
n.
- Insufficient production of thyroid hormones.
- A pathological condition resulting from severe thyroid insufficiency, which may lead to cretinism or myxedema.
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American Heritage Dictionary:
hy·po·thy·roid·ism |

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Oxford Food & Nutrition Dictionary:
hypothyroidism |
Underactivity of the thyroid gland, leading to reduced secretion of thyroid hormones and a reduction in basal metabolic rate. Commonly associated with goitre due to iodine deficiency. In hypothyroid adults there is a characteristic moon-faced appearance, lethargy, and mental apathy. In infants, hypothyroidism can lead to severe mental retardation, cretinism. See also thyrotoxicosis.
Oxford Companion to the Body:
hypothyroidism |
Hypothyroidism is due to underactivity of the thyroid gland, and results from its failure to secrete sufficient thyroid hormones into the bloodstream.
For normal function, the thyroid gland relies upon stimulation by a hormone from the pituitary gland known appropriately as thyroid stimulating hormone (TSH). Primary hypothyroidism is due to failure of the thyroid itself, whilst secondary hypothyroidism occurs when the pituitary secretes inadequate TSH. Primary hypothyroidism is the usual reason for thyroid underactivity.
There are several potential causes of primary hypothyroidism. It may for example be due to insufficient intake of iodine in the diet, since iodine is an essential constituent of thyroid hormones. This is a major health problem in many regions of the underdeveloped world and ranks first as a global cause of thyroid deficiency. In contrast, congenital hypothyroidism is due to a rare failure of the thyroid gland to develop during fetal life. Another infrequent cause of hypothyroidism is a failure in the complex biosynthetic pathway which leads to the secretion of its hormones by the thyroid gland (thyroid dyshormonogenesis). But if there is sufficient dietary iodine, the most common cause of hypothyroidism is autoimmune destruction of the cells which make up the basic functional unit of the thyroid gland — namely, the thyroid follicle. The thyroid gland is particularly prone to autoimmune disorders. Thus in Hashimoto's thyroiditis, which in the UK afflicts about 1 in 10 women, but only 1 in 100 men, there is progressive hypothyroidism with declining secretion of thyroid hormones. The thyroid is gradually infiltrated by lymphocytes and the follicular architecture of the gland breaks down. At the same time, the overall mass of the gland can increase, and if untreated a large multinodular goitre sometimes develops. Hashimoto's thyroiditis is named after the Japanese surgeon who gave the first clear description of the condition in 1912. In 1956 it was demonstrated by Doniach, Roitt, and Campbell in London that Hashimoto's thyroiditis is further characterized by the presence in the circulating blood of thyroid autoantibodies (anti-thyroglobulin and anti-thyroid peroxidase).
Most of the symptoms of hypothyroidism in adults are the result of lowered cellular metabolism, due to the inadequate output of thyroid hormones. Typically, the patient feels cold, lethargic, and depressed. There is often weight gain, a puffy appearance (myxoedema), dry hair, and maybe a goitre. The pulse tends to be slow, cardiac output is reduced, and in women (the majority of sufferers) there may be menstrual irregularities. In children, since thyroid hormones are required for growth, there is stunted growth along with lethargy and obesity. One of the particular problems of this condition is that because hypothyroidism develops slowly these symptoms are insidious; they can go unnoticed or be wrongly attributed, for example, to the menopause or to natural ageing.
Inadequacy of thyroid hormones is particularly serious for the fetus, because they are required for the development of the nervous system in utero. In iodine-deficient regions of the world, this leads to the birth of neurological cretins, who have suffered major and irreversible damage to their central nervous system. It is estimated that, even in these days, 100 000 such cretins are born each year. In contrast, the incidence of neonatal hypothyroidism in iodine-replete Western society — a condition often referred to as ‘sporadic cretinism’ — is about 1 in 4000 live births; this is due to failure of the fetal thyroid to develop. This congenital hypothyroidism, unlike the neurological cretin, is amenable to treatment with thyroid hormones.
Hypothyroidism can readily be treated by oral thyroxine, which is one of the two hormones synthesized by the thyroid gland. This was first demonstrated by George Murray, a physician in Hartlepool. In 1891 he reported to the Newcastle Medical Research Society the beneficial effects of administering extracts of sheep thyroids to his profoundly hypothyroid patients. This was the first example of hormone replacement therapy.
