Iodine deficiency diseases and endemic goiter

Iodine deficiency disorders (endemic goiter) - a condition occurring in certain geographic areas with iodine deficiency in the environment and characterized by enlargement of the thyroid gland (sporadic goiter develops in individuals living outside goiter-endemic areas). This form of goiter is widespread in all countries.

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Epidemiology

According to the WHO, there are over 200 million patients with endemic goiter in the world. The disease is common in mountainous (Alps, Altai, Himalayas, Caucasus, Carpathians, Cordillera, Tien Shan) and lowland regions (Central Africa, South America, Eastern Europe). The first information about endemic goiter in Russia is available in Lezhnev's work "Goiter in Russia" (1904). The author not only cited data on its prevalence in the country, but also suggested that it was a disease of the entire body. In the territory of the former USSR, endemic goiter is found in the central regions of Russia, Western Ukraine, Belarus, Transcaucasia, Central Asia, Transbaikalia, in the valleys of large Siberian rivers, in the Urals, and the Far East. An area is considered endemic if more than 10% of the population has clinical signs of goiter. Women are more likely to suffer from it, but in areas of severe endemia, men often suffer from it as well.

The prevalence of the disease is determined by the number of affected women, the degree of enlargement of the thyroid gland in patients, the frequency of nodular goiter and the ratio of men and women with goiter (Lenz-Bauer index). Endemicity is considered severe if the incidence of the population is over 60%, the Lenz-Bauer index is 1/3-1/1, and the incidence of nodular goiters is above 15%, and there are cases of cretinism. An indicator of its severity can be a study of the iodine content in urine. Its results are calculated in μg%. The norm is 10-20 μg%. In areas of severe endemicity, the iodine level is below 5 μg%. In mild endemic conditions, the incidence of the population is above 10%, the Lenz-Bauer index is 1/6, and nodular forms occur in 5% of cases.

To assess goiter endemicity, the indicator proposed by M. G. Kolomiytseva is also used. It is based (the coefficient of tension of goiter endemicity) on the ratio of the number of initial forms of goiter (I-II degree) to the number of cases of its subsequent forms (III-IV degree), expressed as a percentage. The result is a multiple value showing how many times the initial degrees of thyroid gland enlargement prevail over the subsequent ones. If the Kolomiytseva coefficient is less than 2, the endemicity is of high tension, between 2 and 4 - medium, more than 4 - weak.

The International Council on Iodine Deficiency Disorders, using data on the prevalence and clinical manifestations of iodine deficiency, recommends distinguishing three degrees of severity of iodine deficiency. In the mild degree, goiter occurs from 5 to 20% in the population, the average level of iodine excretion in urine is 5-9.9 mg%, the frequency of congenital hypothyroidism is from 3 to 20%.

The average severity is characterized by a goiter frequency of 20-29%, iodine excretion level of 2-4.9%, and congenital hypothyroidism frequency of 20-40%. In severe cases, the goiter frequency is more than 30%, the iodine excretion level in urine is below 2 μg%, and the congenital hypothyroidism frequency is more than 40%. Cretinism occurs with a frequency of up to 10%.

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Causes Iodine deficiency diseases (endemic goiter)

In the mid-19th century, Chatin and Prevost put forward the theory that endemic goiter was caused by iodine deficiency. In subsequent years, the iodine deficiency theory was further confirmed by research by other scientists and is now widely accepted.

In addition to iodine deficiency, the development of endemic goiter is significantly affected by the intake of goitrogenic substances (thiocyanates and thio-oxyzolidones contained in certain types of vegetables), iodine in a form unavailable for absorption, genetic disorders of intrathyroid iodine metabolism and biosynthesis of thyroid hormones, and autoimmune mechanisms. The occurrence of the disease is significantly affected by the reduced content of microelements in the biosphere, such as cobalt, copper, zinc, molybdenum, which was shown in detail in the studies of V. N. Vernadsky and A. P. Vinogradov, as well as bacterial and helminthic pollution of the environment. Familial goiter and a high frequency of goiter in monozygotic twins compared to dizygotic twins suggest the presence of genetic factors.

