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Levothyroxine Pregnancy

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Last Updated: 20 September 2020

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Primary hypothyroidism is common, occurring in 3 to 10 percent of women, frequently with its onset during childbearing years. 1 2 estimate 1 to 2 percent of all pregnant women receive levothyroxine therapy for hypothyroidism. Epidemiologic studies indicate that 0. 4 percent of pregnant women have serum thyrotropin concentrations above 10 U per milliliter at 15 to 18 weeks of gestation. 3 4 Thus, in the United States alone, minimum of 12 000 to 16 000 infants are born each year to women with either inadequately treated or undiscovered primary hypothyroidism. 5 6 During pregnancy, Women's Thyroid physiology undergoes well - defined changes, including an approximate doubling in thyroxine - binding globulin concentrations due to increases in estradiol concentrations, as well as a 30 to 40 percent increase in plasma volume. 7 - 11 these changes result in a significant increase in total thyroxine pool, primarily during the first trimester. This increment may be provided largely by thyroid stimulation induced by human chorionic gonadotropin, 7 810 since slight increase in free thyroxine and reduction in thyrotropin occur at 9 to 12 weeks of gestation. 8 12 in general, however, thyrotropin concentration stays within normal range for the remainder of pregnancy, despite an estimated 30 to 50 percent increase in levothyroxine requirement. 9 10 13 - 15 although this process is now recognized by endocrinologists and some hypothyroid patients are alert to the need for such an increase, many pregnant women are found to have high serum thyrotropin concentration at time of their initial obstetrical examination, at 8 to 12 weeks of gestation. 3 410 13 16 - 22 Thus, current practice permits transient period of Maternal hypothyroxinemia in the first trimester, which is time when free thyroxine concentration is typically slightly increase. It is known that a pregnant woman is the sole source of fetal supply of Thyroid hormones from conception to approximately 13 weeks of gestation when fetal Thyroid function has develop. Give possible association between gestational hypothyroidism and impaired intellectual and cognitive development in offspring, as well as increased rate of fetal death in women with elevated thyrotropin concentration, 3 20 23 24 current approach is suboptimal. In this prospective study, we seek to delineate precise timing and pattern of increased thyroid hormone requirement during pregnancy in order to determine appropriate recommendations for preventing first - trimester hypothyroidism. We use a strategy involving frequent monitoring of serum thyrotropin concentrations with concomitant adjustments in dose of levothyroxine to maintain thyrotropin at preconception concentrations. Women with primary hypothyroidism who desired pregnancy were recruited from Endocrine outpatient clinics at Brigham and Women's Hospital, Boston. Maternal Thyroid function, estradiol, and human chorionic gonadotropin were measured before and during pregnancy. Our goal was to assess biochemical thyroid status after first miss menstrual cycle, every two weeks throughout first trimester, and monthly thereafter until completion of pregnancy. This aim was achieved in most, but not all, subjects. At each visit, two aliquots of serum were obtain. First was frozen and saved for batch analysis at completion of study.

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8. Cautions with other medicines

Some medicines can interfere with Thyroid Hormones, so the dose of levothyroxine may need to be change. They include: medicines for seizures, carbamazepine and phenytoin rifampicin amiodarone oestrogens - such as in combined contraceptive pills or hormone replacement therapy levothyroxine can change how other medicines work, so their doses may need to be alter. These medicines include: medicines for diabetes - either insulin or tablets blood thinning medicine, warfarin Some medicines shouldn't be taken at the same time of day as levothyroxine as they can reduce the amount of levothyroxine your body takes in, including: antacids, calcium salts, iron salts, orlistat, medicine Use for weight loss sucralfate, medicine Use to treat stomach ulcers some cholesterol - lowering medicines such as colestyramine, colestipol or colesevelem read Information Leaflet supply with these medicines or speak to your pharmacist for advice on how much time to leave between taking these medicines and taking levothyroxine. The thyroid gland in your neck makes a hormone called thyroxine. Thyroxine controls how much energy your body Use. It's also involved in digestion, how your heart and muscles work, brain development and bone health. When the thyroid gland doesn't make enough thyroxine, many of the body's functions slow down. Some of the most common symptoms of underactive Thyroid gland are: tiredness, feeling cold, difficulty concentrating, weight gain, feeling depressed. Levothyroxine is a synthetic version of thyroxine. You take levothyroxine tablets to replace thyroxine that your thyroid gland can't produce and prevent symptoms of hypothyroidism. If you have underactive Thyroid, you are entitled to free prescriptions for all of your medicines. To claim your free prescriptions you 'll need to have a medical exemption certificate. The application form for medical exemption certificate is called FP92A. You can get this from your doctor's surgery. You will need to fill in the form, then your doctor will sign it and send it off. It's having underactive thyroid that causes hair loss - not treatment with levothyroxine. Because the natural hair growth cycle takes several months, hair loss related to Thyroid disease might only be seen months after illness has begin. If treatment with levothyroxine has already start, it may seem like medicine - rather than underlying illness - is causing hair loss. Hair usually regrow after treatment with levothyroxine, but it may take many months.


