|
|
This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (June 2013) |
| Hypothyroidism |
| Classification and external resources |
Thyroxine (T4) normally produced in 20:1 ratio to triiodothyronine (T3)
|
| ICD-10 |
E03.9 |
| ICD-9 |
244.9 |
| DiseasesDB |
6558 |
| MedlinePlus |
000353 |
| eMedicine |
med/1145 |
| MeSH |
D007037 |
Hypothyroidism // is a state in which the thyroid gland does not produce enough of the thyroid hormones thyroxine (T4) and triiodothyronine (T3).
Iodine deficiency is often cited as the most common cause of hypothyroidism worldwide but it can be caused by many other factors. It can result from the 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.
A 2011 study concluded that about 8% of women over 50 and men over 65 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]
Contents
- 1 Signs and symptoms
- 1.1 Earlier
- 1.2 Later
- 1.3 Uncommon
- 2 Causes
- 2.1 Stress and hypothyroidism
- 3 Pathophysiology
- 3.1 Pregnancy and fertility
- 4 Diagnosis
- 4.1 Classification
- 4.2 Subclinical hypothyroidism
- 5 Treatment
- 5.1 Treatment controversies
- 5.1.1 Desiccated thyroid extract
- 5.1.2 T3 only and combination T3 treatments
- 5.1.3 Slow-release T3
- 5.1.4 Dose to treat the patient's symptoms or lab results?
- 5.2 Subclinical hypothyroidism
- 5.3 Non-human presentation
- 6 Epidemiology
- 7 See also
- 8 References
- 9 Further reading
- 10 External links
Signs and symptoms[edit]
Early hypothyroidism is often asymptomatic and can have very mild symptoms. Hypothyroidism can be associated with a number of symptoms. These symptoms can relate to the underlying pathological cause of the hypothyroidism, a mass effect of a thyroid goitre, or direct effects of having insufficient thyroid hormones. Symptoms include:[2][3][4]
Earlier[edit]
- Appearance: thin, brittle fingernails; dry, itchy skin; weight gain, water retention,[5][6][7] myxedema, hair loss
- Neurological: depression, rapid thoughts.
- Neuromuscular: depressed reflexes, hypotonia, muscle cramps, joint pain, mood instability, irritability, constipation[citation needed]
- Constitutional: fatigue,[8] sleepiness, cold intolerance, decreased sweating
- Cardiovascular: bradycardia, elevated serum cholesterol.
- Endocrine: female infertility, menstrual irregularities, hyperprolactinemia, and galactorrhea.
Later[edit]
- Appearance: thinning of the outer third of the eyebrow, dry 'puffy' facial skin
- Neurological: slow speech and hoarse voice, deepening of the voice due to Reinke's Edema
- Neuromuscular: carpal tunnel syndrome and bilateral paresthesia
- Constitutional: low basal body temperature
- Cardiovascular: hypotension
- Endocrine: goiter (depending on cause[citation needed]), decreased libido in men[9] due to impairment of testicular testosterone synthesis.
Uncommon[edit]
- Appearance: yellowing of the skin due to impaired conversion of beta-carotene[10] to vitamin A (carotoderma), puffy face, hands and feet (late, less common symptoms), enlarged tongue[11]
- Neurological: impaired memory.[12] and inattentiveness,[13] decreased sense of taste and smell, deafness[14]
- Neuromuscular: difficulty swallowing, shortness of breath with a shallow and slow respiratory pattern, acute psychosis, (myxedema madness) (a rare presentation of hypothyroidism)
- Cardiovascular: anemia caused by impaired haemoglobin synthesis (decreased erythropoietin levels), impaired intestinal iron and folate absorption, or Vitamin B12 deficiency[15] from pernicious anemia
- Endocrine: reactive (or post-prandial) hypoglycemia,[16] impaired renal function with decreased glomerular filtration rate.
