Desiccated thyroid extract

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Desiccated thyroid extract
Combination of
Thyroxine Thyroid hormone
Triiodothyronine Thyroid hormone
Clinical data
Trade names Armour Thyroid, NP Thyroid, Nature-Throid
Other namesNatural thyroid, natural thyroid hormones, pork thyroid, thyroid USP, thyroid BP
AHFS/Drugs.com Monograph
License data
Routes of
administration 		By mouth
ATC code
  • None
Legal status
Legal status
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CAS Number

Desiccated thyroid extract (DTE), is thyroid gland that has been dried and powdered for medical use. [1] It is used to treat hypothyroidism, [1] but less preferred than levothyroxine. [1] It is taken by mouth. [1] Maximal effects may take up to three weeks to occur. [1]

Contents

Side effects may occur from excessive doses. [1] This may include weight loss, fever, headache, anxiety, trouble sleeping, arrhythmias, and heart failure. [1] Other side effects may include allergic reactions. [1] Use in pregnancy and breastfeeding is generally safe. [2] Regular blood tests are recommended to verify the appropriateness of the dose. [1] They contain a mixture of thyroxine (T4) and triiodothyronine (T3). [1]

Desiccated thyroid has been used since the late 1800s. [3] It is usually made from pigs, sheep, or cows. [4] It is available as a generic medication. [1] In 2022, it was the 137th most commonly prescribed medication in the United States, with more than 4 million prescriptions. [5] [6] Usage has decreased since the 1960s. [3]

Medical uses

The American Association of Clinical Endocrinologists [7] and the Royal College of Physicians [8] recommend against the use of thyroid extract for the treatment of hypothyroidism. Concerns include the potential for adverse effects from superphysiological levels of T3 and the absence of long-term safety data from randomized clinical trials. They recommend levothyroxine as the preferred treatment. Some practitioners refuse to use desiccated thyroid. [9]

Each 64.8 mg (one grain) of thyroid extract contains approximately 38 μg and 9 μg of measurable levothyroxine (T4) and liothyronine (T3), respectively. [1]

Arguments against desiccated thyroid include:

  1. Desiccated thyroid preparations have a greater variability from batch to batch than synthetic ones. [9]
  2. Desiccated thyroid has roughly a 4:1 ratio of thyroxine (T4) to triiodothyronine (T3). In humans, the ratio is 11:1. [10]
  3. A combination of various ratios of T4 and T3 might not provide benefits over T4 alone. Some controlled trials have shown inconsistent benefits of various ratios of T4 and T3. [11] [12]
  4. The use of desiccated thyroid is usually accompanied with the practice of dosing according to symptoms instead of dosing to achieve "ideal" lab results (e.g. serum levels of TSH). While there is debate as to what the ideal serum levels are, dosing according to symptoms often results in higher dosages. Most endocrinologists are opposed to these higher dosages as there may be risks of hyperthyroidism and osteoporosis. [13]
  5. The preference for "natural" treatment seems to stem from philosophical belief as opposed to science. [14]

Arguments for desiccated thyroid include:

  1. Desiccated thyroid contains all the hormones produced exclusively by the thyroid gland, including calcitonin. [ citation needed ]
  2. Desiccated thyroid therapy can be combined with synthetic thyroxine (T4) to balance out the T4/T3 correctly.

Chemistry

Desiccated thyroid has been described in the United States Pharmacopoeia for a century as "the cleaned, dried, and powdered thyroid gland previously deprived of connective tissue and fat... obtained from domesticated animals that are used for food by man" (USP XVI). [15] In the last few decades, pork alone is the usual source. Before modern assays, the potency was specified only by iodine content ("not less than 0.17% and not more than 0.23%"), rather than hormonal content or activity. [16]

History

The earliest oral treatment for hypothyroidism consisted of thyroid extract. George Redmayne Murray of the United Kingdom first described treatment of myxedema with thyroid extract in 1891, and published a description of long-term successful treatment (28 years) of a patient with myxedema (severe hypothyroidism) in 1920 [17] His treatment was quickly adopted in North America and Europe. The first recorded American use dates to 1891 by a woman who was still taking it 52 years later at 84 years of age [18]

Desiccated thyroid extract is prepared from pig thyroid glands. The glands are dried (desiccated), ground to powder, combined with binder chemicals, and pressed into pills. This was a new use for parts that were previously unwanted slaughterhouse offal, and Armour and Company, the dominant American meatpacker in the 20th century, supplied the best-known brand of thyroid extract. [ citation needed ]

Replacement by thyroid extract in hypothyroidism was one of the most effective treatments of any disease available to physicians before the middle of the 20th century, [ citation needed ] and in severe cases afforded dramatic relief of the myriad symptoms. The decision to treat was usually based on the presence of signs and symptoms of hypothyroidism because there were no accurate, readily available laboratory tests of thyroid function. Many less severe cases of hypothyroidism went untreated.[ citation needed ] Dosage was regulated by improvement of symptoms.

