Hypocalcemia

Introduction When serum calcium is less than 2 mmol/L, it is called hypocalcemia. Hypocalcemia is often caused by parathyroid dysfunction, which reduces or loses the role of normal blood calcium. More common in patients with parathyroid injury or idiopathic atrophy, but also due to thyroid surgery caused by hypoparathyroidism, accounting for about 2%. Clinical manifestations of hypoparathyroidism are often less pronounced, and clinical symptoms only occur when parathyroid function needs to be increased (eg, pregnancy, breastfeeding).

Cause

Classification of causes:

(1) Parathyroid hormone (PTH) deficiency or blocked function:

Primary or idiopathic hypoparathyroidism is rare. It is an autoimmune disease. DiGeorge syndrome is called when the thymus is not developed. If both thyroid and adrenal insufficiency are combined, multiple endocrine dysfunction is called. disease. It is more common in patients with clinical secondary hypoparathyroidism. It is common in patients with hyperthyroidism who are treated with radioactive iodine or thyroidectomy.

(2) Vitamin D deficiency or metabolic abnormalities:

1. Vitamin D deficiency: seen in food, lack of intestinal absorption, exposure to too little sunlight, multiple pregnancies, long-term breastfeeding.

2. Hydroxylation of vitamin D: seen in liver cirrhosis, renal failure, hereditary L-a hydroxylase deficiency, and the latter is a vitamin D-dependent rickets type I.

3. Vitamin D resistance: The terminal target organ is not sensitive to 1,25(OH)2D3 and is a vitamin D-dependent rickets type II.

(3) Chronic renal insufficiency.

(D) acute pancreatitis.

mechanism:

The daily calcium requirement is 0.5 ~ 1 g. The calcium content is increased in children, pregnancy and lactation. The calcium intake is mainly absorbed in the upper part of the duodenum and jejunum. The factors determining calcium absorption are vitamin D and the body. The amount of calcium required. The absorbed vitamin D is inactive, and it needs to be activated by hydroxylation of the liver and kidney to 1,25(H)2?D3. Active 1,25(OH)2D3 can promote the absorption of calcium and phosphorus, regulate calcium and phosphorus metabolism and bone metabolism. PTH has an important regulatory effect on calcium and phosphorus metabolism. The secretion of PTH is mainly regulated by feedback of serum Ca2+ levels. The basic function of PTH is to mobilize bone calcium, promote intestinal absorption of calcium, excrete urinary phosphorus, maintain blood calcium levels, and promote renal transformation 25 (OH) D3 to 1.25 (OH) 2? D3, promote renal tubular to calcium back absorb. Therefore, hypoparathyroidism, vitamin D deficiency or metabolic abnormalities can cause hypocalcemia.

The incidence of hypocalcemia in chronic renal failure is mainly related to decreased glomerular filtration rate, blocked phosphate discharge, leading to elevated blood phosphorus; hydroxylation of vitamin D in renal tubules; decreased absorption of calcium by the intestine; The sensitivity of PTH is reduced, and the mechanism of bone calcium mobilization into the blood is blocked. In acute pancreatitis, due to inflammation and necrosis of the pancreas, the fatty acids released combine with calcium to form calcium soap; and pancreatitis can cause excessive secretion of glucagon, which stimulates the increase of calcitonin secretion, which is associated with hypocalcemia. related.

an examination

(1) medical history

Should pay attention to the presence or absence of chronic renal insufficiency, hyperthyroidism after surgery or radiation therapy, other thyroid and neck surgery, liver disease, intestinal malabsorption, inadequate intake, lack of light, multiple pregnancy, long-term breastfeeding history. Long-term use of anti-epileptic drugs (such as epilepsy, phenytoin, phenobarbital, carbamazepine) or protamine, heparin, repeated infusion of sodium-containing sodium can cause hypocalcemia. In addition, you should ask about the history of hand and foot episodes and paresthesia, as well as bone calcification disorders.

