Sporadic goiter

Introduction to sporadic goiter Sporadic goiter is a type of simple goiter, which is a compensatory goiter caused by iodine deficiency, thyroid mass or related enzyme defects, without obvious hyperthyroidism or diminished. Also known as non-toxic goiter, it is characterized by exudation in non-endemic goiter epidemic areas, and is not associated with tumors and inflammation, the thyroid gland is mostly diffuse enlargement in the early stage of the disease, and can later develop multi-nodular enlargement. basic knowledge The proportion of illness: 0.013% Susceptible people: no special people Mode of infection: non-infectious Complications: difficulty swallowing

Causes of sporadic goiter

Iodine deficiency (25%):

There was mild iodine deficiency in childhood, and in adulthood, even if iodine intake has returned to normal, it can still cause thyroid disease to continue to develop.

Enzyme deficiency (15%):

Congenital defects or acquired defects in certain enzymes during thyroid hormone synthesis can cause sporadic goiter, such as iodide transport enzyme deficiency, peroxidase deficiency, dehalogenase deficiency, and iodine tyrosine coupling defects.

Drugs (18%):

Iodide, fluoride, lithium salt, aminopyrine, aminoglutethimide, sulfonamides, phenylbutazone, amiodarone, sulfabutyramide, propylthiouracil and other drugs can cause sporadic goiter, pregnant women with toxic goiter After taking propylthiouracil, propylthiouracil can not pass through the placental barrier, but the maternal blood T4, T3 levels decrease, so that the fetal blood T4, T3 levels also decrease, stimulating fetal TSH levels rise, can occur congenital thyroid swollen.

Smoking (15%):

Smoking can cause sporadic goiter because the inhalation contains thiocyanate, a form of goiter that causes smokers to have higher levels of serum thyroglobulin than non-smokers.

Genetic factors (8%):

Brix (1999) has studied more than 5,000 monozygotic and twin-oval twins in non-endemic goiter areas, and found that genetic susceptibility to simple goiter accounted for 82%, only 18% attributed Based on environmental factors, the results of this study are important evidence that sporadic goiter can be caused by genetic factors. The genetic factors associated with the onset of sporadic goiter are currently found to be 14q, multinodular goiter gene-1, 3q26, Xp22, thyroid. Globulin genes, etc.

Increased thyroxine requirement (14%):

During puberty or pregnancy, the body's need for thyroid hormones increases, and the synthesis of thyroid hormones is relatively insufficient, and simple goiter can occur.

Other diseases (10%):

Sporadic goiter can occur in patients with hypercortisolism, acromegaly, and end-stage renal disease.

Pathogenesis

1. Pathogenesis: The pathogenesis of sporadic goiter is still inconclusive, there may be multiple factors, and multiple mechanisms are involved.

(1) Stimulation of TSH: Some patients with sporadic goiter have iodine intake or intake of goiter-producing drugs, thyroid hormone synthesis decreases, feedback stimulates pituitary secretion of TSH, TSH stimulates thyroid cell hypertrophy, this part of patients supplement Iodine or thyroxine can inhibit TSH.

(2) Increased sensitivity of thyroid to TSH: Most patients with sporadic goiter have normal serum T3 and T4 levels, and serum TSH levels are normal. A reasonable explanation is that some subgroups of thyroid follicular cells have increased sensitivity to TSH stimulation. This part of the patient's supplementation with iodine or thyroxine does not inhibit TSH.

(3) Similar substances in TSH: Growth-stimulating Abs and thyroid-stimulating peptides can be detected in a considerable number of patients with sporadic goiter. These substances have a similar TSH effect, but not Rely on the TSH receptor.

(4) Growth factors: During the occurrence of sporadic goiter, thyroid endocrine, some growth factors secreted by the extrathyroid gland may be involved.

1 insulin-like growth factor-1 (IGF-1): Minuto (1989) found that patients with sporadic goiter had immunoreactive IGF-1 levels that were 2-fold higher than in the normal population, but not elevated in patients with Graves' disease. , Maiorano (1994) found that elevated levels of IGF-1 in patients with sporadic goiter are mainly located in thyroid follicular cells. In vitro cell culture studies have shown that thyroid follicular cells secrete IGF-1, but do not rely on exogenous IGF-1. This indicates that there is autocrine IGF-I in thyroid proliferative diseases. In vitro and in vivo studies have also shown that IGF-1 and TSH synergistically stimulate thyroid growth and function properly. Both are indispensable, and the regulation of thyroid autocrine IGF-1 Iodine-related, iodine follicular cells increased secretion of IGF-1.