5. Side effects

Pseudotumor cerebri and slip capital femoral epiphysis have been reported in children receiving levothyroxine therapy. Overtreatment may result in craniosynostosis in infants and premature closure of epiphyses in children with resultant compromise adult height. Seizures have been reported rarely with institution of levothyroxine therapy. Inadequate levothyroxine dosage will produce or fail to ameliorate signs and symptoms of hypothyroidism. Hypersensitivity reactions to inactive ingredients have occurred in patients treated with thyroid hormone products. These include urticaria, pruritus, skin rash, flushing, angioedema, various GI symptoms, fever, arthralgia, serum sickness and wheezing. Hypersensitivity to levothyroxine itself is not known to occur.


Interactions

Many drugs affect thyroid hormone pharmacokinetics and metabolism and may alter therapeutic response to SYNTHROID. In addition, thyroid hormones and thyroid status have varying effects on pharmacokinetics and actions of other drugs. A Listing of drug - thyroidal axis interactions is contained in Table 2. The list of drug - thyroidal axis interactions in Table 2 may not be comprehensive due to the introduction of new drugs that interact with thyroidal axis or discovery of previously unknown interactions. Prescribers should be aware of this fact and should consult appropriate reference sources for additional information if drug - drug interaction with levothyroxine is suspect.

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Results:

Thyroid disease is the second most common endocrine disease to affect women of reproductive age. Thyroid disorders can have adverse reproductive and pregnancy implications. Although gestational hyperthyroidism is uncommon, gestational hypothyroidism occurs in higher prevalence and can lead to neonatal and child neurodevelopmental deficits and maternal obstetric complications. 1 2 in addition to overt thyroid dysfunction, pregnancy may unveil subclinical hyperthyroidism and hypothyroidism. Women who have been diagnosed with Thyroid gland dysfunctions are usually treated and are able to complete a normal pregnancy. Thyroid - relate pathophysiologic changes aggravated by pregnancy, and some obstetric conditions, such as gestational trophoblastic disease or hyperemesis gravidarum, may affect Thyroid gland function and impact maternal - fetal Thyroid hormone balance. Trimester - specific reference intervals for Thyroid function tests are critical for maintaining a delicate balance of Thyroid hormones during pregnancy. Pregnancy induces complex changes in circulating maternal steroid hormones and Thyroid binding globulin concentrations. In addition to the stimulatory effects of estrogen on TBG synthesis, major contribution to increasing TBG concentration during pregnancy is reducing plasma clearance of protein caused by changes in TBG glycosylation induced by estrogen. It is commonly thought that total thyroxine and total triiodothyronine concentration increase in the setting of pregnancy - induced increases in serum TBG concentrations. Concentrations of TBG double by weeks 16 to 20 of gestation. 3 in addition to 2 - to 3 - fold increase in serum TBG, modest decreases in both serum transthyretin and albumin are commonly found in pregnancy. 4 Free T3 and Free T4 levels are slightly lower in the second and third trimesters. Thyroid - stimulating hormone levels are low - normal in the first trimester, with normalization in the second trimester. Delivery leads to rapid reversal of this process, resulting in serum TBG, T4, and T3 concentrations returning to pregestational levels within 4 to 6 weeks. To detect abnormalities in thyroid hormone concentrations during progression of pregnancy, it is necessary to determine their normal ranges throughout pregnancy by defining reference intervals for each trimester. Reference intervals will be different when the population is Iodine deficient. Maternal overt and subclinical Thyroid disorders and dysfunction are associated with complications of pregnancy and both short - and long - term consequences for mother and child. These risks seem to be increased in women with euthyroid autoimmune Thyroid disease. Hypothyroidism during pregnancy is associated with gestational hypertension and low birth weight. Women who are on Thyroid replacement therapy before pregnancy may require an increase in dosage during pregnancy. Pregnant women with chronic autoimmune thyroiditis have a higher incidence of spontaneous miscarriage. Women with high TSH levels had a > 3 - fold increase in risk of very preterm delivery, and in some analyses, girls who tested positive for antithyroglobulin antibody at entry to prenatal care also had a > 2 - fold increased risk of very preterm delivery. 2 5 Women with autoimmune Thyroid disease before pregnancy are at increased risk for Thyroid insufficiency during pregnancy and postpartum thyroiditis and should be monitored with TSH measurements during pregnancy.