Causes[edit]
Iodine deficiency is the most common cause of hypothyroidism worldwide.[17][18] In iodine-replete areas of the world, hypothyroidism is most commonly caused by Hashimoto's thyroiditis,[18][19] or otherwise as a result of either an absent thyroid gland or a deficiency in stimulating hormones from the hypothalamus or pituitary. Congenital hypothyroidism is a rare cause of hypothyroidism and may result from thyroid agenesis and has an incidence of approximately 1 in 4000 births.[18]
Hypothyroidism can be caused by medications such as lithium-based mood stabilizers, a medication usually used to treat bipolar disorder.[17] In fact, lithium has occasionally been used to treat hyperthyroidism.[20] Other drugs that may produce hypothyroidism include amiodarone, interferon alpha, interleukin-2, rifampicin, sunitinib, and thalidomide.[17][18] Temporary hypothyroidism can be due to the Wolff-Chaikoff effect. A very high intake of iodine can be used to temporarily treat hypothyroidism, 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.
Exposure to radioactive iodine-131 can induce a state of hypothyroidism and this effect is used to medically treat hyperthyroidism.[21] De Quervain's thyroiditis, thought to be viral in origin, is a condition that can transiently cause hyperthyroidism and later progress to hypothyroidism.[22][23]
Hypothyroidism can result from postpartum thyroiditis up to 9 months after giving birth, characterized by transient hyperthyroidism followed by transient hypothyroidism. The syndrome is seen in 5 to 9% of women. 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, 25 to 30% will develop permanent hypothyroidism requiring lifelong thyroxine replacement therapy.[24]
Stress and hypothyroidism[edit]
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.[citation needed] Stress's effect on thyroid function can be indirect, through its effects on blood sugar levels (dysglycemia),[25] but it can also have more direct effects. Stress may cause hypothyroidism or reduced thyroid functioning by disrupting the HPA axis which down-regulates thyroid function,[26] reducing the conversion of T4 to T3,[27] weakening the immune system thus promoting autoimmunity,[28] causing thyroid hormone resistance,[29] and resulting in hormonal imbalances. Indeed, excess estrogen in the blood caused by chronic cortisol elevations can result in hypothyroid symptoms by decreasing levels of active T3.[30] Stress also affects thyroid functioning through the sympathetic nervous system.[31] A 1994 study of refugees from East Germany who experienced chronic stress found them 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.[32] TSH levels correlate positively with physiological stress.[33][34]
Adrenal insufficiency can also result in hypothyroid symptoms without affecting the thyroid itself.[35]
Pathophysiology[edit]
The synthesis of thyroid hormones requires sufficient circulating iodine in the presence of thyroid stimulating hormone (TSH). The iodine is taken up into the thyroid gland and incorporated into thyroglobulin molecules. Insufficient iodine, or insufficient TSH, can result in decreased production of thyroid hormones.[citation needed].
The hypothalamic–pituitary–thyroid axis plays a key role in maintaining thyroid output. Thyrotropin-releasing hormone is released from the hypothalamus, which stimulates the production of TSH by the pituitary. TSH in turn stimulates thyroid activity. If the hypothalamus or pituitary are damaged, then this will impair the activity of the thyroid gland.[citation needed]
A second important cause of hypothyroidism is Hashimoto's thyroiditis. In this condition, there is an autoimmune reaction against thyroid tissue. This results in destruction of the thyroid tissue.[citation needed]
Pregnancy and fertility[edit]
Main article: Thyroid disease in pregnancy
During pregnancy, there is a substantially increased need of thyroid hormones and a substantial risk that previously unnoticed subclinical or latent hypothyroidism will progress to overt hypothyroidism.
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.[36] In subclinical hypothyroidism, supplementation with levothyroxine results in significantly higher delivery rate, with a pooled relative probability of 2.76.[37]
Even mild or subclinical hypothyroidism is known to adversely affect fertility.[citation needed]
Diagnosis[edit]
Main article: Thyroid function tests
One test to diagnose primary hypothyroidism is to measure thyroid-stimulating hormone (TSH) and free thyroxine (T4).[38]
However, these levels can be affected by non-thyroidal illnesses, so diagnosing hypothyroidism based on TSH levels alone has been criticized by patient advocates and some doctors. One article argues that thyroid hormone trial therapy is the best method for achieving diagnostic certainty.[39]
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:
- Free triiodothyronine (fT3)
- Free thyroxine (fT4)
- Total T3
- Total T4
Additionally, the following measurements may be needed:
- Free T3 from 24-hour urine catch[40]
- Antithyroid antibodies – for evidence of autoimmune diseases that may be damaging the thyroid gland
- Serum cholesterol – which may be elevated in hypothyroidism
- Prolactin – as a widely available test of pituitary function
- Testing for anemia, including ferritin
- Basal body temperature
Classification[edit]
Hypothyroidism is often classified by association with the indicated organ dysfunction (see below):[41][42]
| Type |
Origin |
|
| Primary |
Thyroid gland |
The most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodinetherapy 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 cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery.[17] Secondary hypothyroidism accounts for less than 5%[43] or 10%[44] 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.[43] |
Subclinical hypothyroidism[edit]
Subclinical hypothyroidism occurs when thyroid stimulating hormone(TSH) levels are elevated but thyroxine (T4) and triiodothyronine (T3) levels are normal.[45] 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.