2 fibroblast growth factor (FGF): Thompson (1998) found that sporadic goiter follicular cells express FGF-1, FGF-2 and FGFR-1, and the expression level is higher than normal thyroid tissue, animal experiments show that FGF -1 can significantly increase the weight of the thyroid gland and reduce the activity of deiodinase.

3 transforming growth factor- (TGF-): In vitro cell culture studies found that TGF- inhibited the growth of thyroid follicular cells, but TGF-1 secreted by thyroid follicular cells can enhance fibroblasts around follicular cells. The proliferation of the follicles around the follicles leads to fibrosis and excessive deposition of the matrix in sporadic goiter tissue.

4 Epidermal growth factor (EGF): In vitro cell culture experiments showed that EGF can stimulate the proliferation of thyroid follicular cells. TSH can enhance the binding of EGF to EGF-R on the surface of thyroid cells, and enhance the mitosis of EGF on thyroid cells.

5 angiogenic factors: thyroid follicular epithelial hyperplasia requires vascular bed hyperplasia to maintain nutrient supply, therefore, angiogenic factors are involved in the process of sporadic goiter, thyroid follicular cells can stimulate endothelium through FGF Cell proliferation, in vitro experiments show that TSH can stimulate the secretion of vascular endothelial growth factor (VEGF) in thyroid cells, thereby promoting endothelial cell proliferation.

6 endothelin (ET): ET-1 is mainly synthesized by vascular endothelium. ET-2 and ET-3 are mainly synthesized by vascular smooth muscle cells. ET receptors include ETA and ETB, and ETA is expressed on vascular smooth muscle cells. Vasoconstriction, ETB expression on vascular endothelial cells, involvement in the production of nitric oxide (NO), prostacyclin and natriurotic peptide (ANP), expression of nitric oxide synthase gene (NOS I, NOSIII) The level can be increased. For example, the addition of NOS inhibitor can reduce the proliferation of blood vessels. In vitro experiments show that ANP can inhibit the release of thyroglobulin from thyroid cells, while TSH can down-regulate the number of ANP receptors in thyroid cells. In addition, both ET-1 and ANP can be used. Regulates the synthesis of VEGF in endothelial cells, ET-1 stimulates the synthesis of VEGF, and ANP inhibits the synthesis of VEGF. Therefore, during the process of goiter, VEGF, ET-1 and ANP interact to regulate angiogenesis.

7 Hepatocyte growth factor (HGF): Thyroid cells secrete HGF, which is a strong mitogen of thyroid cells.

In the pathogenesis of endemic goiter, elevated levels of TSH caused by iodine deficiency play a key role, while for sporadic goiter, serum TSH levels generally do not increase, and TSH interacts with multiple growth factors to determine The occurrence and development of sporadic goiter, low intracellular iodine levels may be the result of sporadic goiter, not a cause.

(5) Autoimmune: sporadic goiter tissue can express HLA-DR antigen, and epithelial cells expressing HLA-DR antigen can present antigens themselves, stimulate autoimmune reactions, and produce autoantibodies. These autoantibodies stimulate thyroid cell growth. effect.

2. Pathology: The histological changes of the disease vary depending on the etiology and stage of the disease. In the early stage, the thyroid gland is diffusely mild or moderately hypertrophic, with increased blood vessels, hypertrophy of the gland cells, when the disease persists or repeatedly deteriorates and relieves. The thyroid gland gradually develops nodules due to irregular hyperplasia or regeneration. As the disease progresses, a large amount of colloid (colloidal goiter) accumulates in the acinus, forming a huge acinus, and the follicular epithelial cells are flat and connective tissue between the acinus And blood vessels are reduced. In the later stage, some glands may undergo necrosis, hemorrhage, cystic changes, fibrosis or calcification. At this time, the thyroid is not only significantly increased in volume, but also has different sizes, nodules of different textures, thyroid structure and The heterogeneity of function, a certain degree of functional autonomy is the characteristics of the late stage of the disease.

