Iodine-induced hyperthyroidism

Introduction to iodine-derived hyperthyroidism Iodine-induced hyperthyroidism (IIH) refers to hyperthyroidism associated with increased iodine intake, referred to as iodothyroid, also known as iodine-induced thyroidosis or iodine-induced thyrotoxicosis (IIT). In terms of the amount of iodine, there are three cases of iodothyronine: the first one is one or more large doses of iodine intake causing iodine, such as amiodarone or other iodine-containing drugs or contrast agents, which can be used. Occurred in people with normal iodine nutrition, those with sudden nodules are more likely to occur; the second is the intake of higher doses of iodine, mostly in high iodine areas, iodothyroidism occurs due to long-term intake of higher doses of iodine; The third type is the intake of general dose of iodine (which can be the iodine intake in the physiological range), which is found in patients with iodine deficiency (including marginal iodine deficiency) after taking iodized salt; After iodine; patients with existing hyperthyroidism have relapsed after taking iodine. basic knowledge The proportion of illness: the incidence rate is about 0.001% - 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: hyperthyroidism

Iodine-induced hyperthyroidism

(1) Causes of the disease

Iodine is closely related to the thyroid gland; the former is a raw material for the synthesis of thyroid hormone, the daily iodine requirement for adults is about 70 g, and the adolescent is 150-200 g. The synthesis of thyroid hormone increases with the increase of iodine supply in a certain dose range, but if If the supply of iodine exceeds a certain limit (normal mg 5 mg/d, hyperthyroidism patient 2 mg/d), the opposite result may occur.

1 In the short-term, large doses of iodine can cause acute inhibition of thyroid hormone release. This inhibitory effect, also known as Woff-Chaikoff effect, may be a temporary protective mechanism to avoid release and synthesis of excessive hormones; This effect is often used to treat hyperthyroidism.

2 Long-term overdose of iodine, the Woff-Chaikoff effect gradually disappears, the so-called "release phenomenon", the synthesis and release of thyroid hormone after escape can return to normal, and even accelerate, sometimes iodothyroidism occurs.

There are two situations in which iodine causes hyperthyroidism:

1 In areas of iodine deficiency, endemic goiter is treated with iodide and accounts for the majority of iodothyroid.

2 In non-iodine-deficient areas, occasionally in some patients with non-toxic multinodular goiter, in addition, long-term use of amiodarone and other iodine-containing drugs, is also a common cause of non-iodine-deficient areas of iodine.

(two) pathogenesis

The pathogenesis of IIH is still controversial, and possible hypotheses include:

1. Iodine thyroidism after iodine supplementation in iodine-deficient areas. The past explanation is that iodine deficiency leads to thyroid thyroid hormone deficiency and TSH compensatory secretion. Once iodine is supplemented, thyroid hormone secretion is excessive under TSH stimulation. According to this hypothesis, hyperthyroidism should be temporary, once, non-persistent, IIH patients may be lack of self-feedback regulation of excessive iodine in the thyroid gland, large doses of iodine in the thyroid gland can not feedback to inhibit further iodine, so that The thyroid gland produces an excess of thyroid hormone that causes hyperthyroidism.

2. In recent years, studies have shown that individuals with iodothyronide have increased the synthesis of reactive thyroid hormones after iodine supplementation, and have not exerted a normal negative feedback effect on the thyroid (through TSH), ie, certain thyroid tissues of these individuals become In order to have "autonomy", which is not regulated by TSH, it occurs under the long-term stimulation of TSH, the exposure of thyroid cells to higher mutagenic loads (such as free radicals) and the effects of other local cytokines. Stimulate thyroid cell proliferation and differentiation, induce the expression of specific thyroid genes, including iodine carrier, thyroid peroxidase, thyroglobulin, TSH receptor, transcription factor, etc., thyroid gland produces multiple autonomous regions or single high function Nodules, these cells are not regulated by TSH, synthesize and secrete too much thyroid hormone when there is sufficient supply of iodine, leading to IIT. The occurrence of hyperthyroidism in autonomic nodules depends on the size of the nodules, the cells Functional status and supply of iodide, when iodine intake increases, large enough nodules cause increased thyroid hormone secretion and cause hyperthyroidism, namely: The greater the nodule, the more iodine intake, the more likely the hyperthyroidism occurs.

