Endemic goiter

Introduction to endemic goiter Endemic goiter is a type of goiter. The goiter can be divided into local and sporadic by regional distribution. Endemic goiter is caused by a specific environment-induced goiter in a region (mainly iodine deficiency). Therefore, a certain proportion of people living in this area have goiter, and a certain proportion refers to local school age. The rate of goiter in children is more than 5%, that is, the presence of goiter has constituted a public health problem. Generally speaking, less than 5% is a sporadic goiter, mostly caused by non-iodine deficiency factors. basic knowledge Sickness ratio: 2% Susceptible people: no specific people Mode of infection: non-infectious Complications: thyroid cancer

Cause of endemic goiter

Iodine deficiency (55%)

At present, the main cause of this disease in the world is iodine deficiency. The disease is mainly found in mountainous areas far from the coast and high altitude. The soil in the endemic areas, water and food contain very little iodine. This disease is closely related to iodine deficiency. The rate is inversely proportional to the amount of iodine, and the use of iodized salt can prevent the disease.

Excessive iodine intake (20%)

In the natural iodine-rich areas, this disease is also prevalent, mainly because of excessive intake of iodine, which hinders the organic process of iodine in the thyroid gland, inhibits the synthesis of T4, promotes the secretion of TSH and produces goiter, called high iodine. Sexual goiter.

Biochemical factors (20%)

Calcium, fluoride, and magnesium in water can also cause goiter, and some monovalent anions similar to I-such as: SCN-, F-, Br-, At-, C104-, ReO4-, TeO4-, BF4-, etc. The competition of iodine reduces the ability of the thyroid to concentrate iodine, reduces the synthesis of thyroxine, and stimulates the secretion of TSH from the pituitary gland, causing the thyroid gland to enlarge.

Pathogenesis:

The goiter formed by insufficient iodine intake should not be regarded as a disease alone. The thyroid has an adaptive compensation process for iodine deficiency, and the goiter is actually the result of this adaptive compensation. In the process of compensatory (physiological) decompensation (pathological damage), the basic physiological changes of the disease include:

1. When the blood iodine concentration decreases, the iodine uptake capacity of the thyroid epithelium is compensatory, so the iodine absorption rate increases at 24h. In severe iodine deficiency, the concentration of inorganic iodine in the epithelium still decreases, that is, less than the normal value (0.25mg/g). ), the increase in iodine absorption rate is not only manifested in patients with swells and disease, but also the iodine absorption rate of so-called normal people in those wards, reflecting that all people in the ward are victims of iodine deficiency. As Zhu Xianyu said, the so-called normal person in the ward, although there is no goiter, but the iodine deficiency caused by iodine metabolism, the function of the pituitary-thyroid axis system, this is the theory that all the people in the ward should eat iodized salt. according to.

2. Iodine iodine, that is, the iodine organication process is enhanced, the MIT synthesis is increased, and the DIT is relatively reduced. The perchlorate experiment is normal, indicating that there is no problem in the iodine organication process, but Coutras found that it has been routinely In the case of chlorate, KI is released at the same time as thyroid. The thyroid liberates blood more iodine than normal, indicating that the organic process may also have defects, which may partly explain why under the same iodine deficiency condition, some people have goiter and some people are not swollen.

3. The iodine tyrosine coupling process is enhanced. As the MIT/DIT ratio increases, T3 synthesis increases, T4 decreases, that is, T3, T4 increase, and the absolute amount of T4 decreases, which is one of the important manifestations of iodine deficiency disease. From the perspective of compensation, it has two meanings: 1 more synthetic T3 less synthetic T4 can save iodine, T3 is relatively normal to ensure that the surrounding tissue does not appear hypothyroidism. The biological activity of 2T3 is 4-5 times larger than that of T4. Due to the normal or compensatory increase of T3, there is no obvious hypothyroidism or mucinous edema in the surrounding tissues. However, since the brain tissue mainly uses T4 instead of T3, the low T4 pair The maintenance of brain development and brain function is extremely dangerous. The findings of the ward also confirmed that the patient (inflammation or cretinism) showed more T3 normal or compensatory increase, T4, especially FT4, FTI4 (free T4 The index) has dropped significantly.

4. The synthesis of thyroglobulin is compensatory. Therefore, thyroid follicles often show glial retention as the main manifestation, but the glial usually contains iodine incomplete or insufficiently mature thyroglobulin, and the gelatin is updated more normally. Fast.

