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Selenium deficiency epidemiology and demographics

2016-06-03T15:23:33Z

Donald Szlosek: Created page with "__NOTOC__ == Overview== '''Selenium deficiency''' is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported. ==Epidemiology and prev..."

__NOTOC__
== Overview==
'''[[Selenium]] deficiency''' is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.
==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>
==References==
{{reflist}}

Selenium deficiency history and symptoms

2016-06-03T15:22:31Z

Donald Szlosek: Created page with " ==History and symptoms== Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency..."

==History 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>

==References==
{{reflist}}

Selenium deficiency medical therapy

2016-06-03T15:17:35Z

Donald Szlosek: Created page with " ==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..."

==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>

==References==
{{reflist}}

Selenium deficiency causes

2016-06-03T15:16:11Z

__NOTOC__
== Overview==
'''[[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>

==References==
{{reflist}}

Selenium deficiency overview

2016-06-03T15:14:15Z

Donald Szlosek: Created page with "== Overview== '''Selenium deficiency''' is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported. ==References== {{reflist}}"

== Overview==
'''[[Selenium]] deficiency''' is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.

==References==
{{reflist}}

Template:Selenium deficiency

2016-06-03T15:11:51Z

Donald Szlosek: Created page with "{| class="infobox bordered" style="width: 15em; text-align: left; font-size: 90%; background:AliceBlue" |- | colspan="1" style="text-align:center; background:DarkGray" | '''S..."

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'''Selenium Deficiency Microchapters'''
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[[Selenium Deficiency |Home]]
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[[Selenium Deficiency (patient information)|Patient Information]]
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[[Selenium Deficiency overview|Overview]]
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[[Selenium Deficiency historical perspective|Historical Perspective]]
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[[Selenium Deficiency classification|Classification]]
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[[Selenium Deficiency pathophysiology|Pathophysiology]]
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[[Selenium Deficiency causes|Causes]]
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[[Selenium Deficiency differential diagnosis|Differentiating Selenium Deficiency from other Diseases]]
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[[Selenium Deficiency epidemiology and demographics|Epidemiology and Demographics]]
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[[Selenium Deficiency risk factors|Risk Factors]]
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[[Selenium Deficiency screening|Screening]]
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[[Selenium Deficiency natural history, complications and prognosis|Natural History, Complications and Prognosis]]
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Diagnosis
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[[Selenium Deficiency history and symptoms|History and Symptoms]]
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[[Selenium Deficiency physical examination|Physical Examination]]
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[[Selenium Deficiency laboratory findings|Laboratory Findings]]
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[[Selenium Deficiency electrocardiogram|Electrocardiogram]]
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[[Selenium Deficiency chest x ray|Chest X Ray]]
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[[Selenium Deficiency CT|CT]]
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[[Selenium Deficiency MRI|MRI]]
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[[Selenium Deficiency echocardiography or ultrasound|Echocardiography or Ultrasound]]
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[[Selenium Deficiency other imaging findings|Other Imaging Findings]]
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[[Selenium Deficiency other diagnostic studies|Other Diagnostic Studies]]
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Treatment
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[[Selenium Deficiency surgery|Surgery]]
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[[Selenium Deficiency medical therapy|Medical Therapy]]
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[[Selenium Deficiency Radiation therapy|Radiation therapy]]
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[[Selenium Deficiency primary prevention|Primary Prevention]]
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[[Selenium Deficiency secondary prevention|Secondary Prevention]]
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[[Selenium Deficiency cost-effectiveness of therapy|Cost-Effectiveness of Therapy]]
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[[Selenium Deficiency future or investigational therapies|Future or Investigational Therapies]]
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Case Studies
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[[Selenium Deficiency case study one|Case #1]]
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{{PAGENAME}} On the Web
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Selenium deficiency

2016-06-03T15:10:56Z

Donald Szlosek:

__NOTOC__
{{ Selenium Deficiency }}

{{CMG}}

==[[Selenium Deficiency overview|Overview]]==

==[[Selenium Deficiency historical perspective|Historical Perspective]]==

==[[Selenium Deficiency classification|Classification]]==

==[[Selenium Deficiency pathophysiology|Pathophysiology]]==

==[[Selenium Deficiency causes|Causes]]==

==[[Selenium Deficiency differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Selenium Deficiency epidemiology and demographics|Epidemiology and Demographics]]==

