hypoparathyroidism
Introduction
Introduction to hypoparathyroidism Hypoparathyroidism (hypoparathyroidism) is a clinical syndrome of reduced and/or dysfunction of parathyroid hormone (PTH), a major clinically common form of hypoparathyroidism. There are idiopathic hypoparathyroidism, secondary hypoparathyroidism, hypomagnesemia and hypoparathyroidism and neonatal hyperparathyroidism. Other rare cases include pseudohypothyroidism, pseudo-false parathyroidism, and pseudo-speciality. Hair loss, etc. basic knowledge The proportion of illness: 0.0003% Susceptible people: no special people Mode of infection: non-infectious Complications: epilepsy neurosis cataract
Cause
Cause of hypoparathyroidism
(1) Causes of the disease
1. Insufficient secretion of PTH
(1) Surgical parathyroidism: any neck surgery, including thyroid, parathyroid or neck malignant tumor resection, can be caused by insufficient resection of the parathyroid gland, injury or blood supply, resulting in insufficient PTH production. Postoperative hypoparathyroidism, the incidence of which varies depending on the scope of surgery, time and the surgeon's technical experience, mostly temporary hypoparathyroidism, from days to weeks or even months after surgery, postoperative permanent Reduction of parathyroidism, most reports are <1%, individual reports are higher, the highest group in the literature is 33%, excessive parathyroid hyperplasia or re-neck surgery, permanent hypoparathyroidism The risk is higher, a parathyroidism can occur after treatment of hyperthyroidism with radioactive 131I, but very rare after treatment of thyroid cancer, and only occurs in the parathyroid gland thyroid tissue, because of 131I radiation of beta rays The range is only 2mm, and the parathyroidism is more than 5 to 18 months after radiation therapy.
(2) idiopathic hypoparathyroidism: idiopathic parathyroidism can be divided into familial and sporadic according to the mode of onset, and there are early onset and late onset according to the age of onset, among which sporadic and delayed onset is more common. The cause of glandular destruction is still unclear. Most patients have only a parathyroid gland atrophy. A few patients have autoimmune polyadenotrophic endocrine diseases. Early-onset patients are mostly familial, and the genetic pattern is still unknown. Most people think that it is common. Chromosomal recessive inheritance, histologically showing parathyroid atrophy and being replaced by adipose tissue; some patients can detect autoantibodies against parathyroid surface antigenic determinants, as well as anti-endothelial cell antibodies, which may be late or Early onset of adrenal gland, thyroid gland, gonads, islets and other glandular autoimmune endocrine insufficiency and pernicious anemia, and often occur in chronic skin mucosal candidiasis.
(3) Functional hypoparathyroidism: The following conditions may cause a reversible decline in the synthesis and/or release of PTH.
1 Magnesium metabolism abnormalities: magnesium deficiency can be seen in chronic alcoholism, malabsorption syndrome, selective gastrointestinal magnesium absorption defects, aminoglycoside antibiotics (magnesium renal clearance increased), long-term intravenous high nutrition and diuretics and In the case of platinum treatment, the release (not synthesis) of PTH in the absence of magnesium is inhibited, and the peripheral tissues may be resistant to PTH, and thus may be associated with hypocalcemia. Conversely, some authors have found that magnesium is found. Too high may also inhibit the secretion of PTH and cause hypocalcemia. For example, after intravenous magnesium injection in patients with gestational toxicosis, hypocalcemia may occur at the same time as hypermagnesemia.
2 pregnant women with hypercalcemia, the fetal parathyroid gland is inhibited by long-term hypercalcemia, which can cause a transient hyperparathyroidism in the newborn, which usually returns to normal within 1 week.
3 patients with parathyroid adenoma, the normal parathyroid gland due to inhibition of hypercalcemia, after the removal of adenoma may have temporary hypoparathyroidism.
4 hypercalcemia of non-parathyroidism, its parathyroid gland is also functionally inhibited, once the parathyroid gland and hypercalcemia are temporarily inhibited, such as the use of pucamycin (paicamycin) for the treatment of malignant tumors Hypercalcemia, blood calcium often suddenly decreases.
