Hypothyroidism , also called underactive thyroid or low thyroid , is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormone. This can cause a number of symptoms, such as poor ability to tolerate cold, fatigue, constipation, depression, and weight gain. Sometimes there may be swelling in the front of the neck due to goiter. Untreated hypothyroidism during pregnancy can cause delays in growth and intellectual development in infants or cretinism.
Around the world, too little iodine in the diet is the most common cause of hypothyroidism. In countries with sufficient iodine in the diet, the most common cause of hypothyroidism is autoimmune conditions of thyroiditis Hashimoto. Less common causes include: previous treatment with radioactive iodine, injury to the hypothalamus or anterior pituitary gland, certain drugs, lack of thyroid function at birth, or previous thyroid surgery. Diagnosis of hypothyroidism, when suspected, can be confirmed by a blood test measuring thyroid-stimulating hormone (TSH) and thyroxine levels.
Iodized salt has prevented hypothyroidism in many populations. Hypothyroidism can be treated with levothyroxine. Dose adjusted for symptoms and normalization of thyroxine and TSH levels. The thyroid drug is safe in pregnancy. While some dietary iodine is important, excessive amounts can exacerbate certain types of hypothyroidism.
Worldwide about one billion people are estimated to be iodine deficient; However, it is unknown how often this results in hypothyroidism. In the United States, hypothyroidism occurs in 0.3-0.4% of people. Subclinical hypothyroidism, a milder form of hypothyroidism characterized by normal thyroxine levels and elevated levels of TSH, is estimated to occur in 4.3-8.5% of people in the United States. Hypothyroidism is more common in women than men. People over the age of 60 are more affected. Dogs are also known to develop hypothyroidism and in rare cases in cats and horses. The word "hypothyroidism" comes from the Greek hypo - which means "lessened", thyreos for "shield", and eidos for "shapes."
Video Hypothyroidism
Signs and symptoms
People with hypothyroidism often have no or only mild symptoms. Many symptoms and signs are associated with hypothyroidism, and can be attributed to underlying causes, or direct effects because they do not have enough thyroid hormone. Hashimoto's thyroiditis may present with a thyroid mass effect (enlarged thyroid gland).
Delays of relaxation after testing ankle reflexes are typical signs of hypothyroidism and are associated with the severity of hormone deficits.
Myxedema coma
Myxedema coma is a rare but life-threatening state of extreme hypothyroidism. This may occur in those who are known to have hypothyroidism when they develop other ailments, but that could be the first presentation of hypothyroidism. The disease is characterized by a very low body temperature without shivering, confusion, slow heart rate and reduced breathing effort. There may be physical signs that indicate hypothyroidism, such as skin changes or tongue enlargement.
Pregnancy
Even mild or subclinical hypothyroidism leads to the possibility of infertility and an increased risk of miscarriage. Hypothyroidism in early pregnancy, even with limited or no symptoms, may increase the risk of preeclampsia, offspring with lower intelligence, and risk of infant mortality around the time of birth. Women are affected by hypothyroidism in 0.3-0.5% of pregnancies. Subclinical hypothyroidism during pregnancy is also associated with gestational diabetes and childbirth before 37 weeks of pregnancy.
Children
Newborn children with hypothyroidism may have normal birth weight and height (although the head may be larger than expected and the posterior fontanel may be open). Some may experience drowsiness, decreased muscle tone, hoarse cry, difficulty eating, constipation, enlarged tongue, umbilical hernia, dry skin, decreased body temperature and jaundice. Mumps are rare, although they may occur later in children with thyroid gland that do not produce thyroid hormone function. Mumps can also develop in children who grow in areas with iodine deficiency. Normal growth and development may be delayed, and not treating infants can cause intellectual impairment (IQ 6-15 points lower in severe cases). Other issues include the following: large scale and fine motor skills and coordination, reduced muscle tone, squinting, reduced attention span, and delayed speech. Dental eruption may be delayed.
In older children and adolescents, hypothyroid symptoms may include fatigue, cold intolerance, drowsiness, muscle weakness, constipation, growth delay, overweight for height, pallor, coarse and thick skin, body hair increase, menstrual cycle regularly on girls, and delayed puberty. Signs may include relaxation of ankle reflex relaxation and a slow heartbeat. Mumps may be present with a fully expanded thyroid gland; sometimes only a portion of the thyroid is enlarged and can be prominent.
