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{{Infobox medical condition | |||
{{Infobox | | Name = Selenium deficiency | ||
| Name = | | Image = Se-TableImage.png | ||
| ICD10 | | Caption = [[Selenium]] | ||
| ICD9 | | DiseasesDB = 11941 | ||
| | | ICD10 = {{ICD10|E|59||e|50}} | ||
| | | ICD9 = {{ICD9|269.3}} | ||
| | | ICDO = | ||
| | | OMIM = | ||
| | | MedlinePlus = | ||
| | | eMedicineSubj = | ||
| eMedicineTopic = | |||
| MeshID = | |||
}} | }} | ||
'''[[Selenium]] deficiency''' is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported. | |||
== | ==Causes== | ||
It can occur in patients with severely compromised [[intestine|intestinal]] function, those undergoing [[total parenteral nutrition]], those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90).<ref>{{cite journal |first1=Giovanni |last1=Ravaglia |first2=Paola |last2=Forti |first3=Fabiola |last3=Maioli |first4=Luciana |last4=Bastagli |first5=Andrea |last5=Facchini |first6=Erminia |last6=Mariani |first7=Lucia |last7=Savarino |first8=Simonetta |last8=Sassi |first9=Domenico |last10=Lenaz |first10=G |last9=Cucinotta |title=Effect of micronutrient status on natural killer cell immune function in healthy free-living subjects aged ≥90 y |journal=American Journal of Clinical Nutrition |pmid=10648276 |url=http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=10648276 |year=2000 |volume=71 |issue=2 |pages=590–8|display-authors=8 }}</ref> | |||
People dependent on food grown from selenium-deficient soil may be at risk for deficiency. | |||
== | For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with [[cholesterol]]-lowering drugs (e.g., [[statins]]) may resemble the pathology of selenium deficiency.<ref>{{cite journal |pmid=15031036 |year=2004 |last1=Moosmann |first1=B |last2=Behl |first2=C |title=Selenoprotein synthesis and side-effects of statins |volume=363 |issue=9412 |pages=892–4 |doi=10.1016/S0140-6736(04)15739-5 |journal=Lancet}}</ref><ref>{{cite journal |pmid=15542379 |year=2004 |last1=Moosmann |first1=B |last2=Behl |first2=C |title=Selenoproteins, cholesterol-lowering drugs, and the consequences: Revisiting of the mevalonate pathway |volume=14 |issue=7 |pages=273–81 |doi=10.1016/j.tcm.2004.08.003 |journal=Trends in Cardiovascular Medicine}}</ref> | ||
==Reference ranges== | |||
In the USA, the [[Dietary Reference Intake]] for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma [[glutathione peroxidase]]. [[Selenoprotein P]]<ref name="pmid17508906">{{cite journal |doi=10.1089/ars.2007.1528 |title=From Selenium to Selenoproteins: Synthesis, Identity, and Their Role in Human Health |year=2007 |last1=Papp |first1=Laura Vanda |last2=Lu |first2=Jun |last3=Holmgren |first3=Arne |last4=Khanna |first4=Kum Kum |journal=Antioxidants & Redox Signaling |volume=9 |issue=7 |pages=775–806 |pmid=17508906}}</ref> is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.<ref name="pmid15817859">{{cite journal |pmid=15817859 |year=2005 |last1=Xia |first1=Y |last2=Hill |first2=KE |last3=Byrne |first3=DW |last4=Xu |first4=J |last5=Burk |first5=RF |title=Effectiveness of selenium supplements in a low-selenium area of China |volume=81 |issue=4 |pages=829–34 |journal=The American Journal of Clinical Nutrition}}</ref> | |||
== | ==Signs and symptoms== | ||
Selenium deficiency in combination with [[Coxsackievirus]] infection can lead to [[Keshan disease]], which is potentially fatal. Selenium deficiency also contributes (along with [[iodine deficiency]]) to [[Kashin-Beck disease]].<ref name=":0">{{Cite web|url = http://www.atsdr.cdc.gov/toxprofiles/tp92-c3.pdf|title = Toxicological Profile for Selenium|date = September 2003|accessdate = 7 Sep 2015|website = Agency for Toxic Substances and Disease Registry|publisher = U.S. Department of Health and Human Services|last = |first = }}</ref> The primary symptom of Keshan disease is [[myocardium|myocardial]] [[necrosis]], leading to weakening of the heart. [[Kashin-Beck disease]] results in [[atrophy]], degeneration and [[necrosis]] of [[cartilage]] tissue.<ref>{{cite journal |doi=10.1056/NEJM199810153391604 |title=Kashin–Beck Osteoarthropathy in Rural Tibet in Relation to Selenium and Iodine Status |year=1998 |last1=Moreno-Reyes |first1=Rodrigo |last2=Suetens |first2=Carl |last3=Mathieu |first3=Françoise |last4=Begaux |first4=Françoise |last5=Zhu |first5=Dun |last6=Rivera |first6=Maria T. |last7=Boelaert |first7=Marleen |last8=Nève |first8=Jean |last9=Perlmutter |first9=Noémi |last10=Vanderpas |first10=Jean |journal=New England Journal of Medicine |volume=339 |issue=16 |pages=1112–20 |pmid=9770558|display-authors=8 }}</ref> Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases. | |||