Generally subclinical hypothyroidism with TSH under 10mU/l does not require treatment.[46]
Treatment[edit]
Main article: Medical use of thyroid hormones
Hypothyroidism is treated with the levorotatory forms of thyroxine (levothyroxine) (L-T4) and triiodothyronine (liothyronine) (L-T3). Synthroid, produced by Abbott Laboratories, is the brand name counterpart to the generic Levothyroxine. Synthroid is also the most common pill prescribed by doctors that has the synthetic thyroid hormone in it, and it is taken by over 40% of people with hypothyroidism.[8] 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, the generic form of synthroid, is best taken 30–60 minutes before breakfast, as some food can diminish absorption. Calcium can inhibit the absorption of levothryoxine.[47] Compared to water, coffee reduces absorption of levothyroxine by about 30 percent.[48] 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.[49] There are several different treatment protocols in thyroid-replacement therapy:
- T4 only
- This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is currently the standard treatment in mainstream medicine.[50]
- T4 and T3 in combination
- This treatment protocol involves administering both synthetic L-T4 and L-T3 simultaneously in combination.[51]
- Desiccated thyroid extract
- Desiccated thyroid extract is an animal-based thyroid extract, most commonly from a porcine source. It is also a combination therapy, containing natural forms of L-T4 and L-T3. It also contains calcitonin, L-T1 and L-T2, which are not present in synthetic hormone medication.[52]
Treatment controversies[edit]
Patient advocates and some doctors oppose many of the practices of the mainstream endocrinology community[citation needed]. Critics[who?] argue that there is a dissatisfaction among patients regarding unnecessarily high levels of underdiagnosis and suboptimal patient outcomes. They argue that professional associations have behaved irrationally in continuing practices that are not supported by empirical evidence.[citation needed]
[edit]
Proponents argue that desiccated thyroid improves symptoms in most patients compared to conventional synthetic T4 treatments. There is at least one double-blind study that supports these claims.[53] Most endocrinologists and professional associations are opposed to the usage of desiccated thyroid.[citation needed]
T3 only and combination T3 treatments[edit]
The potential benefit from substituting some T3 for T4 has been investigated, but no conclusive benefit for combination therapy has been shown.[54][55]
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 µg/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".[56] Doctors however often assume that if a 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.
Slow-release T3[edit]
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.[57]
Dose to treat the patient's symptoms or lab results?[edit]
The currently accepted practice is to adjust the dosage of medication until serum hormone levels are at an "ideal" value. There is some disagreement as to what the ideal values should be. Patient advocates argue that doctors should adjust dosage to optimize the patient's symptoms.[58] Endocrinologists argue that they have a duty not to harm patients. Overdosage can lead to hyperthyroidism and may increase the risk of osteoporosis.