Desiccated Thyroid became a commercial treatment option in 1934 with Westhroid,[ citation needed ]. In the early 1960s, desiccated thyroid hormones (thyroid extract) began to be replaced by levothyroxine (synthetic T4), or by combinations of T4 and T3. Replacement occurred faster in the United Kingdom than in North America, but by the 1980s more patients were being prescribed synthetic T4 (levothyroxine) or synthetic T4/T3 combinations than desiccated thyroid extract.[ citation needed ]

Several reasons have been identified as to why prescriptions changed from desiccated thyroid treatment.

Thyroid care changed in other ways as well. Accurate T4 and T3 measurements became widely used in the 1970s, and by the late 1980s, TSH measurement had become sensitive enough to detect mild degrees of hyperthyroidism and overtreatment.[ citation needed ] Blood levels of thyroid hormones and TSH were found to be the best predictors of objective benefits from thyroid replacement[ improper synthesis? ]: those with the most severe measurable deficiency enjoyed the most dramatic and sustained benefits.[ citation needed ] It was also discovered that even mild hyperthyroidism as defined by a suppressed TSH level, whether due to disease or overtreatment, was associated with poorer bone density in women, and with higher rates of atrial fibrillation in elderly patients.[ citation needed ]

Society and culture

Names

This product is sometimes referred to as thyroid USP, thyroid BP. Brands differing only in binders and fillers.[ citation needed ]

Related Research Articles

<span class="mw-page-title-main">Hyperthyroidism</span> Clinical syndrome caused by excessive thyroid hormone

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon but life-threatening complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature; this often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.

<span class="mw-page-title-main">Thyroid</span> Endocrine gland in the neck; secretes hormones that influence metabolism

The thyroid, or thyroid gland, is an endocrine gland in vertebrates. In humans, it is a butterfly-shaped gland located in the neck below the Adam's apple. It consists of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the isthmus. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid.

<span class="mw-page-title-main">Hypothyroidism</span> Insufficient production of thyroid hormones by the thyroid gland

Hypothyroidism is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormones. It can cause a number of symptoms, such as poor ability to tolerate cold, extreme fatigue, muscle aches, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goitre. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.

<span class="mw-page-title-main">Iodothyronine deiodinase</span> Class of enzymes

Iodothyronine deiodinases (EC 1.21.99.4 and EC 1.21.99.3) are a subfamily of deiodinase enzymes important in the activation and deactivation of thyroid hormones. Thyroxine (T4), the precursor of 3,5,3'-triiodothyronine (T3) is transformed into T3 by deiodinase activity. T3, through binding a nuclear thyroid hormone receptor, influences the expression of genes in practically every vertebrate cell. Iodothyronine deiodinases are unusual in that these enzymes contain selenium, in the form of an otherwise rare amino acid selenocysteine.

<span class="mw-page-title-main">Congenital hypothyroidism</span> Thyroid hormone deficiency present at birth

Congenital hypothyroidism (CH) is thyroid hormone deficiency present at birth. If untreated for several months after birth, severe congenital hypothyroidism can lead to growth failure and permanent intellectual disability. Infants born with congenital hypothyroidism may show no effects, or may display mild effects that often go unrecognized as a problem. Significant deficiency may cause excessive sleeping, reduced interest in nursing, poor muscle tone, low or hoarse cry, infrequent bowel movements, significant jaundice, and low body temperature.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Triiodothyronine</span> Chemical compound

Triiodothyronine, also known as T3, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.

<span class="mw-page-title-main">Hashimoto's thyroiditis</span> Autoimmune disease

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, Hashimoto's disease, and autoimmune thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed.

<span class="mw-page-title-main">Levothyroxine</span> Thyroid hormone

Levothyroxine, also known as L-thyroxine, is a synthetic form of the thyroid hormone thyroxine (T4). It is used to treat thyroid hormone deficiency (hypothyroidism), including a severe form known as myxedema coma. It may also be used to treat and prevent certain types of thyroid tumors. It is not indicated for weight loss. Levothyroxine is taken orally (by mouth) or given by intravenous injection. Levothyroxine has a half-life of 7.5 days when taken daily, so about six weeks is required for it to reach a steady level in the blood.