(4) Insufficient secretion of PTH caused by other causes:
1 Parathyroid metastases can cause damage to the parathyroid glands. Autopsy found that up to 12% of malignant tumors occur in parathyroid metastases. The most common primary tumor is breast cancer.
2 drug parathyroidism: tumor chemotherapy, especially with doxorubicin hydrochloride and cytarabine can reduce the secretion of PTH, there are cases reported in the literature, the use of propylthiouracil to treat hyperthyroidism, in the occurrence of granulocytosis At the same time as the rash, PTH reduction and hypocalcemia can also occur.
3 congenital thymus is not developed (Digeorgc disease): Some authors have classified it as one of the causes of idiopathic hypoparathyroidism, the disease is due to congenital third and IV sac developmental disorders, leading to thymus and parathyroid The gland is absent, mostly due to severe hypocalcemia and/or infection within 1 to 2 years of age.
4 iron deposition, such as hemochromatosis and excessive blood transfusion, in addition to causing dysfunction of the gonads and islet cells, parathyroid gland can also occur invasive destruction.
5 Hepatolenticular degeneration (Wilson's disease): due to the extensive deposition of copper, it can also infiltrate the parathyroid gland and cause its function to decline.
2. Bioactive PTH According to the literature, hypocalcemia may also feedback excitatory parathyroid glands to secrete non-biologically active PTH. In the literature, hypothyroidism caused by FSH caused by familial gene mutation However, only one family has been initially proven to have a genetic defect in PTH.
3. PTH resistance - pseudo-parathyroidism.
(two) pathogenesis
Insufficient PTH production and secretion cause hypocalcemia, hyperphosphatemia, decreased urinary calcium and phosphorus emissions, insufficient PTH, weakened osteoclastism, reduced bone calcium mobilization and release, and insufficient PTH to reduce 1,25-(OH)2D3 production At the same time, renal phosphorus is reduced, blood phosphorus is increased, and the production of 1,25-(OH)2D3 is reduced, intestinal calcium absorption is decreased, renal tubular reabsorption of calcium is reduced, and hypocalcemia is caused by multiple pathways above, due to low Blood calcium, urinary calcium discharge decreased, PTH is insufficient, renal tubular reabsorption of phosphorus increased, so blood phosphorus increased, urinary phosphorus decreased, hypocalcemia and alkalosis reached a certain degree, neuromuscular excitability increased, appearing The hands and feet are weak, and the longer course is often accompanied by optic disc edema, increased intracranial pressure, rough skin, cracked nails, sparse hair and abnormal ECG.
Prevention
Hypoparathyroidism prevention
The prevention of this disease is mainly in the thyroid surgery, to avoid injury or mistaken resection of the parathyroid gland; in the parathyroid surgery, the diagnosis of parathyroid lesions must be reliable, well-defined, familiar with the anatomy of the parathyroid gland before surgery, detailed and Probing and performing surgical procedures to avoid excessive or total removal of the parathyroid glands. After the diagnosis of hypothyroidism, vitamin D preparation and calcium supplementation should be applied in time to correct hypocalcemia to relieve symptoms and prevent complications of hypocalcemia.
Complication
Parathyroid hypofunction complications Complications epileptic neuropathy cataract
Psychiatric performance
The mild cases are rickets-like episodes, and the severe cases are severe psychosis. These patients are often misdiagnosed and sent to psychiatric hospitals for treatment. In order to prevent such misdiagnosis, mental patients should routinely check blood calcium and blood phosphorus, since blood biochemical automatic analyzer Since the application, it has been very easy to routinely check blood calcium and blood phosphorus. It is very important to improve the understanding of this disease. Pay attention to the occurrence of hand, foot and ankle in the process of observing patients. If you find hand, foot and foot, you should check blood calcium immediately. Prove that hand, foot and ankle are caused by hypocalcemia, and slowly intravenously or instilled with calcium and glucose. Calcium treatment can quickly relieve hand, foot and sputum, this "hand and foot sputum - hypocalcemia - calcium treatment - relief Sequential observation is important for understanding the presence of hypocalcemia and further obtaining a correct diagnosis by hypoparathyroidism.