Subclinical hypothyroidism[edit]
Whilst previously there was has been some debate on the biochemical and symptomatic point at which to treat with levothyroxine, the typical treatment for overt hypothyroidism, the American Association of Clinical Endocrinologists (AACE) has stated that "the upper limit of TSH should remain at 4.5 mIU/L, rather than 3.0-3.5 as some other organizations have suggested".[59]
There is always the risk of overtreatment and hyperthyroidism. Some studies have suggested that subclinical hypothyroidism does not need to be treated. A 2002 meta-analysis looking into whether subclinical hypothyroidism may increase the risk of cardiovascular disease, as has been previously suggested,[60] found a possible modest increase and suggested further studies be undertaken with coronary-heart disease as an end point "before current recommendations are updated."[61] 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."[62]
Consensus American and British opinion since 2008, has been that in general patients with TSH under 10mU/l do not require treatment.[46][59]
Non-human presentation[edit]
Hypothyroidism is also a relatively common disease in domestic dogs, with some specific breeds having a definite predisposition.[63]
Epidemiology[edit]
Hypothyroidism is estimated to affect between 3.8-4.6% of the general population.[18] 0.3% of the general American population have overt hypothyroidism, and 4.3% have subclinical hypothyroidism.[64] 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).[65] Data from the CDC spanning the years 1999 to 2010 yield similar numbers: hypothyroidism is four times as common among women as among men.[8]
Estimates of subclinical hypothyroidism range between 3% and 8%, increasing with age; the median age of someone with hypothyroidism is 58.[8][66]
See also[edit]
- Hyperthyroidism
- Pituitary disease
- Subacute lymphocytic thyroiditis
- Thyroid hormone resistance
References[edit]
- ^ "100,000 Older People Missing Thyroid Treatment – Study". BBC News. 2011-01-24.
- ^ ATA 2003, p. 4
- ^ MedlinePlus Encyclopedia Hypothyroidism – primary – see list of Symptoms
- ^ "Hypothyroidism – In-Depth Report". New York Times. 2008. Retrieved 2012-06-18.
- ^ "Hypothyroidism" (PDF). American Association of Clinical Endocrinologists.
- ^ Yeum, C; Kim, SW; Kim, NH; Choi, KC; Lee, J (2002). "Increased expression of aquaporin water channels in hypothyroid rat kidney". Pharmacological Research 46 (1): 85–8. doi:10.1016/S1043-6618(02)00036-1. PMID 12208125.
- ^ "Thyroid and Weight" (PDF). The American Thyroid Association. Retrieved 2012-06-18.
- ^ a b c d fact sheet CDC medical records on VoxHealth. Retrieved on 2013-01-01
- ^ Velázquez, E. M.; Arata, G. Bellabarba (1997). "Effects of Thyroid Status on Pituitary Gonadotropin and Testicular Reserve in Men". Systems Biology in Reproductive Medicine 38: 85–92. doi:10.3109/01485019708988535.
- ^ Lavalle, James B. Cracking the Metabolic Code 1. p. 100. ISBN 1-4429-5039-0.
- ^ American College of Psychiatrists 2010 PRITE (Psychiatry Resident In-Training Exam) question 38.
- ^ Samuels, Mary H (2008). "Cognitive function in untreated hypothyroidism and hyperthyroidism". Current Opinion in Endocrinology, Diabetes and Obesity 15 (5): 429–33. doi:10.1097/MED.0b013e32830eb84c. PMID 18769215.
- ^ Rubin, Devon I; Aminoff, Michael J; Ross, Douglas S; Wilterdink, Janet L (November 12, 2009). "Neurologic manifestations of hypothyroidism".
- ^ Clinical Medicine by Kumar and Clark, "Thyroid Axis Endocrinology," p. 610.
- ^ Jabbar, A; Yawar, A; Waseem, S; Islam, N; Ul Haque, N; Zuberi, L; Khan, A; Akhter, J (2008). "Vitamin B12 deficiency common in primary hypothyroidism". JPMA. the Journal of the Pakistan Medical Association 58 (5): 258–61. PMID 18655403.
- ^ Hofeldt FD, Dippe S, Forsham PH (1972). "Diagnosis and classification of reactive hypoglycemia based on hormonal changes in response to oral and intravenous glucose administration" (PDF). Am. J. Clin. Nutr. 25 (11): 1193–201. PMID 5086042.
- ^ a b c d ATA 2003, p. 6
- ^ a b c d e Chakera, AJ; Pearce, SH; Vaidya, B (2012). "Treatment for primary hypothyroidism: current approaches and future possibilities.". Drug design, development and therapy 6: 1–11. doi:10.2147/DDDT.S12894. PMID 22291465.
- ^ Gaberscek, S; Zaletel, K (September 2011). "Thyroid physiology and autoimmunity in pregnancy and after delivery.". Expert review of clinical immunology 7 (5): 697–706. doi:10.1586/eci.11.42. PMID 21895480.
- ^ Offermanns, Stefan; Rosenthal, Walter (2008). Encyclopedia of Molecular Pharmacology, Volume 1 (2nd ed.). Springer. p. 189. ISBN 978-3-540-38916-3.