==[[Selenium Deficiency risk factors|Risk Factors]]==

==[[Selenium Deficiency screening|Screening]]==

==[[Selenium Deficiency natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Selenium Deficiency history and symptoms|History and Symptoms]] | [[Selenium Deficiency physical examination|Physical Examination]] | [[Selenium Deficiency laboratory findings|Laboratory Findings]] | [[Selenium Deficiency electrocardiogram|Electrocardiogram]] |[[Selenium Deficiency chest x ray|Chest X Ray]] | [[Selenium Deficiency CT|CT]] | [[Selenium Deficiency MRI|MRI]] | | [[Selenium Deficiency other imaging findings|Other Imaging Findings]] | [[Selenium Deficiency other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Selenium Deficiency medical therapy|Medical Therapy]] | [[Selenium Deficiency surgery|Surgery]] | [[Selenium Deficiency primary prevention|Primary Prevention]] | [[Selenium Deficiency secondary prevention|Secondary Prevention]] | [[Selenium Deficiency cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Selenium Deficiency future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Selenium Deficiency case study one|Case #1]]

[[Category:Projects]]
[[Category:Help]]

{{WH}}
{{WS}}

Sandbox/01

2016-06-03T15:10:25Z

Donald Szlosek:

{{Infobox medical condition
| Name = Selenium deficiency
| Image = Se-TableImage.png
| Caption = [[Selenium]]
| 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==
{{reflist|2}}

{{Nutritional pathology}}

[[Category:Mineral deficiencies]]
[[Category:Selenium]]

Rickets medical therapy

2016-06-03T14:45:43Z

Donald Szlosek: Created page with " ==Medical Therapy== ===Diet and sunlight=== [[Cholecalciferol (D3)]] [[Ergocalciferol (D2)]]..."

==Medical Therapy==
===Diet and sunlight===
[[Image:Cholecalciferol.png|thumb|left|[[Cholecalciferol]] (D3)]]
[[Image:Ergocalciferol.png|thumb|left|[[Ergocalciferol]] (D2)]]
Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet light (sunshine), [[cod liver oil]], halibut-liver oil, and [[Ergosterol|viosterol]] are all sources of vitamin D.

A sufficient amount of ultraviolet in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned babies need to be exposed longer to the [[ultraviolet|ultraviolet rays]]. The replacement of vitamin D has been proven to correct rickets using these methods of [http://pediatrics.aappublications.org/cgi/content/full/112/2/e132 ultraviolet light therapy]and medicine.

Recommendations are for 200 [[international unit]]s (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.

===Supplementation===
Sufficient vitamin D levels can also be achieved through dietary supplementation. Vitamin D3 ([[cholecalciferol]]) is the preferred form since it is more readily absorbed than vitamin D2. Most [[dermatology|dermatologists]] recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure.

According to the [[American Academy of Pediatrics]] (AAP), infants who are breast-fed may not get enough vitamin D from breast milk alone. For this reason, the AAP recommends that infants who are exclusively breast-fed receive daily supplements of vitamin D from age 2 months until they start drinking at least 17 ounces of vitamin D-fortified milk or formula a day [http://aappolicy.aappublications.org/cgi/content/full/pediatrics;111/4/908]. This requirement for supplemental vitamin D is not a defect in the evolution of human breastmilk but is instead a result of the modern-day infant's decreased exposure to sunlight.

Rickets laboratory findings

2016-06-03T14:44:23Z

Donald Szlosek: Created page with "==Laboratory Findings== *Blood tests: **Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high..."

==Laboratory Findings==
*Blood tests:
**Serum [[calcium]] may show low levels of calcium, serum [[phosphorus]] may be low, and serum [[alkaline phosphatase]] may be high.
*[[Arterial blood gas]]es may reveal [[metabolic acidosis]]
*[[X-ray]]s of affected bones may show loss of calcium from bones or changes in the shape or structure of the bones.
*Bone biopsy is rarely performed but will confirm rickets.

Rickets other imaging findings

2016-06-03T14:42:52Z

Donald Szlosek: Created page with " '''Patient #1: Radiographs of the knee in a patient with rickets''' ==Imaging Findings== <gallery> Image:Rickets-001.jpg Image:Rickets-002.jpg </gallery> '''Patient #2: Ra..."

'''Patient #1: Radiographs of the knee in a patient with rickets'''
==Imaging Findings==

<gallery>
Image:Rickets-001.jpg
Image:Rickets-002.jpg
</gallery>

'''Patient #2: Radiographs of the knee in a patient with rickets'''
<gallery>
Image:

Rickets-201.jpg

Image:

Rickets-202.jpg

</gallery>

'''Patient #3: Radiograph of the chest in a patient with rickets'''
<gallery>
Image:

Rickets-301.jpg

</gallery>

Rickets history and symptoms

2016-06-03T14:38:06Z

Donald Szlosek: Created page with "==History and Symptoms== [[Radiograph of a two-year old rickets sufferer, with a marked genu varum (bowing of the femurs)..."