2. Epileptic seizures and other neurological symptoms
In addition to observing hypocalcemia and its clinical manifestations, X-ray or CT examination of brain calcification lesions is helpful for diagnosis.
3. Chronic hand, foot and ankle
If it occurs in children, it should be checked whether the skin is dry, desquamation, abnormal nails, rough hair, and should further check the occurrence, development and pathology of the teeth, combined with chronic hypocalcemia, can be diagnosed and treated early.
4. Poor eyesight
Cataracts should be checked for cataracts, and cataracts are irreversible, and early treatment can stop their development.
5. A parathyroid heart disease
In severe cases, heart failure can occur and death, so to be vigilant, ECG can be used as a preliminary examination method, non-invasive cardiac function test, or color Doppler heart function test can provide more detailed cardiac function.
Symptom
Symptoms of hypoparathyroidism Common symptoms Diarrhea, abdominal distension, abdominal pain, depression, libido, dry skin, tachycardia, constipation, swallowing, limb convulsions
Post-operative hypoparathyroidism can occur in the short-term after surgery, but also after the first episode 30 years, which is related to the local damage caused by surgery, blood flow disorder and the degree of parathyroid loss, whether it is post-operative hypothyroidism or special A parathyroidism can be subclinical for a long period of time, that is, it does not show symptoms, but symptoms appear under certain incentives, such as after menstruation, after infection, high fever, fatigue, cold and mood changes, etc. As a cause, it induces hand and foot spasms.
Hand, foot and ankle
Onset, numbness of the hands and feet, muscle pain, wrist flexion, metacarpophalangeal joint flexion, interphalangeal joint straightening, thumb straight, adduction, oblique across the palm, slamming muscles may cause muscle contraction, throat is the most Dangerous conditions, resulting in hypoxia, suffocation, and even death, visceral muscle function abnormalities often cause biliary colic or diarrhea.
Hand, foot and ankle are caused by increased neuromuscular excitability due to hypocalcemia. When the hand and foot are not attacking, the following methods can be used to induce an increase in neuromuscular excitability and induce hand and foot spasm.
(1) Chvostek sign: use the percussion sputum or finger to slap the facial nerve, the position is 2 to 3 cm in front of the ear, causing the mouth twitching to be a positive reaction, the mouth twitching is divided into 1 to 4, 1 is only detectable mouth twitching, 2 is Obvious mouth twitching, 3 is slightly twitching on the facial muscles, 4 is obvious convulsions on the facial muscles, about 10% of healthy people have a positive reaction, so careful observation of the intensity of the reaction, combined with medical history and blood calcium levels are important for diagnosis. .
(2) Trousseau sign: the method of measuring the blood pressure is the same as that of measuring the blood pressure. The inflation is pressurized to 2.67 kPa above the systolic pressure. Most of the requirements are for 3 minutes, and the requirement is 5 minutes. If the athlete's foot is induced, it is positive. The Trousseau sign is positive because the inflatable arm band causes ischemia and excitatory nerves in the compression, rather than due to forearm ischemia. This can be proved by the use of a double-armed belt test and is helpful for diagnosis. The method is to make the inflatable arm band. The test was as described above, and the positive reaction was immediately placed on the arm of the first inflatable arm band with another inflatable arm band, inflated, and the first inflatable arm band was immediately deflated, and the hand, foot and ankle disappeared, after a few minutes. Another occurrence, the double-armed belt test is used to test the method of camouflage the hand and foot squats. The scammers generally do not show the positive-negative-positive reaction procedure of the arms test, and the healthy person does not have the Trousseau sign positive.
(3) Erb sign: less than 6 mA cathode current, can cause - the motor nerve reaction is positive.
The above three methods are used to detect occult hand and foot sputum and induce it to assist in diagnosis.
2. Eye performance
The most common eye manifestation is cataract, which is due to lens calcification. Even after treatment, hypocalcemia is improved, cataract is difficult to disappear. Patients with hypoparathyroidism have hypocalcemia but soft tissue calcification may occur. This may be due to hyperphosphatemia. For the sake of the disease, fundus examination may have papilledema and pseudo-brain tumors.