— N. J. Marshall
Gale Encyclopedia of Children's Health:
Hypothyroidism |
Definition
Hypothyroidism, or underactive thyroid, develops when the thyroid gland fails to produce or secrete as much thyroxine (T4) and triiodothyonine (T3) as the body needs. Because these thyroid hormones regulate such essential functions as heart rate, digestion, physical growth, and mental development, an insufficient supply of this hormone can slow metabolic processes, damage organs and tissues in every part of the body, and lead to life-threatening complications.
Description
Hypothyroidism is one of the most common chronic diseases in the United States. Symptoms may not appear until years after the thyroid has stopped functioning and often are mistaken for signs of other illnesses. Although this condition is believed to affect up to 11 million adults and children, as many as two out of every three people with hypothyroidism may not know they have the disease.
Nicknamed "Gland Central" because it influences almost every organ, tissue, and cell in the body, the thyroid is shaped like a butterfly and located just below the larynx, or Adam's apple, and in front of the trachea, or windpipe. The thyroid stores iodine that the body obtains from food, and uses this mineral to create the thyroid hormones. Low thyroid hormone levels can alter weight, appetite, sleep patterns, body temperature, and a variety of other physical, mental, and emotional characteristics.
Although hypothyroidism is most common in women who are middle-aged or older, the disease can occur at any age. In addition, an infant can be born with congenital hypothyroidism, i.e., without a functioning thyroid. In older children, the development of hypothyroidism may progress slowly and it may be several years before the disease is diagnosed.
Demographics
The most common cause of hypothyroidism in mid-to late-childhood and adolescence is Hashimoto's thyroiditis, which occurs in up to 1.2 percent of the school age population. Congenital hypothyroidism is less common. One out of every 4,000–5,000 infants is born without a properly functioning thyroid gland. Congenital hypothyroidism is twice as common in girls as in boys and about five times more common in whites than in blacks.
Causes and Symptoms
Congenital hypothyroidism is a disorder that affects infants from birth, resulting from the loss of thyroid function due to the failure of the thyroid gland to develop correctly. Sometimes the thyroid gland is absent or is ectopic, i.e., in an abnormal location. This congenital defect means that the infant does not produce sufficient thyroid hormones, resulting in abnormal growth and development as well as slower mental function.
Hypothyroidism may also be caused by an abnormality of the immune system that results in damage and destruction of the thyroid gland (Hashimoto's thyroiditis). This process can result in either loss of thyroid tissue or enlargement of the thyroid. In most cases, there is no pain or tenderness associated with this disease, although sometimes persons affected complain of difficulty in swallowing, as if they had a lump in the throat.
Less often, hypothyroidism develops when the pituitary gland fails and does not release enough thyroid-stimulating hormone (TSH), which stimulates the thyroid to produce and secrete normal amounts of T4 and T3. TSH may be deficient for several reasons:
Other causes of hypothyroidism include:
Often babies with congenital hypothyroidism will appear normal at birth, which is why screening is vital. However, some infants may have one of more of the following symptoms:
Children born with symptoms have a greater risk of developmental delay than children born without symptoms. The longer a child with hypothyroidism remains untreated, the greater is the loss of intellectual capacity, as measured by the standard intelligence testing (IQ). The ultimate IQ has been shown to be significantly higher in children whose hypothyroidism was detected and treated prior to six weeks of age, compared to those children whose hypothyroidism went untreated for six to 12 weeks.
Hypothyroidism that develops after birth is sometimes referred to as a silent disease because early symptoms may be so mild that no one realizes anything is wrong. Untreated symptoms become more noticeable and severe, and can lead to confusion and mental disorders, breathing difficulties, heart problems, fluctuations in body temperature, and death.
A child or adolescent who has hypothyroidism may have one or more of the following symptoms:
Although hypothyroidism usually develops gradually, when the disease results from surgery or other treatment for hyperthyroidism, symptoms may appear suddenly and include severe muscle cramps in the arms, legs, neck, shoulders, and back.
People whose hypothyroidism remains undiagnosed and untreated may eventually develop myxedema. Symptoms of this rare, but potentially deadly, complication include enlarged tongue, swollen facial features, hoarseness, and physical and mental sluggishness. Myxedema coma can cause unresponsiveness; irregular, shallow breathing; low blood sugar; and drops in blood pressure and body temperature. The onset of this medical emergency can be sudden in children with undiagnosed hypothyroidism; it can be brought on by illness, injury, surgery, use of sedatives or anti-depressants, or exposure to very cold temperatures. Without immediate medical attention, myxedema coma can be fatal.
