What Are the Common Armour Thyroid Side Effects?

Primary hyperparathyroidism is easily ignored in clinical practice, but when unknown bone pain, pathological fractures, urinary stones, hematuria, urinary tract infections, hypercalcemia, or refractory peptic ulcers In other cases, the disease should be thought of and the corresponding examination should be done to confirm the diagnosis. The treatment principles for different etiologies are different. Primary adenoma should be surgically removed as soon as possible. Those who are not suitable for surgery should choose different drugs according to the complications. Secondary hyperparathyroidism is mainly for the treatment of primary disease, and secondary hyperparathyroidism should be performed as a subtotal parathyroidectomy.

Basic Information

English name

primary hyperparathyroidism

Visiting department

Endocrinology

Common causes

Head and Neck Radiation Therapy, Alcohol, Drugs, Genetics, etc.

Common symptoms

Bone and joint damage, urethral stones, renal colic, hematuria, polyuria, polydipsia, anorexia, nausea, vomiting and constipation, etc.

Causes of primary hyperparathyroidism

The cause is unknown, and the possible causes are as follows:

Head and neck radiation therapy

10% to 30% of patients with hyperthyroidism have a history of radiation therapy, and often have thyroid nodule disease. Among them, benign thyroid disease accounts for 20% to 50%, and malignant lesions are 6% to 11%.

Alcoholism

3. Drug

Thiazine diuretics, glucocorticoids, thiouracil, glucagon, etc. can all lead to increased PTH.

4. Genetics

There may be more than one member in a family with parathyroidism, some multiple endocrine adenomas (MEN). MENI refers to multiple endocrine adenomas of the pituitary, pancreas, parathyroid glands, and adrenal cortex. Deletion of alleles; MENII is paranasal hyperplasia or adenoma accompanied by medullary thyroid tumors and / or pheochromocytomas, a genetic defect on the 10th pair of chromosomes.

Clinical manifestations of primary hyperparathyroidism

Bone and joint damage

Systemic diffuse osteopathy, mostly bones that bear gravity, such as the lower limbs and lumbar spine. Physical examination may have tenderness in the long bones and spontaneous fractures, especially in cystic lesions, which often occur in the long bones. Arthralgia is caused by subchondral fractures or invasive arthritis, which is easily misdiagnosed as rheumatoid arthritis.

2. Urinary system

About two-thirds of patients may have kidney damage. The most common are recurrent urinary tract stones, renal colic, hematuria, polyuria, polydipsia, and increased blood calcium, which can cause diabetes insipidus in severe cases. Repeated urinary tract infections are prone to irreversible renal failure.

3. Digestive system

The patient has indigestion, anorexia, nausea, vomiting and constipation. May be accompanied by recurrent peptic ulcer, drug treatment is ineffective. The parathyroid adenoma can be cured after removal. 5% to 10% of patients have acute and chronic pancreatitis.

4. Cardiovascular system

Hypercalcium causes contraction of vascular smooth muscle, calcification of blood vessels, and formation of hypertension. Endocardial and myocardial calcification reduce cardiac function.

5. Neuropsychiatric disorders

When blood calcium is 3 to 4mmol / l, there are symptoms of mental weakness. At 4mmol / l, he was mentally ill, with delirium and insanity. Near 5mmol / l unconscious. A few have headaches, strokes, extrapyramidal diseases, and paralysis, which may be related to intracranial calcification.

6. Muscle system

Muscle weakness, proximal muscle pain, atrophy, and nonspecific changes in muscle biopsy. EMG can be reported as myogenic or neurogenic and can be misdiagnosed as peripheral neuritis.

Examination of primary hyperparathyroidism

Qualitative inspection

(1) Serum calcium and hypercalcemia are the most important biochemical indicators of the disease, and have the most diagnostic value. Many patients need to repeat the test several times in the same laboratory to find out. Hypercalcemia can only be diagnosed if blood calcium is> 2.6mmol / l. If free calcium can be measured, it is more favorable for the diagnosis of hypercalcemia.

(2) Serum phospholipids are 0.97 to 1.45 mmol / l in normal adults and 1.29 to 2.10 mmol / l in children. 80% of patients with hyperparathyroidism have decreased blood phosphorus, which is caused by PTH's "bone dissolving phosphorus" effect. It must be emphasized that the fasting blood phosphorus decreases.

(3) 24-hour urinary calcium excretion: The 24-hour urinary calcium excretion of adults in China increases during parathyroidism when 1.9 to 5.6 mmol (75 to 225 mg). 24-hour urine calcium> 250 mg (female) and 300 mg (male) are diagnostically significant.