3. Neuropathy
(1) epileptic seizures: hypocalcemia causes increased neuromuscular excitability, and may have paroxysmal extremity twitching or convulsions on one side of the limbs, screaming before the attack, and the like, but the symptoms of epileptic seizures Loss, cyanosis or urinary incontinence, etc., are not effective with antiepileptic drugs.
(2) rickets-like episodes: often after the work is tense, there is a rickety-like episode, which is characterized by twitching of the mouth, limbs twitching, and dance-like movements.
(3) neurasthenia syndrome; may have dizziness, headache, shallow sleep, insomnia, multiple dreams, fatigue, memory loss, hi quiet, lack of interest in all things, loss of libido, depression, irritability and other symptoms of nervous failure.
(4) peripheral nerves and muscle symptoms; feelings of hyposensitivity or allergies, numbness around the mouth, soreness of the limbs, numbness, pain, tendon and so on.
(5) autonomic symptoms; intestinal fistula, accelerated peristalsis, abdominal pain, abdominal distension, diarrhea, constipation, difficulty swallowing, arrhythmia, tachycardia.
(6) Central nervous system: extrapyramidal symptoms due to calcification of brain tissue, such as involuntary movement, movement of hands and feet, twisting of convulsions, tremors, cerebellar ataxia, gait instability.
(7) Psychiatric-like manifestations: irritations due to hypocalcemia, depression, fanaticism, and even severe severe psychosis. EEG is abnormal, but not specific. The most common ones are high-voltage slow waves. Frequent rapid development, EEG correction after blood calcium correction is also normal, children's poor academic performance is also a manifestation.
(8) Heart: If hypotension occurs, it is ineffective by using a booster drug or a common method such as increasing blood volume. When the calcium is used, the blood pressure is restored. The typical electrocardiogram is the extension of the ST segment and the QT interval is prolonged, and the QRS interval is extended. There is no change, and the T wave can have non-specific changes.
(9) Large cell anemia: large cell anemia can occur in patients with hypoparathyroidism, and the Schilling test is not normal. The reason is that B12 is poorly bound to internal factors in hypocalcemia, so there is a lack of B12, and there are groups. Amine-resistant gastric acid deficiency, the above situation can be improved after serum calcium is normal.
4. Other
(1) Skin: dry skin, desquamation, thick and brittle nails and hair, scarce eyebrows, oral mucosa Candida albicans infection can be seen in idiopathic hyperparathyroidism, generally not seen after surgery.
(2) Tooth: abnormal tooth is common. The earlier the onset is, the more obvious the symptoms and signs are. The tooth development is poor, the tooth root formation is defective, the tooth enamel hyperplasia is poor, and there are bands or caves around the crown and crown. , or the permanent teeth do not grow out, the detection of abnormal teeth can help estimate the time of onset.
(3) soft tissue calcification: calcium deposition around the joint is also common, cartilage also see calcification, localized stimulation of calcified tissue can be expressed as pseudogout.
(4) diarrhea and poor fat absorption: also seen in the parathyroidism, after treatment to improve the symptoms of hypocalcemia improved.
Symptoms and signs of hypothyroidism are extensive and variable, so it is easy to be misdiagnosed. There are many types of parathyroidism and pseudohypothyroidism. In order to confirm the diagnosis, the etiology and pathology should be further identified.
Examine
Examination of hypoparathyroidism
1. Blood calcium reduction and blood phosphorus increase
Insufficient PTH can weaken the role of osteoclasts, reduce bone calcium mobilization, and reduce the production of 1,25-(OH)2D3 and the reabsorption of calcium by renal tubules and the reduction of phosphorus excretion. High blood phosphorus, only a small number of oral antacids or blood phosphorus in the diet can be normal.
2. Urinary calcium and urinary phosphorus reduction
The reduction of urinary calcium caused by parathyroidism is less than the reduction of urinary calcium in rickets, because the former is secondary to lowering blood calcium, while the latter's blood PTH is mostly increased, which can promote renal tubular reabsorption of calcium. PTH can inhibit the reabsorption of phosphorus by renal tubules, so the reabsorption of urinary phosphorus increases and the phosphorus excretion decreases when PTH is insufficient.
