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Thyroid hormones are easy to take. Because it stays in your system for a long time, it can be taken just once a day, and this results in very stable levels of Thyroid hormone in the blood stream. When Thyroid hormone is used to treat hypothyroidism, goal of treatment is to keep thyroid function within the same range as people without Thyroid problems. Keeping TSH level in normal range do this. The best time to take Thyroid hormone is probably first thing in the morning on an empty stomach. This is because food in the stomach can affect absorption of thyroid hormone. However, most important thing is to be consistent, and take your thyroid hormones at same time, and in the same way, every day. If you are taking several other medications, you should discuss the timing of your Thyroid hormone dose with your physician. Sometimes taking your Thyroid hormone at night can make it simpler to prevent your Thyroid hormone from interacting with food or other medications. Do not stop your thyroid hormones without discussing this with your physician. Most Thyroid problems are permanent, and therefore, most patients require Thyroid hormones for life. If you miss dose of thyroid hormone, it is usually best to take the missed dose as soon as you remember. It is also safe to take two pills the next day; one in the morning and one in the evening. It is very important that your Thyroid hormone and TSH levels are checked periodically, even if you are feeling fine, so that your dose of Thyroid hormone can be adjusted if needed. Taking other medications can sometimes cause people to need higher or lower doses of Thyroid hormone. Medications that can potentially cause people to need different doses of thyroid hormone include birth control pills, estrogen, testosterone, some anti - seizure medications, and some medications for depression. Yet other products can prevent absorption of full dose of Thyroid hormone. These include iron, calcium, soy, certain antacids and some cholesterollowering medications. For all these reasons, it is important for people taking Thyroid hormone to keep their physician up to date with any changes in medications or supplements they are taking. Since thyroid hormone is a hormone normally present in the body, it is absolutely safe to take while pregnant. Indeed, it is very important for pregnant women, or women who are planning to become pregnant, to have normal thyroid function to provide an optimum environment for their baby. Women who are taking Thyroid hormone often need increased dose of Thyroid hormone during their pregnancy, so it is important to have Thyroid hormone and TSH levels measured once you know that you are pregnant. You should discuss the timing of Thyroid blood tests with your physician, but often thyroid function is checked at least every trimester. Desiccate animal thyroid, now mainly obtained from pigs, was the most common form of Thyroid therapy before individual active Thyroid hormones were discover.
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Hypothyroidism is a condition classified by underactive Thyroid gland when the thyroid does not produce enough hormones. There are various treatments available depending on the cause of insufficient hormone production, but the standard of care is the sameinitiating Thyroid hormone Replacement therapy. To best understand the purpose of Thyroid hormone Replacement therapy, it helps to appreciate the role and interaction of T3 and T4the, two primary Thyroid hormones. T3 and T4 full names of T3 are triiodothyronine, and T4's full name is tetraiodothyronine or thyroxine. T3 and T4 control your body's metabolism. If you don't have enough of these hormones, then your metabolism slows down. Your metabolic rate dictates how quickly you process food, how fast your heart beats, how much heat your body producesand even how quickly you can think. In essence, T3 and T4 are in charge of how your body uses energy. T3 and T4 are not equal in strength; T3 is the more active hormone of the two. While T3 is stronger, taking synthetic T4 hormone has been considered standard treatment for Hypothyroidism. The reason for this is because most of T3 in our bodies actually used to be T4. When T4 hormones come into contact with other cells in the bloodstream, they give up iodine atom to interact with those cells. When T4 loses iodine atom, it becomes T3. When this T4 To T3 conversion occurs, T3 then conveys metabolic message to other cells throughout the body. The benefit of taking only T4 therapy is that you re allow your body to perform some of the actions it is meant to do, which is taking T4 and changing it into T3. The half - life of T4 is also longer compared to T3,. That means that it will stay for longer time in your body after ingestion. However, there is growing consensus among experts that providing supplement of both T3 and T4 is beneficial for many patients who have had total thyroidectomy. If you are prescribed a form of Thyroid hormone Replacement therapy, goal is to compensate for lack of hormone secreted by your Thyroid gland. In most cases, you will take a daily dose of T4 in pills orally. But it's important to understand that every patient's therapy may be different. There is no cookie - cutter dosage or treatment plan when it comes to Thyroid hormone Replacement therapy. How the body absorbs hormones, along with the amount of hormones needed to help the body function properly, is very varied. Your treatment plan will be individualistic. As such, you should expect some degree of adjustment when it comes to finding the dosage and form of therapy that works best for you. Though synthetic T4 supplements have been the most prescribed form of Thyroid hormone Replacement therapy, there are a variety of forms, including animal Thyroid supplements.