The definition of autonomous thyroid nodules is as follows: the obvious nodules on the boundary often show an increase in radioactive iodine uptake; the uptake of radioactive iodine is independent of TSH; the thyroid tissue outside the nodule responds to TSH stimulation; Serum TSH is reduced, response to TRH is slow, "autonomy" can occur in a region of the entire nodule or nodule (autonomous area); it may not be a nodule but a functionally autonomous follicular population or A cluster of autonomous cells.

3. In recent years, it has been noted that iodine may induce or aggravate the autoimmune response of the thyroid gland. In patients with autoimmune thyroid disease, excessive iodine intake may aggravate the disease, but the pathogenesis of hyperthyroidism is not iodine but autoimmune mechanism. .

4. Amiodarone can cause hyperthyroidism caused by two types of type I in excess of iodine, which is more common in patients with existing goiter; type II is temporary caused by amiodarone destroying thyroid follicles and releasing thyroid hormone. Hyperthyroidism, more common in patients with normal thyroid gland, will eventually result in permanent hypothyroidism due to glandular fibrosis.

Iodine-induced hyperthyroidism prevention

1. With appropriate iodine intake, the ideal iodine intake can prevent local cretinism and endemic hyperthyroidism without causing excessive IIH, WHO, UNICEF, ICCIDD according to different people's iodine Nutritional requirements and IIH after salt iodization, the recommended daily intake of iodine is as follows: 0 to 1 year old 50g; 2 to 6 years old 90g; 7 to 12 years old 120g; 12 years old and above 150g; pregnant women and lactating women 200g It is recommended that the concentration of iodine in salt should be 20-40 mg/kg, that is, the average level of urinary iodine in school-age children should be kept at 100-200 g/L. This iodine level minimizes the incidence of IIH (not disappears). Urine iodine higher than 200g / L is greater than the appropriate amount, but the incidence of IIH may be increased in some patients with nodular hyperthyroidism; when the urinary iodine is greater than 300g / L (especially greater than 500g / L) will definitely The incidence of iodothymidine is elevated.

2. In areas with high iodine, after the health authorities have organized expert argumentation, the iodized salt will be deactivated after being reported to the provincial government for approval.

3. The need for non-iodine salt should be met for a specific population, ie, for patients with other thyroid diseases or other unsuitable iodized salt, non-iodized salt should be purchased, and each community should have a store that sells non-iodized salt ( This is clearly stated in the salt iodization regulations).

4. Strict daily monitoring of iodized salt, using salt iodine concentration of 15 ~ 20mg / kg, according to the monitoring results should adjust the concentration of iodine in the production of iodized salt to avoid iodine deficiency or excessive iodine, that is, take appropriate And constantly adjusting the iodine interventions to meet the needs of the population for iodine, but also to minimize the risk of IIH.

5. To improve the understanding of iodine, the occurrence of iodothyroid is related to functional autonomic nodules, and the formation of "autonomy" is caused by long-term iodine deficiency, and it shows hyperthyroidism after iodine supplementation; therefore, iodine is iodine One of the manifestations of lack of disease is inevitable in the prevention and treatment of IDD. In view of the transient nature of iodine, it is generally reduced to the level before iodine after several years of prevention and treatment of iodized salt (3 to 5 years); The harm has become a public health problem for the whole people. It affects the brain development of the next generation and is related to the quality of the nation and the progress of society. Therefore, the prevention and treatment of iodine deficiency is still the focus of current work. The prevention and treatment of iodine hyperthyroidism cannot be ignored. When special attention is paid to iodoformam, there should be no delay, and the implementation of the iodized salt control plan should be abandoned or stopped.

Iodine-induced hyperthyroidism complications Complications, hyperthyroidism

Hyperthyroidism

16 to 73 years old can be onset, the incidence rate of 13.4% to 21.8% of patients with hyperthyroidism, often occurs 2 to 3 years after hyperthyroidism, in addition to the typical clinical manifestations of hyperthyroidism, the electrocardiogram often has sinus tachycardia, atrial fibrillation Tremor, atrial flutter, atrioventricular block, ventricular premature contraction, myocardial damage and cardiac hypertrophy. The enlarged heart can be aortic valve type, or left and right heart enlargement type. After the treatment of hyperthyroidism, heart disease can be improved. This disease should be diagnosed with myocarditis, coronary heart disease, rheumatic heart disease and other heart enlargement diseases.