3. Determination of PTH in blood
Most of the clinical hypothyroidism due to PTH deficiency, blood PTH is lower than normal, but some patients can also be in the normal range, because non-parathyroidism hypocalcemia has a strong stimulating effect on the parathyroid gland, which is low There is a significant negative correlation between blood calcium and PTH in the blood. Therefore, even if the PTH in the blood is in the normal range, it indicates that the parathyroid gland is dysfunctional. However, the parathyroid glands secrete non-bioactive PTH and PTH. When the hypothyroidism caused by resistance, PTH has a compensatory increase in secretion, the former can measure the increase of iPTH, the latter can measure the increase of biologically active PTH.
4. Reduced cAMP in urine
CAMP in the urine is a functional indicator of PTH. Therefore, the cAMP in the urine of patients with hypoparathyroidism is mostly lower than normal.
5. Normal alkaline phosphatase in the blood
ALP is elevated in patients with hyperparathyroidism with serum alkaline phosphatase (ALP), and ALP in patients with low parathyroid is normal.
6. ECG shows ST segment extension, QT interval extension and T wave change.
7. Imaging examination
About 20% of the skull X-ray shows basal ganglia calcification, and a few patients still have pineal and choroid plexus calcification; CT scan is more sensitive than X-ray, and can detect intracranial calcification earlier and more.
Diagnosis
Diagnosis and differentiation of hypoparathyroidism
Diagnostic criteria
Diagnosis The symptoms and signs of hypoparathyroidism are extensive, variable, and easily misdiagnosed.
1. Hypocalcemia caused by hypoparathyroidism can cause increased neuro-muscle excitability, may have paroxysmal limb convulsions or convulsions on one side of the limbs, screaming and other symptoms before the attack, easily misdiagnosed as epilepsy, need to be Clinically, observe the loss of consciousness, cyanosis or urinary incontinence, etc., if there is no clinical manifestation of these epileptic seizures, should be alert to the possibility of hypoparathyroidism, routinely check blood calcium and Blood phosphorus, if the patient has hand and foot convulsions, blood calcium should be measured immediately to determine whether hand and foot convulsions are caused by hypocalcemia. If calcium or glucose is added slowly by intravenous injection or infusion, the rapid relief of hand and foot convulsions is extremely Help, if necessary, determine parathyroid hormone (PTH).
2. Due to hypocalcemia, irritability, depression, fanaticism, and even severe manifestations of severe psychosis, EEG can be abnormal, the most common is high voltage slow wave and intermittent speed Hair, easy to be misdiagnosed as a mental illness, in order to avoid this misdiagnosis, mental patients should routinely check blood calcium and blood phosphorus, if the EEG is abnormal but not specific, or after the hypocalcemia correction, the EEG is designed to be normal The possibility of parathyroidism, if necessary, to determine the diagnosis of PTH.
3. Extrapyramidal symptoms may occur due to calcification of brain tissue, such as involuntary movement, hand and foot movement, twisting twitch, tremor, cerebellar ataxia, gait instability, etc., easily misdiagnosed as neurological lesions, should be carefully observed No hypocalcemia and its corresponding clinical manifestations, as well as X-ray or CT examination of brain calcification lesions, will be conducive to the diagnosis of hypoparathyroidism.
4. Intestinal fistula, intestinal peristalsis, abdominal pain, abdominal distension, diarrhea and poor fat absorption, constipation, etc., easily misdiagnosed as intestinal disease or autonomic neuropathy, if hypocalcemia and its corresponding clinical manifestations, After treatment, the above intestinal symptoms can be obviously improved after the improvement of hypocalcemia, and the possibility of parathyroid disease should be considered.
5. There may be hypotension, T wave changes, prolonged QT interval, heart failure, etc., easily misdiagnosed as heart disease, if the patient's hypotension is not effective with conventional therapy such as booster drug or expansion, T wave is non-specific change, Although the QT interval is prolonged, the ST segment is prolonged, the QRS interval is unchanged, and heart failure is refractory digitalis without response. It should be highly alert to hypoparathyroidism, such as hypocalcemia after treatment, treated with calcium. Recoverable blood pressure, etc. will help diagnose hypoparathyroidism.