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Statistical Analysis

Descriptive statistical data were compared with use of the Wilcoxon rank - sum test or chi - square test and are presented according to subject or pregnancy, as appropriate. Changes in results of Thyroid - Function tests, human chorionic gonadotropin and estradiol concentrations, and levothyroxine doses throughout pregnancy were graphed with use of locally weighted polynomial regression to achieve best - fit curve throughout pregnancy, with no attempt to document statistical significance. To assess the statistical significance of changes in various response variables during pregnancy, results before pregnancy and at 10 20 30, and 38 weeks of gestation were analyzed by repeat - measures analysis of variance and by post hoc subgroup comparisons with use of the Newman - Keuls test. All data was analyzed with the use of SPSS software, version 11. 0 P values of less than 0. 05 were considered to indicate statistical significance.

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Continued

For women inheriting this genetic mutation, pregnancy can be problematic. If her baby does not inherit mutation, her excess thyroid hormones will be excessive for the fetus, Refetoff explains. This group of women represents a very unique opportunity to study this problem, he say. His research group analyzed medical records for 167 members of this family, including 36 couples. They compare pregnancies of affected mothers or affected fathers against those without mutation - looking at miscarriage rates, and at newborns ' birth weights and Thyroid hormone levels. If pregnancy had affected the mother, there were more miscarriages - 23% more, compared with 2% For pregnancies where the father was affected and 4% in pregnancies with unaffected mothers. Babies born to affected mothers were significantly smaller than babies born to unaffected mothers. Because of mothers ' high levels of Thyroid hormone, newborn infants with normal Thyroid systems respond by not making Thyroid hormone of their own. Within a few weeks of life, they start to make their own Thyroid hormone. Unaffected mothers had normal rates of miscarriages and deliveries; they gave birth to equal numbers of affected and unaffected babies. Normal miscarriages for the general population is 8%, he add. His data shows that high levels of this hormone can exert a direct toxic effect on fetal development, writes Refetoff. It is important to recognize that overreplacement appears to be. Detrimental. Nevertheless, thyroid problems are important but manageable, seely say. We don't want to panic Women who have Thyroid problems and are planning to get pregnant should discuss changes in Thyroid hormone dose with their doctor. If you find yourself pregnant and haven't planned it, get a blood test right away, she advise. The test is called the Thyroid - stimulating hormone test. It usually has a turnaround of 24 hours. Then you can get dosage adjustment make. Most miscarriages are caused by chromosomal defects - not by factors such as hormone levels, points out Ashi Daftary, MD, professor of Maternal and fetal Medicine at University of Pittsburgh School of Medicine. Most women taking Thyroid Medicine won't require change during pregnancy, he told WebMD. Instead of making a 30% adjustment in her medication - based on the mere fact that she's pregnant, doctor should follow her very closely very early, so appropriate adjustments can be make. A sizeable number of women taking Thyroid medication will not need any increase in dosage.