Sporadic 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.

Sporadic goiter complications Complications, difficulty swallowing

Patients with larger glandular enlargement may have hernia or dysphagia, and may be accompanied by a small number of growth retardations accompanied by hoarseness, accompanied by symptoms of hypothyroidism. Such as mental retardation, facial swelling, bone age, etc.

Symptoms of sporadic goiter Common symptoms thyroid gland and smooth... Thyroid nodules tracheal compression goiter dyspnea dyspnea facial edema sound hoarseness internal bleeding dysphagia

1. Goiter or neck mass: Goiter is a characteristic clinical manifestation of non-toxic goiter. Patients often complain that the neck is thick or the collar is tight. The thyroid is located in the front of the neck, easy to grow outward, sometimes goiter. Can be developed downward into the sternum, which may be due to negative pressure in the thoracic cavity; occasionally the goiter occurs in the vagus thyroid tissue, the early stage of the disease is diffuse goiter, the body surface is swollen, the thyroid surface is smooth, soft, With swallowing up and down activities, no tremor and vascular murmur, puberty, gestation, lactation patients with thyroid enlargement significantly increased, with the development of the disease, thyroid nodular enlargement, generally asymmetry, multi-nodular Multiple nodules can be gathered together, showing a neck mass, varying sizes of nodules, varying textures, different positions, and no pain in goiter. If there is bleeding in the nodules, pain can occur. The nodule is hard and the activity is not good. It should be vigilant.

2. Compression symptoms: Compression symptoms are the most important clinical manifestations of non-toxic goiter. Compression symptoms usually appear in the late stage of the disease, but compression symptoms can occur in the early stage of the retrosternal goiter.

(1) compression of the trachea: mild tracheal compression is usually asymptomatic, heavy pressure can cause wheezing, difficulty breathing, cough, began to appear during activity, and later developed to rest, also caused by retrosternal goiter Wheezing and dyspnea often occur at night, and can occur with changes in body position (such as the upper limb of a patient). When the patient has a narrow airway, hemorrhage in the nodular sac or bronchitis can aggravate the symptoms of dyspnea.

(2) compression of the esophagus: the esophagus position is relatively low, generally not easy to be compressed, such as goiter growing backwards, can compress the esophagus, causing difficulty swallowing.

(3) compression of the recurrent laryngeal nerve: unilateral recurrent laryngeal nerve compression can cause vocal cord paralysis, hoarseness, bilateral recurrent laryngeal nerve compression can also cause breathing difficulties, recurrent laryngeal nerve compression symptoms can be transient, but also For permanent, there is a symptom of retinal nerve compression, and it is necessary to be highly vigilant.

(4) compression of blood vessels: huge goiter, especially the retrosternal goiter can compress the jugular vein, subclavian vein or even the superior vena cava, causing facial edema, neck and upper chest shallow vein expansion.

(5) compression of the phrenic nerve: retrosternal thyroid can compress the phrenic nerve, causing hiccups, sputum swelling, sacral nerve compression is less common.

(6) compression of the cervical sympathetic chain: retrosternal goiter can compress the cervical sympathetic chain, causing Horners syndrome, cervical sympathetic chain pressure is less common.

Examination of sporadic goiter

Its purpose is to determine the functional status of the thyroid gland, because the goiter can be accompanied by clinical or subclinical hypothyroidism, but also with clinical or subclinical hyperthyroidism.

1. Serum TSH, T3, T4 detection: patients with sporadic goiter usually have normal serum TSH, T3, T4 levels. When late autonomic function is formed, serum TSH levels decrease, FT4 levels increase, or FT4 levels are normal and FT3 levels are elevated. ,

2.131I uptake rate: 131I uptake rate is normal or elevated,

3. Serum TPOAb, TgAb is generally negative, a few can be positive, suggesting that its onset may be related to autoimmune response, in addition, it may be suggested that it is more likely to have hypothyroidism in the future.