==History and Symptoms==
[[Image:XrayRicketsLegssmall.jpg|thumb|left|[[Radiograph]] of a two-year old rickets sufferer, with a marked [[genu varum]] (bowing of the [[femur]]s) and decreased bone [[opacity]], suggesting poor [[bone mineralization]].|right]]
Signs and symptoms of rickets include:
*Bone pain or tenderness
*[[tooth|dental]] problems
*[[muscle]] weakness (rickety myopathy or "floppy baby syndrome")
*increased tendency for [[fracture]]s (easily broken bones), especially [[greenstick fracture]]s
*Skeletal deformity
**Toddlers: Bowed legs ([[genu varum]])
**Older children: Knock-knees ([[genu valgum]]) or "windswept knees"
**Cranial, spinal, and pelvic deformities
*Growth disturbance
*[[Hypocalcemia]] (low level of calcium in the blood), and
*[[Tetany (medical sign)|Tetany]] (uncontrolled muscle spasms all over the body).
*[[Craniotabes]] (soft skull)
*[[Costochondral]] swelling (aka "[[rickety rosary]]" or "[[rachitic rosary]]")
*[[Harrison's groove]]
*Double malleoli sign due to metaphyseal hyperplasia [http://medicalpics.blogspot.com/2007/04/double-malleoli-sign-of-rickets.html]

An [[X-ray]] or [[radiography|radiograph]] of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance. These deformities persist into adult life if not treated.

Long-term consequences include permanent bends or disfiguration of the long bones, and a [[Scoliosis|curved back]].

Rickets epidemiology and demographics

2016-06-03T14:36:02Z

Donald Szlosek: Created page with "__NOTOC__ ==Overview== '''Rickets''' is a softening of the bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood dise..."

__NOTOC__
==Overview==
'''Rickets''' is a softening of the bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a [[vitamin D]] deficiency, but lack of adequate [[calcium]] in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe [[malnutrition]], usually resulting from [[famine]] or [[starvation]] during the early stages of childhood.
[[Osteomalacia]] is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.
The origin of the word "rickets" is unknown. The Greek derived word "rachitis" (meaning "inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound.
==Epidemiology==
[[Image:Rickets wrist.jpg|thumb|left|"rachitis" The "wrist widening" of rickets]]
Those at higher risk for developing rickets include:
*Breast-fed infants whose mothers are not exposed to sunlight
*Breast-fed infants who are not exposed to sunlight
*Individuals not consuming fortified milk, such as those who are [[lactose intolerant]]
Individuals with red hair have a decreased risk for rickets due to their greater production of vitamin D in sunlight.<ref>[http://www.derm.med.ed.ac.uk/06_teaching/redhairgen.htm Red hair and genetics]</ref>

==References==
{{reflist}}

Rickets overview

2016-06-03T14:34:54Z

Donald Szlosek: Created page with " ==Overview== '''Rickets''' is a softening of the bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in..."

==Overview==

'''Rickets''' is a softening of the bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a [[vitamin D]] deficiency, but lack of adequate [[calcium]] in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe [[malnutrition]], usually resulting from [[famine]] or [[starvation]] during the early stages of childhood.
[[Osteomalacia]] is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.

The origin of the word "rickets" is unknown. The Greek derived word "rachitis" (meaning "inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound.