Maps Hypothyroidism
Cause
Hypothyroidism is caused by inadequate glandular function itself (primary hypothyroidism), inadequate stimulation of thyroid stimulating hormone from the pituitary gland (secondary hypothyroidism), or insufficient release of thyrotropin-releasing hormones from the hypothalamus of the brain (tertiary hypothyroidism). Primary hypothyroidism is about a thousand times more common than central hypothyroidism.
Iodine deficiency is the most common cause of primary hypothyroidism and endemic goiter worldwide. In regions of the world with sufficient dietary iodine, hypothyroidism is most commonly caused by autoimmune thyroiditis Hashimoto disease (chronic autoimmune thyroiditis). Hashimoto may be related to mumps. It is characterized by infiltration of the thyroid gland with T lymphocytes and autoantibodies against specific thyroid antigens such as thyroid peroxidase, thyroglobulin and TSH receptors.
After the woman gives birth, about 5% develops postpartum thyroiditis which can occur up to nine months later. This is characterized by a brief period of hyperthyroidism followed by a period of hypothyroidism; 20-40% remains permanent hypothyroid.
Autoimmune thyroiditis is associated with other immune-mediated diseases such as type 1 diabetes mellitus, pernicious anemia, myasthenia gravis, celiac disease, rheumatoid arthritis and systemic lupus erythematosus. This can occur as part of the autoimmune polyendocrine syndrome (type 1 and type 2).
In consumptive hypothyroidism, high levels of type 3 deiodinase disable thyroid hormones and cause hypothyroidism. High levels of type 3 deiodinase generally occur as a result of hemangioma. Conditions are very rare.
Pathophysiology
Thyroid hormones are required for the normal functioning of many tissues in the body. In healthy individuals, the main thyroid gland secretes thyroxine (T 4 ), which is converted into triiodothyronine (T 3 ) in other organs by enzymes that depend on selenium iodothyronine deiodinase. Triiodothyronine binds to the thyroid hormone receptor in the cell nucleus, where it stimulates the activation of certain genes and the production of specific proteins. In addition, the hormone binds integrin? V? 3 on the cell membrane, thus stimulating sodium-hydrogen antiporter and processes such as blood vessel formation and cell growth. In the blood, almost all thyroid hormones (99.97%) are bound to plasma proteins such as thyroxine-binding globulin; only unrestricted free thyroid hormones are biologically active. Overexpression of deiodinase can lead to consumptive hypothyroidism.
The thyroid gland is the only source of thyroid hormones in the body; the process requires iodine and amino acid tyrosine. Iodine in the bloodstream is taken up by the gland and inserted into the thyroglobulin molecule. This process is controlled by thyroid stimulating hormone (TSH, thyrotropin), which is secreted by the pituitary. Not enough iodine, or not enough TSH, can cause a decrease in thyroid hormone production.
The hypothalamic-pituitary-thyroid axis plays a key role in maintaining thyroid hormone levels within normal limits. TSH production by the anterior pituitary gland is stimulated alternately by thyrotropin-releasing hormone (TRH), released from the hypothalamus. Production of TSH and TRH decreases due to thyroxine through a negative feedback process. Not enough TRH, which is rare, can lead to insufficient TSH and thus insufficient production of thyroid hormones.
Pregnancy causes marked changes in the physiology of the thyroid hormone. Glands increased in size by 10%, thyroxine production increased by 50%, and iodine requirements increased. Many women have normal thyroid function but have immunological evidence of autoimmune thyroid (as evidenced by autoantibodies) or iodine deficiency, and develop evidence of hypothyroidism before or after childbirth.
Diagnosis
Laboratory testing of thyroid stimulating hormone levels in the blood is considered the best preliminary test for hypothyroidism; a second TSH level is often obtained a few weeks later for confirmation. Levels may be abnormal in the context of other illnesses, and TSH tests in hospitalized people are not recommended unless thyroid dysfunction is highly suspect. Increased levels of TSH indicate that the thyroid gland does not produce enough thyroid hormones, and free T4 levels are often obtained. Measuring T 3 is not recommended by AACE in the assessment for hypothyroidism. There are a number of symptom assessment scales for hypothyroidism; they provide a level of objectivity but have limited use for diagnosis.