5. In the absence of iodine, the secretion of thyroid hormone is accelerated. When the content of organic iodine in the thyroid gland drops to less than half or less than normal (10 mg/g), T3 and T4 decrease significantly. Therefore, the amount of thyroid hormone secreted into the blood is reduced. In addition, after deiodination of iodinated tyrosine, the iodine recovery rate is increased, and the amount of iodine leakage (into the blood) is greatly reduced.

6. Because of the decrease of T4, feedback increases TSH, which is one of the most important manifestations of iodine deficiency. T4 decreases, and the rise of TSH fully reflects the hypothyroidism of patients. TSH has two types of effects, one is to promote thyroid. The function is expressed in the intake of iodine, the synthesis of T3 and T4, the secretion of hormones, etc. One type is the long-term increase of TSH and shows the effect of promoting growth of thyroid cells (slow effect), that is, the epithelium changes from cubic to high. Columnar, cell number, cell volume increase, so the epithelial protein, RNA synthesis accelerates, the slow effect of TSH is often gradually appearing after several weeks or months of persistent low iodine, with the degree of iodine deficiency and the body's reactivity Generally speaking, within 2 to 3 months of severe iodine deficiency, the patient may have goiter. The change of TSH is negatively correlated with T4, and has no obvious correlation with T3. It is worth noting that iodine deficiency is not serious or patient compensation In good times, TSH is mildly elevated or at a normal high level, ie subclinical hypothyroidism, which is an iodine-deficient injury that is often overlooked.

The above adaptation compensation changes are in the process of development. Low T4 high TSH has the meaning of damage. When the thyroid gland forms nodules, the meaning of compensation gradually disappears and further transforms into injury factors (such as: induced hyperthyroidism, oppression, Cancer, etc.).

Endemic goiter prevention

At present, the following methods are often used to prevent:

1 Iodized salt: Sodium iodide or potassium iodide is added to the salt, and the concentration is from 1:1 to 1:20,000.

2 Iodized drinking water: Potassium iodide is added to the drinking water, and 1 g of potassium iodide is added according to 100,000 L of water (that is, 10 g of potassium iodide per liter of water).

3 Iodine oil injection is suitable for areas with low incidence, no need for general iodine, injection of iodized oil dose, 125mg under 1 year old; 250mg from 1 to 5 years old; 750mg from 6 to 10 years old; over 10 years old and adult, 1000mg.

4 Eat more foods rich in iodine, such as kelp, seaweed, seaweed, sea fish and shrimp.

Endemic goiter complications Complications thyroid cancer

1. Hypothyroidism in many patients with hyperthyroidism is more normal in clinical practice (compensation), but since the application of radioimmunoassay to determine hormones, it has been confirmed that most patients with hyperthyroidism, even non-surgical patients, have varying degrees of hypothyroidism, in Guizhou Province. The results of the investigation in Majiang County are worthy of attention. Among the 18 pregnant women with thyroid swelling, the detection rate of neonatal hypothyroidism among their children was 38.9%. Liu Jiaxuan and Tan Yubin also provided the fetus in the iodine deficiency area for the first time in the world. Changes in thyroid function, they found 30 cases of abortion fetus in the province found that 23 cases showed a decrease in T4, elevated TSH, which will undoubtedly cause different degrees of brain development disorders.

2. The incidence of hyperthyroidism in patients with hyperthyroidism is not high. It is only seen in patients with toxic nodular hyperthyroidism over 40 years old. The symptoms of hyperthyroidism are the same as those of general hyperthyroidism. Radionuclide scanning can be found to be concentrated. The hot nodules of iodine, the symptoms are generally lighter than Graves' disease, easy to cure, and not easy to relapse after surgery.

3. Whether thyroid cancer is related to thyroid cancer, there has been controversy. Tan Yubin reported that the incidence of thyroid cancer in 997 cases of nodular hyperthyroidism in Longhua County, Hebei Province was 1.2%. Ma Rong was found in 3304 cases in Shaanxi. It is only 1.59%, and the incidence rate is not higher than that of non-disease areas. It is worthy of high attention that the possibility of carcinogenesis of nodular goiter is large, especially for single nodules. According to reports from all over the world, areas lacking iodine The incidence of follicular and undifferentiated carcinomas (anaplastic) is high, while the incidence of papillary carcinoma is low; however, after iodine supplementation, in areas with adequate iodine or high iodine, the incidence of follicular and undifferentiated carcinomas is low, but papillary The incidence of cancer is high.