Healthy TSH levels are usually an indicator that the whole system is working as it should. Thyroid disorders are complicate, fickle, and highly individual, meaning thyroid issues are going to look very different for each person. In any case, it is important to have a basic understanding of how thyroid gland works and the hormones it produce. This understanding can help you advocate for yourself and ask the right questions when you visit your healthcare provider. It can also clue you into some of those mysterious symptoms you may be experiencing. First things first: thyroid gland is part and parcel of the endocrine system, which is a collection of glands that produce all - important hormones responsible for metabolism, growth, sexual function, sleep, and your mood. The gland, which is tiny and butterfly - shaped, is found at bottom front of your neck. It has two main thyroid hormones, triiodothyronine and thyroxine, both of which have a major hand on your energy levels, internal temperature, hair, skin, weight, and more. For this reason, T3 and T4 are definitely not to be taken for grant and you probably know this already if you have experienced any of the frustrating symptoms of thyroid disorder. According to Dr. Cory Rice, DO, internal Medicine physician and certified practitioner with BioTE Medical, when thyroid hormone levels are off, several issues can arise. You can have overactive Thyroid gland where too much Thyroid hormone is produce. An example of this is Graves disease. You can also have underactive Thyroid gland in which too little Thyroid hormone is produce. An example of this is Hashimoto's thyroiditis.
Radioactive IODINE UPTAKE Because T4 contains IODINE, thyroid gland must pull large amounts of IODINE from the bloodstream in order to make the appropriate amount of T4. Thyroid has developed a very active mechanism for doing this. Therefore, this activity can be measured by having an individual swallow a small amount of IODINE, which is RADIOACTIVE. Radioactivity allows doctors to track where IODINE go. By measuring the amount of radioactivity that is taken up by the thyroid gland, doctors may determine whether the gland is functioning normally. Very high RAIU is seen in individuals whose Thyroid gland is overactive, while low RAIU is seen when the Thyroid gland is underactive. In addition to RADIOACTIVE IODINE UPTAKE, thyroid scan may be obtain, which shows picture of the thyroid gland and reveals what parts of the thyroid have taken up IODINE. There are many medications that can affect thyroid function testing. Some common examples include: estrogens, such as in birth control pills, or in pregnancy, cause high levels of Total T4 and T3. This is because estrogens increase the level of binding proteins. In these situations, it is better to ask both for TSH and FREE T4 for Thyroid evaluation, which will typically be in the normal range. Biotin, commonly taken over - counter supplement, can cause measurement of several Thyroid function TESTS to appear abnormal, when they are in fact normal in blood. Biotin should not be taken for 2 days before blood is drawn for Thyroid function testing to avoid this effect.
Enlarge thyroid - also called goiter - can be a sign of iodine deficiency that hasn't yet affected function of the thyroid. But it could also be a sign of overactive thyroid or underactive thyroid, where too many or too few hormones are made respectively. Nodules that can be felt from outside may also be a sign of thyroid problem. But sometimes people have enlarged thyroid gland or nodules without it affecting the function of their thyroid gland. So this palpation examination can only tell us whether there might be a thyroid problem. Further tests and examinations are needed in order to be sure.
Thyroid Tests Blood Tests to measure Thyroid hormones are readily available and widely used Not all Thyroid Tests are useful in all situations. Tsh Test best way to initially test thyroid function is to measure TSH level in blood sample. Changes in TSH can serve as an early warning system - often occurring before the actual level of Thyroid hormones in the body becomes too high or too low. High TSH levels indicate that the thyroid gland is not making enough Thyroid Hormone. On the other hand, low TSH levels usually indicate that the thyroid is producing too much Thyroid Hormone. Occasionally, low TSH may result from abnormality in the pituitary gland, which prevents it from making enough TSH to stimulate thyroid. In most healthy individuals, normal TSH value means that the thyroid is functioning properly.
