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T4 Thyroxine Sodium 50 mcg , (Thyroxine Sodium Anhydrous) by GlaxoSmithKline

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Thyroxine Sodium Anhydrous
15.00 Grams
100 tabs. / pack (50 mcg)
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Product Description

Thyroid hormone

The thyroid hormonestriiodothyronine (T3) and thyroxine (T4), are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism. Iodine is necessary for the production of T3 and T4. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as goitre. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3. The ratio of T4 to T3 released into the blood is roughly 20 to 1. T4is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a).


  • 1
     Medical use
    • 1.1 Formulations
  • 2 Circulation and transport
    • 2.1 Plasma transport
    • 2.2 Membrane transport
    • 2.3 Intracellular transport
  • 3 Function
  • 4 Related diseases
  • 5 Measurement
  • 6 Production
    • 6.1 Central
    • 6.2 Peripheral
    • 6.3 Initiation of production in fetuses
  • 7 Effect of iodine deficiency on thyroid hormone synthesis
  • 8 Anti-thyroid drugs
  • 9 Effects of thyroxine
  • 10 Herbs
  • 11 References
  • 12 External links

    Medical use

    Both T3 and T4 are used to treat thyroid hormone deficiency (hypothyroidism). They are both absorbed well by the gut, so can be given orally. Levothyroxine is the pharmaceutical name (INN) of physiological thyroxine (T4), which is metabolised more slowly than T3 and hence usually only needs once-daily administration. Natural desiccated thyroid hormones are derived from pig thyroid glands, and are a "natural" hypothyroid treatment containing 20% T3 and traces of T2, T1 and calcitonin. Also available are synthetic combinations of T3/T4 in different ratios (such as liotrix) and pure-T3 medications (INN: liothyronine). Levothyroxine is usually the first course of treatment tried. Some patients feel they do better on desiccated thyroid hormones, however, this is based on anecdotal evidence and no clinical trials have shown any benefit over the biosynthetic forms.

    Thyronamines have no medical usages yet, though their use has been proposed for controlled induction of hypothermia, which causes thebrainto enter a protective cycle, useful in preventing damage during ischemic shock.

    Synthetic thyroxine was first successfully produced by Charles Robert Harington and George Barger in 1926.



    Today most patients are treated with levothyroxine, or a similar synthetic thyroid hormone. However, natural thyroid hormone supplements from the dried thyroids of animals are still available. Natural thyroid hormones have become less popular, due to evidence that varying hormone concentrations in the thyroids of animals before they are slaughtered leads to inconsistent potency and stability. Levothyroxine contains T4 only and is therefore largely ineffective for patients unable to convert T4 to T3. These patients may choose to take natural thyroid hormone as it contains a mixture of T4 and T3, or alternatively supplement with a synthetic T3 treatment. In these cases, synthetic liothyronine is preferred due to the potential differences between drug lots of natural thyroid products. Also it would be counterintuitive to supplement with a T4/T3 combination if the patient cannot convert T4 to T3. Some natural thyroid hormone brands are F.D.A. approved, but some are not. Thyroid hormones are generally well tolerated. Thyroid hormones are usually not dangerous for pregnant women or nursing mothers, but should be given under a doctor's supervision. In fact, if a woman who is hypothyroid is left untreated, her baby is at a higher risk for birth defects. When pregnant, a woman with a low functioning thyroid will also need to increase her dosage of thyroid hormone. One exception is that thyroid hormones may aggravate heart conditions, especially in older patients; therefore, doctors may start these patients on a lower dose & work up to avoid risk of heart attack.


    Circulation and transport

    Plasma transport

    Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free (unbound) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value.