2. Hyperthyroidism periodic paralysis

This disease occurs mostly in male young adults, often mixed with hyperthyroid myopathy, hyperthyroidism with normal potassium, abnormal electromyogram, and hyperthyroidism periodic paralysis: 1 blood potassium <3.5mmol / L, Abnormal potassium metabolism; 2 abnormal potassium distribution: elevated blood glucose can shift potassium from the cell to the cell; 3 excitability of the central nervous system is enhanced, vagus nerve can promote the release of insulin to promote further abnormality of potassium distribution; 4 immune factors can cause IATS The levels of LATS-P, T3 and T4 are elevated, and thyroid hormones promote potassium levels. 5 The high adrenergic state of hyperthyroidism promotes the decrease of potassium levels and the occurrence of hyperthyroidism. This type should be differentiated from Bartterssyndrome, familial periodic paralysis, hypomagnesemia, hyperaldosteronism, myasthenia gravis, and drug-induced hypokalemia.

3. Hyperthyroidism

The incidence of hyperthyroidism accounts for 1% to 2% of hyperthyroidism. The elderly are more common, often associated with infection, trauma, surgery, childbirth, overwork, sudden withdrawal, drug reaction and other complications, resulting in hyperthyroidism, sympathetic activity. The function is strengthened and the crisis is caused. In the early stage of crisis, the fever can reach more than 39 °C, the pulse rate is 120-160 beats/min, restlessness, loss of appetite, nausea, vomiting, diarrhea, mental paralysis, sweating, lethargy, development to semi-coma and coma. A comatose patient indicates that there is a crisis and is very dangerous. Elevated white blood cells, abnormal liver function, GPT, GOT, bilirubin, etc. can be elevated, including dehydration, hypotension, electrolyte imbalance, acidosis, heart failure and pulmonary edema. Serum T3, T4, FT3, FT4 can be elevated, the mortality rate is high, and must be rescued locally.

Symptoms of iodine-induced hyperthyroidism Common symptoms High-metabolism group Iodine

The clinical manifestations of iodothymidine are similar to those of Graves' disease, except that the former is older, mostly occurs in the elderly, and less frequently in children (there are reported that 50,000 children who received iodine treatment did not have IIH), the ratio of male to female 1:6~1 : 10, similar to Graves' disease, (in patients with iodine deficiency, most patients with thyroid nodules, 15% to 30% have small or no goiter, some patients have no nodules), the condition is relatively light, the thyroid is not Tenderness, thyroid examination can be seen nodular goiter or single nodules, generally no exophthalmos, and there are few vascular murmurs and tremors in the thyroid area, cardiovascular symptoms and signs are obvious, serum anti-thyroid antibody is negative, thyroid scan can be found The existence of "hot zone" is characterized by a decrease in thyroid iodine uptake rate of 24 h < 3%. Because of the large range of normal urinary iodine values, the determination of urinary iodine does not contribute much to the diagnosis.

Examination of iodine-derived hyperthyroidism

1. Recently, there has been a history of increased iodine intake. Patients have hyperthyroidism: tachycardia, sweating, weight loss, and lethargy and weakness.

2. Laboratory examination of blood FT4 increased, FT3 also increased, but not proportional to the increase in T4; TSH decreased; iodine absorption rate decreased.

3. Thyroid scan can reveal the presence of a "hot zone".

4. Hyperthyroidism caused by other causes should be excluded.

Diagnostic identification of iodine-derived hyperthyroidism

diagnosis

Diagnosis can be based on the cause, related symptoms, and test results.

Differential diagnosis

1. Hyperthyroidism combined with pregnancy often has the following conditions

(1) Patients with hyperthyroidism have a very low chance of conception, but those with milder disease can still conceive even without any treatment, leading to hyperthyroidism combined with pregnancy.