<span class="mw-page-title-main">Thyroid disease</span> Medical condition

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

<span class="mw-page-title-main">Carbimazole</span> Medication used for hyperthyroidism

Carbimazole (brand names Neo-Mercazole, Anti-Thyrox, etc.) is used to treat hyperthyroidism. Carbimazole is a pro-drug as after absorption it is converted to the active form, methimazole. Methimazole prevents thyroid peroxidase enzyme from iodinating and coupling the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4 (thyroxine).

Thyroid storm is a rare but severe and life-threatening complication of hyperthyroidism. It occurs when an overactive thyroid leads to hypermetabolism, which can cause death from cardiac arrest or multiple organ failure.

<span class="mw-page-title-main">Liothyronine</span> Chemical compound

Liothyronine is a manufactured form of the thyroid hormone triiodothyronine (T3). It is most commonly used to treat hypothyroidism and myxedema coma. It can be taken by mouth or by injection into a vein.

Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. TFTs may be requested if a patient is thought to suffer from hyperthyroidism or hypothyroidism, or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requested routinely in conditions linked to thyroid disease, such as atrial fibrillation and anxiety disorder.

<span class="mw-page-title-main">Hypothalamic–pituitary–thyroid axis</span> Part of the neuroendocrine system

The hypothalamic–pituitary–thyroid axis is part of the neuroendocrine system responsible for the regulation of metabolism and also responds to stress.

An antithyroid agent is a hormone inhibitor acting upon thyroid hormones.

Euthyroid sick syndrome (ESS) is a state of adaptation or dysregulation of thyrotropic feedback control wherein the levels of T3 and/or T4 are abnormal, but the thyroid gland does not appear to be dysfunctional. This condition may result from allostatic responses of hypothalamus-pituitary-thyroid feedback control, dyshomeostatic disorders, drug interferences, and impaired assay characteristics in critical illness.

<span class="mw-page-title-main">Thyroid hormones</span> Hormones produced by the thyroid gland

Thyroid hormones are any hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine, derived from food. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre.

Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

<span class="mw-page-title-main">Hypothyroidism in dogs</span> Medical condition

Hypothyroidism is an endocrine disorder in which the thyroid gland fails to produce sufficient thyroid hormones. Hypothyroidism is one of the most common endocrinopathies in dogs. It is either acquired or congenital.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 "Thyroid Monograph for Professionals". Drugs.com. American Society of Health-System Pharmacists. Retrieved 8 April 2019.
  2. ↑ "Thyroid desiccated Use During Pregnancy". Drugs.com. Retrieved 9 April 2019.
  3. 1 2 Jameson JL, Groot LJ (2010). Endocrinology - E-Book: Adult and Pediatric. Elsevier Health Sciences. p. 1608. ISBN   9781455711260.
  4. ↑ Thomas JA, Keenan EJ (2012). Principles of Endocrine Pharmacology. Springer Science & Business Media. p. 78. ISBN   9781468450361.
  5. ↑ "The Top 300 of 2022". ClinCalc. Archived from the original on 30 August 2024. Retrieved 30 August 2024.
  6. ↑ "Thyroid Drug Usage Statistics, United States, 2013 - 2022". ClinCalc. Retrieved 30 August 2024.
  7. ↑ Garber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, et al. (December 2012). "Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association" (PDF). Thyroid. 22 (12): 1200–1235. doi:10.1089/thy.2012.0205. PMID   22954017. Archived from the original (PDF) on 14 January 2016. Retrieved 8 November 2014.
  8. ↑ "Thyroid disorders 'misdiagnosed'". BBC News. 27 March 2009. Retrieved 30 March 2009. the only accurate way to diagnose a thyroid disorder is via a blood test which measures hormone levels, and the only scientifically proven way of treating the condition is by topping up a patient's natural thyroxine levels with a synthetic form of the hormone.
  9. 1 2 "Endocrine Today Blog". Endocrinetoday.com. Retrieved 24 July 2014.
  10. ↑ Repas, Thomas. Desiccated thyroid in the management of hypothyroidism: Part I.
  11. ↑ Baskin HJ, Cobin RH, Duick DS, Gharib H, Guttler RB, Kaplan MM, Segal RL (2002). "American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism" (PDF). Endocrine Practice. 8 (6): 457–469. doi:10.4158/1934-2403-8.6.457. PMID   15260011. Archived from the original (PDF) on 8 December 2015. Retrieved 3 February 2015.
  12. ↑ Clyde PW, Harari AE, Getka EJ, Shakir KM (December 2003). "Combined levothyroxine plus liothyronine compared with levothyroxine alone in primary hypothyroidism: a randomized controlled trial". JAMA. 290 (22): 2952–2958. doi:10.1001/jama.290.22.2952. PMID   14665656.
  13. ↑ "Endocrine Today Blog". Endocrinetoday.com. Retrieved 24 July 2014.
  14. ↑ "Endocrine Today Blog". Endocrinetoday.com. Retrieved 24 July 2014.
  15. ↑ US Pharmacopeia Natural Formulary USP 37 N32 2014 Volume 3 May 1, 2014. The United States Pharmacopeial Convention. 2014. ISBN   9781936424221.
  16. ↑ Tory DB (2006). Remington The Science and Practice of Pharmacy (21st ed.). Philadelphia, PA: Lippincott Williams and Wilkins. pp. 1460, 1461. ISBN   0781763789.
  17. ↑ Murray GR. The life history of the first case of myxoedema treated by thyroid extract. Br Med J 1920;i:359-60.
  18. ↑ Burgess AM. Myxedema-- controlled by thyroid extract for fifty-two years: report of a case. Ann. Intern. Med. 1946; 25:146.
  19. ↑ Means JH, DeGroot LJ, Stanbury JB. The Thyroid and its Diseases. 3rd ed. New York:McGraw Hill, 1963. See chapter 9 for a lengthy discussion of the difficulties of assessing treatment in the era before effective tests, as well as the doctors' impressions of the superiority of the new synthetic thyroxine that had just become available.
  20. ↑ Macgregor AG (February 1961). "Why does anybody use thyroid B.P.?". Lancet. 1 (7172): 329–332. doi:10.1016/s0140-6736(61)91498-2. PMID   13764789.
  21. ↑ Catz B, Ginsburg E, Salenger S (January 1962). "Clinically inactive thyroid U.S.P. A preliminary report". The New England Journal of Medicine. 266: 136–137. doi:10.1056/nejm196201182660308. PMID   13877407.
  22. ↑ Pileggi VJ, Golub OJ, Lee ND (July 1965). "Determination of Thyroxine and Triiodothyronine in Commercial Preparations of Desiccated Thyroid and Thyroid Extract". The Journal of Clinical Endocrinology and Metabolism. 25 (7): 949–956. doi:10.1210/jcem-25-7-949. PMID   14319377.
  23. ↑ Mangieri CN, Lund MH (January 1970). "Potency of United States Pharmacopeia desiccated thyroid tablets as determined by the antigoitrogenic assay in rats". The Journal of Clinical Endocrinology and Metabolism. 30 (1): 102–104. doi: 10.1210/jcem-30-1-102 . PMID   5409525.
  24. ↑ Rees-Jones RW, Rolla AR, Larsen PR (February 1980). "Hormonal content of thyroid replacement preparations". JAMA. 243 (6): 549–550. doi:10.1001/jama.1980.03300320041023. PMID   7351788.
  25. ↑ Braverman LE, Ingbar SH, Sterling K (May 1970). "Conversion of thyroxine (T4) to triiodothyronine (T3) in athyreotic human subjects". The Journal of Clinical Investigation. 49 (5): 855–864. doi: 10.1172/jci106304 . PMC   535757 . PMID   4986007.
  26. ↑ Saberi M, Utiger RD (November 1974). "Serum thyroid hormone and thyrotropin concentrations during thyroxine and triiodothyronine therapy". The Journal of Clinical Endocrinology and Metabolism. 39 (5): 923–927. doi:10.1210/jcem-39-5-923. PMID   4422006.
  27. ↑ Penny R, Frasier SD (January 1980). "Elevated serum concentrations of triiodothyronine in hypothyroid patients. Values for patients receiving USP thyroid". American Journal of Diseases of Children. 134 (1): 16–18. doi:10.1001/archpedi.1980.02130130008003. PMID   7350782.
  28. 1 2 Capiferri R, Evered D (March 1979). "Investigation and treatment of hypothyroidism". Clinics in Endocrinology and Metabolism. 8 (1): 39–48. doi:10.1016/S0300-595X(79)80008-0. PMID   371874.
  29. ↑ Surks MI, Schadlow AR, Oppenheimer JH (December 1972). "A new radioimmunoassay for plasma L-triiodothyronine: measurements in thyroid disease and in patients maintained on hormonal replacement". The Journal of Clinical Investigation. 51 (12): 3104–3113. doi: 10.1172/jci107137 . PMC   332992 . PMID   4539287.
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