Selenium is also necessary for the conversion of the thyroid hormone [[thyroxine]] (T4) into its more active counterpart, [[triiodothyronine]],<ref name=":0" /> and as such a deficiency can cause symptoms of [[hypothyroidism]], including extreme [[Fatigue (medicine)|fatigue]], mental slowing, [[goiter]], [[cretinism]], and [[habitual abortion|recurrent miscarriage]].<ref>{{cite web|title = Selenium: Dietary Supplement Fact Sheet|url = http://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/|publisher = National Institutes of Health|accessdate = July 4, 2013}}</ref> | |||
== | ==Epidemiology and prevention== | ||
These diseases are most common in certain parts of China where the intake is low<ref name="urlSelenium: Mineral Deficiency and Toxicity: Merck Manual Professional">{{cite web |url=http://www.merck.com/mmpe/sec01/ch005/ch005i.html |title=Selenium: Mineral Deficiency and Toxicity: Merck Manual Professional |work= |accessdate=2008-11-29}}</ref> because the soil is extremely deficient in selenium. Studies in [[Jiangsu Province]] of China have indicated a reduction in the prevalence of these diseases by taking selenium supplements.<ref>{{Cite web|title = Dietary Supplement Fact Sheet: Selenium — Health Professional Fact Sheet|url = http://ods.od.nih.gov/factsheets/selenium.asp|website = ods.od.nih.gov|accessdate = 2015-09-08}}</ref> In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils.<ref>{{Cite journal|url = http://ajcn.nutrition.org/content/48/2/324.full.pdf|title = Selenium intake and serum selenium in Finland: effects of soil fertilization with selenium|date = 1988|accessdate = 8 September 2015|journal= American Journal of Clinical Nutrition|last = Varo|first = Pertti|last2 = Alfihan|first2 = Georg|last3 = Ekholm|first3 = Paivi|last4 = Aro|first4 = Antti|last5 = Koivistoinen|first5 = Pekka}}</ref> | |||
==Selenium deficiency in non-human animals== | |||
In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and the southeastern US), selenium deficiency in some animal species is common unless supplementation is carried out.<ref name=NRCsheep1985>{{cite book | url = https://books.google.com/books?id=UMb4ZwEACAAJ | title = Nutrient Requirements of Sheep | author1 = Subcommittee On Sheep Nutrition. National Research Council | year = 1985}}</ref> Selenium deficiency is responsible (either alone or together with vitamin E deficiency) for many of the cases of WMD ("white muscle disease"), evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides.<ref>{{cite book | url = https://books.google.com/books?id=yhgBwjoJ8WoC | title = Jensen and Swift's diseases of sheep | isbn = 9780812110999 | author1 = Kimberling | first1 = Cleon V | year = 1988}}</ref> Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible.<ref>{{cite journal | url = https://books.google.com/books?id=epjiKYkgbIAC | title = The Mineral Nutrition of Livestock | isbn = 9780851991283 | author1 = Underwood | first1 = Eric John | last2 = Suttle | first2 = N. F | year = 1999}}</ref> In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain.<ref name=NRCsr2007>National Research Council, Committee on Nutrient Requirements of Small Ruminants. 2007. Nutrient requirements of small ruminants. National Academies Press, Washington. 362 pp.</ref> Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep.<ref name=NRCsr2007/> Because of selenium's role in certain peroxidases (converting hydroperoxides to alcohols) and because of the antioxidant role of vitamin E (preventing hydroperoxide formation), a low level of Se can be somewhat (but not wholly) compensated by a high level of vitamin E. (In the animal, localization of peroxidases and vitamin E differs, partly because of the fat-solubility of vitamin E.) Some studies have indicated that about 0.12 or 0.23 mg Se per kg of dry matter intake may be sufficient for avoiding Se deficiency in sheep in some circumstances.<ref name=NRCsheep1985/> However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed.<ref>Whanger, P. D., P. H. Weswig, J. E. Oldfield, P. R. Cheeke and O. H. Muth. 1972. Factors influencing selenium and white muscle disease: forage types, salts, amino acids and dimethyl sulfoxide. Nutr. Rep. Int. 6; 21-37.</ref> The cyanogenic glycosides in some white clover ([[Trifolium repens]]) varieties may influence the Se requirement,<ref name=NRCsr2007/> presumably because of cyanide from the aglycone released by glucosidase activity in the rumen<ref>Coop, I. E. and R. L. Blakely. 1949. The metabolism and toxicity of cyanides and cyanogenic glycosides in sheep. N. Z. J. Sci. Technol. 30: 277-291.</ref> and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the [[glutathione]] moiety.<ref>{{cite journal | pmid = 7426660 | year = 1980 | last1 = Kraus | first1 = RJ | last2 = Prohaska | first2 = JR | last3 = Ganther | first3 = HE | title = Oxidized forms of ovine erythrocyte glutathione peroxidase. Cyanide inhibition of a 4-glutathione:4-selenoenzyme | volume = 615 | issue = 1 | pages = 19–26 | journal = Biochimica et Biophysica Acta | doi=10.1016/0005-2744(80)90004-2}}</ref> | |||