Many cases of hypothyroidism are associated with a mild increase in creatine kinase and liver enzymes in the blood. They usually return to normal when hypothyroidism has been completely treated. Cholesterol levels, low-density lipoprotein and lipoprotein (a) may increase; the impact of subclinical hypothyroidism on lipid parameters is poorly defined.
Extremely severe hypothyroidism and myxedema coma are typically associated with low blood sodium levels along with increased antidiuretic hormones, and worsening of acute renal function for a number of causes.
The diagnosis of hypothyroidism without lumps or mass in the thyroid gland does not require thyroid imaging; However, if the thyroid feels abnormal, diagnostic imaging is then recommended. The presence of antibodies against thyroid peroxidase (TPO) makes it more likely that thyroid nodules are caused by autoimmune thyroiditis, but if there is any doubt, needle biopsy may be necessary.
Middle
If normal or low TSH levels and serum levels of T 4 are low, this indicates central hypothyroidism (not enough TSH or TRH secretion by the pituitary gland or hypothalamus). There may be other features of hypopituitarism, such as menstrual cycle abnormalities and adrenal insufficiency. There may also be symptoms of pituitary mass such as headache and vision changes. Central hypothyroidism should be investigated further to determine the underlying cause.
Overt
In clear primary hypothyroidism, the TSH level is high and the rate of T 4 and T 3 is low. Excessive hypothyroidism can also be diagnosed with those who have TSH on multiple occasions greater than 5mIU/L, the precise symptoms, and only the lower bound of T 4 . It can also be diagnosed with those with TSH greater than 10mIU/L.
Subclinical
Subclinical hypothyroidism is a milder form of hypothyroidism characterized by elevated serum TSH levels, but with normal serum-free thyroxine levels. This lighter form of hypothyroidism is most commonly caused by Hashimoto's thyroiditis. In adults it is diagnosed when TSH levels are greater than 5 mIU/L and less than 10mIU/L. Presentation of subclinical hypothyroidism is the signs and symptoms of variable and classic hypothyroidism may not be observed. People with subclinical hypothyroidism, the proportion will develop clear hypothyroidism every year. In those with detectable antibodies against thyroid peroxidase (TPO), this occurred in 4.3%, whereas in those undetectable antibodies, this occurred at 2.6%. Those with subclinical hypothyroidism and detectable anti-TPO antibodies that do not require treatment should repeat the thyroid function tests more frequently (eg yearly) than those who do not have antibodies.
Pregnancy
During pregnancy, the thyroid gland must produce 50% more thyroid hormone to provide enough thyroid hormones for the developing fetus and pregnant mother. In pregnancy, free thyroxine levels may be lower than anticipated due to increased binding of thyroid binding globulin and decreased binding to albumin. They should be corrected for the stage of pregnancy, or the total thyroxine level should be used instead for diagnosis. TSH values ​​may also be lower than normal (especially in the first trimester) and the normal range should be adjusted for the pregnancy stage.
In pregnancy, subclinical hypothyroidism is defined as TSH between 2.5 and 10 mIU/l with normal thyroxine levels, whereas those with TSH above 10 mIU/l are considered blatant hypothyroid even if the thyroxine level is normal. Antibodies to TPOs may be important in making decisions about treatment, and therefore should be determined in women with abnormal thyroid function tests.
Determination of TPO antibodies may be considered part of the assessment of recurrent miscarriage, because subtle thyroid dysfunction may be associated with miscarriage, but this recommendation is not universal, and the presence of thyroid antibodies may not predict future outcomes.
Prevention
Hypothyroidism can be prevented in the population by adding iodine to commonly used foods. This public health action has eliminated the endemic childhood hypothyroidism in countries where it was once common. In addition to promoting the consumption of iodine-rich foods such as milk and fish, many countries with iodine deficiency are applying universal iodized salts (USI). Driven by the World Health Organization, 130 countries now have USI, and 70% of the world's population receive iodized salt. In some countries, iodized salt is added to bread. Despite this, iodine deficiency has reappeared in some Western countries as a result of efforts to reduce salt intake.