6. Can appear large cell anemia, vitamin B12 deficiency, histamine-resistant gastric acid deficiency, and Schilling test is abnormal, easily misdiagnosed as blood disease, for patients with anemia should routinely determine blood calcium and blood phosphorus, if patients have low calcium The diagnosis of hypoparathyroidism will be facilitated by the improvement of the above-mentioned conditions after the serum calcium is normal and the corresponding clinical manifestations.
7. Due to hypocalcemia and hyperphosphatemia, calcification of the lens may occur, resulting in cataract, which causes vision loss and is easily misdiagnosed as an ophthalmic disease. Therefore, blood calcium and blood phosphorus should be measured in patients with cataract, if the patient has hypocalcemia and The corresponding clinical manifestations will contribute to the diagnosis of hypoparathyroidism. At this time, fundus examination may have optic disc edema and pseudo-brain tumors.
8. There may be tooth dysplasia, tooth root defect, tooth enamel hyperplasia, banding or cave around the crown and crown, or permanent teeth do not grow, easily misdiagnosed as dental disease, therefore, for dental patients Blood calcium and blood phosphorus should be measured. If the patient has hypocalcemia and its corresponding clinical manifestations will help diagnose the hypoparathyroidism, checking the abnormalities of the teeth will help to estimate the hypoparathyroidism. Onset time.
9. For patients with hypocalcemia, should not immediately diagnose hypoparathyroidism, should first exclude hypoalbuminemia, and then measure blood phosphorus, alkaline phosphatase, urea nitrogen, if the patient is hypocalcemia, Low blood phosphorus, alkaline phosphatase increased, normal urea nitrogen, malnutrition, intestinal malabsorption or liver disease, should be alert to the possibility of vitamin D deficiency, at this time measured PTH increased, urinary calcium decreased, urine cAMP increased, 25 -(0H)D3 and 1,25-(OH) 2 D3 decrease, which is helpful for the diagnosis of vitamin D deficiency; if the patient is hypocalcemia, hyperphosphatemia, elevated alkaline phosphatase, elevated urea nitrogen, should Considered for renal insufficiency, at this time, PTH increased, urinary calcium decreased, urinary cAMP increased, 1,25-(OH)2D3 decreased, but 25-(OH)D3 was normal, and increased serum creatinine would contribute to renal function. Incomplete diagnosis.
10. For patients with hypoparathyroidism who have been diagnosed, due to the high number of hypoparathyroidism and pseudohypothyroidism, the identification of the cause and type should be further confirmed for the diagnosis. PTH is reduced in idiopathic hypoparathyroidism. , in the hypothyroidism and false idiopathic hyperparathyroidism, in the pseudo-false parathyroidism normal, PHT stimulation test in idiopathic hypoparathyroidism, pseudo-false parathyroidism, pseudo Idiopathic hypoparathyroidism is normal, in pseudohypoparathyroidism, PHT antibody is positive in idiopathic parathyroidism, Gs protein is abnormal in hypoparathyroidism type Ia, in pseudohypoparathyroidism Ib, Ic type and False idiopathic parathyroidism is normal, and the false-false hypothyroidism is reduced.
For the diagnosis of parathyroidism, it is necessary to improve clinical vigilance. For patients with history of neck surgery, polyadenotrophic endocrine insufficiency, chronic mucocutaneous candidiasis, cataract, finger numbness and tightness, facial muscles or hands and feet have spontaneity and induction. Sexual sputum and other symptoms should be repeatedly measured blood calcium and blood phosphorus, there are typical hand and foot sputum, low blood calcium, high blood phosphorus, urinary calcium and phosphorus are reduced without renal dysfunction, it is strongly suggestive of parathyroidism Diagnosis.
Differential diagnosis
The clinical and blood changes at the low side are mainly hypocalcemia, and the causes are various.
The most important causes of chronic hypocalcemia are low parathyroidism, vitamin D deficiency and chronic renal failure.
