of calcium in the intestine, often occurring after 4-6 hours of action. CT has the opposite effect on PTH. It inhibits osteoclast activity, reduces bone resorption, and inhibits the absorption of calcium and phosphorus by the renal tubules. It also inhibits the activity of la-hydroxylase in the kidney.

Early changes in hypercalcemia are impaired renal concentrating function. Calcium is an orange antagonist of cAMP. Hypercalcemia can reduce the effect of ADH in the collecting duct and hinder the binding of ADH to the receptor, thereby interfering with the normal effect of ADH. Hypercalcemia also reduces renal blood flow and glomerular filtration rate. After 48 hours of hypercalcemia, ultrastructural changes of the kidney can be seen, and Henry ascending branch, distal renal tubule, collecting tube edema, basement membrane calcification, epithelial necrosis and so on. Renal tubular fibrosis occurs in the late stage.

an examination

Related inspection

Parathyroid hormone (PTH) parathyroid hormone calcitonin serum chromium (Cr) parathyroid imaging

(1) Medical history:

You should be aware of the history of primary hyperparathyroidism, such as recurrent renal colic, hematuria, systemic bone pain, and pathological fractures. There is no family history of hypercalcemia. The kidney is quite sensitive to hypercalcemia, and renal dysfunction is associated with many clinical manifestations of hypercalcemia. Patients with malignant tumors should pay attention to the presence or absence of hypercalcemia.

(2) Physical examination:

In addition to the signs of the primary disease, the main signs of hypercalcemia are mood changes, depression, increased reflexes, decreased pain, weakness of the proximal muscles, and gait instability. In addition, attention should be paid to the symptoms of impaired renal function and changes in cardiac function.

(3) Laboratory inspection:

1. Determination of serum calcium:

Multiple determinations of serum calcium exceeded 2.75 mmol / L. UL$ calciumemia can be established. The effect of serum albumin on serum total calcium should be corrected. Serum albumin increased or decreased by 10 g/L, serum calcium increased or decreased by 0.2 mmol / L, and serum ionized calcium was not affected by this.

2. Serum phosphorus determination:

Serum phosphorus is reduced in patients with primary hyperparathyroidism, but blood phosphorus can be elevated with renal insufficiency.

3. Serum PTH determination:

The majority of patients with primary hyperparathyroidism have elevated serum PTH and serum calcium. Serum PTH is also elevated in some patients with malignant tumors and hypercalcemia.

(four) device inspection

1. X-ray inspection:

Patients with hyperparathyroidism often show bone decalcification, renal calcium deposition, and multiple urinary calculi. Malignant tumors can be seen in bone metastases, and multiple myeloma can be seen with multiple rounded bone defects.

2. ECG check:

The QT interval was shortened in patients with hypercalcemia, and the T wave was low and the P-Q interval was prolonged.

Differential diagnosis

1. Symptoms are more important than absolute calcium levels.

2. The blood calcium measurement value of the laboratory must be corrected according to the serum albumin level [calcium calcium correction value = blood calcium measured value + 0.02 × (40 - serum albumin concentration) mmol / L; blood calcium correction value = blood calcium measured Value +0.8X (4-serum albumin concentration) mg/dl].

3. It is necessary to pay close attention to the state of the volume and renal function, and consider other factors other than the primary malignant tumor that cause high calcium.

4. False hypercalcemia is rare:

(1) The calcium of the star has combined with the plasma protein of non-albumin, resulting in an increase in total serum calcium.

(2) The increase in "M" protein found in MM and MGUS.

(3) Plasma ionized calcium is normal, and the abnormal formula is obtained by calculating the correction formula of albumin.

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