    When thyroid hormone is bound, it is not active, so the amount of free T3/T4 is what is important. For this reason, measuring total thyroxine in the blood can be misleading.

    bound to thyroxine-binding globulin (TBG) 70%
    bound to transthyretin or "thyroxine-binding prealbumin" (TTR or TBPA) 10-15%
    paraalbumin 15-20%
    unbound T4 (fT4) 0.03%
    unbound T3 (fT3) 0.3%

    T3 and T4 cross the cell membrane easily as they are lipophilic molecules, and function via a well-studied set of nuclear receptors in the nucleus of the cell, the thyroid hormone receptors.

    T1a and T0a are positively charged and do not cross the membrane; they are believed to function via the trace amine-associated receptor TAAR1 (TAR1, TA1), a G-protein-coupled receptor located in the cell membrane.

    Another critical diagnostic tool is measurement of the amount of thyroid-stimulating hormone (TSH) that is present.

    Membrane transport

    Contrary to common belief, thyroid hormones can not traverse cell membranes in a passive manner like other lipophilic substances. The iodine in o-position makes the phenolic OH-group more acidic, resulting in a negative charge at physiolocical pH. However, at least 10 different active, energy dependent and genetic regulated iodothyronine transporters have been identified in humans. They guarantee that intracellular levels of thyroid hormones are higher than in blood plasma or interstitial fluids.

    Intracellular transport

    Little is known about intracellular kinetics of thyroid hormones. However, recently it could be demonstrated that the crystallin CRYM binds 3,5,3′-triiodothyronine in vivo.


    The thyronines act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone) and neuronal maturation, and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis.

    Thyroid hormone leads to heat generation in humans. However, the thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour ofbirds. One effect of administering the thyronamines is a severe drop in body temperature.


    Related diseases

    Both excess and deficiency of thyroxine can cause disorders.

    • Hyperthyroidism (an example is Graves Disease) is the clinical syndrome caused by an excess of circulating free thyroxine, free triiodothyronine, or both. It is a common disorder that affects approximately 2% of women and 0.2% of men. Thyrotoxicosis is often used interchangeably with hyperthyroidism, but there are subtle differences. Although thyrotoxicosis also refers to an increase in circulating thyroid hormones, it can be caused by the intake of thyroxine tablets or by an over-active thyroid, whereas hyperthyroidism refers solely to an over-active thyroid.
    • Hypothyroidism (an example is Hashimoto's thyroiditis) is the case where there is a deficiency of thyroxine, triiodiothyronine, or both.
    • Clinical depression can sometimes be caused by hypothyroidism. Some research has shown that T3 is found in the junctions of synapses, and regulates the amounts and activity of serotonin, norepinephrine, and Gamma-aminobutyric acid (GABA) in the brain.

    Preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones, at a time when their own thyroid is unable to meet their postnatal needs.



    Thyroxine and triiodothyronine can be measured as free thyroxine and free triiodothyronine, which are indicators of thyroxine and triiodothyronine activities in the body. They can also be measured as total thyroxine and total triiodothyronine, which also depend on the thyroxine and triiodothyronine that is bound to thyroxine-binding globulin. A related parameter is the free thyroxine index, which is total thyroxine multiplied by thyroid hormone uptake, which, in turn, is a measure of the unbound thyroxine-binding globulins.




    Thyroid hormones (T4 and T3) are produced by the follicular cells of the thyroid gland and are regulated byTSH made by the thyrotrophs of the anterior pituitary gland. Because the effects of T4 in vivo are mediated via T3 (T4 is converted to T3 in target tissues), T3 is 3- to 5- fold more active than T4.

    Thyroxine (3,5,3',5'-tetraiodothyronine) is produced by follicular cells of the thyroid gland. It is produced as the precursor thyroglobulin (this is not the same as TBG), which is cleaved by enzymes to produce active T4.

    Thyroxine is produced by attaching iodine atoms to the ring structures of tyrosine molecules. Thyroxine (T4) contains four iodine atoms. Triiodothyronine (T3) is identical to T4, but it has one less iodine atom per molecule.