Acute hypocalcemia
When hypocalcemia of hand, foot and ankle occurs, it must be treated with intravenous calcium. The calcium used for injection in China is calcium chloride injection (5%, 10ml, containing elemental calcium 90mg) and calcium gluconate injection (10%). , 10ml, containing elemental calcium 90mg), the first intravenous injection should be injected with elemental calcium 180mg, concentrated calcium solution is irritating to the vein, if it escapes the vein, it will cause serious inflammation to the soft tissue, so it is best to use glucose 50 ~ 100ml, calcium injection Dilution, intravenous injection in 5 ~ 10min, such as hypocalcemia persists, or repeated occurrence of hand, foot and ankle, intravenous calcium can be repeated in 6 ~ 8h, or intravenous infusion with dilute calcium solution, and in the course of treatment Check the blood calcium to adjust the dose of calcium injection. If the patient used the digitalis preparation within 3 weeks, it is more appropriate to take calcium intravenously. Blood calcium should be kept at a normal low level because hypercalcemia makes the heart to digitalis. More sensitive, prone to arrhythmia or even sudden death, if the diagnosis of idiopathic hypoparathyroid has been determined, or the necessity of long-term replacement therapy is clear, then vitamin D or its derivatives can be given at the same time as calcium treatment. Oral dihydrogen Dihydrotachysterol (DHT) is 0.5 to 1 mg per day. It is the most convenient and effective treatment. If hypocalcemia is 2mmol/L, there is no hand or foot spasm or only mild neuromuscular symptoms. Oral calcium can be used. 2g, divided into serving), or add oral vitamin D or its derivatives.
2. Chronic hypocalcemia
(1) Principles of treatment: The treatment of chronic hypocalcemia referred to here is mainly for the treatment of hypocalcemia caused by hypoparathyroidism. For the treatment of chronic hypoparathyroidism, injection of PTH is reasonable, but due to the high price of PTH. It is difficult to obtain, so this kind of therapy can not be applied. The transplanted parathyroid gland has little permanent effect and needs to be studied. Therefore, the treatment method is mainly vitamin D or its derivatives, and calcium treatment. The purpose of treatment is: 1 Control symptoms; 2 reduce the incidence of low side complications; 3 to avoid vitamin D poisoning, in order to achieve the purpose of 3 points, it is appropriate to maintain blood calcium in the treatment of 2.13 ~ 2.25mmol / L, and vitamin D as small as possible The dose, at this blood calcium level, most patients are asymptomatic, when the serum calcium is 2.25 ~ 2.5mmol / L, the urinary calcium is discharged three times as normal, so it is prone to urinary stones, in general, according to the above It is required to maintain the minimum amount of vitamin D. When mild symptoms of hypocalcemia occur due to mood fluctuations, vomiting, physical exertion, menstruation and other factors, the dosage of calcium can be increased. If the symptoms of hypocalcemia persist, then Continuous blood calcium Adjustment of the dose of vitamin D, when there are pregnant, breast-feeding, clothing hydrochlorothiazide or antiepileptic drug regimens should be adjusted.
(2) Vitamin D and derivatives: Vitamin D and its derivatives can promote intestinal calcium absorption, and there are many varieties:
1 Vitamin D2 (calciferol, calciferol, ergocalciferol) injection 400,000 U / ml, according to USP regulations, each milligram equivalent to 40,000 USP units or international units (IU).
2 Vitamin D3 (cholecalciferol) injection has 300,000 U / ml and 600,000 U / ml two dosage forms, the above vitamin D2 and D3 are oil agents for intramuscular injection, the two have the same effect.
3DHT contains 120,000 equivalent units per mg, with 0.125, 0.2, 0.4 mg pellets, 0.125 mg capsules and 0.25 mg/ml oil.
425-hydroxyvitamin D3 [25-(OH)D3], 20 g / granule, 50 g / capsule and 50 g / ml oil, the usual amount of hypoparathyroidism is 25 ~ 200 g / d.
51,25 dihydroxyvitamin D3 (1,25-(OH)2D3) is available in Rocaltrol (calcitriol), containing 0.25/g per capsule, usually with 0.25 g/d, gradually increasing the dose and The blood calcium is adjusted to a suitable maintenance amount (0.36 to 1.5 g/d).