Template:Rickets

2016-06-03T14:31:21Z

{| class="infobox bordered" style="width: 15em; text-align: left; font-size: 90%; background:AliceBlue"
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'''Rickets Microchapters'''
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[[Rickets |Home]]
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[[Rickets (patient information)|Patient Information]]
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[[Rickets overview|Overview]]
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[[Rickets historical perspective|Historical Perspective]]
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[[Rickets classification|Classification]]
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[[Rickets pathophysiology|Pathophysiology]]
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[[Rickets causes|Causes]]
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[[Rickets differential diagnosis|Differentiating Rickets from other Diseases]]
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[[Rickets epidemiology and demographics|Epidemiology and Demographics]]
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[[Rickets risk factors|Risk Factors]]
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[[Rickets screening|Screening]]
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[[Rickets natural history, complications and prognosis|Natural History, Complications and Prognosis]]
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Diagnosis
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[[Rickets history and symptoms|History and Symptoms]]
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[[Rickets physical examination|Physical Examination]]
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[[Rickets laboratory findings|Laboratory Findings]]
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[[Rickets electrocardiogram|Electrocardiogram]]
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[[Rickets chest x ray|Chest X Ray]]
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[[Rickets CT|CT]]
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[[Rickets MRI|MRI]]
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[[Rickets echocardiography or ultrasound|Echocardiography or Ultrasound]]
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[[Rickets other imaging findings|Other Imaging Findings]]
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[[Rickets other diagnostic studies|Other Diagnostic Studies]]
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Treatment
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[[Rickets surgery|Surgery]]
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[[Rickets medical therapy|Medical Therapy]]
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[[Rickets Radiation therapy|Radiation therapy]]
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[[Rickets primary prevention|Primary Prevention]]
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[[Rickets secondary prevention|Secondary Prevention]]
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[[Rickets cost-effectiveness of therapy|Cost-Effectiveness of Therapy]]
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[[Rickets future or investigational therapies|Future or Investigational Therapies]]
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Case Studies
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[[Rickets case study one|Case #1]]
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|- bgcolor="PaleGoldenrod "
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{{PAGENAME}} On the Web
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&db=pubmed&term={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}} Most recent articles]
|-
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|- bgcolor="LightYellow"
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[http://scholar.google.com/scholar?ie=UTF-8&oe=utf-8&q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}&qt_s=Search&sa=N&tab=ps Most cited articles]
|-
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[http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=search&db=pubmed&term={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}%20AND%20systematic%5Bsb%5D Review articles]
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[http://www.google.com/search?hl=en&client=firefox-a&rls=org.mozilla:en-US:official&q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}+more:health_continuing_education&cx=disease_for_health_professionals&sa=N&oi=coopctx&resnum=0&ct=col3&cd=2 CME Programs]
|-
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|- bgcolor="LightYellow"
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[http://www.google.com/search?q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}+ppt&ie=utf-8&oe=utf-8&aq=t&rls=org.mozilla:en-US:official&client=firefox-a Powerpoint slides]
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[http://images.google.com/images?q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}&ie=UTF-8&oe=utf-8&rls=org.mozilla:en-US:official&client=firefox-a&um=1&sa=N&tab=wi Images]
|-
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American Roentgen Ray Society Images of {{PAGENAME}}
:[http://goldminer.arrs.org/search.php?query={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}} All Images]
:[http://goldminer.arrs.org/search.php?query={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}} X-ray}}}} X-rays]
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[http://clinicaltrials.gov/search/open/condition={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}} Ongoing Trials at Clinical Trials.gov]
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[http://www.cdc.gov/search.do?queryText={{urlencode:{{#if:{{{1|}}}|{{{1}}}|{{PAGENAME}}}}}}&searchButton.x=33&searchButton.y=6&action=search CDC on {{PAGENAME}}]
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Rickets

2016-06-03T14:30:13Z

Donald Szlosek:

__NOTOC__
{{ Rickets }}

{{CMG}}

==[[Rickets overview|Overview]]==

==[[Rickets historical perspective|Historical Perspective]]==

==[[Rickets classification|Classification]]==

==[[Rickets pathophysiology|Pathophysiology]]==

==[[Rickets causes|Causes]]==

==[[Rickets differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Rickets epidemiology and demographics|Epidemiology and Demographics]]==

==[[Rickets risk factors|Risk Factors]]==

==[[Rickets screening|Screening]]==

==[[Rickets natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Rickets history and symptoms|History and Symptoms]] | [[Rickets physical examination|Physical Examination]] | [[Rickets laboratory findings|Laboratory Findings]] | [[Rickets electrocardiogram|Electrocardiogram]] |[[Rickets chest x ray|Chest X Ray]] | [[Rickets CT|CT]] | [[Rickets MRI|MRI]] | | [[Rickets other imaging findings|Other Imaging Findings]] | [[Rickets other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Rickets medical therapy|Medical Therapy]] | [[Rickets surgery|Surgery]] | [[Rickets primary prevention|Primary Prevention]] | [[Rickets secondary prevention|Secondary Prevention]] | [[Rickets cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Rickets future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Rickets case study one|Case #1]]

[[Category:Projects]]
[[Category:Help]]

{{WH}}
{{WS}}

Sandbox/01

2016-06-03T14:29:03Z

Donald Szlosek:

__NOTOC__
{{Infobox Disease
| Name = Rickets
| ICD10 = {{ICD10|E|55| |e|50}}
| ICD9 = {{ICD9|268}}
| Image = Rickets USNLM.gif
| Caption = A family with rickets. Paris, 1900.
| DiseasesDB = 9351
| MedlinePlus = 000344
| MeshName = Rickets
| MeshNumber = D012279
}}
{{SI}}
{{CMG}}

==Overview==

'''Rickets''' is a softening of the bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a [[vitamin D]] deficiency, but lack of adequate [[calcium]] in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe [[malnutrition]], usually resulting from [[famine]] or [[starvation]] during the early stages of childhood.
[[Osteomalacia]] is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.
The origin of the word "rickets" is unknown. The Greek derived word "rachitis" (meaning "inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound.