Pregnant and lactating women, who require 66% more daily need for iodine than women who are not pregnant, may still not get enough iodine. The World Health Organization recommends a daily intake of 250 Âμg for pregnant and lactating women. Since many women will not achieve this from dietary sources alone, the American Thyroid Association recommends a daily supplement of 150 Âμg orally.
Screening
Screening for hypothyroidism is performed in newborn periods in many countries, generally using TSH. This has led to early identification of many cases and thus the prevention of developmental delays. This is the most widely used newborn screening test in the world. Although TSH-based screening will identify the most common cause, the addition of T 4 testing is required to take less frequent causes of neonatal hypothyroidism. If the determination of T 4 is included in the screening at birth, it will identify cases of congenital hypothyroidism from the central origin in 1: 16,000 to 1: 160,000 children. Considering that these children usually have other pituitary hormone deficiencies, early identification of these cases can prevent complications.
In adults, extensive screening in the general population is a matter of debate. Some organizations (such as the United States Prevention Service Task Force) state that evidence is insufficient to support routine checks, while others (such as the American Thyroid Association) recommend intermittent testing over a certain age in either sex or only in women. Targeted screening may be appropriate in a number of situations where general hypothyroidism: other autoimmune diseases, a strong family history of thyroid disease, those who have received radioiodine or other radiation therapy to the neck, those who have previously undergone thyroid surgery, those with abnormal thyroid examinations, those with psychiatric disorders, people taking amiodarone or lithium, and those with a number of health conditions (such as certain heart and skin conditions). The annual thyroid function tests are recommended in people with Down syndrome, as they are at higher risk for thyroid disease.
Management
Hormone replacement
Most people with symptoms of hypothyroidism and thyroxine deficiency are confirmed to be treated with a synthetic long-acting tiro form, known as levothyroxine ( L -thyroxine). In young and healthy people with blatant hypothyroidism, a full replacement dose (adjusted for weight) can be started immediately; in the elderly and people with heart disease, lower initial doses are recommended to prevent excessive supplementation and the risk of complications. Lower doses may be enough in those with subclinical hypothyroidism, while people with central hypothyroidism may require higher doses than average.
Thyroxine and blood-free TSH levels are monitored to help determine if the dose is adequate. This is done 4-8 weeks after the start of treatment or changes in levothyroxine dose. Once an adequate replacement dose has been established, the test may be repeated after 6 and then 12 months, unless there is a change in symptoms. In people with central/secondary hypothyroidism, TSH is not a reliable marker for hormone replacement and decisions are based primarily on free T 4 levels. Levothyroxine should be taken 30-60 minutes before breakfast, or four hours after meals, as certain substances such as food and calcium may inhibit levothyroxine absorption. There is no direct way to increase thyroid hormone secretion by the thyroid gland.
Liothyronine
Adding liothyronine (synthetic T 3 ) to levothyroxine has been suggested as a measure to provide better symptom control, but this has not been confirmed by the study. In 2007, the British Thyroid Association stated that combination therapy T 4 and T 3 carries a higher rate of side effects and no benefit over T 4 alone. Similarly, American guidelines prevent combination therapy due to lack of evidence, although they recognize that some people feel better when receiving combination treatments. Treatment with liothyronine alone has not received sufficient studies to make recommendations for its use; because the shorter half-life needs to be taken more often.
People with hypothyroidism who do not feel well despite optimal levothyroxine doses may request additional treatment with liothyronine. The 2012 Guideline of the European Thyroid Association recommends that support should be offered with regard to the chronic nature of the disease and that other causes of the symptoms should be excluded. The addition of liothyronine should be regarded as experimental, initially only for a 3 month trial period, and in the ratio prescribed with the current levothyroxine dose. This guide explicitly aims to improve the security of this approach and to counter random use.
Dryed animal thyroid
The dried thyroid extract is an animal-based thyroid gland extract, most commonly from pigs. This is a combination therapy, which contains the form T 4 and T 3 . It also contains calcitonin (a hormone produced in the thyroid gland involved in the regulation of calcium levels), T 1 and T 2 ; this is not in synthetic hormone drugs. This extract has been a major hypothyroidism treatment, but its current use is not supported by evidence; The British Thyroid Association and American professional guides do not recommend its use.