4. Tracheal softening This is the result of long-term compression of the trachea of the enlarged thyroid gland. The hard or calcified thyroid nodules directly compress the trachea, which is the main cause of softening. The main symptom of the patient is difficulty breathing (71.6%), or even supine. (16.4%), more than half of the patients also had flustered, shortness of breath and other cardiovascular symptoms. The sputum was diagnosed with thyroid complications when surgery was performed in Shaanxi Province for 11,500 thyroid swollen surgery.

Another complication of endemic goiter is follicular cell degenerative carcinoma and its sarcoma. After treatment with iodine supplementation, the incidence is reduced and the course of the disease is increased.

Symptoms of endemic goiter Common symptoms Iodine sputum hoarseness goiter thyroid nodules dyspnea dysphagia iodine dysphagia

No obvious clinical symptoms in the early stage, mild thyroid, moderate diffuse enlargement, soft, no tenderness, very few patients with obvious swelling may have compression symptoms, such as difficulty breathing, difficulty swallowing, hoarseness, irritating cough, etc. Goiter may have symptoms of esophageal or superior vena cava compression, and thyroid function is basically normal, but about 5% of patients suffer from hypothyroidism due to insufficient thyroid function, which affects intelligence and growth. A small number of endemic goiter patients have long-term Serum, TSH levels increased, when iodine was added, thyroxine was synthesized too much to form iodothyronidine.

Examination of endemic goiter

There are many examination items for patients with hyperthyroidism, and each examination has certain clinical significance. It is very important to select some items for inspection according to the different conditions of each patient.

1. Metabolic state of the body

Basal metabolic rate (BMR) determination; blood cholesterol, triglycerides, and creatinine determination.

2. Serum thyroid hormone levels

Serum total T3 (TT3) determination, serum total T4 (TT4) determination, serum free T3 (FT3) determination, serum free T4 (FT4) determination, serum anti-T3 (rT3) determination.

3. Pituitary - thyroid axis regulation

Thyroid absorbing 131 iodine rate and thyroid inhibition test (including T3 inhibition test and thyroid tablet inhibition test), serum hypersensitivity thyroid stimulating hormone test (S-TSH), thyroid stimulating hormone releasing hormone stimulation test (TRH stimulation test).

4. Goiter enlargement

Thyroid B-mode ultrasonography, thyroid radionuclide development examination, etc.

5. Thyroid immunological examination

Determination of thyroid stimulating receptor antibodies, such as thyroid stimulating immunoglobulin assay (TRAb), thyroglobulin antibody assay (TGAb), thyroid microsomal antibody (TMAb) or anti-thyroid peroxidase antibody (TPOAb) assay.

6. The nature of thyroid disease.

7. Electrolyte condition.

Diagnosis and diagnosis of endemic goiter

Diagnostic criteria

1. The patient is from a prevalent area of goiter.

2. The thyroid is diffusely enlarged and the thyroid function is basically normal.

3. Children with iodine deficiency, urinary iodine discharge decreased, less than 50g / d.

4.131I uptake rate is higher than normal.

5. Blood T4 is normally lower or lower than normal, blood T3 is increased or normal, and TSH is increased or normal.

Differential diagnosis

1. Nodular goiter The thyroid gland is nodular hyperplasia with clinical manifestations of hyperthyroidism and hyperthyroidism.

2. Sporadic goiter is not prevalent in the region. It is more common in pre-pubertal and adolescent children with faster growth and development or substances that have used goiter, and urinary iodine is not reduced.

3. Chronic lymphocytic thyroiditis swollen thyroid texture is flexible, most of the functions are normal, a few years later, hypothyroidism, very few hyperthyroidism, thyroid antibody TGAb and TPOAb (TMAb), blood iodine does not decrease.

4. Familial enzyme-deficient cretinism has clinical manifestations of goiter and hypothyroidism, serum T3, T4 decreased, TSH increased, and urinary iodine did not decrease.

5. Hyperthyroidism caused by various causes of thyrotoxicosis, thyroid enlargement, soft texture, accompanied by clinical manifestations of hyperthyroidism, blood T3, T4 can be increased, TSH decreased.

6. Deafness - Goiter syndrome (Pendred syndrome) Deafness with dumb after birth, goiter in childhood, normal or low thyroid function, this disease is an autosomal recessive disorder, the birth defects of congenital iodine, There is an increase in iodine tyrosine in the blood, and the ratio of MIT/DIT and iodine tyrosine/iodolinine is increased, and urinary iodine is not reduced.

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