(2) Before pregnancy, the patient has suffered from hyperthyroidism and is receiving anti-thyroid drugs. If the clinical symptoms subsided, the thyroid function has basically returned to normal, and the chance of conception is high. After pregnancy, hyperthyroidism may recur or worsen.

(3) There is a history of hyperthyroidism, which has now healed and caused hyperthyroidism after pregnancy.

(4) There is no history of hyperthyroidism, and hyperthyroidism occurs after pregnancy. Specifically, the first two cases belong to hyperthyroidism combined with pregnancy, and the latter two cases belong to hyperthyroidism after pregnancy, but in any case, pregnancy can aggravate the condition of hyperthyroidism. To complicate the diagnosis and treatment of the disease.

Some clinical manifestations during normal pregnancy may resemble hyperthyroidism, so it often causes difficulties in differential diagnosis: First, due to physiological hypertrophy and placental hormone secretion in the pituitary gland during normal pregnancy, there may be a high metabolic syndrome similar to hyperthyroidism, such as Excessive sweat, heat, appetite, heart rate, sometimes thyroid can be slightly larger, after 4 months of pregnancy, the basal metabolic rate is gradually increased, up to 25%, and the estrogen level is elevated during pregnancy, blood The thyroid hormone-binding globulin (TBG) is also increased, so the levels of TT3 and TT4 in the serum are correspondingly increased. Therefore, TT3 and TT4 in serum are generally not used as a standard for the diagnosis of hyperthyroidism.

The diagnostic criteria for hyperthyroidism combined with pregnancy are as follows:

1 typical clinical manifestations: in addition to high metabolic signs, when patients with exophthalmos, thyroid enlargement, even with vascular murmur, weight loss, muscle weakness and other symptoms, support the diagnosis of hyperthyroidism,

2 FT3 in serum, FT4 increased,

3 Hypersensitivity TSH: TSH in the serum of patients with hyperthyroidism is inhibited, even in the case of combined pregnancy, the detection of hypersensitivity TSH is often less than 0.1mU / L, but some reports show that normal women may occasionally appear in the 8th to 14th week of pregnancy TSH is mildly inhibited, but not less than 0.1 mU/L.

Among the above three points, FT3, FT4 and TSH are the most valuable. When the TSH is less than 0.1 mU/L and the FT3 or FT4 is increased, the diagnosis of hyperthyroidism is basically established.

The preferred drug treatment is safe and effective; it can be treated surgically if it is unavoidable; 131I treatment is prohibited.

medical treatement

1 anti-thyroid drugs. Thioureas are preferred. Although such drugs can adversely affect the fetus through the placenta, they are safe and effective as long as they are used properly. Propylthiouracil (PTU) is currently preferred because it has less placental permeability than methimazole (tabazole). The minimum effective dose should be used as much as possible. The daily dose of propylthiouracil (PTU) should not exceed 200 mg, because the thyroid gland of the fetus can receive the excitement of TSH at 3 months of pregnancy, if there is a sufficient dose of propylthiouracil (PTU) Gathering in the thyroid gland of the fetus can cause thyroid dysfunction, which in turn causes goiter; the former can affect brain development, and the latter can cause dystocia. In terms of disease control, pregnant women with hyperthyroidism do not have to control their heart rate and basal metabolic rate to normal as in general hyperthyroidism patients. The basic heart rate of 100 to 110 beats/min does not adversely affect delivery. FT3 and FT4 are It can be within the critical range. Pregnant women who still take propylthiouracil (PTU) in the second trimester of pregnancy should not be breast-feeding after birth because these drugs can affect the baby through milk.

2 about thyroxine. It is necessary to properly supplement the thyroid preparation. However, there have been differences in opinions on this issue, because exogenous thyroid hormone is not easy to pass through the placenta, so the combination of thyroxine does not guarantee that the fetus does not have goiter and stagnation.

3 about propranolol. Although it has been reported that propranolol can cause fetal intrauterine growth retardation and neonatal hypoglycemia, it is generally considered safe to be less than 30 mg per day. For pregnant women whose small doses of propylthiouracil (PTU) cannot control symptoms, propranolol can be added as appropriate. Because propranolol can increase uterine activity and delay cervical dilation, it should be used with caution before delivery.