In areas where selenium deficiency in livestock is a concern, selenium (as selenite) may be supplemented in feed. In some countries, e.g. the US and Canada, such supplementation is regulated. Neonate ruminants at risk of WMD may be administered both Se and vitamin E by injection; some of the WMD myopathies respond only to Se, some only to vitamin E, and some to either.<ref>Kahn, C. M. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.</ref> | |||
==References== | |||
== References == | |||
{{reflist|2}} | {{reflist|2}} | ||
{{Nutritional pathology}} | {{Nutritional pathology}} | ||
[[Category: | [[Category:Mineral deficiencies]] | ||
[[Category: | [[Category:Selenium]] | ||
Revision as of 15:10, 3 June 2016
Template:Infobox medical condition Selenium deficiency is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.
Causes
It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90).[1]
People dependent on food grown from selenium-deficient soil may be at risk for deficiency.
For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs (e.g., statins) may resemble the pathology of selenium deficiency.[2][3]
Reference ranges
In the USA, the Dietary Reference Intake for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma glutathione peroxidase. Selenoprotein P[4] is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.[5]
Signs and symptoms
Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes (along with iodine deficiency) to Kashin-Beck disease.[6] The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue.[7] Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.
Selenium is also necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart, triiodothyronine,[6] and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.[8]
Epidemiology and prevention
These diseases are most common in certain parts of China where the intake is low[9] because the soil is extremely deficient in selenium. Studies in Jiangsu Province of China have indicated a reduction in the prevalence of these diseases by taking selenium supplements.[10] In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils.[11]
Selenium deficiency in non-human animals
In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and the southeastern US), selenium deficiency in some animal species is common unless supplementation is carried out.[12] Selenium deficiency is responsible (either alone or together with vitamin E deficiency) for many of the cases of WMD ("white muscle disease"), evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides.[13] Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible.[14] In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain.[15] Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep.[15] Because of selenium's role in certain peroxidases (converting hydroperoxides to alcohols) and because of the antioxidant role of vitamin E (preventing hydroperoxide formation), a low level of Se can be somewhat (but not wholly) compensated by a high level of vitamin E. (In the animal, localization of peroxidases and vitamin E differs, partly because of the fat-solubility of vitamin E.) Some studies have indicated that about 0.12 or 0.23 mg Se per kg of dry matter intake may be sufficient for avoiding Se deficiency in sheep in some circumstances.[12] However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed.[16] The cyanogenic glycosides in some white clover (Trifolium repens) varieties may influence the Se requirement,[15] presumably because of cyanide from the aglycone released by glucosidase activity in the rumen[17] and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the glutathione moiety.[18]
In areas where selenium deficiency in livestock is a concern, selenium (as selenite) may be supplemented in feed. In some countries, e.g. the US and Canada, such supplementation is regulated. Neonate ruminants at risk of WMD may be administered both Se and vitamin E by injection; some of the WMD myopathies respond only to Se, some only to vitamin E, and some to either.[19]
References
- ↑ Ravaglia, Giovanni; Forti, Paola; Maioli, Fabiola; Bastagli, Luciana; Facchini, Andrea; Mariani, Erminia; Savarino, Lucia; Sassi, Simonetta; et al. (2000). "Effect of micronutrient status on natural killer cell immune function in healthy free-living subjects aged ≥90 y". American Journal of Clinical Nutrition. 71 (2): 590–8. PMID 10648276.