==Epidemiology==
[[Image:Rickets wrist.jpg|thumb|left|"rachitis" The "wrist widening" of rickets]]
Those at higher risk for developing rickets include:
*Breast-fed infants whose mothers are not exposed to sunlight
*Breast-fed infants who are not exposed to sunlight
*Individuals not consuming fortified milk, such as those who are [[lactose intolerant]]

Individuals with red hair have a decreased risk for rickets due to their greater production of vitamin D in sunlight.<ref>[http://www.derm.med.ed.ac.uk/06_teaching/redhairgen.htm Red hair and genetics]</ref>

==Etiology==
Vitamin D is required for proper calcium absorption from the gut. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in [[hypocalcemia]], leading to skeletal and dental deformities and [[neuromuscular]] symptoms, e.g. hyperexcitability.

A rare [[X-linked dominant]] form exists called [[X-linked hypophosphatemia|Vitamin D resistant rickets]].

==Presentation==
[[Image:XrayRicketsLegssmall.jpg|thumb|left|[[Radiograph]] of a two-year old rickets sufferer, with a marked [[genu varum]] (bowing of the [[femur]]s) and decreased bone [[opacity]], suggesting poor [[bone mineralization]].|right]]
Signs and symptoms of rickets include:
*Bone pain or tenderness
*[[tooth|dental]] problems
*[[muscle]] weakness (rickety myopathy or "floppy baby syndrome")
*increased tendency for [[fracture]]s (easily broken bones), especially [[greenstick fracture]]s
*Skeletal deformity
**Toddlers: Bowed legs ([[genu varum]])
**Older children: Knock-knees ([[genu valgum]]) or "windswept knees"
**Cranial, spinal, and pelvic deformities
*Growth disturbance
*[[Hypocalcemia]] (low level of calcium in the blood), and
*[[Tetany (medical sign)|Tetany]] (uncontrolled muscle spasms all over the body).
*[[Craniotabes]] (soft skull)
*[[Costochondral]] swelling (aka "[[rickety rosary]]" or "[[rachitic rosary]]")
*[[Harrison's groove]]
*Double malleoli sign due to metaphyseal hyperplasia [http://medicalpics.blogspot.com/2007/04/double-malleoli-sign-of-rickets.html]

An [[X-ray]] or [[radiography|radiograph]] of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance. These deformities persist into adult life if not treated.

Long-term consequences include permanent bends or disfiguration of the long bones, and a [[Scoliosis|curved back]].

==Diagnosis==
A doctor may diagnose rickets by:

*Blood tests:
**Serum [[calcium]] may show low levels of calcium, serum [[phosphorus]] may be low, and serum [[alkaline phosphatase]] may be high.
*[[Arterial blood gas]]es may reveal [[metabolic acidosis]]
*[[X-ray]]s of affected bones may show loss of calcium from bones or changes in the shape or structure of the bones.
*Bone biopsy is rarely performed but will confirm rickets.

'''Patient #1: Radiographs of the knee in a patient with rickets'''
<gallery>
Image:Rickets-001.jpg
Image:Rickets-002.jpg
</gallery>

'''Patient #2: Radiographs of the knee in a patient with rickets'''
<gallery>
Image:

Rickets-201.jpg

Image:

Rickets-202.jpg

</gallery>

'''Patient #3: Radiograph of the chest in a patient with rickets'''
<gallery>
Image:

Rickets-301.jpg

</gallery>

==Ricketts: Microscopical Findings==
{{#ev:youtube|y7iA0_jkOTI}}
==Treatment and prevention==
===Diet and sunlight===
[[Image:Cholecalciferol.png|thumb|left|[[Cholecalciferol]] (D3)]]
[[Image:Ergocalciferol.png|thumb|left|[[Ergocalciferol]] (D2)]]
Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet light (sunshine), [[cod liver oil]], halibut-liver oil, and [[Ergosterol|viosterol]] are all sources of vitamin D.

A sufficient amount of ultraviolet in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned babies need to be exposed longer to the [[ultraviolet|ultraviolet rays]]. The replacement of vitamin D has been proven to correct rickets using these methods of [http://pediatrics.aappublications.org/cgi/content/full/112/2/e132 ultraviolet light therapy]and medicine.

Recommendations are for 200 [[international unit]]s (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.

===Supplementation===
Sufficient vitamin D levels can also be achieved through dietary supplementation. Vitamin D3 ([[cholecalciferol]]) is the preferred form since it is more readily absorbed than vitamin D2. Most [[dermatology|dermatologists]] recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure.

According to the [[American Academy of Pediatrics]] (AAP), infants who are breast-fed may not get enough vitamin D from breast milk alone. For this reason, the AAP recommends that infants who are exclusively breast-fed receive daily supplements of vitamin D from age 2 months until they start drinking at least 17 ounces of vitamin D-fortified milk or formula a day [http://aappolicy.aappublications.org/cgi/content/full/pediatrics;111/4/908]. This requirement for supplemental vitamin D is not a defect in the evolution of human breastmilk but is instead a result of the modern-day infant's decreased exposure to sunlight.