61-hydroxyvitamin D3 [1-(OH)D3] is still in the application study, the dose is the same as that of Luo calcium, because it is easier to synthesize, this drug is promising.
If the biological activity of calciferol is 1, compared with the activity of other derivatives: DHT is 3,25-(OH)D3 is 10-15; 1,25-(OH)2D3 and 12-(OH)D3 For 1000-1500, because each person's physiological functions are different, the comparison of the above biological activities is only an approximate value. Vitamin D and its derivatives are similar in chemical structure, and the medical practitioners can understand the chemical structure of them. Increased understanding of physiological effects.
(3) Calcium: Calcium for intravenous injection is used for the treatment of hand, foot and ankle. As has been described above, it is preferred to use oral vitamins for the treatment of chronic hypocalcemia while using vitamin D or its derivative.
(4) Choice and mastery of treatment methods: The efficacy of vitamin D and its derivatives is affected by many factors. Vitamin D2 or D3 is converted to 25-(OH)D in the liver, and then 25-OH 1 hydroxylase in the kidney. The effect is changed to 1,25-(OH)2D, so the effect of vitamin D is weakened in patients with liver or kidney disease. The effect of 1-hydroxylase depends on PTH. Therefore, when PTH is completely deficient, vitamin D can only be converted to 25-(OH)D, but can not produce 1,25-(OH)2D, its efficacy depends only on the action of 25-(OH)D, so the amount of vitamin D required is very large, various vitamin D The effect of derivatives on calcium and phosphorus metabolism depends on the sum of intestinal absorption function, renal excretion function and bone resorption function. Therefore, the therapeutic dose of vitamin D cannot be accurately calculated, and the dose can only be gradually adjusted during the treatment. To achieve the purpose of treatment, however, if the patient's kidney function is very bad, or PTH is seriously lacking, the use of DHT, 1-(OH)D3 or 1,25-(OH)2D3 is the best policy.
1 After surgery, the hypothyroidism is low and the symptoms are very mild. One to 2 g of elemental calcium per day can be asymptomatic. In some patients, the parathyroid function gradually recovers and even the calcium can be reduced or stopped.
2 The symptoms of heavier hypothyroidism (including postoperative and idiopathic) require an average of 80,000 U (50,000 to 100,000 U/d) of calcified alcohol per day. The vitamin D dosage form of China, D2 is 400,000 U/ml. D3 is 300,000 U/ml, often 1 ml per week or 1 ml per 2 weeks. The therapeutic dose must be adjusted according to the degree of symptom control and blood calcium level. In addition, it must be taken daily. Calcium tablets, daily elemental calcium 1 ~ 1.5g.
3DHT and 1-(OH)D3 need only 25-hydroxyl in vivo, without the action of 1-hydroxylase, the effect is rapid and stable, and the average dose of DHT is 0.75mg (0.51mg/d). At the same time take calcium tablets, daily elemental calcium 1 ~ 1.5g, Luo calcium full dose has been seen before, the above drugs are oral, more convenient.
4 During the above dose treatment, most of them are relatively stable, and vitamin D toxic hypercalcemia rarely occurs, but blood calcium and phosphorus should be checked weekly at the beginning of treatment until the blood calcium level reaches the therapeutic purpose and is stable. Then, review it every 3 to 6 months.
5 Some patients need to use larger doses of vitamin D or its derivatives to achieve therapeutic purposes, but higher doses are more prone to hypercalcemia, so regular review is more necessary.
6 a small number of severe idiopathic hypoparathyroidism occurs with vitamin D "resistance", that is, treatment is not reactive, and this resistance can also be unstable, for example: resistance at the beginning of treatment, and then resistance disappears, There are also treatments that are very stable, but they are resistant. If resistance occurs, the therapeutic drugs can be changed. For example, if vitamin D3 is changed to DHT or calcium, the therapeutic effect can be restored.
7 If vitamin D toxic hypercalcemia occurs, the treatment is the same as the treatment of hyperparathyroidism.