When to Call the Doctor
The doctor should be called if signs of hypothyroidism or myxedema are present. Every child who has a decrease in rate of growth in height during childhood and adolescence should be tested to determine if the growth problem is caused by hypothyroidism.
Diagnosis
In the United States, newborn infants between 24 and 72 hours old are tested for congenital thyroid deficiency (cretinism) using a test that measures the levels of thyroxine in the infant's blood. If the levels are low, the physician will likely repeat the blood test to confirm the diagnosis. The physician may take an x ray of the infant's legs. In an infant with hypothyroidism, the ends of the bones have an immature appearance. Treatment within the first few months of life can prevent mental retardation and physical abnormalities.
Older children who develop hypothyroidism may suddenly stop growing. If the child was above average height before the disease occurred, he or she may now be short compared to other children of the same age. Therefore, the most important feature of hypothyroidism in a child is a decrease in the rate of growth in height. If the disease is recognized early and adequately treated, the child will grow at an accelerated rate until reaching the same growth percentile where the child measured before the onset of hypothyroidism. Diagnosis of hypothyroidism is based on the patient's observations, medical history, physical examination, and thyroid function tests. Doctors who specialize in treating thyroid disorders (endocrinologists) are most likely to recognize subtle symptoms and physical indications of hypothyroidism. A diagnostic evaluation may include a blood test known as a thyroid-stimulating hormone (TSH) assay, thyroid nuclear medicine scan, thyroid ultrasound, or needle aspiration biopsy (which is also used to provide information on thyroid masses). All patients should be sure their doctors are aware of any recent procedures involving radioactive materials or contrast media.
The blood test is extremely accurate, but some doctors doubt its ability to detect mild hypothyroidism. They advise patients to monitor their basal (resting) body temperature for below-normal readings that could indicate the presence of hypothyroidism.
Alternative Treatment
Alternative treatments are primarily aimed at strengthening the thyroid but will not eliminate the need for thyroid hormone medications. Herbal remedies to improve thyroid function and relieve symptoms of hypothyroidism include bladder wrack (Fucus vesiculosus), which can be taken in capsule form or as a tea. The shoulder stand yoga position (done at least once daily for 20 minutes) is believed to improve thyroid function.
Nutritional Concerns
Because the thyroid makes T4 from iodine in food, an iodine-deficient diet can cause hypothyroidism. Adding iodine to table salt and other common foods has eliminated iodine deficiency in the United States. Some foods, including cabbage, rutabagas, radishes, peanuts, peaches, soybeans, and spinach, can interfere with thyroid hormone production. Anyone with hypothyroidism may want to avoid these foods. A high-fiber diet along with regular exercise is recommended to help maintain thyroid function and prevent constipation.
Prognosis
Thyroid hormone replacement therapy generally maintains normal thyroid hormone levels unless treatment is interrupted or discontinued.
Prevention
Hypothyroidism usually cannot be prevented, but the symptoms and effects of the disease can be controlled by prompt diagnosis and treatment.
Parental Concerns
Parents must ensure that medication is taken on a routine basis by making the process a part of the family's lifestyle. Taking the medication as prescribed helps assure the child's optimal growth and development.
Resources
Books
Gomez, Joan. Thyroid Problems in Women and Children: Self-Help and Treatment. Alameda, CA: Hunter House, 2003.
Langer, Stephen, and James F. Scheer. Hypothyroidism: The Unsuspected Illness. New Canaan, CT: Keats Publishing, 1995.
Pratt, Maureen. The First Year—Hypothyroidism: An Essential Guide for the Newly Diagnosed. New York: Marlowe and Company, 2003.
Rosenthal, M. Sara. The Hypothyroid Sourcebook: Everything You Need to Know. New York: McGraw Hill, 2002.
Shomon, Mary J. Living Well with Hypothyroidism: What Your Doctor Doesn't Tell You...That You Need to Know. New York: Harper Resource, 2000.
Wood, Lawrence C., et al. Your Thyroid: A Home Reference. New York: Ballantine Books, 1996.
Organizations
American Thyroid Association. Montefiore Medical Center, 111 E. 210th St., Bronx, NY 10467. Web site: www.thyroid.org.
Endocrine Society. 4350 East West Highway, Suite 500, Bethesda, MD 20814-4410. (301) 941-0200. Web site: www.endosociety.org.
Thyroid Foundation of America, Inc. Ruth Sleeper Hall, RSL 350, Boston, MA 02114-2968. (800) 832-8321 or (617) 726-8500. Web site: www.tsh.org.