(4) 24-hour urinary phosphorus discharge: Normal 24-hour urinary phosphorus is less than 1 g, and parathyroidism often increases. However, due to dietary factors, its diagnostic significance is not as important as urine calcium output. Urinary phosphorus clearance (Cp) has a diagnostic significance of 60 to 70% for parathyroidism.

(5) Urine cAMP (cyclic adenosine monophosphate) measurement cAMP increased in urine in 80% of patients with parathyroidism. The excretion rate of urinary cAMP reflects the concentration of biologically active PTH in the circulation.

(6) When the renal tubular reabsorption phosphorus test (TRP) is normal, if 800-900 mg of phosphorus is taken daily, phosphorus is filtered from the glomerulus, and the renal tubule can absorb 80% -90%, that is, TRP80% -90% . PTH inhibits renal tubular reabsorption of phosphorus. When parathyroidism is suppressed to 10% to 70%, less than 78% is diagnostic.

(7) Determination of urinary hydroxyproline (HOP) PTH can dissolve bone and dissolve bone organic matrix, so the HOP in urine increases.

(8) PTH measurement iPTH was significantly increased in the serum of 55% to 95% of patients with primary parathyroidism. Such as increased PTH when serum calcium is elevated has special diagnostic significance for parathyroidism.

(9) Calcium stress test: After intravenous calcium infusion in normal people, blood calcium concentration increases and PTH decreases. However, patients with parathyroidism have negative feedback disorders of PTH. Therefore, PTH does not decrease or slightly decrease after calcium load. Normal people dropped significantly, and even suppressed to 0. This test is only used in suspicious patients with elevated PTH and insignificant increase in blood calcium.

(10) Cortisol inhibition test: It is mainly used to identify hypercalcemia caused by other causes. Patients with hyperparathyroidism take large doses of glucocorticoids (prednisone 60mg / day) for one week, and the blood calcium does not decrease. For other reasons such as vitamin D poisoning, myeloma, etc., milk alkali poisoning can inhibit blood calcium. Most patients with parathyroidism cannot be suppressed.

(11) X-ray examination: X-ray examination of each part must be performed on bone and mixed patients. The earliest X-ray sign is subperiosteal bone resorption, which can occur before osteoporosis.

2. Positioning check

Because most of the primary hyperparathyroidism is parathyroid adenoma, imaging examination can suggest that the lesion is conducive to surgical exploration.

(1) The effective rate of B ultrasound is 70% to 79%, and tumors of 0.5 to 1 cm can be found, and the false positive rate is only 4%. But it is not easy to find ectopic and parasternal lesions behind the sternum.

(2) CT of the neck and mediastinum revealed a positive rate of 67% on the mediastinum and the smallest lesion found was 1.6 cm.

(3) Radionuclide inspection In recent years, thorium-99 ( ^99m Tc-MIBI) has replaced the original dual radionuclide subtraction scans of thorium-99m (99m-Tc) and gadolinium ( ²⁰¹ TI). Can detect lesions of more than 1cm in diameter.

(4) Selective thyroid vein blood test for iPTH This test is traumatic. The peak of blood iPTH is the position of the parathyroid gland reflecting the lesion.

(5) Selective thyroid angiography: Because this test can cause serious complications, it should be treated with caution.

Surgical exploration can be considered after localization and diagnosis, and exploration by an experienced surgeon is required. Before reoperation, cervical ultrasound and radionuclide MIBI examination and mediastinal CT examination still have some significance.

Treatment of primary hyperparathyroidism

(A) surgical exploration

It is an effective method to treat hyperparathyroidism.

(Two) medical treatment

When severe cardiovascular disease and severe hypercalcemia are temporarily inoperable, medication can be used first to create conditions for surgery.

1. Limit intake of foods containing high calcium

2. Inhibit PTH secretion

(1) Propranolol, a ₃ adrenergic receptor inhibitor.

(2) The effect of cimetidine is not reliable.

3 Inhibit the effect of PTH on bone

(1) Phosphate phosphate increases blood phosphorus, causes calcium salts to be deposited in bones and causes a decrease in blood calcium; secondly, it inhibits the production of 1,25 (OH) ₂ D ₃ , resulting in a decrease in intestinal calcium absorption and a decrease in blood calcium. Due to the response of phosphorus preparations to the gastrointestinal tract, and the stimulation of PTH secretion by phosphorus preparations can cause side effects such as ectopic calcification of soft tissues, it is currently not recommended for the treatment of primary parathyroidism.

(2) Estrogen is suitable for menopausal women. To balance the use, it is recommended to use selective estrogen receptor modulator-ranoxifene.

(3) Bisphosphonate inhibits osteoclast activity and reduces blood calcium.