- ↑ Moosmann, B; Behl, C (2004). "Selenoprotein synthesis and side-effects of statins". Lancet. 363 (9412): 892–4. doi:10.1016/S0140-6736(04)15739-5. PMID 15031036.
- ↑ Moosmann, B; Behl, C (2004). "Selenoproteins, cholesterol-lowering drugs, and the consequences: Revisiting of the mevalonate pathway". Trends in Cardiovascular Medicine. 14 (7): 273–81. doi:10.1016/j.tcm.2004.08.003. PMID 15542379.
- ↑ Papp, Laura Vanda; Lu, Jun; Holmgren, Arne; Khanna, Kum Kum (2007). "From Selenium to Selenoproteins: Synthesis, Identity, and Their Role in Human Health". Antioxidants & Redox Signaling. 9 (7): 775–806. doi:10.1089/ars.2007.1528. PMID 17508906.
- ↑ Xia, Y; Hill, KE; Byrne, DW; Xu, J; Burk, RF (2005). "Effectiveness of selenium supplements in a low-selenium area of China". The American Journal of Clinical Nutrition. 81 (4): 829–34. PMID 15817859.
- ↑ 6.0 6.1 "Toxicological Profile for Selenium" (PDF). Agency for Toxic Substances and Disease Registry. U.S. Department of Health and Human Services. September 2003. Retrieved 7 Sep 2015.
- ↑ Moreno-Reyes, Rodrigo; Suetens, Carl; Mathieu, Françoise; Begaux, Françoise; Zhu, Dun; Rivera, Maria T.; Boelaert, Marleen; Nève, Jean; et al. (1998). "Kashin–Beck Osteoarthropathy in Rural Tibet in Relation to Selenium and Iodine Status". New England Journal of Medicine. 339 (16): 1112–20. doi:10.1056/NEJM199810153391604. PMID 9770558.
- ↑ "Selenium: Dietary Supplement Fact Sheet". National Institutes of Health. Retrieved July 4, 2013.
- ↑ "Selenium: Mineral Deficiency and Toxicity: Merck Manual Professional". Retrieved 2008-11-29.
- ↑ "Dietary Supplement Fact Sheet: Selenium — Health Professional Fact Sheet". ods.od.nih.gov. Retrieved 2015-09-08.
- ↑ Varo, Pertti; Alfihan, Georg; Ekholm, Paivi; Aro, Antti; Koivistoinen, Pekka (1988). "Selenium intake and serum selenium in Finland: effects of soil fertilization with selenium" (PDF). American Journal of Clinical Nutrition. Retrieved 8 September 2015.
- ↑ 12.0 12.1 Subcommittee On Sheep Nutrition. National Research Council (1985). Nutrient Requirements of Sheep.
- ↑ Kimberling, Cleon V (1988). Jensen and Swift's diseases of sheep. ISBN 9780812110999.
- ↑ Underwood, Eric John; Suttle, N. F (1999). "The Mineral Nutrition of Livestock". ISBN 9780851991283.
- ↑ 15.0 15.1 15.2 National Research Council, Committee on Nutrient Requirements of Small Ruminants. 2007. Nutrient requirements of small ruminants. National Academies Press, Washington. 362 pp.
- ↑ Whanger, P. D., P. H. Weswig, J. E. Oldfield, P. R. Cheeke and O. H. Muth. 1972. Factors influencing selenium and white muscle disease: forage types, salts, amino acids and dimethyl sulfoxide. Nutr. Rep. Int. 6; 21-37.
- ↑ Coop, I. E. and R. L. Blakely. 1949. The metabolism and toxicity of cyanides and cyanogenic glycosides in sheep. N. Z. J. Sci. Technol. 30: 277-291.
- ↑ Kraus, RJ; Prohaska, JR; Ganther, HE (1980). "Oxidized forms of ovine erythrocyte glutathione peroxidase. Cyanide inhibition of a 4-glutathione:4-selenoenzyme". Biochimica et Biophysica Acta. 615 (1): 19–26. doi:10.1016/0005-2744(80)90004-2. PMID 7426660.
- ↑ Kahn, C. M. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.