As a response of the body to prolonged and severe iodine deficiency, goiter develops, a number of adaptation mechanisms are activated, the main ones being an increase in the thyroid clearance of inorganic iodine, hyperplasia of the thyroid gland, a decrease in the synthesis of thyroglobulin, modification of iodine-containing amino acids in the gland, an increase in the synthesis of triiodothyronine by the thyroid gland, an increase in the conversion of T4 _to T3 _in peripheral tissues and the production of thyroid hormone.

Increased iodine metabolism in the body reflects stimulation of the thyroid gland by thyroid-stimulating hormone. However, the mechanisms of regulation of thyroid hormone synthesis mainly depend on the intrathyroidal iodine concentration. In pituitary-ectomized rats kept on a diet with insufficient iodine, an increase in the absorption of ¹³¹ 1 by the thyroid gland was observed.

In neonates and children in endemic areas, epithelial hyperplasia of the thyroid gland without cellular hypertrophy and relative reduction of follicles is observed. In regions of moderate iodine deficiency, parenchymatous goiters with the formation of nodes on a hyperplastic base are found in adults. A progressive decrease in iodine content is revealed, respectively, an increase in the ratio of monoiodotyrosine to diiodotyrosine (MIT/DIT) and a decrease in iodothyronines. Another important result of the decrease in iodine concentration is an increase in the synthesis of T3 _and the maintenance of its level in the serum, despite the decrease in the level of T4 _. In this case, the TSH level can also be increased, sometimes very significantly.

G. Stockigt believes that there is a direct correlation between the size of the goiter and the content of TSH.

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Pathogenesis

In endemic goiter, the following morphological variants of goiter are encountered.

Diffuse parenchymatous goiter occurs in children. The gland enlargement is expressed to varying degrees, but most often its mass is 1.5-2 times greater than the mass of thyroid tissue in a healthy child of the same age. In section, the substance of the gland is of a homogeneous structure, soft elastic consistency. The gland is formed by small closely located follicles lined with cubic or flat epithelium; colloid, as a rule, does not accumulate in the cavity of the follicle. In individual lobules, interfollicular islets are found. The gland is abundantly vascularized.

Diffuse colloid goiter is a gland weighing 30-150 g or more with a smooth surface. On section, its substance is amber-yellow, shiny. Large colloid inclusions, from several millimeters to 1-1.5 cm in diameter, surrounded by thin fibrous strands are easily distinguishable. Large stretched follicles lined with flat epithelium are detected microscopically. Their cavities are filled with poorly or non-resorbable oxyphilic colloid. In areas of resorption, the epithelium is mostly cubic. Among the large follicles, there are foci of small functionally active follicles lined with cubic, sometimes proliferating epithelium. In the largest follicles, iodination of thyroglobulin is impaired.

Nodular colloid goiter - can be solitary, multinodular and conglomerate, when the nodes are intimately fused together, unlike multinodular goiter. Such goiters can reach 500 g or more. The surface of the gland is uneven, covered with a dense fibrous capsule. The diameter of the nodes varies from several millimeters to several centimeters. Their number varies, sometimes they replace the entire gland. The nodes are usually located in goitrous thyroid tissue. They are formed by follicles of different sizes, lined with epithelium of varying height. Large nodes cause compression of the surrounding thyroid tissue and vascular network with the development of ischemic necrosis, interstitial fibrosis, etc. In the foci of necrosis and outside it, part of the follicular cells is loaded with hemosiderin. Ossification can be observed in areas of lime deposition. Fresh and old hemorrhages and atheromas are often found in follicles. Local damage induces follicular hyperplasia. Thus, the basis of the pathological process in nodular colloid goiter is the processes of degeneration and regeneration. In recent years, lymphoid infiltration of the stroma of nodes and especially the surrounding thyroid tissue with changes observed in autoimmune thyroiditis has become a common occurrence.

Against the background of nodular goiter, in the nodes themselves and/or in the surrounding tissue, in approximately 17-22% of cases, adenocarcinomas are formed, more often microfoci of highly differentiated cancers. Thus, the main complications of nodular goiter are acute hemorrhages, sometimes with a sudden increase in the gland, lymphoid infiltration with autoimmune struma, more often focal, and the development of cancers.

Familial goiter is one of the variants of endemic goiter with autosomal recessive inheritance. This form of the disease is verified histologically. It is characterized by uniform, usually medium-sized follicles lined with cubic epithelium, pronounced hygroscopic vacuolization of the cytoplasm, nuclear polymorphism; increased neoformation of follicles is often noted. The colloid is liquid with many parietal vacuoles. Cases with signs of cancer are not uncommon: areas of glandular tissue from anaplastic cells, phenomena of angioinvasion and penetration of the gland capsule, psammoma bodies.

