What Is Hypoparathyroidism?

Parathyroid glands are mostly endocrine glands located behind the thyroid lateral lobe in the front of the human neck. About 80% of people have 4 parathyroid glands. The hormone secreted by the parathyroid glands is parathyroid hormone, which mainly regulates calcium Phosphorus metabolism and bone metabolism. Hypoparathyroidism is referred to as hypoparathyroidism. Parathyroid hormone (PTH) is reduced or defective due to various reasons. Hypocalcemia and hyperphosphatemia are the main laboratory abnormalities. The patient's performance is abnormal. For repeated tremors and seizures, calcium and vitamin D preparations have been taken orally for a long time to control the condition.

Basic Information

Visiting department
Endocrinology
Common locations
Parathyroid glands
Common causes
Insufficient parathyroid hormone secretion, inactive parathyroid hormone, parathyroid hormone resistance-pseudoparathyroidism
Common symptoms
Numbness and tingling of fingertips or mouth, muscle cramps, etc.
Contagious
no

Causes of hypoparathyroidism

1. hypoparathyroidism
Congenital hypoparathyroidism can cause hypoparathyroidism, which develops in newborns. Parathyroidism may occur singly, or there may be immunodeficiency and congenital heart abnormalities with congenital thymus atrophy.
2. Parathyroid Gland Injury
More common in radical thyroid cancer or hyperparathyroidism after multiple surgery, resection or damage to the parathyroid tissue, affecting the parathyroid blood supply. There are two cases of temporary and permanent parathyroidism. The incidence of parathyroidism caused by anterior cervical or thyroid surgery is about 0.2% to 5.8%. Patients with primary hyperparathyroidism have a permanent parathyroidism reduction of about 0.5% after surgery. Very few cases are due to hypoparathyroidism following cervical radiation therapy.
3. Metal poisoning
Such as hemochromatosis (iron), thalassemia (iron) and hepatolenticular degeneration (Wilson's disease, copper), etc.
4. Parathyroid Infiltrative Diseases
Such as amyloidosis, tuberculosis, sarcoidosis, granulomas or tumor infiltration.
5. Autoimmune polyglandular disease
Such as familial endocrine lesions-hypoparathyroidism, Addison's disease and mucosal skin candidiasis syndrome.
6. Parathyroid hormone secretion defects
Gene abnormalities such as calcium-sensitive receptors and parathyroid hormones cause disorders in the regulation and synthesis of PTH secretion.
7. Abnormal regulation of parathyroid hormone secretion
(1) The mother has a newborn with hyperparathyroidism;
(2) Patients with hyperparathyroidism after surgery;
(3) Hypomagnesemia.
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 can be primary to hypoparathyroidism or secondary to hypomagnesemia.

Clinical manifestations of hypoparathyroidism

1. Increased neuromuscular stress
In the early stage, there are numbness, tingling, and ants walking. In severe cases, the hands and feet are convulsed, and even the whole body muscles contract and there is a seizure. Symptoms often occur when the serum free calcium concentration is 0.95mmol / L (3.8mg / dl), or the total blood calcium value is 1.88mmol / L (7.5mg / dl). May also be accompanied by dysfunction of autonomic nerves, such as sweating, glottic spasm, tracheal and respiratory muscle spasm, and bile, bowel and bladder smooth muscle spasm. Signs were positive for facial nerve tapping (Chvostek sign) and positive for beam compression test (Trousseau sign).
2. Nervous system performance
Seizures are classified into major, minor, psychomotor and seizure states. Accompanied by increased muscle tone and trembling hands. Mental symptoms include excitement, anxiety, fear, irritability, euphoria, depression, memory loss, delusions, hallucinations, and delirium. About 15% of the cases have mental decline, about 5% see optic nipple edema, occasionally increased intracranial pressure, electroencephalogram shows general rhythmic slow waves, explosive slow waves, and sharp waves, spikes, and epileptiform discharge changes.
3. Vegetative degeneration of ectoderm tissue
Such as low-calcium cataracts, delayed teething, hypoplasia of teeth, shortened molar roots, more caries, even missing teeth, hyperkeratosis, brittle nails, roughness and cracks, and hair loss.
4. Bone changes
Long-term and severe illness may have bone pain, more common in the lower back and hip. Bone density is normal or increased.
5. Gastrointestinal dysfunction
Nausea, vomiting, abdominal pain and constipation.
6. Cardiovascular abnormalities
Hypocalcium stimulation of the vagus nerve can lead to myocardial spasm and sudden death. The patient's heart rate increased or arrhythmia. The ECG showed that the QT interval was prolonged. Severe patients may have hypoparathyroidism cardiomyopathy and heart failure.
7. Metastatic calcification
More common in the basal ganglia of the brain (pale bulb, putamen and caudate nucleus), often distributed symmetrically. The positive rate of brain CT examination is high, about 50%. In severe cases, scattered calcifications can also be seen in the brain parenchyma of the cerebellum, dentate nucleus, frontal and parietal lobes of the brain. Calcification can occur in other soft tissues, tendons, and paraspinal ligaments.
8. Special manifestations of pseudoparathyroidism
Typical patients often have the so-called AHO body shape (short stature, overweight body, round face, short neck, shield-shaped chest), deformities of the fingers and phalanges (mostly the 4th and 5th metacarpals or metatarsals). Soft tissue calcification and ossification are more common than secondary and idiopathic parathyroidism.