Surgery In order to avoid miscarriage and premature delivery, surgery is not recommended for the first 3 months and 3 months after pregnancy. If surgery is necessary, it should be performed within 4 to 6 months of pregnancy. If preoperative iodine preparation is required, it usually does not exceed 10 days. In order to avoid postoperative hypothyroidism and other adverse effects, dry thyroxine tablets can be added.

2. Newborn hyperthyroidism

Newborns born to pregnant women with hyperthyroidism may have hyperthyroidism, the incidence rate is about 1%, and the child often relieves itself 1 to 3 months after birth. Recent data indicate that the risk of neonatal hyperthyroidism and TRAb in the mother The concentration is closely related; however, there are very few mothers with no history of hyperthyroidism, but there is often a positive family history, and the hyperthyroidism of such children is generally not relieved by themselves.

(1) Pathogenesis: It is currently believed that neonatal hyperthyroidism is caused by the TRAb of the mother with Graves disease affecting the fetus through the placenta. It is not related to TSH. Many data indicate that more than 95% of the children have strong TRAb. Positive, and the severity of hyperthyroidism in children is proportional to the concentration of TRAb in the mother.

(2) Clinical manifestations: Children often have low body weight at birth, and symptoms appear after birth. They are characterized by irritability, flushing of skin color, tachycardia, excessive appetite but no increase in body weight. People with severe goiter may have tracheal obstruction. The performance of a patient who is extremely ill and not properly treated may die due to arrhythmia and heart failure.

The TRAb in the child is mostly positive, but since these TRAbs are obtained from the mother and have a half-life of only about 16 days, they are generally only transient hyperthyroidism. The symptoms are most obvious at the first week of birth, lasting 4 to 12 weeks. After that, it will relieve itself.

(3) Diagnosis: For pregnant women with hyperthyroidism or previous history of hyperthyroidism, close observation of their babies after delivery, especially within 10 days after birth, pregnant women with high TRAb should be alert to neonatal hyperthyroidism before delivery. Occurs to prevent suffocation or death from arrhythmia due to goiter.

(4) For children with mild symptoms, they can be observed temporarily, but for those who are heavier, they need to be treated with drugs. Generally, antithyroid drugs and iodine are used at the same time; methimazole (tazodazole) is 0.5 to 1.0 mg per day. Kg, taken in 3 times; iodine / potassium iodide (combined iodine solution) 3 times / d, 1 drop each time, such as thyroid enlargement affects breathing, emergency tracheal incision is required, sedatives may be used if necessary.

3. Children's armor

Children with hyperthyroidism account for 1% to 5% of all hyperthyroidism, and those less than 3 years old are rare. After 3 to 4 years old, the incidence rate is gradually increased, and the highest is 11 to 16 years old. The ratio of male to female is similar to that of Graves' disease, which is about 1:5. Children with hyperthyroidism are almost all Graves' disease, most of them have exophthalmia, but most of them are non-invasive. Other clinical manifestations are similar to those of adults, but those who start from the age of 10 may have obvious growth acceleration and accelerated bone formation. It is related to the role of thyroxine in promoting synthesis, and puberty also occurs early, especially in girls.

For children with hyperthyroidism, anti-thyroid drugs should be used, but the recurrence rate after stopping the drug is higher than that of adults, and the curative effect is also poor; generally no surgical treatment is needed, and radioactive iodine treatment is a contraindication.

4. Apathetic hyperthyroidism

Also known as occult or weakness type hyperthyroidism, more common in the elderly, more women, this type of patients with high metabolic signs, eye disease, goiter are not obvious, often insidious onset, manifested as apathy, unresponsive, lethargy , weight loss is obvious, even cachexia; dry skin, wrinkles, can have stained pigmentation; muscles are thin, often with severe proximal myopathy, involving the muscles of the shoulders and hips; pulse rate is only slightly increased Fast or normal, rarely more than 110 beats / min; the heart tends to expand, a small number of patients can be associated with angina or even myocardial infarction, the incidence of advanced atrial fibrillation is quite high.