These changes are especially pronounced in congenital goiter with impaired iodine organification. Such a gland has a finely lobulated structure. The lobules are formed by strands and clusters of large atypical epithelial cells with polymorphic, often malformed nuclei, of embryonic and, less frequently, fetal or follicular structure. Follicular cells have pronounced hygroscopic vacuolization of the cytoplasm, and the nuclei are polymorphic, often hyperchromic. These goiters may recur (with partial thyroidectomy).

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Symptoms Iodine deficiency diseases (endemic goiter)

Symptoms of endemic goiter are determined by the shape, size of the goiter, and the functional state of the thyroid gland. Patients are bothered by general weakness, increased fatigue, headaches, and discomfort in the heart area. With large goiters, symptoms of pressure on nearby organs occur. When the trachea is compressed, attacks of suffocation and a dry cough may be observed. Sometimes there are difficulties in swallowing due to compression of the esophagus.

There are diffuse, nodular and mixed forms of goiter. According to consistency, it can be soft, dense, elastic, cystic. In areas of severe endemia, nodes appear early and are found in 20-30% of children. Often, especially in women, the thyroid gland is represented by multiple nodes and a clear decrease in the synthesis of thyroid hormones is noted with the appearance of clinical signs of hypothyroidism.

^{In endemic goiter, an increase in the absorption of 131} 1 by the thyroid gland is observed. When conducting a test with triiodothyronine, suppression of the absorption of I is revealed, which indicates the autonomy of the thyroid nodules. In regions of moderate endemia, with diffuse goiters, a lack of response of the thyroid-stimulating hormone to the introduction of thyroliberin is found. Sometimes in areas of iodine deficiency, patients with an unenlarged thyroid gland, increased thyroid clearance of ¹³¹ 1 and its further growth after the introduction of TSH are encountered. The mechanism of development of thyroid atrophy remains unknown to this day.

In regions of pronounced endemicity, the most typical manifestation of endemic goiter is hypothyroidism. The appearance of patients (puffy pale face, pronounced dryness of the skin, hair loss), lethargy, bradycardia, muffled heart sounds, hypotension, amenorrhea, slow speech - all indicate a decrease in thyroid function.

One of the manifestations of hypothyroidism in endemic goiter, especially in severe cases, is cretinism, the frequency of which fluctuates from 0.3 to 10%. The close relationship between endemic goiter, deaf-muteness and cretinism in one area suggests that the main cause of the latter is iodine deficiency. Conducting iodine prophylaxis in endemic areas leads to a clear decrease in its frequency. Cretinism is associated with deep pathology, beginning in the prenatal period from early childhood.

Its characteristic features are: pronounced mental and physical retardation, short stature with disproportionate development of individual parts of the body, severe mental deficiency. Cretins are sluggish, sedentary, with impaired coordination of movements, they have difficulty making contact. McKarrison identified two forms of cretinism: "myxedema" cretinism with a pronounced picture of hypothyroidism and growth defect and less common "nervous" cretinism with pathology of the central nervous system. Characteristic features of both types are mental retardation and deaf-muteness. In the endemic regions of Central Africa, "myxedema" and athyrogenic cretinism are more common, while in the mountainous regions of America and the Himalayas, the form of "nervous" cretinism is more common.

In "myxedematous" cretins, the clinical picture is characterized by pronounced signs of hypothyroidism, mental retardation, growth defects, and delayed bone maturation. The thyroid gland is usually not palpable; when scanning, its residual tissue is in the usual location. Low plasma T3, T4, and significantly elevated TSH levels are noted.

Clinical manifestations of "nervous" cretinism are described in detail by R. Horna-brook. There is an initial slowdown in neuromuscular maturation, delayed development of ossification nuclei, hearing and speech disorders, strabismus, and intellectual retardation. Most have goiters, the functional state of the thyroid gland is euthyroid. Patients have normal body weight.