Levothyroxine is mainly absorbed in the small intestine, more specifically through the duodenum, jejunum and ileum. 10 11 Very little is absorbed in the stomach. Consequently, patients with shorter small intestines have reduced absorption and require higher Levothyroxine doses. 12 time to maximum concentration occurs at approximately 2 hours in euthyroid volunteers while it is delayed to approximately 3 hours in hypothyroid patients. 13 Food also delayed Tmax. 13 14 bioavailability of Levothyroxine is approximately 60 - 80% in euthyroid volunteers. 14 - 16 It may be slightly higher in hypothyroid and hyperthyroid patients, 15 16 and is decrease in presence of food from 79% under fasted conditions to 64% under fed conditions for 100 mcg dose. 14 Absorption of Levothyroxine appears to be influenced by gastric pH. 17 18 Centanni et al. Demonstrate that in euthyroid patients suffering from nontoxic multinodular Goiter, impaired gastric acid secretion or use of omeprazole was associated with increased dosing requirements in order to adequately suppress TSH. 17 Similarly, Sachmechi and colleagues show that chronic lansoprazole use in hypothyroid patients also results in increased Levothyroxine dose requirements to maintain targeted TSH levels. 18 Although T 4 is subject to multiple metabolic reactions, 20 - 22 main metabolic route for T 4 involves deiodination reactions by deiodinase enzymes. 23 - 25 Removal of iodine from carbon 5 of the outer ring transforms T 4 to T 3, thus T 4 can be regarded somewhat as pro - hormone for T 3. Deiodination of the inner ring of T 4 can also occur, leading to formation of inactive reverse T 3. Approximately half of deiodinised T 4 is metabolise to rT 3 and half to T 3. 25 26 Both T 3 and rT 3 are further metabolise to diiodothyronine, iodothyronamine and reverse T 2 and T 1. 25 26 daily turnover rate for T 4 is approximately 10% while it is approximately 50 - 70% for T 3, with a slightly faster turnover rate in normal volunteers compared with patients with primary hypothyroidism. 1 2 this equates to half - life for T 4 of 7. 5 days in hypothyroid patients and 6. 2 days in euthyroid individuals, while T 3 half - life is approximately 1. 4 and 1. 0 days for hypothyroid and euthyroid volunteers, respectively. 19 Clearance for T 4 was similar to 0. 056 and 0. 054 L / H in hypothyroid and euthyroid subjects, respectively. 19 these values are similar to other values reported in hypothyroid patients 27 and in normal control subjects. 28 29 Both T 4 and T 3 are highly bind to plasma proteins at greater than 99. 8% in both euthyroid and primary hypothyroid volunteers. 1 19 30 31 Both T 4 and T 3 bind predominantly to thyroxine - binding globulin, and to a lesser extent to thyroxine - binding prealbumin and albumin. 1 30 Benvenga and Robbins have also demonstrated binding to lipoproteins such as high - density lipoprotein.
However, some patients and clinicians have an interest in replacing T3 along with T4. Reasons include persistence of hypothyroid symptoms despite achieving biochemically normal serum TSH concentrations with levothyroxine therapy, desire to have more options for therapy, or concern about possibly having type II deiodinase polymorphism. Although there is some evidence that patients prefer use of regimens containing T3, outcomes evaluating quality of life or psychological endpoints have been inconsistent. Some might have a preference for animal - derive, nonsynthetic, natural forms of treatment, such as desiccated thyroid extract from bovine and porcine sources, which contain both T3 and T4 at an approximate physiologic ratio of 1: 4. Dte has been in use since at least 1891, before the FDA in 1938 was required to begin regulating the efficacy and safety of new medications in the United States. Thus, DTE formulations are considered grandfather drugs, which technically remain FDA - unapproved for thyroid hormone replacement to this day.