- ^ Rivkees, SA (2010). "Pediatric Graves' disease: controversies in management". Hormones research in pediatrics 74 (5): 305–311. doi:10.1159/000320028. PMID 20924158.
- ^ Sharma, M; Aronow, WS; Patel, L; Gandhi, K; Desai, H (April 2011). "Hyperthyroidism". Medical science monitor 17 (4): RA85–RA91. doi:10.12659/MSM.881705. PMID 21455118.
- ^ Thyroiditis from Columbia University Medical Center, Department of Surgery, New York, NY. Retrieved Mars 2011
- ^ Lazarus JH, Parkes AB, Premawardhana LD (May 2002). "Postpartum thyroiditis". Autoimmunity 35 (3): 169–73. PMID 12389641.
- ^ Rettori, V.; Jurcovicova, J.; McCann, S. M. (1987). "Central action of interleukin-1 in altering the release of tsh, growth hormone, and prolactin in the male rat". Journal of Neuroscience Research 18 (1): 179–83. doi:10.1002/jnr.490180125. PMID 3500324.
- ^ Sapolsky, R. M.; Krey, L. C.; McEwen, B. S. (1986). "The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis". Endocrine Reviews 7 (3): 284–301. doi:10.1210/edrv-7-3-284. PMID 3527687.
- ^ Ongphiphadhanakul, B; Fang, SL; Tang, KT; Patwardhan, NA; Braverman, LE (1994). "Tumor necrosis factor-alpha decreases thyrotropin-induced 5'-deiodinase activity in FRTL-5 thyroid cells". European journal of endocrinology 130 (5): 502–7. doi:10.1530/eje.0.1300502. PMID 8180680.
- ^ Guhad, FA; Hau, J (1996). "Salivary IgA as a marker of social stress in rats". Neuroscience letters 216 (2): 137–40. doi:10.1016/0304-3940(96)13037-8. PMID 8904802.
- ^ Kimura, Hiroaki; Caturegli, Patrizio (2007). "Chemokine Orchestration of Autoimmune Thyroiditis". Thyroid 17 (10): 1005–11. doi:10.1089/thy.2007.0267. PMID 17910527.
- ^ Steingold KA, Matt DW, DeZiegler D, Sealey JE, Fratkin M, Reznikov S (August 1991). "Comparison of transdermal to oral estradiol administration on hormonal and hepatic parameters in women with premature ovarian failure". J. Clin. Endocrinol. Metab. 73 (2): 275–80. doi:10.1210/jcem-73-2-275. PMID 1906893.
- ^ Klecha, Alicia Juana; Barreiro Arcos, María Laura; Frick, Luciana; Genaro, Ana María; Cremaschi, Graciela (2008). "Immune-Endocrine Interactions in Autoimmune Thyroid Diseases". Neuroimmunomodulation 15 (1): 68–75. doi:10.1159/000135626. PMID 18667802.
- ^ Bauer, M; Priebe, S; Kürten, I; Gräf, KJ; Baumgartner, A (1994). "Psychological and endocrine abnormalities in refugees from East Germany: Part I. Prolonged stress, psychopathology, and hypothalamic-pituitary-thyroid axis activity". Psychiatry Research 51 (1): 61–73. doi:10.1016/0165-1781(94)90047-7. PMID 8197271.
- ^ Peeters RP, van der Geyten S, Wouters PJ, et al. (December 2005). "Tissue thyroid hormone levels in critical illness". J. Clin. Endocrinol. Metab. 90 (12): 6498–507. doi:10.1210/jc.2005-1013. PMID 16174716.
- ^ Stouthard JM, van der Poll T, Endert E, et al. (November 1994). "Effects of acute and chronic interleukin-6 administration on thyroid hormone metabolism in humans". J. Clin. Endocrinol. Metab. 79 (5): 1342–6. doi:10.1210/jc.79.5.1342. PMID 7962327.
- ^ Abdullatif, HD; Ashraf, AP (2006). "Reversible subclinical hypothyroidism in the presence of adrenal insufficiency". Endocrine practice 12 (5): 572. PMID 17002934.