    Iodide is actively absorbed from the bloodstream by a process called iodide trapping. In this process,sodium is cotransported with iodide from the basolateral side of the membrane into the cell and then concentrated in the thyroid follicles to about thirty times its concentration in the blood. Via a reaction with the enzyme thyroperoxidase, iodine is bound to tyrosine residues in the thyroglobulin molecules, formingmonoiodotyrosine (MIT) and diiodotyrosine (DIT). Linking two moieties of DIT produces thyroxine. Combining one particle of MIT and one particle of DIT produces triiodothyronine.

    • DIT + MIT → r-T3 (biologically inactive)
    • MIT + DIT → triiodothyronine (usually referred to as T3)
    • DIT + DIT → thyroxine (referred to as T4)

    Proteases digest iodinated thyroglobulin, releasing the hormones T4 and T3, the biologically active agents central to metabolic regulation.


    Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T3. T4 is converted as required in the tissues by iodothyronine deiodinase. Deficiency of deiodinase can mimic an iodine deficiency. T3 is more active than T4 and is the final form of the hormone, though it is present in less quantity than T4.

    Initiation of production in fetuses

    Thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) start being secreted from the fetal hypothalamus and pituitary at 18-20 weeks of gestation, and fetal production of thyroxine (T4) reach a clinically significant level at 18–20 weeks. Fetal triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks of gestation, and increases to 50 ng/dL at term. Fetal self-sufficiency of thyroid hormones protects the fetus against e.g. brain development abnormalities caused by maternal hypothyroidism.


    Effect of iodine deficiency on thyroid hormone synthesis

    If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (goiter)endemic colloid goiter. This has the effect of increasing the thyroid's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.


    Anti-thyroid drugs

    Iodine uptake against a concentration gradient is mediated by a sodium-iodine symporter and is linked to a sodium-potassium ATPase. Perchlorate and thiocyanate are drugs that can compete with iodine at this point. Compounds such as goitrin can reduce thyroid hormone production by interfering with iodine oxidation.


    Effects of thyroxine

  • Increases cardiac output
  • Increases heart rate
  • Increases ventilation rate
  • Increases basal metabolic rate
  • Potentiates the effects of catecholamines (i.e. increases sympathetic activity)
  • Potentiates brain development
  • Thickens endometrium in females
  • increase metabolism of proteins and carbohydrates

  • Herbs

    There are no herbs (plant chemicals) that contain thyroid hormone. Therefore, while there are some herbs that may provide some help for a sluggish thyroid (i.e. if the thyroid is producing a low amount of thyroid hormone, but has not stopped completely), myxedema requires treatment with synthetic or desiccated natural thyroid hormones.However, there are many edible plants that have high concentrations of iodine (e.g., seaweed and kelp). Iodine is an irreplaceable precursor to the biosynthesis of thyroid hormones.