The immune system of the body normally protects us from foreign invaders such as bacteria and viruses by destroying these invaders with substances called antibodies produced by blood cells known as lymphocytes. In many patients with hypothyroidism or hyperthyroidism, lymphocytes react against thyroid and make antibodies against thyroid cell proteins. Two common antibodies are the thyroid peroxidase antibody and the THYROGLOBULIN antibody. Measuring levels of thyroid antibodies may help diagnose the cause of thyroid problem. For example, positive anti - thyroid peroxidase and / or anti - THYROGLOBULIN antibodies in patients with hypothyroidism result in diagnosis of Hashimotos thyroiditis. While detecting antibodies is helpful in initial diagnosis of hypothyroidism due to autoimmune thyroiditis, following their levels over time is not helpful in detecting development of hypothyroidism or response to therapy. Tsh and FT4 are what tell us about actual thyroid function or levels. A different antibody that may be positive in patients with hyperthyroidism is the stimulatory TSH receptor antibody. This antibody causes thyroids to be overactive in Graves Disease. If you have Graves Disease, your doctor might also order a thyrotropin receptor antibody test, which detects both stimulating and blocking antibodies. Following antibody levels in Graves patients may help to assess response to treatment of hyperthyroidism, to determine when it is appropriate to discontinue antithyroid medication, and to assess risk of passing antibodies to the fetus during pregnancy. Thyroglobulin THYROGLOBULIN is a protein produced by normal thyroid cells and thyroid cancer cells. It is not a measure of thyroid function and it does not diagnose thyroid cancer when thyroid gland is still present. It is used most often in patients who have had surgery for thyroid cancer in order to monitor them after treatment. Tg is included in this brochure of thyroid function TESTS to communicate that, although measured frequently in certain scenarios and individuals, Tg is not the primary measure of thyroid hormone function.
At front of your neck lie thyroid, butterfly - shaped gland that makes the hormone T4. When released into the bloodstream, T4 converts to T3, most active form of thyroid hormone. Having sufficient levels of these hormones is important because the thyroid regulate body temperature, metabolism, blood pressure, and heart rate. Hypothyroidism occurs when the thyroid is underactive. It affects as many as five in 100 people. Symptoms of hypothyroidism include fatigue, cold intolerance, constipation, dry skin, hair loss, muscle weakness, weight gain, and fertility problems. In my primary care practice, I am finding that more and more of my patients are reporting feeling tired and concerned about whether they have hypothyroidism. Some patients request many different thyroid blood tests to diagnose and treat hypothyroidism. But are these tests really necessary?
Thyroid gland takes its direction from both the hypothalamus and pituitary gland, pea - size gland at the base of your skull. In complex dance, hypothalamus releases something called thyrotropin - releasing Hormone, which then triggers the pituitary gland to produce something called Thyroid Stimulating Hormone. That is then what helps your Thyroid gland release T4 and T3. Without TSH, system would fail. Thyroxine is responsible for your metabolism, mood, and body temperature, among other things. T3, too, is made in thyroid gland, and it can also be made in other tissues within the body by converting T4 into T3. This hormone is at the center of your digestive and metabolic function, and it also oversees bone health. So, if your T3 and T4 levels are too low, pituitary gland will release more TSH. If theyre too high, gland will release less TSH, but this give and take system only works if everything is functioning properly.
Although Thyroid gland produces T4 and T3, LT4 monotherapy has been the mainstay of Thyroid hormone replacement since the 1970s, replacing desiccated Thyroid extract which had been used for many years prior. This is because it is easily administer, well absorbed by oral route and its long half - life allows for once daily dosing with very stable serum levels. It was also shown to be converted to T3 within the body, alleviating the need to add LT3, which does not have the same stable pharmacological profile. Furthermore, it has also been shown that the majority of circulating T3 comes from peripheral conversion of T4 to T3 and not secretion of T3 from Thyroid, hence T4: T3 secretion ratio of approximately 14: 1 appears average in humans, suggesting only a small role for secreted T3. However, there is a small group of patients who do not feel back to their euthyroid well - being despite having Thyroid function tests suggestive of adequate replacement on LT4. There are also several studies showing that on LT4 monotherapy serum T3 levels are significantly lower for same TSH in euthyroid patients, although the clinical significance of this is unknown. Another study showed it was not possible to normalise serum TSH, T3 and T4 levels or tissue T3 levels in laboratory animals giving them LT4 monotherapy. Because of this, there have now been at least 13 randomized control trials comparing the efficacy of combination LT4 / LT3 therapy versus LT4 monotherapy for Thyroid hormone replacement. There has also been one trial comparing DTE to LT4 monotherapy. Trials differ significantly in study population size, method of substituting LT3 for LT4, dose, length of study and outcomes measure. There have now been 4 systematic reviews / meta - analyses of these studies attempting to clarify the findings. Overall, these meta - analyses have suggested there is no significant benefit of combination LT4 / LT3 therapy compared to LT4 monotherapy in terms of mood, health - related quality of life or cognitive function. This provides reasonable evidence that at population level there is no benefit of using combination therapy over monotherapy. However, different methods of replacing LT4 with LT3 and smaller size and hence the power of some studies should be consider. There was no increase in adverse events in combination groups in this admittedly short period of follow up. There is one randomized cross - over trial comparing DTE with levothyroxine monotherapy in 70 patients for 16 weeks each arm. This does not show any significant benefit of DTE over LT4 in symptoms and neurocognitive markers. There was an increase in preference for DTE over LT4, However it is unclear what this signifies given the overall lack of improvement in symptoms. The study was too small to pick up subgroups responding to T3 and future studies in this area may consider having synthetic T4 / T3 arm also to determine if any benefit is due to the addition of T3 or DTE itself.