Thyroid Society for Education and Research. 7515 S. Main St., Suite 545, Houston, TX 77030. (800) THYROID or (713) 799-9909. Web site: www.the-thyroid-society.org.
Web Sites
Thyroid Diseases. National Institutes of Health. Available online at: www.nlm.nih.gov/medlineplus/thyroiddiseases.html.
[Article by: Judith Sims, M.S. Maureen Haggerty]
Gale Encyclopedia of Public Health:
Hypothyroidism |
Hypothyroidism is the condition that reflects decreased concentrations of thyroid hormones, due to any cause. The resulting hypometabolic state causes decreased heat production and generally slows many of the bodies' processes. Its prevalence is 1 to 3 percent of young to middle-aged adults, mainly women, and its incidence rises with age. Severe hypothyroidism occurs in 2 to 4 percent of women older than seventy years of age, and milder forms of disease in 8 to 15 percent. Outside of North America, iodine deficiency is a major cause of hypothyroidism. In the United States, causes include Hashimoto's disease and treatment of hyperthyroidism—either by surgery or radioactive iodine (I-131). Treatment for hypothyroidism consists of hormone supplementation, generally synthetic l-thyroxine, taken once per day.
(SEE ALSO: Goiter; Hyperthyroidism; Iodine; Thyroid Disorders; Thyroid Function Tests)
Bibliography
Shapiro, L. (1999). "Hypothyroidism." In Atlas of Clinical Endocrinology, Vol. 1: Thyroid Diseases, ed. M. I. Surks. Philadelphia, PA: Current Medicine.
— MARTIN I. SURKS
Oxford Dictionary of Biochemistry:
hypothyroidism |
| hypothetical protein, hypothalamus, hypothalamic | |
| hypotonic, hypovolemia, hypox |
Saunders Veterinary Dictionary:
hypothyroidism |
Deficiency of thyroid gland activity, with underproduction of thyroxine, or the condition resulting from it. Common in adult dogs, particularly certain breeds, as a result of an idiopathic atrophy of the thyroid or a lymphocytic thyroiditis. Alopecia, weight gain, mental dullness, fatigue, cold intolerance, infertility and neurological deficits are seen. In food animals the syndrome is classical neonatal colloid goiter. See also goiter.
Mosby's Dental Dictionary:
hypothyroidism |
Diminished activity of the thyroid gland with decreased secretion of thyroxin, resulting in lowered basal metabolic rate, lethargy, sleepiness, dysmenorrhea in females, and a tendency toward obesity. Occasionally there is accompanying gingival hyperplasia. The condition is called cretinism in children and myxedema in adults.
Random House Word Menu:
categories related to 'hypothyroidism' |

Wikipedia on Answers.com:
Hypothyroidism |
| Hypothyroidism | |
|---|---|
| Classification and external resources | |
Thyroxine (T4) normally produced in 20:1 ratio to triiodothyronine (T3) |
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| ICD-10 | E03.9 |
| ICD-9 | 244.9 |
| DiseasesDB | 6558 |
| eMedicine | med/1145 |
| MeSH | D007037 |
Hypothyroidism (pronounced /ˌhaɪpɵˈθaɪrɔɪdɪzəm/) is a condition in which the thyroid gland does not make enough thyroid hormone.
Iodine deficiency is often cited as the most common cause of hypothyroidism worldwide but it can be caused by many other factors. Excessive iodine intake has been shown to induce hypothyroidism in population studies. And in Japan, hypothyroidism has been reversed by severely restriciting iodine intake[citation needed]. It can result from a lack of a thyroid gland or from iodine-131 treatment, and can also be associated with increased stress. Severe hypothyroidism in infants can result in cretinism. Many antibacterial chemicals in toothpastes and soaps have been shown to block thyroid receptors thereby inducing a new type of hypothyroidism.
A 2011 study concluded that about 8% of people in the UK suffer from an under-active thyroid and that as many as 100,000 of these people could benefit from treatment they are currently not receiving.[1]
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Contents
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Hypothyroidism is often classified by association with the indicated organ dysfunction (see below):[2][3]
| Type | Origin | Description |
|---|---|---|
| Primary | Thyroid gland | The most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodine therapy for hyperthyroidism. |
| Secondary | Pituitary gland | Occurs if the pituitary gland does not create enough thyroid-stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine. Although not every case of secondary hypothyroidism has a clear-cut cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery.[4] Secondary hypothyroidism accounts for less than 5%[5] or 10%[6] of hypothyroidism cases. |
| Tertiary | Hypothalamus | Results when the hypothalamus fails to produce sufficient thyrotropin-releasing hormone (TRH). TRH prompts the pituitary gland to produce thyroid-stimulating hormone (TSH). Hence may also be termed hypothalamic-pituitary-axis hypothyroidism. It accounts for less than 5% of hypothyroidism cases.[5] |
Early hypothyroidism is often asymptomatic and can have very mild symptoms. Subclinical hypothyroidism is a state of normal thyroid hormone levels, thyroxine (T4) and triiodothyronine (T3), with mild elevation of thyrotropin, thyroid-stimulating hormone (TSH). With higher TSH levels and low free T4 levels, symptoms become more readily apparent in clinical (or overt) hypothyroidism.