  • ^ "Thyroxine-triiodothyronine combination therapy versus thyroxine monotherapy for clinical hypothyroidism: meta-analysis of randomized controlled trials." Grozinsky-Glasberg S; Fraser A; Nahshoni E; Weizman A; Leibovici L. J Clin Endocrinol Metab. 2006 Jul;91(7):2592-
  • ^ Robert Lloyd Segal, MD Endocrinologist
  • a b c "preferred thyroid hormone --Levothyroxine Sodium (Synthroid, Levoxyl, Levothroid, Unithroid)", Retrieved on 2009-3-27
  • a b c d "Hypothyroidism Causes, Symptoms, Diagnosis, Treatment Information Produced by Medical Doctors", Retrieved on 2009-3-27
  • ^ Clyde, PW; Harari AE, Mohamed Shakir KM. (2004). "Synthetic Thyroxine vs Desiccated Thyroid -Reply". JAMA 291 (12): 1445. doi:10.1001/jama.291.12.1445-b.
  • ^ Cooper, DS (1989). "Thyroid hormone treatment: new insights into an old therapy.".JAMA 261 (18): 2694–2695. doi:10.1001/jama.1989.03420180118042.
  • ^ Thyroid hormone replacement therapy
  • a b "Consequences of Not Taking Thyroid Medications - Implications of Failing to Take Prescription Thyroid Drugs", Retrieved on 2009-3-27
  • ^ "Armour Thyroid", Retrieved on 4-1-2009
  • ^ "Nature-Throid", Retrieved on 4-1-2009
  • ^ "Armour Thyroid Shortages Worsening: What Can Thyroid Patients Do?", Retrieved on 2009-3-27
  • ^ Liothyronine
  • ^ "Thyroid Information", Retrieved on 2009-3-27
  • ^ "Desiccated thyroid in a nutritional supplement | Journal of Family Practice | Find Articles at BNET", Retrieved on 2009-3-27
  • ^ "Nature-Throid", Retrieved on 4-1-2009
  • ^ Dietrich, J. W., K. Brisseau und B. O. Boehm (2008). "Resorption, Transport und Bioverfügbarkeit von Schilddrüsenhormonen" [Absorption, transport and bio-availability of iodothyronines]. Deutsche Medizinische Wochenschrift 133 (31/21): 1644-8. DOI 10.1055/s-0028-1082780
  • ^ Satoru Suzuki, Nobuyoshi Suzuki, Jun-ichirou Mori, Aki Oshima, Shinichi Usami and Kiyoshi Hashizume. μ-Crystallin as an Intracellular 3,5,3′-Triiodothyronine Holder in Vivo. MMolecular Endocrinology April 1, 2007 vol. 21 no. 4 885-894. PMID 17264173
  • ^ References used in image are found in image article in Commons:Commons:File:Thyroid_systbcvhxcxcfffgem.png#References.
  • ^ Kirkegaard C, Faber J (1998). "The role of thyroid hormones in depression". Eur J Endocrinol 138 (1): 1–9. doi:10.1530/eje.0.1380001. PMID 9461307.
  • ^ Dratman M, Gordon J (1996). "Thyroid hormones as neurotransmitters". Thyroid 6 (6): 639–47. doi:10.1089/thy.1996.6.639. PMID 9001201.
  • ^ Berbel P, Navarro D, Ausó E, Varea E, Rodríguez AE, Ballesta JJ, Salinas M, Flores E, Faura CC, de Escobar GM. (2010). Role of late maternal thyroid hormones in cerebral cortex development: an experimental model for human prematurity. Cereb Cortex. 20(6):1462-75. PMID 19812240.
  • ^ Military Obstetrics & Gynecology > Thyroid Function Tests In turn citing: Operational Medicine 2001, Health Care in Military Settings, NAVMED P-5139, May 1, 2001, Bureau of Medicine and Surgery, Department of the Navy, 2300 E Street NW, Washington, D.C., 20372-5300
  • ^ Chapter 48, "SYNTHESIS OF THYROID HORMONES" in: Walter F., PhD. Boron (2003). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. pp. 1300. ISBN 1-4160-2328-3.
  • ^ How Iodide Reaches its Site of Utilisation in the Thyroid Gland – Involvement of Solute Carrier 26A4 (Pendrin) and Solute Carrier 5A8 (Apical Iodide Transporter) - a report by Bernard A Rousset. Touch Brieflings 2007
  • a b Page 493 (Table 33-3) in: Eugster, Erica A.; Pescovitz, Ora Hirsch (2004). Pediatric endocrinology: mechanisms, manifestations and management. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4059-2.
  • ^ Zoeller RT (April 2003). "Transplacental thyroxine and fetal brain development". J. Clin. Invest. 111 (7): 954–7. doi:10.1172/JCI18236. PMC 152596.PMID 12671044.
  • ^ Spiegel C, Bestetti GE, Rossi GL, Blum JW (September 1993). "Normal circulating triiodothyronine concentrations are maintained despite severe hypothyroidism in growing pigs fed rapeseed presscake meal". J. Nutr. 123 (9): 1554–61.PMID 8360780.
  • a b "Thyroid Disease: A Natural/Herbal Perspective -- Interview with Shasta Tierra-Tayam, L.Ac", Retrieved on 2009-3-27
  • ^ “WikiAnswers - Is there are natural herb to take for a sluggish thyroid”, Retrieved on 2009-3-27
  • ^ "Hypothyroidism Causes, Symptoms, Diagnosis, Treatment Information Produced by Medical Doctors", Retrieved on 2009-3-27
  • External links