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Methods

From 630 articles retrieve, we include three trials with data on 220 patients. One of these three trials states live delivery as outcome. Lt4 treatment resulted in a significantly higher delivery rate, with a pooled relative risk of 2. 76, pool absolute risk difference of 36. 3% and summary number need to treat of 3 in favour of LT4 supplementation. Lt4 treatment significantly lowers the miscarriage rate with a pooled RR of 0. 45, pool ARD of 31. 3% and summary NNT of 3 in favour of LT4 supplementation. Lt4 treatment had no effect on clinical pregnancy. In ART setting, no data is available on effects of LT4 supplementation on premature delivery, arterial hypertension, placental abruption or pre - eclampsia.

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Introduction

Thyroid disorders are common in pregnancy and relate to maternal and fetal complications. Hyperthyroidism occurs in 0. 1 - 0. 4% of pregnant women. Whereas about 2 - 3% of pregnant women are hypothyroid, of whom 0. 3 - 0. 5% have overt hypothyroidism and 2 - 2. 5% present subclinical hypothyroidism. At least 5 - 10% of women are positive for Thyroid antibodies and have an increased risk of developing a certain degree of Thyroid insufficiency during pregnancy. Thyroid function is influenzed by pregnancy and its dysfunction is associated with maternal and fetal morbidity. Moreover, role of subclinical hypothyroidism in developing fetal and maternal complications is not univocal. Indeed, subclinical hyperthyroidism is not associated with adverse outcomes. Thyroid autoimmunity appears to be associated with increased risk of miscarriage and preterm delivery. In this article we aim to review possible adverse maternal and fetal outcomes of Thyroid during pregnancy and proper management of these conditions to avoid such complications.

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Thyroid Function Tests in Pregnancy

What ARE NORMAL CHANGES in THYROID FUNCTION associated WITH PREGNANCY? Hormone CHANGES. Thyroid FUNCTION tests change DURING NORMAL PREGNANCY due to the influence of two main hormones: human chorionic gonadotropin and estrogen. Because hCG can weakly stimulate THYROID, high circulating hCG levels in the first trimester may result in low TSH that return to NORMAL throughout the duration OF PREGNANCY. Estrogen increases the amount of THYROID HORMONE binding proteins, and this increases total THYROID HORMONE levels, but free HORMONE usually remains NORMAL. Thyroid functions normally if TSH and Free T4 remain in Trimester - specific NORMAL ranges throughout PREGNANCY. Thyroid SIZE CHANGES. Thyroid gland can increase in size DURING PREGNANCY. However, PREGNANCY - associate goiters occur much more frequently in iodine - deficient areas of the world. It is relatively uncommon in the United States. If very sensitive imaging techniques ARE used, it is possible to detect an increase in THYROID volume in some women. This is usually only a 10 - 15% increase in SIZE and is not typically apparent on physical examination by a physician. However, sometimes significant goiters may develop and prompt doctors to measure tests OF THYROID FUNCTION. For the first 18 - 20 weeks of PREGNANCY, baby is completely dependent on mother for production OF THYROID HORMONE. By mid - PREGNANCY, babys THYROID begin to produce THYROID HORMONE on its own. The baby, however, remains dependent on the mother for ingestion OF adequate amounts of iodine, which is essential to make THYROID hormones. The World Health Organization recommends iodine intake OF 250 micrograms / day DURING PREGNANCY to maintain adequate THYROID HORMONE production. Because iodine intakes in PREGNANCY ARE currently low in the United States, ATA recommends that US women who ARE planning to become pregnant, who ARE pregnant, or breastfeeding, should take daily supplement containing 150 mcg OF iodine. What ARE the MOST COMMON CAUSES OF HYPOTHYROIDISM DURING PREGNANCY? Overall, COMMON cause OF HYPOTHYROIDISM is an autoimmune disorder known as Hashimotos thyroiditis. Hypothyroidism can occur DURING PREGNANCY due to initial presentation OF Hashimotos thyroiditis, inadequate treatment OF woman already known to have HYPOTHYROIDISM from a variety OF CAUSES, or over - treatment OF hyperthyroid women WITH anti - THYROID medications. Approximately, 2. 5% OF women will have a TSH OF greater than 6 mIU / L and 0. 4% will have TSH greater than 10 mIU / L DURING PREGNANCY. Untreated, or inadequately treat, HYPOTHYROIDISM has increased the risk OF miscarriage, and has been associated with maternal anemia, myopathy, congestive heart failure, pre - eclampsia, placental abnormalities, and postpartum hemorrhage. These complications ARE more likely to occur in women WITH severe HYPOTHYROIDISM. Some risks also appear to be higher in women WITH antibodies against THYROID peroxidase. Women WITH mild HYPOTHYROIDISM may have no symptoms or attribute symptoms they have to PREGNANCY. Thyroid HORMONE is critical for brain development in baby. Children born WITH congenital HYPOTHYROIDISM can have severe cognitive, neurological and developmental abnormalities if the condition is not recognized and treated promptly.