(2) Physical examination

Increased neuromuscular excitability during hypocalcemia, may occur in hand and foot convulsions, tendons, throat, convulsions, as well as irritability, emotional instability, hallucinations and other mental symptoms. Patients with hypocalcemia can show positive signs of Chvostek and Trousseau, but about one-third of patients can be negative. Hypocalcemia with calcium deficiency in the body can cause bone calcification disorders. Children can develop rickets, hysteresis, skeletal deformities, and can be characterized by osteomalacia, fibrotic osteitis, and osteoporosis. Neonatal hypocalcemia can be complicated by heart failure.

(3) Laboratory inspection

1. Determination of blood calcium: serum protein concentration is normal, serum calcium <2.2mmol / L (8.5mg / dl), called hypocalcemia.

2. Determination of serum phosphorus: increased serum phosphorus and decreased blood calcium due to acute or chronic renal failure or idiopathic, pseudohypoparathyroidism, and hypocalcemia with decreased serum phosphorus is more common in malabsorption, vitamin D Lack of polyuria in acute pancreatitis and acute renal failure.

3. Urine phosphorus determination: low blood calcium and increased urinary phosphorus are more common in vitamin D deficiency, malabsorption, etc., urinary phosphorus reduction is mostly idiopathic or pseudohypoparathyroidism and magnesium deficiency.

4. Determination of serum PTH: elevated serum PTH is more common in vitamin D deficiency, malabsorption, acute or chronic renal failure. Pseudohypoparathyroidism, etc., serum PTH reduction is mostly idiopathic hyperparathyroidism, acute pancreatitis and magnesium deficiency. 5.25-hydroxycholecalciferol determination This normal reference value is 15-80 g/ml. 25(OH)?D3 production is reduced in hepatobiliary diseases, the main biochemical characteristic of vitamin D deficiency rickets is plasma 25(OH)?D3 deficiency, and 25(OH)D3 in blood of patients with pseudovitamin D deficiency The concentration is normal.

(four) device inspection

1. Electrocardiogram examination: hypocalcemia electrocardiogram showed prolonged QT time, ST segment lengthening, T wave low level or inverted.

2. CT scan and X-ray examination: no special findings, occasionally thick bone plate thickening. For example, it shows that cerebral calcification and basal calcification are mostly idiopathic or pseudohypoparathyroidism.

Differential diagnosis

The total calcium concentration at the time of diagnosis of hypocalcemia must be the corrected calcium concentration after serum albumin correction, and the free calcium concentration can be determined if necessary.

Corrected calcium concentration (mg/dl) = total calcium (mg/dl) - 0.8 x [4.0 - serum albumin concentration (g/dl)].

According to medical history, physical examination and laboratory tests (such as blood phosphorus, PTH, liver and kidney function, albumin, etc.), the cause of the disease can often be clarified. For example, most patients with low calcium, high phosphorus and normal renal function often have primary or secondary hypoparathyroidism; the parathyroid gland should be suspected in the history of neck surgery; magnesium content, nutritional status, massive blood transfusion Chemotherapy, acute pancreatitis, gastrointestinal lesions, medication history, vitamin D deficiency, and other endocrine abnormalities are helpful for diagnosis. Skeletal radiographs can understand the nature and extent of bone disease, and can also determine whether there is a metastatic tumor.

1. Hypocalcemia refers to serum ionized calcium concentrations below normal or serum total calcium below 2.1 mmol/L. Note that ionized calcium is inconsistent with serum total calcium in both pathological conditions: hypoproteinemia and acidosis.

2. The body has a huge bone calcium reservoir and dietary calcium intake, usually without hypocalcemia. When low calcium is found clinically, the two major calcium-lowering hormones should be used to find the cause, namely parathyroid hormone deficiency and vitamin D deficiency or hydroxylation disorders. Pay attention to several special cases unrelated to hormone deficiency: acute pancreatitis, fluorosis, massive input of citrate anticoagulation, alkalosis, osteogenic bone metastasis, Gram-negative sepsis and toxic shock.

3. Long-term seizures may be caused by hypocalcemia, in which symptomatic epilepsy is completely relieved after low calcium correction. If epilepsy still has seizures, consider the long-term low calcium-induced intracerebral calcification, and further reasons should be sought.

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