Subclinical hypothyroidism
There is little evidence of whether there is benefit from treating subclinical hypothyroidism, and whether this offsets the risk of overtreatment. Untreated subclinical hypothyroidism may be associated with a moderate increase in the risk of coronary artery disease. A 2007 review found no benefit of thyroid hormone replacement except for "some lipid profile parameters and left ventricular function". There is no association between subclinical hypothyroidism and an increased risk of fracture, nor is there any association with cognitive decline.
Since 2008, the American consensus and British opinion is that in general people with TSH below 10 mIU/l do not require treatment. The American Guidelines recommend that treatment should be considered in people with symptoms of hypothyroidism, detectable antibodies to thyroid peroxidase, history of heart disease or on increased risk for heart disease, if TSH is elevated but below 10 mIU/l.
Myxedema coma
Myxedema coma or severe decompensated hypothyroidism usually requires intensive care, rigorous observation and treatment of respiratory disorders, temperature control, blood pressure, and sodium levels. Mechanical ventilation may be necessary, such as fluid replacement, vasopressor agent, cautious warming, and corticosteroids (for possible adrenal insufficiency that may occur along with hypothyroidism). Careful correction of low sodium levels can be achieved with hypertonic saline solutions or vasopressin receptor antagonists. For rapid treatment of hypothyroidism, levothyroxine or liothyronine may be administered intravenously, especially if the level of consciousness is too low to safely ingest the drug. Although administration via a nasogastric tube is possible, it may be unsafe and not recommended.
Pregnancy
In women with known hypothyroidism becoming pregnant, it is recommended that serum TSH levels be closely monitored. Levothyroxine should be used to keep TSH levels within the normal range for the trimester. The first normal trimester range below 2.5 mIU/L and the second and third trimesters of the normal range is below 3.0 mIU/L. Treatment should be guided by total thyroxine (not free) or with T 4 free. Similarly for TSH, the thyroxine yield should be interpreted according to the appropriate reference range for the stage of pregnancy. Dose of levothyroxine often needs to be improved after pregnancy is confirmed, although this is based on limited evidence and some recommend that it is not always necessary; decisions may need to be based on TSH levels.
Women with anti-TPO antibodies that attempt to conceive (naturally or with help) may require thyroid hormone supplementation even if the TSH level is normal. This is especially true if they have had a previous miscarriage or have had hypothyroidism in the past. Additional Levothyroxine may reduce the risk of preterm birth and the possibility of miscarriage. This recommendation is stronger in pregnant women with subclinical hypothyroidism (defined as TSH 2.5-10 mIU/l) that is anti-TPO positive, given the overt risk of hypothyroidism. If a decision is made untreated, close monitoring of thyroid function (every 4 weeks in the first 20 weeks of pregnancy) is recommended. If anti-TPO is not positive, treatment for subclinical hypothyroidism is currently not recommended. It has been suggested that many of the recommendations mentioned above may lead to unnecessary treatment, in the sense that the TSH cutoff rate may be too tight in some ethnic groups; there may be little benefit from the treatment of subclinical hypothyroidism in certain cases.
Epidemiology
Worldwide about one billion people are estimated to be iodine deficient; However, it is unknown how often this results in hypothyroidism. In large population-based studies in Western countries with sufficient dietary iodine, 0.3-0.4% of the population had blatant hypothyroidism. A larger proportion, 4.3-8.5%, has subclinical hypothyroidism. People with subclinical hypothyroidism, 80% have TSH levels below 10 mIU/l considered a threshold for treatment. Children with subclinical hypothyroidism often return to normal thyroid function, and a small fraction develops blatant hypothyroidism (as predicted by antibody evolution and TSH levels, celiac disease, and mumps).
Women are more likely to develop hypothyroidism than men. In population-based studies, women were seven times more likely than men to have TSH levels above 10 mU/l. 2-4% of people with subclinical hypothyroidism will develop into open hypothyroidism every year. The risk is higher in those who have antibodies to thyroid peroxidase. Subclinical hypothyroidism is thought to affect about 2% of children; in adults, subclinical hypothyroidism is more common in older people, and in Caucasians. There is a much higher rate of thyroid disorders, the most common being hypothyroidism, in individuals with Down syndrome and Turner syndrome.
Severe hypothyroidism and myxedema coma are rare, with estimates occurring at 0.22 per million people per year. Most cases occur in women over the age of 60, although it can occur in all age groups.