The pathogenesis of apathetic hyperthyroidism is unknown, probably because hyperthyroidism has not been treated for a long time, and the body is seriously depleted. It may also be that the sympathetic nerves of elderly patients are not sensitive to thyroid hormone or catecholamine depletion.

Laboratory tests are similar to those of common type of hyperthyroidism. TT3, TT4, FT3 and FT4 are both increased, and hypersensitivity TSH is reduced. Therefore, as long as you can think of indifferent hyperthyroidism, it is generally not difficult to diagnose, but the disease is easily missed and misdiagnosed. Most of them are Atypical symptoms interfere with the disease, because it can not be diagnosed and treated in time, the disease is more likely to sneak into the crisis, the indifferent type of hyperthyroidism crisis is also different from the common type of hyperthyroidism, body temperature, pulse can not increase, no signs of madness, and Eventually there may be stupidity or coma.

The treatment is similar to that of common type of hyperthyroidism, and its thyroid function is easier to control, but such patients should pay attention to systemic support treatment, such as vitamin supplementation, due to long-term consumption and age.

5.T3 type hyperthyroidism

Most patients with hyperthyroidism have elevated T3 and T4 in their blood, but a few patients have only T3 increased, but T4 is normal, called T3 hyperthyroidism. This disease was first reported by Maclagan in 1957, and the incidence rate was different. It accounts for 3% to 20% of hyperthyroidism; some people think that elderly patients are more likely to occur.

(1) Pathogenesis:

1 Clinically, if T3 type hyperthyroidism is not treated for a long time, most patients can eventually evolve into common type hyperthyroidism, that is, T4 is also elevated. This phenomenon suggests that T3 type hyperthyroidism may be a precursor of common type hyperthyroidism, because in the early stage of hyperthyroidism T3 rises faster and faster than T4.

2 Some patients have not evolved into common type hyperthyroidism, and the mechanism is unknown. It may be related to excessive T3 synthesis by the thyroid itself.

3 T3 type hyperthyroidism occurred during the treatment, mostly due to the early and rapid decline of T4 after drug treatment.

4 According to some statistics, the proportion of T3 type hyperthyroidism in iodine-deficient areas is obviously higher, which may be due to the fact that the synthesis of T3 requires less iodine than T4, and the biological activity of T3 is large.

(2) Clinical manifestations: T3 type hyperthyroidism is common in all kinds of hyperthyroidism (including toxic thyroid adenoma, Plummer disease, Graves disease, and even thyroid cancer, etc.) in the early stage of the disease, during the course of treatment or early relapse, and the clinical manifestations are similar to those of the common type. May be associated with eye problems, goiter, but mild symptoms.

(3) Diagnostic criteria:

1 has symptoms and signs of hyperthyroidism.

2T4, FT4 is normal or low, while T3, FT3 is elevated.

3 Hypersensitive TSH decline or TRH excitation test showed a low flat curve.

(4) Same as common type of hyperthyroidism, usually treated with drugs; the chance of recurrence is less than that of normal type hyperthyroidism.

6.T4 type hyperthyroidism

Contrary to T3 type hyperthyroidism, some patients have only T4 increased, T3 is normal, called T4 type hyperthyroidism, the disease is more common in the elderly or patients with chronic diseases, first proposed in 1978.

T4 type hyperthyroidism is more common in two cases:

1 Iodothymidine, about 30% of patients with iodothyronidine, T3 is normal, T4 is increased, probably due to large doses of iodine load leading to a large number of thyroid synthesis of T3 and T4, but in fact T4 synthesis and release more than T3, thus High T4emia,

2 Hyperthyroidism combined with chronic complications, the ability of T4 to T3 transformation in peripheral blood of patients with hyperthyroidism is weakened or lost, T3 in the body can only be derived from the direct synthesis of thyroid, so although T4 is elevated, T3 is normal or even decreased, Because of the inhibition of 5' monoiodine deiodinase, the rT3 in the blood of such patients is abnormally increased. When the chronic disease is restored, rT3 is decreased, and T3 is increased. It should be noted that some chronic patients have no hyperthyroidism. However, the phenomenon of elevated T4 may occasionally occur in the course of the disease, and it needs to be differentiated from T4 type hyperthyroidism, which can be judged according to the level of TSH.

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