- ^ Van Den Boogaard, E.; Vissenberg, R.; Land, J. A.; Van Wely, M.; Van Der Post, J. A. M.; Goddijn, M.; Bisschop, P. H. (2011). "Significance of (sub)clinical thyroid dysfunction and thyroid autoimmunity before conception and in early pregnancy: A systematic review". Human Reproduction Update 17 (5): 605–619. doi:10.1093/humupd/dmr024. PMID 21622978. edit
- ^ [1] Velkeniers, B.; Van Meerhaeghe, A.; Poppe, K.; Unuane, D.; Tournaye, H.; Haentjens, P. (2013). "Levothyroxine treatment and pregnancy outcome in women with subclinical hypothyroidism undergoing assisted reproduction technologies: Systematic review and meta-analysis of RCTs". Human Reproduction Update 19 (3): 251–258. doi:10.1093/humupd/dms052. PMID 23327883. edit
- ^ Allahabadia, A.; Razvi, S.; Abraham, P.; Franklyn, J. (2009). "Diagnosis and treatment of primary hypothyroidism". BMJ 338: b725. doi:10.1136/bmj.b725. PMID 19325179.
- ^ http://www.query.com/terp/TSH_Test.pdf
- ^ Baisier, W. V.; Hertoghe, J.; Eeckhaut, W. (June 2000). "Thyroid Insufficiency. Is TSH Measurement the Only Diagnostic Tool?". Journal of Nutritional and Environmental Medicine 10 (2): 105–13. doi:10.1080/13590840050043521.
- ^ Simon H (2006-04-19). "Hypothyroidism". University of Maryland Medical Center. Retrieved 2008-02-28.
- ^ Department of Pathology (June 13, 2005). "Pituitary Gland – Diseases/Syndromes". Virginia Commonwealth University (VCU). Archived from the original on 2008-02-06. Retrieved 2008-02-28.
- ^ a b Agabegi, Elizabeth D; Agabegi, Steven S. (2008). Step-Up to Medicine. Step-Up. Hagerstwon MD: Lippincott Williams & Wilkins. p. 160. ISBN 0-7817-7153-6.
- ^ Burness, Christine E.; Shaw, Pamela J. (2008). "Thyroid Disease and the Nervous System". In Aminoff, Michael Jeffrey. Neurology and General Medicine. Churchill Livingstone. pp. 357–81. ISBN 978-0-443-06707-5.
- ^ Jack DeRuiter (2002). "Thyroid pathology" (PDF). Endocrine Module (PYPP 5260). Auburn University School of Pharmacy. p. 30.
- ^ a b The Royal College of Physicians, The Association for Clinical Biochemistry The Society for Endocrinology, The British Thyroid Association et al (19 November 2008). "The Diagnosis and Management of Primary Hypothyroidism" (pdf). Retrieved 2013-06-16.
- ^ Nippoldt, Todd. "Hypothyroidism (underactive thyroid)". Maco Clinic. Retrieved 01/23/2012.
- ^ Benvenga, Salvatore; Bartolone, Luigi; Pappalardo, Maria Angela; Russo, Antonia; Lapa, Daniela; Giorgianni, Grazia; Saraceno, Giovanna; Trimarchi, Francesco (2008). "Altered Intestinal Absorption of L-Thyroxine Caused by Coffee". Thyroid 18 (3): 293–301. doi:10.1089/thy.2007.0222. PMID 18341376.
- ^ Yamamoto, Toshihide (2003). "Tablet Formulation of Levothyroxine Is Absorbed Less Well Than Powdered Levothyroxine". Thyroid 13 (12): 1177–81. doi:10.1089/10507250360731596. PMID 14751040.
- ^ American Association of Clinical Endocrinologists (November/December 2002). "Medical Guidelines For Clinical Practice For The Evaluation And Treatment Of Hyperthyroidism And Hypothyroidism" (PDF). Endocrine Practice 8 (6): 457–69. PMID 15260011.
- ^ Bunevičius, Robertas; Kažanavičius, Gintautas; Žalinkevičius, Rimas; Prange, Arthur J. (February 1999). "Effects of Thyroxine as Compared with Thyroxine plus Triiodothyronine in Patients with Hypothyroidism". New England Journal of Medicine 340 (6): 424–9. doi:10.1056/NEJM199902113400603. PMID 9971866.