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Preconception Counseling

Subclinical hypothyroidism is a mild form of hypothyroidism defined as elevated TSH concentration in conjunction with normal free thyroxine levels. It is a common diagnosis among women of reproductive age and, as such, it can affect women planning conception and pregnant women. Owing to the nonspecific nature of hypothyroidism - related symptoms, diagnosis of SCH is based on laboratory testing. In contrast to the negative impact on conception and pregnancy of overt hypothyroidism, in which TSH is elevated and FT4 level is below normal, impact of SCH remains unclear. In some studies, it has been associated with infertility, increased risk of adverse pregnancy and neonatal outcomes, and possibly with increased risk of neurocognitive deficits in offspring. However, other studies have not found Association of SCH with Adverse outcomes. The Recommend treatment for maternal overt hypothyroidism is administration of oral Levothyroxine. The question that clinicians are called to answer is the following: Is SCH also a disease requiring treatment or is it just biochemical diagnosis with no clinical consequences? Although there are few observational studies suggesting the beneficial effect of LT4 treatment in pregnant women with SCH, results from large randomized trials suggest the opposite. This review discusses evidence informing clinical strategy for using LT4 in women with SCH during pregnancy and those who are planning conception, focusing on benefits and risks of treatment. We also consider issues relating to monitoring and duration of treatment.


CONCLUSION

Sch is associated with multiple adverse pregnancy and neonatal outcomes. Lt4 treatment has been associated with better reproductive outcomes in women undergoing artificial reproductive techniques and decreased risk for pregnancy loss and preterm delivery when TSH is > 4. 0 mIU / L. However, well - conduct, large randomized trials with LT4 intervention at an early stage of pregnancy or preconception are still needed in this field to refine available information. In the meantime, both clinicians and patients with SCH in pregnancy still face uncertainty about the effect of thyroid hormone treatment on maternal and neonatal outcomes. During consultation, clinicians and patients should engage in long and careful consideration of current evidence in the context of patients ' values and preferences to determine whether LT4 therapy initiation is the best next step.

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Hyperthyroidism

What ARE the MOST COMMON CAUSES OF HYPERTHYROIDISM DURING PREGNANCY? Overall, most COMMON cause OF HYPERTHYROIDISM in women of childbearing age is Graves Disease, which occurs in 0. 2% OF pregnant patients. In addition to other usual CAUSES OF HYPERTHYROIDISM, very high levels OF hCG, seen in severe forms of morning sickness, may cause transient HYPERTHYROIDISM in early PREGNANCY. Correct diagnosis is based on careful review OF history, physical exam and laboratory testing. Go to HYPERTHYROIDISM in PREGNANCY Brochure > WHAT ARE MOST COMMON CAUSES OF HYPOTHYROIDISM DURING PREGNANCY? Overall, COMMON cause OF HYPOTHYROIDISM is an autoimmune disorder known as Hashimotos thyroiditis. Hypothyroidism can occur DURING PREGNANCY due to initial presentation OF Hashimotos thyroiditis, inadequate treatment OF woman already known to have HYPOTHYROIDISM from a variety OF CAUSES, or over - treatment OF hyperthyroid women with anti - Thyroid medications. Approximately, 2. 5% OF women will have a TSH OF greater than 6 mIU / L and 0. 4% will have TSH greater than 10 mIU / L DURING PREGNANCY. Go to HYPOTHYROIDISM in PREGNANCY Brochure >