== References ==
{{reflist|2}}
<references/>

== External links ==
*[http://aappolicy.aappublications.org/cgi/content/full/pediatrics;111/4/908 AAP Recommendations on Vitamin D Supplementation]
*[http://courses.washington.edu/bonephys/hypercalU/opmal2.html Dr. Susan Ott's website on osteomalacia]
*[http://www.healthvitaminsguide.com/deficiencies/rickets.htm Rickets - Symptoms, Causes, Treatment]
*[http://dictionary.reference.com/search?q=osteomalacia Dictionary.com - Osteomalacia]
*[http://www.fluoridealert.org/health/bone/fluorosis/osteomalacia.html Fluoride & Osteomalacia]
*[http://www.beyonddiscovery.org/content/view.txt.asp?a=414 History of Vitamin D and the battle against Rickets]
* {{Chorus|00906}}

{{Nutritional pathology}}

[[Category:Malnutrition]]
[[Category:Pediatrics]]
[[Category:Skeletal disorders]]
[[Category:Gastroenterology]]

[[de:Rachitis]]
[[es:Raquitismo]]
[[fi:Riisitauti]]
[[fr:Rachitisme]]
[[ko:구루병]]
[[it:Rachitismo]]
[[ja:くる病]]
[[nl:Rachitis]]
[[no:Rakitt]]
[[pl:Krzywica]]
[[pt:Raquitismo]]
[[ru:Рахит]]
[[simple:Rickets]]
[[sv:Rakitis]]
[[tr:Raşitizm]]
[[zh:佝僂病]]

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Pyridoxine deficiency history and symptoms

2016-06-03T14:13:18Z

Donald Szlosek: Created page with "== History and Symptoms == *Advanced Age *Alcoholism *Catabolic state *Celiac Disease *Chronic Renal Failure *Drugs- Isoniazid *Extrahepatic biliary obstruction *..."

== History and Symptoms ==
*Advanced Age
*Alcoholism
*Catabolic state
*[[Celiac Disease]]
*[[Chronic Renal Failure]]
*Drugs- [[Isoniazid]]
*Extrahepatic biliary obstruction
*Hemodialysis
*[[Hepatocellular Carcinoma]]
*[[Hepatitis]]
*Hospitalization
*Hyperoxaluria
*Kidney transplant
*Peritoneal dialysis
*Severe malnutrition <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:310</ref>

==References==
{{reflist|2}}

Pyridoxine deficiency laboratory findings

2016-06-03T14:11:18Z

Donald Szlosek: Created page with "==Laboratory Findings== A positive diagnosis test for pyridoxine deficiency can be assertained by measuring erythrocyte levels of aspartate aminotransferase and transk..."

==Laboratory Findings==
A positive diagnosis test for pyridoxine deficiency can be assertained by measuring [[erythrocyte]] levels of [[aspartate aminotransferase]] and transketolase in [[blood plasma|serum]].

Pyridoxine deficiency causes

2016-06-03T14:09:32Z

Donald Szlosek: Created page with "__NOTOC__ ==Overview== The classic clinical syndrome for '''Pyridoxine deficiency''' (or '''B6 deficiency''') is a seborrheic dermatitis-like eruption, atrophic glossitis with..."

__NOTOC__
==Overview==
The classic clinical syndrome for '''Pyridoxine deficiency''' (or '''B6 deficiency''') is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy.<ref>Andrews' Diseases of the Skin, 10th Edition, Elsevier.</ref>
Vitamin B6 is a co-factor for glutamic acid decarboxylase, an enzyme that converts Glutamate to GABA. Therefore, the concurrent increase in the excitatory neurotransmitter, Glutamate, and decrease in inhibitory neurotransmitter, GABA, resultant from B6 deficiency, may manifest itself in the form of seizures.

==Causes==
*Supporters of a debated medical condition known as [[Pyroluria]] believe it may be one potential cause of vitamin B6 deficiency.
*Another cause of vitamin B6 deficiency is the use of the tuberculostatic medication [[isoniazid]], and for this reason, it is recommended to supplement with vitamin B6 when using this drug.
*Grumpiness and irritability are also often symptomatic of a deficiency according to "Body, Mind, and the B Vitamins" by Ruth Adams and Frank Murray.
*A [[meta-analysis]] of three databases ([[MEDLINE]], [[EMBASE]], and [[Cochrane Library]]), including only [[double-blind]], randomized controlled trials, found that vitamin B6 has a significant effect compared to [[placebo]]s in treating [[morning sickness]], similar to that of [[ginger]].<ref>[http://www.medicalnewstoday.com/medicalnews.php?newsid=22469 Pregnancy Morning Sickness - Ginger as Effective as Vitamin B6 (open)] [http://www.greenjournal.org/cgi/content/abstract/105/4/849 Effectiveness and Safety of Ginger in the Treatment of Pregnancy-Induced Nausea and Vomiting (subscription)], Borrelli ''et al.'', ''Obstetrics & Gynecology'', 2005;105:849-856</ref>