Propylthioracil and methimazole are medications used to treat overactive thyroid. They work by slowing down production of thyroid hormones and do not cause permanent damage. When taken appropriately, these medications can control hyperthyroidism in just a few weeks;. However, main problem with anti - thyroid medications lies with the fact that the underlying problem returns once they are discontinue. Therefore, many people are encouraged to seek more permanent treatments, such as radioactive iodine treatment or surgical removal. Side effects of anti - thyroid medications include skin rash, upset stomach, drowsiness, and bitter aftertaste. Rare but serious side effects include sore throat, fever, chills, jaundice, decreased white blood cells, and liver disease. Your doctor may also prescribe medication called beta blocker to block action of thyroid hormone in your body. While beta blockers will not change levels of thyroid hormones in your blood, they will make you feel better by reducing some of the symptoms of hyperthyroidism, including increased heart rate, shakes, and nervousness. These drugs work within hours and may help to quell these symptoms before other drugs have a chance to take effect. However, speak to your doctor if you have the Raynauds phenomenon, since beta blockers worsen this condition.
This is very well possible. Outcomes might be different by applying different selection Criteria. New RCTs can be envisage restricted to patients with persistent symptoms and / or specific genotypes like Thr92Ala DIO2. Other polymorphisms should be considered as well, like SNPs in brain - specific Thyroid hormone transporter OATP1C1 which have been associated with Fatigue and Depression but not with neurocognitive functioning or preference for T4 + T3. Interestingly, Danish RCT found two SNPs associated with favored treatment: preference for T4 + T3 therapy was 42% when both SNPs were absent, 63% if one SNP was present, and 100% if both SNPs were present.
Poor compliance is the most common reason for continued elevation of TSH level in patients receiving presumably adequate thyroid hormone replacement. Patients who do not regularly take their replacement medication and then try to catch up just before physician visit may restore their free T 4 levels to normal but continue to have elevated TSH level. Very rarely, patients have tissue - level unresponsiveness to thyroid hormone. This condition reflects mutation in the gene that controls receptor for T 3, rendering it unable to bind with hormone. Genetic mutations have been identified in only 300 families. 22 in these patients, adequate amounts of thyroid hormone are produced but are ineffective. Consequently, TSH levels remain elevate, and patients continue to have symptoms of hypothyroidism. These patients should be referred to an endocrinologist for further evaluation and management.