Hypothyroidism and pregnancy

Uncontrolled hyperthyroidism has many effects. It may lead to preterm birth and low birth weight for the baby. Some studies have shown an increase in pregnancy - induced hypertension in women with hyperthyroidism. A severe, life - threatening form of hyperthyroidism, called thyroid storm, may complicate pregnancy. This is a condition in which there are extremely high levels of thyroid hormone that can cause high fever, dehydration, diarrhea, rapid and irregular heart rate, shock and death, if not treat. It is always best to plan for pregnancy and to consult with your physician to ensure your thyroid status and treatment are optimized prior to becoming pregnant and monitored throughout your pregnancy. However, if this does not happen and you find out you are pregnant, you should contact your physician immediately to arrange for increased testing of your thyroid functions and potential change in your medication.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Postpartum Thyroid Dysfunction

Women with subclinical hypothyroidism initially diagnosed during pregnancy comprise between 2 and 15% of pregnant women. Many, but not all, of these women will be Thyroid antibody positive. Once diagnose, recommendation for Thyroid antibody positive Women of Both American Thyroid Association and Endocrine Society is to begin levothyroxine therapy. Study by Abalovich et al. Base its initial treatment recommendations on the level of TSH at diagnosis and does not take Thyroid antibody status into consideration. Specifically, recommendation was to initiate levothyroxine at dose of 1. 20 g / kg / day in women with TSH 4. 2 mIU / L and 1. 42 g / kg / day If TSH is between 4. 2 and 10. 0 mIU / L. My practice is to begin treatment with levothyroxine dose of between 50 and 75 g / day and to reassess TSH in 4 - 6 weeks. In deciding on the postpartum dose of levothyroxine, I postulate that prior to pregnancy, patient had underlying Hashimotos thyroiditis and was either euthyroid with limited reserve or already had subclinical hypothyroidism. At present, literature does not exist informing us what percentage of women diagnosed with subclinical hypothyroidism in gestation were euthyroid prior to pregnancy and what percentage already had subclinical hypothyroidism. In making therapeutic decisions for this group of women, I make treatment decisions under the assumption that it is best to avoid subclinical hypothyroidism in immediate postpartum when woman is lactating and adjusting to the rigors of life with newborn. Therefore, I recommend that all women in this group be maintain on levothyroxine in immediate Postpartum. Once again, it can be assumed that the dose of levothyroxine required following delivery is less than the dose needed to maintain euthyroidism in the third trimester. Consequently, I would recommend that immediately postpartum, levothyroxine dose be decreased to half of the final dose administered during gestation. Follow - up Thyroid function tests should be performed at first postpartum visit.


Impact of Postpartum Thyroiditis

Postpartum thyroiditis is defined as development of hypothyroidism, thyrotoxicosis or both in the year following delivery, in any woman who does not have clinical evidence of thyroid disease before pregnancy. 2 It occurs in 7 - 10% of postpartum women, although this varies depending on iodine intake and genetic factors. 2 investigation for postpartum thyroiditis is recommended if there is clinical suspicion and it should be considered as differential diagnosis in women presenting with depressive symptoms in the postpartum period. Almost 50% of women with antithyroid peroxidase antibodies in early pregnancy will develop postpartum thyroiditis,. Therefore, it is the most useful marker for identifying those at risk. 27 Thyroid function tests are indicated at three and six months postpartum in these women and those with known autoimmune disease, previous postpartum thyroiditis or chronic viral hepatitis. 2 annual TSH tests for 5 - 10 years are recommended for women with a history of postpartum thyroiditis. They have an increased risk of developing permanent overt hypothyroidism.

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Sources

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