Most hypothyroidism is the major in nature. Secondary/secondary hypothyroidism affects 1: 20,000 to 1: 80,000 population, or about one in every thousand people with hypothyroidism.
History
In 1811, Bernard Courtois discovered iodine present in seaweed, and iodine intake was associated with a measure of goiter in 1820 by Jean-Francois Coindet. Gaspard Adolphe Chatin was proposed in 1852 that endemic goitre is the result of insufficient iodine intake, and Eugen Baumann showed iodine in the thyroid tissue in 1896.
The first cases of myxedema were recognized in the mid-19th century (1870s), but their relationship to the thyroid was not discovered until 1880 when myxedema was observed in people after removal of the thyroid gland (thyroidectomy). This link was further confirmed in the late 19th century when people and animals who had undergone their thyroid showed improvements in symptoms with transplantation of animal thyroid tissue. The severity of myxedema, and the associated risk of death and complications, creates an interest in finding effective treatments for hypothyroidism. The transplantation of the thyroid tissue shows some efficacy, but recurrence of hypothyroidism is relatively common, and sometimes it takes several recurrent transplants from the thyroid tissue.
In 1891, British physician George Redmayne Murray introduced a subcutaneously injected therapeutic thyroid extract, followed immediately after oral formulation. The purified thyroxine was introduced in 1914 and by the 1930s synthetic thyroxine became available, although the extract of dry animal thyroid remained widely used. Liothyronine was identified in 1952.
Early attempts for titration therapy for hypothyroidism have proved difficult. After hypothyroidism was found to cause lower basal metabolic rates, it was used as a marker to guide adjustment in therapy in the early 20th century (circa 1915). However, low basal metabolic rates are known to be non-specific, also present in malnutrition. The first laboratory test useful in assessing the status of the thyroid is a serum protein bound to iodine, which began to be used around the 1950s.
In 1971, thyroid stimulating hormone (TSH) radioimmunoassay was developed, which is the most specific marker for assessing thyroid status in patients. Many people who are being treated based on basal metabolic rates, minimizing hypothyroid symptoms, or by serum iodine-bound proteins, are found to have excessive thyroid hormones. The following year, in 1972, radioimmunoassay T3 was developed, and in 1974, a T4 radioimmunoassay was developed.
Other animals
In veterinary practice, dogs are the species most frequently exposed to hypothyroidism. Most cases occur as a result of primary hypothyroidism, where two types are recognized: lymphocytic thyroiditis, which may be immune-driven and lead to the destruction and fibrosis of the thyroid gland, and idiopathic atrophy, leading to the gradual replacement of the gland by fat tissue. There is often lethargy, cold intolerance, exercise intolerance, and weight gain. Furthermore, skin changes and fertility problems are seen in dogs with hypothyroidism, as well as a number of other symptoms. Signs of myxedema can be seen in dogs, with protruding folds of skin on the forehead, and myxedema coma cases are encountered. Diagnosis can be confirmed by blood tests, because clinical impression alone can lead to overdiagnosis. Lymphocytic thyroiditis is associated with detectable antibodies against thyroglobulin, although they usually become undetectable in advanced disease. Treatment is by thyroid hormone replacement.
Other less common species affected include cats and horses, as well as other large domestic animals. In cats, hypothyroidism is usually the result of other medical treatments such as surgery or radiation. In young horses, congenital hypothyroidism has been reported primarily in Western Canada and has been associated with maternal diet.
References
External links
- Hypothyroidism at Curlie (based on DMOZ)
- "Information hypothyroidism for patients". American Thyroid Association . Retrieved 2017/03/25 "UK Guidelines for the use of thyroid function tests" (PDF) . The Association of Clinical Biochemistry, the British Thyroid Association and the British Thyroid Foundation. 2006 . Retrieved 2013/12/25
- Alexander, EK; Pearce, EN; Brent, GA; Brown, RS; Chen, H; Dosiou, C; Grobman, W; Laurberg, P; Lazarus, JH; Mandel, SJ; Peeters, R; Sullivan, S (January 6, 2017). "2016 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Diseases during Pregnancy and Postpartum". Thyroid: the official journal of the American Thyroid Association . 27 : 315-389. doi: 10.1089/thy.2016.0457. PMIDÃ, 28056690
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