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Diagnostics Iodine deficiency diseases (endemic goiter)

The diagnosis of endemic goiter is based on a clinical examination of individuals with an enlarged thyroid gland, information about the prevalence of the disease and place of residence. An ultrasound examination is performed to determine the volume of the thyroid gland and its structure. The functional state of the thyroid gland is assessed based on ¹³¹ 1 diagnostics, TSH and thyroid hormone content.

Differential diagnosis should be made with autoimmune thyroiditis, thyroid cancer. Increased thyroid density, increased titer of antithyroid antibodies, "variegated" picture on the scanogram, puncture biopsy can help in diagnosing autoimmune thyroiditis.

Rapid and uneven tumor development, uneven node contours, tuberosity, limited mobility, weight loss may be suspicious of thyroid cancer. In advanced cases, an increase in regional lymph nodes is observed. For correct and timely diagnosis, the results of a puncture biopsy, gland scanning, and ultrasound echography are important.

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Treatment Iodine deficiency diseases (endemic goiter)

For the treatment of euthyroid goiter in children and adolescents, iodine preparations are used in physiological doses, 100-200 mcg per day. Against the background of iodine treatment, the thyroid gland decreases and normalizes in size. In adults, there are 3 treatment methods: monotherapy with I-thyroxine at a dose of 75-150 mcg per day, monotherapy with iodine (potassium iodide at a dose of 200 mcg per day) and combined treatment with levothyroxine with iodine (iodthyrox contains 100 mcg T ₄ and 100 mcg iodine, 1 tablet per day; thyreocomb - 70 mcg T ₄ and 150 mcg iodine). The thyroid gland usually decreases in size 6-9 months after the start of treatment. The duration of the treatment course should be from 6 months to 2 years. In the future, to prevent relapse, prophylactic doses of iodine preparations of 100-200 mcg are prescribed. Control examinations are carried out at intervals of 3-6 months (measuring the circumference of the neck, palpation of the goiter to detect nodes, ultrasound examination).

Patients with signs of decreased thyroid function are treated with thyroid hormones in doses adequate to compensate for the condition. Treatment is also given to patients with elevated TSH levels, decreased T3, T4, and elevated thyroglobulin antibody titers, i.e. subclinical forms of hypothyroidism and autoimmune thyroiditis are observed.

In case of nodular goiter, its large size and symptoms of compression of surrounding organs, patients are recommended to undergo surgical intervention.

Prevention

Since the 1930s, a network of anti-goiter dispensaries has been created in our country, the activities of which are aimed at organizing measures to prevent and treat endemic goiter. The most convenient method of mass iodine prophylaxis is the use of iodized salt. Scientific justification for iodine prophylaxis was first proposed in 1921 by D. Marine and S. Kimball. In the USSR, O. V. Nikolaev, I. A. Aslanishvili, B. V. Aleshin, I. K. Akhunbaev, Ya. Kh. Turakulov and many others made a great contribution to solving the problem of endemic goiter.

In 1998, a new standard for iodized table salt was adopted in Russia, which requires the addition of 40±15 mg of iodine per 1 kg of salt in the form of a stable salt - potassium iodate. Monitoring of the potassium iodide content in iodized salt is carried out by sanitary and epidemiological stations. Mandatory supply of iodized salt to the population in goiter-affected areas has been organized.

In recent years, due to insufficient attention to iodine prophylaxis in our country, there has been a tendency towards an increase in morbidity. Thus, according to V. V. Talantov, the frequency of endemic goiter of I-II degree is 20-40%, III-IV degree - 3-4%.

In addition to mass prophylaxis, group and individual iodine prophylaxis is carried out in endemic areas. The first - with antistrumin (1 tablet contains 0.001 g of potassium iodide) or the drug potassium iodide 200, 1 tablet daily - is carried out in organized children's groups, pregnant and lactating women, taking into account the increased need of the growing body for thyroid hormones under the control of determining the excretion of iodine in the urine, which reliably reflects the amount of iodine entering the body. Individual iodine prophylaxis is carried out for people who have undergone surgery for endemic goiter; patients who, for some reason, cannot be treated; people temporarily residing in goiter endemic areas.

In tropical countries of the globe, prevention of iodine deficiency diseases by administering iodized oil is widely used. Lipiodol is used - a preparation of iodized oil in capsules for per os administration or ampoules for intramuscular administration.

1 ml of iodized oil (1 capsule) contains 0.3 g of iodine, which provides the body with the required amount for a year.

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