Thyroid Hormone replacement therapy with oral Levothyroxine is standard treatment for patients with hypothyroidism. Goals of treatment include resolution of symptoms and signs of hypothyroidism and normalization of circulating Thyroid - stimulating Hormone levels. Orally administered LT4 is available in several formulations, and LT4 tablets are available in multiple brand and generic forms. Traditional tablet formulations contain LT4 sodium, stable salt, and a variety of inactive excipients, composition of which may affect tablet stability and pharmacokinetics. The US Food and Drug Administration defines generic drug as medication that has the same dosage form, safety, strength, route of Administration, quality, performance characteristics and intended use as already marketed brand - name medication. The European Medicines Agency defines generic drugs as those that have the same qualitative and quantitative composition of active substances and same pharmaceutical form as reference drug and whose bioequivalence with reference drug has been demonstrated by appropriate bioavailability studies. With regard to generic and brand LT4 preparations, endocrinologists around the world differ in their preferences. According to a survey of 880 members of the Endocrine Society, American Thyroid Association and American Association of Clinical Endocrinologists, 49. 9% of respondents prefer the brand - name LT4, while 49. 3% preferred generic LT4. However, among European members, who represent 9. 2% of respondents, proportion of those who prefer brand - name drugs was 58. 8%. At present, FDA uses serum thyroxine levels to establish Bioequivalence of LT4 products. Base on FDA criteria for Bioequivalence, substitution between bioequivalent generic and brand - name LT4 can be automatically performed with no need for dose adjustment. There is ongoing debate around concerns that currently use pharmacokinetic approach for assessing bioequivalence of LT4 products could allow products with clinically significant differences in bioavailability to be declared therapeutically equivalent and interchangeable. Therefore, ATA, ES and AACE have issued joint statement encouraging consistent use of the same brand or generic LT4 formulation in individual patients. These recommendations have since been reinforced by Guidelines From Endocrine Society of Australia, European Thyroid Association and Thyroid Federation International, and are summarized in Table 1. If switch to another LT4 formulation is make, repeat Thyroid function testing is recommend. Switching is considered to be a particular concern in vulnerable populations, including elderly, pregnant and pediatric patients, especially since these patients are often excluded from studies undertaken to establish Bioequivalence. This review describes problems that can be encountered when switching between formulations or when original products are reformulate.
Thyroid hormones undergo minimal placental transfer and human experience does not indicate adverse fetal effects; do not discontinue needed replacement during pregnancy. Also, hypothyroidism diagnosed during pregnancy should be promptly treat. Measure TSH during each trimester to gauge adequacy of Thyroid replacement dosage since during pregnancy Thyroid replacement requirements may increase. Immediately after obstetric delivery, dosage should return to pre - pregnancy dose, monitor serum TSH 6 to 8 weeks postpartum to assess for needed adjustments. Thyroid hormones, like liotrix, are generally compatible with breast - feeding; minimal amounts of Thyroid hormones are excreted in breast milk. Liotrix is a mixture of levothyroxine and liothyronine. The American Academy of Pediatrics considers use of levothyroxine to be compatible with breast - feeding due to lack of reported adverse effects in nursing infants. It should be noted that in general, adequate Thyroid replacement doses are needed to maintain normal lactation and there is no reason maternal replacement should be halt due to lactation alone. Levothyroxine is often the drug of choice to treat hypothyroidism during pregnancy and lactation. However, use caution when administering liotrix to nursing woman; changes in thyroid status in the post - partum period may require careful monitoring and maternal dosage adjustment. Comparisons of levels of TSH and other Thyroid function tests between breast - fed and bottle - fed infants have been publish. Breast milk does not provide sufficient levothyroxine or liothyronine to prevent the effects of congenital hypothyroidism; therefore, serum levels of TSH in breast - fed hypothyroid infants are markedly elevate. Euthyroid babies who were breast - fed do not have differences in TSH levels when compared to euthyroid babies receiving formula feedings.
