Hypoparathyroidism

Introduction Hypoparathyroidism (endocrine) is caused by a lack of synthetic or secreted parathyroid hormone (PTH), or a biologically inactive PTH in the blood circulation, or a PTH target organ insensitivity. It is clinically characterized by clinical syndrome characterized by hand, foot and sputum, ectopic calcification, hypocalcemia, hyperphosphatemia, and reduction of urinary calcium and urinary phosphorus excretion. Long-term application of calcium preparations and vitamin D preparations can control the condition. Diagnosis The symptoms and signs of hypoparathyroidism are extensive and variable, and are easily misdiagnosed.

Cause

(A), parathyroid hypoplasia

Congenital parathyroid hypoplasia can cause parathyroidism, which occurs in neonates. A parathyroidism can occur singly, and there can be immunodeficiencies and congenital heart abnormalities of congenital thymus atrophy.

(B), parathyroid injury

More common in thyroid cancer radical or hyperparathyroidism after multiple operations, resection or damage to the parathyroid tissue, affecting the parathyroid blood supply. If due to surgical bleeding, edema, insufficient blood supply or nerve damage, its function can be gradually restored, called temporary hypoparathyroidism. If the gland is gradually fibrotic and the parathyroid function can be lowered, permanent parathyroidism will occur. The incidence of hypoparathyroidism caused by anterior cervical or thyroid surgery is about 0.2%-5.8%. A permanent hyperparathyroidism occurred in patients with primary hyperparathyroidism after surgery of about 0.5%. A very small number of patients have a parathyroidism after receiving radiation therapy from the neck.

(3) Metal poisoning

Such as hemochromatosis (iron), thalassemia (iron) and hepatolenticular degeneration (Wilson's disease, copper).

(D), parathyroid invasive disease

Caused by amyloidosis, tuberculosis, sarcoidosis, granuloma or tumor infiltration.

(5) Autoimmune polygland disease (APS)

Parathyroidism can be one of the symptoms of APS, and can be accompanied by Edison's disease and mucocutaneous candidiasis.

(6), parathyroid hormone secretion defects

Gene abnormalities such as calcium-sensitive receptors and parathyroid hormones lead to regulation and synthesis of PTH secretion.

(7) abnormal regulation of parathyroid hormone secretion

1. The mother is suffering from hyperparathyroidism in neonates. Neonates with hypercalcemia have hypocalcemia due to inhibition of parathyroid function, and may present with temporary or permanent hypoparathyroidism after birth.

2. The parathyroid gland remaining after surgery in patients with hyperparathyroidism has temporary hyperparathyroidism due to long-term hypercalcemia inhibition. This state rarely lasts for more than a week. Parathyroid injury is also a possible cause of a decrease in transient PTH secretion.

3. Hypomagnesemia, magnesium deficiency may have PTH synthesis and secretion disorders.

(8) Defects in the response of target tissues to the biological effects of PTH

The resistance of the target tissue to the action of PTH may be primary to pseudohypothyroidism or secondary to hypomagnesemia.

an examination

Related inspection

Serum alkaline phosphatase molybdenum target X-ray examination of plasma cyclic adenosine monophosphate Chvostek conjugated anti-thyroglobulin antibody (ATGA)

1. Idiopathic patients have a positive family history, and acquired hypothyroidism has a history of surgery or 131I treatment.

2. The clinical manifestations are weak hands and feet, Chvostek sign, Trousseau sign positive. Dry skin, pigmentation, sparse hair, shedding. The nails are crisp. cataract. Calcification of the teeth is incomplete, the tooth quality is thin, and the tooth enamel is poorly developed. Mental retardation, personality changes.

3. Low blood calcium, high blood phosphorus, serum alkaline phosphatase is normal. Urinary calcium and urinary phosphorus excretion decreased. Urinary CAMP discharge decreased.

4. Serum PTH levels are reduced. The renal tubular phosphorus reabsorption rate increased and the phosphorus clearance rate decreased.

5. X-ray examination: brain basal ganglia, renal calcification, normal bone density, and low polymorphism.

6. Hypocalcemic hand and foot such as renal tubular acidosis, hypomagnesemia, respiratory alkalosis, etc., which must be excluded for other reasons.

Differential diagnosis

At present, the rate of misdiagnosis is as high as 40%, and many misdiagnosed as epilepsy, neurasthenia, rickets, hand, foot and sputum and encephalopathy. A quick urine test for the Sulkowitch test and EKG found that low calcium can be diagnosed in time. Neonatal patients should check their mother blood calcium and phosphorus to confirm the diagnosis. It should be identified with the following diseases:

1. Renal insufficiency: may have low blood calcium, high blood phosphorus, because of acidosis, free calcium is not low, so convulsions are not common. Often there are changes in urine and renal insufficiency, there may be high blood pressure, if necessary, blood PTH is often elevated.

2. Vitamin D deficiency rickets: and severe hypocalcemia may have convulsions, but blood phosphorus is reduced, alkaline phosphatase is elevated, mostly in the spring, X-ray shows skeletal bone changes.

3. Epilepsy: EEG can be identified, when there is low blood calcium in the hypothalamic side, slow waves, spikes appear, blood calcium disappears after normal.

4. Hand and foot spasm that occurs when blood calcium is normal: There may be convulsions in the reduction of free calcium during alkalosis, or low blood magnesium, <0.6mmol/L (1.5mg/dl) may also have convulsions.

5. Rickets: blood calcium, phosphorus normal, there are incentives for emotional fluctuations.

6. porridge-like diarrhea: low calcium can cause diarrhea, atherosclerosis can also be combined with low blood calcium, but the former is treated with calcium and diced vitamins to restore blood calcium, diarrhea is also cured, can be identified.

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