- ^ Baisier, W. V.; Hertoghe, J.; Eeckhaut, W. (September 2001). "Thyroid Insufficiency. Is Thyroxine the Only Valuable Drug?". Journal of Nutritional and Environmental Medicine 11 (3): 159–66. doi:10.1080/13590840120083376.
- ^ Thanh D. Hoang, Cara H. Olsen, Vinh Q. Mai, Patrick W. Clyde and Mohamed K. M. Shakir. [2]Desiccated Thyroid Extract Compared With Levothyroxine in the Treatment of Hypothyroidism: A Randomized, Double-Blind, Crossover Study. The Journal of Clinical Endocrinology & Metabolism 2013;98:1982-90
- ^ Escobar-Morreale, H. F.; Botella-Carretero, JI; Escobar Del Rey, F; Morreale De Escobar, G (2005). "Treatment of Hypothyroidism with Combinations of Levothyroxine plus Liothyronine". Journal of Clinical Endocrinology & Metabolism 90 (8): 4946–54. doi:10.1210/jc.2005-0184. PMID 15928247.
- ^ Joffe, R. T.; Brimacombe, M.; Levitt, A. J.; Stagnaro-Green, A. (2007). "Treatment of Clinical Hypothyroidism With Thyroxine and Triiodothyronine: A Literature Review and Metaanalysis". Psychosomatics 48 (5): 379–84. doi:10.1176/appi.psy.48.5.379. PMID 17878495.
- ^ Laboratory Support for the Diagnosis of Thyroid Disease (PDF), The National Academy of Clinical Biochemistry, 2002
- ^ Todd, C H (2010). "Management of thyroid disorders in primary care: challenges and controversies". Postgraduate Medical Journal 85 (1010): 655–9. doi:10.1136/pgmj.2008.077701. PMID 20075403.
- ^ http://www.stopthethyroidmadness.com/tsh-why-its-useless/
- ^ a b "Subclinical Thyroid Disease". Guidelines & Position Statements. The American Association of Clinical Endocrinologists. April 10, 2013. Retrieved 2013-06-16.
- ^ Biondi B, Palmieri EA, Lombardi G, Fazio S (December 2002). "Effects of subclinical thyroid dysfunction on the heart". Ann. Intern. Med. 137 (11): 904–14. PMID 12458990.
- ^ Ochs N, Auer R, Bauer DC et al. (June 2008). "Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality". Ann. Intern. Med. 148 (11): 832–45. PMID 18490668.
- ^ Villar, Heloisa Cerqueira Cesar Esteves; Saconato, Humberto; Valente, Orsine; Atallah, Álvaro N (2007). Thyroid hormone replacement for subclinical hypothyroidism. In Villar, Heloisa Cerqueira Cesar Esteves. "Cochrane Database of Systematic Reviews". Cochrane database of systematic reviews (Online) (3): CD003419. doi:10.1002/14651858.CD003419.pub2. PMID 17636722.
- ^ Brooks W (01/06/2008). "Hypothyroidism in Dogs". The Pet Health Library. VetinaryPartner.com. Retrieved 2008-02-28.
- ^ Hollowell JG, Staehling NW, Flanders WD, et al. (February 2002). "Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III)". J. Clin. Endocrinol. Metab. 87 (2): 489–99. doi:10.1210/jc.87.2.489. PMID 11836274.
- ^ Vanderpump, MP; Tunbridge, WM; French, JM; Appleton, D; Bates, D; Clark, F; Grimley Evans, J; Hasan, DM et al. (1995). "The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey". Clinical endocrinology 43 (1): 55–68. doi:10.1111/j.1365-2265.1995.tb01894.x. PMID 7641412.
- ^ Fatourechi, V. (2009). "Subclinical Hypothyroidism: An Update for Primary Care Physicians". Mayo Clinic Proceedings 84 (1): 65–71. doi:10.4065/84.1.65. PMC 2664572. PMID 19121255.
Further reading[edit]
- Tchong L, Veloski C, Siraj ES (May 2009). "Hypothyroidism: management across the continuum". J Clin Outcomes Manage 16 (5): 231–5.
- Rayman, Margaret P (July 2000). "The importance of selenium to human health". Lancet 356 (9225): 233–41. doi:10.1016/S0140-6736(00)02490-9. PMID 10963212.