==References==
{{reflist}}

Pyridoxine deficiency overview

2016-06-03T14:08:31Z

Template:Pyridoxine deficiency

2016-06-03T14:04:26Z

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[[Pyridoxine deficiency overview|Overview]]
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[[Pyridoxine deficiency secondary prevention|Secondary Prevention]]
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[[Pyridoxine deficiency cost-effectiveness of therapy|Cost-Effectiveness of Therapy]]
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Pyridoxine deficiency

2016-06-03T14:03:53Z

Donald Szlosek:

__NOTOC__
{{ Pyridoxine deficiency }}

{{CMG}}

==[[Pyridoxine deficiency overview|Overview]]==

==[[Pyridoxine deficiency historical perspective|Historical Perspective]]==

==[[Pyridoxine deficiency classification|Classification]]==

==[[Pyridoxine deficiency pathophysiology|Pathophysiology]]==

==[[Pyridoxine deficiency causes|Causes]]==

==[[Pyridoxine deficiency differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Pyridoxine deficiency epidemiology and demographics|Epidemiology and Demographics]]==

==[[Pyridoxine deficiency risk factors|Risk Factors]]==

==[[Pyridoxine deficiency screening|Screening]]==

==[[Pyridoxine deficiency natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Pyridoxine deficiency history and symptoms|History and Symptoms]] | [[Pyridoxine deficiency physical examination|Physical Examination]] | [[Pyridoxine deficiency laboratory findings|Laboratory Findings]] | [[Pyridoxine deficiency electrocardiogram|Electrocardiogram]] |[[Pyridoxine deficiency chest x ray|Chest X Ray]] | [[Pyridoxine deficiency CT|CT]] | [[Pyridoxine deficiency MRI|MRI]] | | [[Pyridoxine deficiency other imaging findings|Other Imaging Findings]] | [[Pyridoxine deficiency other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Pyridoxine deficiency medical therapy|Medical Therapy]] | [[Pyridoxine deficiency surgery|Surgery]] | [[Pyridoxine deficiency primary prevention|Primary Prevention]] | [[Pyridoxine deficiency secondary prevention|Secondary Prevention]] | [[Pyridoxine deficiency cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Pyridoxine deficiency future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Pyridoxine deficiency case study one|Case #1]]

[[Category:Projects]]
[[Category:Help]]

{{WH}}
{{WS}}

Sandbox/01

2016-06-03T14:02:03Z

Donald Szlosek:

__NOTOC__
{{CMG}}

{{Editor Help}}

==Overview==
{{Infobox_Disease
| Name = Vitamin B6 deficiency
| Image =
| Caption =
| DiseasesDB = 13923
| ICD10 = {{ICD10|E|53|1|e|50}}
| ICD9 = {{ICD9|266.1}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = med
| eMedicineTopic = 1977
| MeshID = D026681
}}
{{SI}}
The classic clinical syndrome for '''Pyridoxine deficiency''' (or '''B6 deficiency''') is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy.<ref>Andrews' Diseases of the Skin, 10th Edition, Elsevier.</ref>

Vitamin B6 is a co-factor for glutamic acid decarboxylase, an enzyme that converts Glutamate to GABA. Therefore, the concurrent increase in the excitatory neurotransmitter, Glutamate, and decrease in inhibitory neurotransmitter, GABA, resultant from B6 deficiency, may manifest itself in the form of seizures.

==Causes==
*Supporters of a debated medical condition known as [[Pyroluria]] believe it may be one potential cause of vitamin B6 deficiency.
*Another cause of vitamin B6 deficiency is the use of the tuberculostatic medication [[isoniazid]], and for this reason, it is recommended to supplement with vitamin B6 when using this drug.
*Grumpiness and irritability are also often symptomatic of a deficiency according to "Body, Mind, and the B Vitamins" by Ruth Adams and Frank Murray.
*A [[meta-analysis]] of three databases ([[MEDLINE]], [[EMBASE]], and [[Cochrane Library]]), including only [[double-blind]], randomized controlled trials, found that vitamin B6 has a significant effect compared to [[placebo]]s in treating [[morning sickness]], similar to that of [[ginger]].<ref>[http://www.medicalnewstoday.com/medicalnews.php?newsid=22469 Pregnancy Morning Sickness - Ginger as Effective as Vitamin B6 (open)] [http://www.greenjournal.org/cgi/content/abstract/105/4/849 Effectiveness and Safety of Ginger in the Treatment of Pregnancy-Induced Nausea and Vomiting (subscription)], Borrelli ''et al.'', ''Obstetrics & Gynecology'', 2005;105:849-856</ref>

===Diagnostic Testing for B6 Deficiency===
A positive diagnosis test for pyridoxine deficiency can be assertained by measuring [[erythrocyte]] levels of [[aspartate aminotransferase]] and transketolase in [[blood plasma|serum]].