4. Fine needle aspiration cytology: patients with non-toxic goiter do not need routine fine needle aspiration cytology, but for the ultra-echo substantive nodules of B-ultrasound, calcified nodules, nodules 3 cm in diameter, Fine needle nodules or rapid growth nodules should be fine needle aspiration cytology, fine needle aspiration cytology is the most effective method for preoperative evaluation of thyroid nodules, sensitivity is 65% to 98%, specificity 72% to 100%,

5. X-ray examination of the neck: Patients with long course of disease, obvious goiter or respiratory obstruction or retrosternal goiter should take a tracheal piece and close the glottis, respectively, in forced exhalation and inhalation. Time film to understand the presence or absence of tracheal displacement, tracheal softening, and to determine the location and size of the retrosternal goiter,

6. Ultrasound examination of the neck: The neck B-ultrasound is the most reliable method for diagnosing goiter. B-ultrasound can detect small nodules of 2 to 4 mm, so B-ultrasound can find nodules that are not touched by physical examination. The incidence of thyroid nodules is 4% to 7%, and B-ultrasound found that nearly 70% of adults have thyroid nodules, many of which have a diameter of 1cm. The thyroid volume should be measured during B-ultrasound examination to observe the presence or absence of nodules. Is it a single nodule or multiple nodules, cystic nodules or substantial nodules, high echo or low echo, with or without calcification, clear boundaries, etc., common manifestations of diffuse goiter:

1 The thyroid gland is diffuse, with increased symmetry, smooth surface, no nodules, and can compress the trachea and neck vessels when significantly enlarged.

2 When the follicle is full of colloid and is highly expanded, multiple anechoic areas are formed. When color Doppler examination, no significant increase in blood flow signal compared with normal thyroid is observed, and a small amount of blood flow signal is scattered.

7. Radionuclide imaging: Radionuclide imaging can evaluate the function of thyroid morphology and thyroid nodules. Diffuse goiter can show enlarged thyroid volume, uniform radioactivity distribution, and nodular goiter can be seen in warm nodules or cold nodules.

8. CT and MRI of the neck: CT or MRI of the neck does not provide more information than B-mode ultrasound, and the price is higher, but it has a higher diagnostic value for retrosternal goiter.

9. Respiratory function test: Giant goiter or retrosternal goiter should be tested for lung function to make a functional evaluation of airway pressure.

Diagnosis and diagnosis of sporadic goiter

Diagnostic criteria

Residents of non-endemic goiter areas, diffuse thyroid enlargement or nodular enlargement, can be diagnosed as sporadic goiter after the exclusion of hyperthyroidism, Hashimoto's goiter, thyroid cancer and other diseases.

1. Goiter classification: The criteria for goiter classification proposed by WHO (1994):

(1) Level 0: No goiter (thyroid can not be seen, can not touch).

(2) Level 1: The neck mass caused by thyroid enlargement can be touched, but it is not seen in the normal position of the neck. The mass moves up when swallowing, and the grade 1 has included nodular goiter.

(3) Level 2: The neck mass can also be seen in the normal position of the neck, which is consistent with the enlargement of the thyroid found by palpation.

2. Evaluation of thyroid function: diagnosis of non-toxic goiter must confirm that thyroid function is normal and serum T3, T4 level is normal, thyroid function status is sometimes difficult to evaluate clinically, because some patients with hyperthyroidism, especially the elderly, have mild clinical manifestations Or not typical.

Serum T3 and T4 levels can be used to evaluate thyroid function, but serum T3 levels in elderly patients with normal thyroid function can be reduced. Serum TSH levels are the best indicator of thyroid function. Subclinical hyperthyroidism serum TSH levels are decreased. TSH is TRH. The reaction is reduced.

Differential diagnosis

1. Hashimoto goiter (chronic lymphocytic thyroiditis): manifested as bilateral unilateral or unilateral diffuse nodular or massive mass, hard texture, TPOAb, TgAb are positive, help with Identification of non-toxic goiter, fine needle aspiration cytology can confirm the diagnosis.

2. Riedel thyroiditis (chronic fibrotic thyroiditis): manifested as a painless thyroid mass, hard texture, fixation, fine needle aspiration cytology is of little significance, requiring surgical biopsy to confirm the diagnosis.

3. Thyroid tumor: manifested as a single thyroid mass, quality and toughness, single-nodal nodules with non-toxic goiter are difficult to identify, fine needle aspiration cytology is helpful to identify.

4. Thyroid cancer: manifested as a single thyroid mass, hard, medullary carcinoma with elevated serum calcitonin levels, pathological examination confirmed.

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