External links[edit]
- "Hypothyroidism Booklet" (PDF). American Thyroid Association. 2003.
|
Endocrine pathology: endocrine diseases (E00–E35, 240–259)
|
|
Pancreas/
glucose
metabolism |
| Hypofunction |
- types:
- type 1
- type 2
- MODY 1 2 3 4 5 6
- complications
- coma
- angiopathy
- ketoacidosis
- nephropathy
- neuropathy
- retinopathy
- cardiomyopathy
- insulin receptor (Rabson–Mendenhall syndrome)
- Insulin resistance
|
|
| Hyperfunction |
- Hypoglycemia
- beta cell (Hyperinsulinism)
- G cell (Zollinger–Ellison syndrome)
|
|
|
Hypothalamic/
pituitary axes |
| Hypothalamus |
- gonadotropin
- Kallmann syndrome
- Adiposogenital dystrophy
- CRH (Tertiary adrenal insufficiency)
- vasopressin (Neurogenic diabetes insipidus)
- general (Hypothalamic hamartoma)
|
|
| Pituitary |
| Hyperpituitarism |
- anterior
- Acromegaly
- Hyperprolactinaemia
- Pituitary ACTH hypersecretion
- posterior (SIADH)
- general (Nelson's syndrome)
|
|
| Hypopituitarism |
- anterior
- Kallmann syndrome
- Growth hormone deficiency
- ACTH deficiency/Secondary adrenal insufficiency
- GnRH insensitivity
- FSH insensitivity
- LH/hCG insensitivity
- posterior (Neurogenic diabetes insipidus)
- general
- Empty sella syndrome
- Pituitary apoplexy
- Sheehan's syndrome
- Lymphocytic hypophysitis
|
|
|
| Thyroid |
| Hypothyroidism |
- Iodine deficiency
- Cretinism
- Congenital hypothyroidism
- Myxedema
- Euthyroid sick syndrome
|
|
| Hyperthyroidism |
- Hyperthyroxinemia
- Thyroid hormone resistance
- Familial dysalbuminemic hyperthyroxinemia
- Hashitoxicosis
- Thyrotoxicosis factitia
- Graves' disease
|
|
| Thyroiditis |
- Acute infectious
- Subacute
- De Quervain's
- Subacute lymphocytic
- Autoimmune/chronic
- Hashimoto's
- Postpartum
- Riedel's
|
|
| Goitre |
- Endemic goitre
- Toxic nodular goitre
- Toxic multinodular goiter
|
|
|
| Parathyroid |
| Hypoparathyroidism |
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Pseudopseudohypoparathyroidism
|
|
| Hyperparathyroidism |
- Primary
- Secondary
- Tertiary
- Osteitis fibrosa cystica
|
|
|
| Adrenal |
| Hyperfunction |
- aldosterone: Hyperaldosteronism/Primary aldosteronism
- Conn syndrome
- Bartter syndrome
- Glucocorticoid remediable aldosteronism
- AME
- Liddle's syndrome
- 17α CAH
- cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome)
- sex hormones: 21α CAH
- 11β CAH
|
|
Hypofunction/
Adrenal insufficiency
(Addison's, WF) |
- aldosterone: Hypoaldosteronism
|
|
|
| Gonads |
- ovarian: Polycystic ovary syndrome
- Premature ovarian failure
- testicular: enzymatic
- 5α-reductase deficiency
- 17β-hydroxysteroid dehydrogenase deficiency
- aromatase excess syndrome)
- Androgen receptor (Androgen insensitivity syndrome
- general: Hypogonadism (Delayed puberty)
- Hypergonadism
- Hypoandrogenism
- Hypoestrogenism
- Hyperandrogenism
- Hyperestrogenism
|
|
|
| Height |
- Dwarfism/Short stature
- Midget
- Laron syndrome
- Psychosocial
- Ateliosis
- Gigantism
|
|
| Multiple |
- Autoimmune polyendocrine syndrome multiple
- Carcinoid syndrome
- Multiple endocrine neoplasia
- Progeria
- Werner syndrome
- Acrogeria
- Metageria
- Woodhouse-Sakati syndrome
|
|
|
|
|
noco (d)/cong/tumr, sysi/epon
|
proc, drug (A10/H1/H2/H3/H5)
|
|
|
|