Hypothyroidism can be associated with the following symptoms:[7][8][9]
Subclinical hypothyroidism occurs when thyrotropin (TSH) levels are elevated but thyroxine (T4) and triiodothyronine (T3) levels are normal.[21] In primary hypothyroidism, TSH levels are high and T4 and T3 levels are low. TSH usually increases when T4 and T3 levels drop. TSH prompts the thyroid gland to make more hormone. In subclinical hypothyroidism, TSH is elevated but below the limit representing overt hypothyroidism. The levels of the active hormones will be within the laboratory reference ranges.
During pregnancy there is a substantially increased need of thyroid hormones and substantial risk that a previously unnoticed, subclinical or latent hypothyroidism will turn into overt hypothyroidism. See thyroid disease in pregnancy for more details.
Subclinical hypothyroidism in early pregnancy, compared with normal thyroid function, has been estimated to increase the risk of pre-eclampsia with an odds ratio (OR) of 1.7 and the risk of perinatal mortality with an OR of 2.7.[22]
Even mild or subclinical hypothyroidism are known to adversely affect fertility.
About three percent of the general American population has hypothyroidism.[21] A 1995 survey in the UK found the mean incidence (with 95% confidence intervals) of spontaneous hypothyroidism in women was 3.5/1000 survivors/year (2.8-4.5) rising to 4.1/1000 survivors/year (3.3-5.0) for all causes of hypothyroidism and in men was 0.6/1000 survivors/year (0.3-1.2).[23]
Estimates of subclinical hypothyroidism range between 3–8%, increasing with age; incidence is more common in women than in men.[24]
Iodine deficiency is the most common cause of hypothyroidism worldwide.[25] In iodine-replete individuals hypothyroidism is frequently caused by Hashimoto's thyroiditis, or otherwise as a result of either an absent thyroid gland or a deficiency in stimulating hormones from the hypothalamus or pituitary.
Factors such as iodine deficiency or exposure to iodine-131 from nuclear fallout, which is absorbed by the thyroid gland like regular iodide and destroys its cells, can increase the risk.
Congenital hypothyroidism is very rare accounting for approximately 0.2‰ and can have several causes such as thyroid aplasia or defects in the hormone metabolism. Thyroid hormone insensitivity (most often T3 receptor defect) also falls into this category although in this condition the levels of thyroid hormones may be normal or even markedly elevated.
Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all women within a year of giving birth.[citation needed] The first phase is typically hyperthyroidism; the thyroid then either returns to normal, or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring life-long treatment.
Hypothyroidism can result from de Quervain's thyroiditis, which, in turn, is often caused by having a bad flu that enters and destroys part, or all, the thyroid.[26]
Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.[citation needed]
Temporary hypothyroidism can be due to the Wolff-Chaikoff effect. A very high intake of iodine can be used to temporarily treat hyperthyroidism, especially in an emergency situation. Although iodide is a substrate for thyroid hormones, high levels reduce iodide organification in the thyroid gland, decreasing hormone production. The antiarrhythmic agent amiodarone can cause hyper- or hypothyroidism due to its high iodine content.