Whereas patients randomized to receive L - T4 monotherapy continued their usual L - T4 dose, in patients randomized to receive L - T4 + L - T3 combination therapy, part of their L - T4 dose was replaced by L - T3. Most frequently, fixed amount of L - T4 was replaced by a fixed amount of L - T3, resulting in a variable ratio of administered T4 to T3 dose by weight in each of these studies. The T4 to T3 dose ratio thus can vary substantially between participants within the same RCT. Other studies replaced the proportion of L - T4 dose by variable L - T3 dose, resulting in a fixed ratio of administered T4 to T3 dose for all participants within trial. The Variation in T4 to T3 dose ratio between studies aiming at fix ratio is large, ranging from 19: 1 to 4: 1. Wide variation in T4 to T3 dose ratio within and between RCTs constitutes potential bias because most studies fail to mimic the ratio of T4 to T3 secretion by human Thyroid gland under physiological conditions, which is close to 13: 1 by weight. Nevertheless, combination therapy was judged not to be better than monotherapy in four trials in meta - analysis applying fixed dose ratio of 19: 1, 15: 1 or 10: 1. Along similar lines, one may look at the ratio of serum free T4 to free T3. To obtain serum TSH values similar to controls during L - T4 monotherapy, serum free T4 concentrations higher than controls are required at serum free T3 values similar to those in controls. Indeed, serum free T4 to free T3 ratios in patients randomized to receive L - T4 monotherapy range from 4. 0 to 5. 5, higher than the value of 3. 3 observe healthy controls. Serum free T4 to free T3 ratio during combination therapy ranges from 2. 2 to 4. 0 in only two RCTs ratios were close to control values, but both studies still fail to demonstrate the superiority of combination therapy over monotherapy. L - T3 doses administered during combination therapy vary between 5 and 25 g daily, with the exception of the oldest study in which 40 - 60 g of L - T3 was give. The daily L - T3 dose was administered as a single dose in all trials except four, in which it was divided into two doses. In 2006, meta - analysis was published of 11 clinical studies in which 1 216 adult hypothyroid patients on L - T4 treatment were randomized to receive L - T4 monotherapy or L - T4 + L - T3 combination therapy. Meta - analysis found NO difference in effectiveness of combination versus monotherapy in any of the following items: bodily pain, Depression, Anxiety, fatigue, quality of life, body weight, total serum cholesterol, triglycerides, low - density lipoprotein, and high - density lipoprotein. Adverse events do not differ between regimens. The authors of meta - analysis conclude: It is doubtful whether further trials evaluating combination therapy are needed because chances that accumulating evidence will change are low. A more recent systematic review in 2009 reached similar conclusions. However, recent RCT observed combination therapy was superior to monotherapy.
Hypothyroidism is a condition characterized by clinical and biochemical manifestations of thyroid hormone deficiency in target tissues of thyroid hormone. The most common cause of hypothyroidism is deficient production of thyroid hormones by the thyroid gland. Thyroxine is produced exclusively by thyroid gland; its daily production rate is about 100 g at an average body surface area of 1. 79 m 2. Daily production rate of triiodothyronine for body surface area of 1. 79 m 2 is about 29 g: 20% is secreted by thyroid gland, and 80% is generated in extrathyroidal tissues by 5 - deiodination of T4. Treatment of hypothyroidism is today predominantly with L - T4: its long half - life of 1 week is advantageous, allowing one daily dose and it generates stable T3 levels by conversion of T4 into T3 in peripheral tissues. In contrast, half - life of T3 is short, and treatment with L - T3 would require several doses per day with wide variation in serum T3 levels along 24 - hour period. Elevate serum T3 concentrations may occur during absorption of L - T3, which can be associated with symptoms of tachycardia and nervousness. Options of treatment with L - T3 or combination of L - T4 and L - T3 therefore have largely been abandon. However, recent developments have rekindled interest in the potential advantages of L - T4 + L - T3 combination therapy over L - T4 monotherapy. On one hand, many practising physicians have experienced that some of their hypothyroid patients have persistent complaints, despite adequate treatment with L - T4 as evident from normalization of TSH, free T4 and T3 concentrations. The creation of special interest groups like that of Hypo but not Happy patients attests this point. A recent randomized clinical trial reported a clear preference of patients for L - T4 + L - T3 combination therapy over L - T4 monotherapy. In recognition of these developments and existing controversies regarding the value of L - T4 + L - T3 combination therapy for hypothyroidism, ETA appointed a task force to systematically approach this issue and establish guidelines according to principles of evidence - base medicine. The Task force acknowledges that L - T4 + L - T3 combination therapy is a highly controversial issue. In fact, as evident from recommendations in this report, evidence base to advocate this treatment modality is very limited indeed. Nevertheless, presently proposed guidelines aim to provide guidance on how to explore persisting symptoms in a systematic manner. They stipulate that combination therapy should be viewed solely as experimental. They recommend much lower L - T3 doses in combination therapy than previously used, thereby enhancing safety. And they show that the thyroid community at large does care about the issue of persistent symptoms. Guidelines should not lead to indiscriminate use of L - T4 + L - T3 combination therapy; in contrast, recommendations made should help physicians to identify relatively few L - T4 - treat hypothyroid patients who might benefit from carefully executed trial with L - T4 + L - T3 combination therapy.
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