Examination of hypoparathyroidism

Blood calcium
The blood calcium level is 2.13mmol / L (8.5mg / dl). For those who have obvious symptoms, the total blood calcium value is generally 1.88mmol / L (7.5mg / dl), and the free blood calcium is 0.95mmol / L (3.8mg / dl).
Blood phosphorus
Most patients increased, and some patients were normal.
3.24 hour urine calcium and phosphorus discharge
Urinary calcium excretion is reduced. Phosphorus reabsorption in the renal tubules increased, and urinary phosphorus output decreased. Some patients were normal.
4. Blood alkaline phosphatase
normal.
5. Blood PTH
Most of them are lower than normal, and they can also be in the normal range. Hypocalcemia is a strong stimulus to the parathyroid glands. When the total blood calcium value is 1.88mmol / L (7.5mg / dl), the blood PTH value should be 5 10-fold increase, so when hypocalcemia, such as blood PTH levels in the normal range, is still hypoparathyroidism, so blood PTH should be measured at the same time, both analysis. Patients with pseudohypoparathyroidism have elevated blood PTH levels. Although patients with primary hyperparathyroidism and sporadic hyperparathyroidism have elevated blood PTH, they also have high calcium and hypophosphatemia.

Treatment of hypoparathyroidism

Early diagnosis and timely treatment should be performed. The goal of treatment is to control the condition and relieve symptoms. Serum calcium is corrected to the normal low limit or close to normal. Urine calcium output is maintained at normal levels. Infants <1.0mmol / 24h (40mg / 24h). Children <0.1 0.15mmol / kg / 24h (4 6mg / kg / 24h), adult 2.5 7.5mmol / 24h (100 300mg / 24h).
1. Application of calcium and vitamin D and their derivatives
This classic treatment plan will also be the main treatment for a long time to come. The therapeutic dose of vitamin D and its derivatives varies from person to person, and individual differences are large, and a treatment plan needs to be formulated as appropriate. When taking calcium and vitamin D preparations, the drug dose should be adjusted for blood calcium and phosphorus levels and urinary calcium excretion. Insufficient treatment will still have complications such as hand-foot convulsions and basal ganglion calcification. Risk of urinary stones. When the blood calcium has not reached the target value and the 24-hour urine calcium has been> 8.75 mmol (350 mg), the addition of dihydrogram urine urine and potassium salts (such as potassium citrate) may be considered to promote the renal tubule's renal tubules for calcium. Reabsorption. Closely monitor blood calcium and phosphorus and 24-hour urine calcium. Pseudoparathyroidism is relatively easy to treat, its blood calcium is more easily corrected and it is less prone to hyperuricemia.
(1) Calcium should be taken orally for a long time. Calcium gluconate, calcium lactate, calcium chloride and calcium carbonate contain elemental calcium 9.3%, 13%, 27% and 40%, respectively. In a few cases, calcium alone can correct hypocalcemia. Taking calcium with meals can help lower blood phosphorus.
(2) Vitamin D and its derivatives Vitamin D 2 or D 3 , individual patients need larger doses. Dihydrotachysterol DHT or AT10 is generally started from a small amount and taken once, and the blood and urine calcium are monitored weekly, and the dose is adjusted as appropriate. Calcitriol (1,25 (OH) 2 D 3 , that is calcitriol). Alfacalcidol (1 (OH) D 3 ) is suitable for patients with normal liver function, and it is taken orally in three times. The therapeutic dose is about 1.6 to 2 times of calcitriol.
2. Parathyroid hormone replacement therapy
In theory, it should be the most ideal treatment for parathyroidism. Human PTH preparations with genetic recombination have been marketed, but currently they are mostly used for osteoporosis treatment. A number of clinical trials suggest that PTH1-34 subcutaneous injection treatment can better achieve the normal range of blood calcium and reduce the occurrence of high urine calcium than traditional calcium supplement and vitamin D treatment, so it can reduce kidney stones and renal insufficiency. Incidence. However, due to its high price and insufficient safety evidence for long-term use, the FDA has not yet approved PTH for children and adults under 24 years of age. Even in adults, the indications for PTH for hypoparathyroidism have not yet been approved by the FDA.
3. Parathyroid Gland Transplant
There are still many problems such as donor source and rejection, so it is still in the research and has not been applied to clinical treatment.

Prognosis of hypoparathyroidism

The prognosis of secondary hypoparathyroidism is closely related to the primary disease. For idiopathic hypoparathyroidism and pseudoparathyroidism, the combined application of calcium and vitamin D can completely control the disease, so the focus of determining the prognosis is whether it can get the correct early diagnosis and reasonable treatment. This not only means eliminating hypocalcemia-related tetany and neurological symptoms, but also preventing and preventing the occurrence and progression of hypocalcic cataracts and basal ganglia calcification.

Prevention of hypoparathyroidism

High-level neck surgery is an important factor in reducing secondary hypoparathyroidism in neck surgery. Controlling the mother's blood calcium level can reduce parathyroidism in the newborn. [1-3]

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