Hypothyroidism can be caused by lithium-based mood stabilizers, usually used to treat bipolar disorder (previously known as manic depression).[25] In fact, lithium has occasionally been used to treat hyperthyroidism.[27] Other drugs that may produce hypothyroidism include interferon alpha, interleukin-2, and thalidomide.[25]
Stress is known to be a significant contributor to thyroid dysfunction: this can be environmental stress as well as lesser-considered homeostatic stress such as fluctuating blood sugar levels and immune problems. Moreover, adrenal stress's effect on thyroid function can be indirect, through its effects on blood sugar levels (dysglycemia),[28][29] but can also have more direct effects. Stress can cause hypothyroidism or reduced thyroid functioning through disrupting the HPA axis which down-regulates thyroid function,[30] reducing the conversion of T4 to T3,[31] weakening the immune system thus promoting autoimmunity,[32] causing thyroid hormone resistance,[33] and resulting in hormonal imbalances:[34] indeed, excess estrogen in the blood caused by chronic cortisol elevations (which reduce the liver's ability to clear excess estrogen[35]), can result in hypothyroid symptoms by decreasing levels of active T3.[36] Stress also affects thyroid functioning through the sympathetic nervous system.[37] Refugees from East Germany in a 1994 study who experienced chronic stress were found to have a very high rate of hypothyroidism or subclinical hypothyroidism, although not all refugees displayed clinical or behavioral symptoms associated with this reduced thyroid functioning.[38] TSH levels correlate positively with physiological stress.[39][40]
Symptoms of adrenal stress include
Weak adrenal glands can also result in hypothyroid symptoms without affecting the thyroid itself.[41]
The only validated test to diagnose primary hypothyroidism, is to measure thyroid-stimulating hormone (TSH) and free thyroxine (T4).[42] However, these levels can be affected by non-thyroidal illnesses.
High levels of TSH indicate that the thyroid is not producing sufficient levels of thyroid hormone (mainly as thyroxine (T4) and smaller amounts of triiodothyronine (T3)). However, measuring just TSH fails to diagnose secondary and tertiary hypothyroidism, thus leading to the following suggested blood testing if the TSH is normal and hypothyroidism is still suspected:
Additionally, the following measurements may be needed:
Hypothyroidism is treated with the levorotatory forms of thyroxine (levothyroxine) (L-T4) and triiodothyronine (liothyronine) (L-T3). Synthroid is, in the US, the most common name form of the pill Levothyroxine. Synthroid is also the most common pill prescribed by doctors that has the synthetic thyroid hormone in it. This medicine can improve symptoms of thyroid deficiency such as slow speech, lack of energy, weight gain, hair loss, dry skin, and feeling cold. It also helps to treat goiter. It is also used to treat some kinds of thyroid cancer along with surgery and other medicines. Both synthetic and animal-derived thyroid tablets are available and can be prescribed for patients in need of additional thyroid hormone. Thyroid hormone is taken daily, and doctors can monitor blood levels to help assure proper dosing. Levothyroxine is best taken 30–60 minutes before breakfast, as some food can diminish absorption. Calcium can inhibit the absorption of levothryoxine. [44] Compared to water, coffee reduces absorption of levothyroxine by about 30 percent.[45] Some patients might appear to be resistant to levothyroxine, when in fact they do not properly absorb the tablets - a problem which is solved by pulverizing the medication.[46] There are several different treatment protocols in thyroid-replacement therapy:
The potential benefit from substituting some T3 for T4 has been investigated, but no conclusive benefit for combination therapy has been shown.[50][51]
The 2002 Laboratory Medicine Practice Guidelines of the National Academy of Clinical Biochemistry state that during pregnancy: "The L-T4 dose should be increased (usually by 50 mcg/day) to maintain a serum TSH between 0.5 and 2.0 mIU/L and a serum FT4 in the upper third of the normal reference interval." Doctors however often assume that if your TSH is in the "normal range", sometimes defined as high as 5.5 mIu/L, it has no effect on fertility. Healthy pregnant women however have a TSH level of around 1.0 mIU/L.
There is a range of opinion on the biochemical and symptomatic point at which to treat with levothyroxine, the typical treatment for overt hypothyroidism. Reference ranges have been debated as well. As of 2003, the American Association of Clinical Endocrinologists (ACEE) considers 0.3–3.0 mIU/L within normal range.[52]
There is always the risk of overtreatment and hyperthyroidism. Some studies have suggested that subclinical hypothyroidism does not need to be treated. A 2007 meta-analysis by the Cochrane Collaboration found no benefit of thyroid-hormone replacement except "some parameters of lipid profiles and left-ventricular function."[53] A 2002 meta-analysis looking into whether subclinical hypothyroidism may increase the risk of cardiovascular disease, as has been previously suggested,[54] found a possible modest increase and suggested further studies be undertaken with coronary-heart disease as an end point "before current recommendations are updated."[55]
Compounded slow-release T3 has been suggested for use in combination with T4, which proponents argue will mitigate many of the symptoms of functional hypothyroidism and improve quality of life. This is still controversial and is rejected by the conventional medical establishment.[56]
Hypothyroidism is also a relatively common disease in domestic dogs, with some specific breeds having a definite predisposition.[57]
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