    • Find TH response elements in DNA sequences.
    • Triiodothyronine bound to proteins in the PDB
    • Thyroxine bound to proteins in the PDB

    Thyroid hormone treatment in thyroid disease

    • Thyroid Hormone Treatment Brochure by the American Thyroid Association
    • Elaborate article about the use of thyroid drugs Written by an MD
    • What is the "Best" Thyroid Drug? Is it Synthroid, Unithroid, Armour, Thyrolar, or Something Else? Article by health activist and patient advocate Mary Shomon
    • Thyroid Disease Manager Collection of elaborate medical articles on thyroid disease, including information on thyroid hormones
    • Stop the thyroid madness Collection of references to articles comparing different treatment methods of hypothyroidism




    Thyroxine-binding proteins

    Thyroxine-binding proteins is a protein which binds thyroid hormone. Examples include:

    • Thyroxine-binding globulin
    • Transthyretin
    • Serum albumin


    Thyroxine-binding globulin

    Thyroxine-binding globulin (TBG) binds thyroid hormone in circulation. It is one of three proteins (along with transthyretinand albumin) responsible for carrying the thyroid hormones thyroxine (T4) and 3,5,3’-triiodothyronine (T3) in the bloodstream. Of these three proteins, TBG has the highest affinity for T4 and T3, but is present in the lowest concentration. Despite its low concentration, TBG carries the majority of T4 in the blood. Due to the very low concentration of T4 & T3 in the blood, TBG is rarely more than 25% saturated with its ligand. Unlike transthyretin and albumin, TBG has a single binding site for T4/T3. TBG is synthesized primarily in the liver as a 54 kDa protein. In terms of genomics, TBG is a serpin; however, it has no inhibitory function like many other members of this class of proteins.


    Role in Diagnosis

    TBG tests are sometimes used in finding the reason for elevated or diminished levels of thyroid hormone. This is done by measuring resin binding to labeled thyroid hormone, which happens only when the labeled thyroid hormone is free.

    The patient's serum is mixed with the labeled thyroid hormone; then, the resin is added to the whole mixture to measure the amount of free labeled thyroid hormone. So, for instance, if the patient is truly hypothyroid, and TBG levels are normal, then there are many sites open for binding on the TBG, since the total thyroid hormone level is low. Therefore, when the labeled hormone is added, it will bind mostly to the TBG, leaving little of it left for binding to the resin. In contrast, however, if the patient is truly hyperthyroid, and TBG levels are normal, the patient's endogenous hormone will saturate the TBG binding sites more, leaving less room for the labeled hormone, which allows greater binding to the resin.

    In the situations described above, TBG testing is not very useful. However, if total thyroid hormone levels point to hypothyroidism or hyperthyroidism in the absence of accompanying symptoms, the utility of TBG testing becomes more evident, since TBG production can be modified by other factors such as estrogen levels, corticosteroid levels, or liver failure. If, for example, the TBG level is high, which can occur when estrogen levels are high, the TBG will bind more thyroid hormone, decreasing the free hormone available in the blood, which leads to stimulation of TSH, and the production of more thyroid hormone. In this case, the total thyroid hormone level will be high. And so, when labeled hormone is added, since TBG is so high, it will bind to the TBG, leaving little free labeled hormone for uptake into the resin. On the converse, in the presence of corticosteroids, which lower TBG levels, the total thyroid hormone (bound and free) in the blood will be low. Thus, when the labeled hormone is added, since so little TBG is available in the blood, only a small portion of it will bind, leaving plenty available for uptake by the resin.

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