== Differential Diagnosis ==
*Advanced Age
*Alcoholism
*Catabolic state
*[[Celiac Disease]]
*[[Chronic Renal Failure]]
*Drugs- [[Isoniazid]]
*Extrahepatic biliary obstruction
*Hemodialysis
*[[Hepatocellular Carcinoma]]
*[[Hepatitis]]
*Hospitalization
*Hyperoxaluria
*Kidney transplant
*Peritoneal dialysis
*Severe malnutrition <ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:310</ref>

==References==
{{reflist|2}}

{{SIB}}
{{Nutritional pathology}}

[[Category:Gastroenterology]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Propionic acidemia medical therapy

2016-06-03T13:59:51Z

Donald Szlosek:

==Medical Therapy==
===Management===
Patients with propionic acidemia should be started as early as possible on a low protein diet. In addition to a protein mixture that is devoid of methionine, threonine, valine, and isoleucine, the patient should also receive L-carnitine treatment and should be given antibiotics 10 days per month in order to remove the intestinal propiogenic flora. The patient should have diet protocols prepared for him with a “well day diet” with low protein content, a “half emergency diet” containing half of the protein requirements, and an “emergency diet” with no protein content. These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states.<ref>Saudubray JM, Van Der Bergh G, Walter J : Inborn Metabolic Diseases Diagnosis and Treatment (2012)</ref>

Liver transplant is gaining a role in the management of these patients, with small series showing improved quality of life.

==References==
{{reflist}}

Propionic acidemia medical therapy

2016-06-03T13:59:20Z

Donald Szlosek: Created page with "==Medical Therapy== ===Management=== Patients with propionic acidemia should be started as early as possible on a low protein diet. In addition to a protein mixture that is de..."

Propionic acidemia epidemiology and demographics

2016-06-03T13:56:58Z

Donald Szlosek:

__NOTOC__
==Overview==
'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an [[autosomal]] [[recessive]]<ref>{{cite journal |pmid=10820128 |date=July 2000 |author1=Ravn K |author2=Chloupkova M |author3= Christensen E |author4=Brandt NJ |author5=Simonsen H |author6=Kraus JP |author7=Nielsen IM |author8=Skovby F |author9=Schwartz M |title=High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase |volume=67 |issue=1 |pages=203–206 |pmc=1287078 |doi=10.1086/302971 |journal=American Journal of Human Genetics}}</ref> [[metabolic disorder]], classified as a [[branched-chain amino acid|branched-chain]] [[organic acidemia]].<ref name="oad">{{cite journal |vauthors =Deodato F, Boenzi S, Santorelli FM, Dionisi-Vici C |title=Methylmalonic and propionic aciduria |journal=[[Am J Med Genet C Semin Med Genet]] |volume=142 |issue=2 |pages=104–112 |year=2006 |pmid=16602092 |doi=10.1002/ajmg.c.30090 }}</ref>
The disorder presents in the early [[neonatal]] period with progressive [[encephalopathy]]. Death can occur quickly, due to secondary [[hyperammonemia]], infection, cardiomyopathy, or basal ganglial stroke.<ref name="pbg">{{cite journal |vauthors =Hamilton RL, Haas RH, Nyhan WC, Powell HC, Grafe MR |title=Neuropathology of propionic acidemia: a report of two patients with basal ganglia lesions |journal=Journal of Child Neurology |volume=10 |issue=1 |pages=25–30 |year=1995 |pmid=7769173 |doi=10.1177/088307389501000107 }}</ref>
Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.
==Genetic prevalence==
Propionic acidemia is inherited in an [[autosomal]] [[recessive]] pattern and is found in about 1 in 35,000<ref name="pamr" /> live births in the [[United States]]. The condition appears to be more common in [[Saudi Arabia]],<ref name="pasa">{{cite journal |vauthors =Al-Odaib AN, Abu-Amaro KK, Ozand PT, Al-Hellani AM |title=A new era for preventive genetic programs in the Arabian Peninsula |journal=Saudi Medical Journal |volume=24 |issue=11 |pages=1168–1175 |year=2003 |pmid=14647548 }}</ref> with a frequency of about 1 in 3,000.<ref name="pamr">[http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm] Barry Lab - Vector and Virus Engineering. ''Gene therapy for Propionic Acidemia''</ref> The condition also appears to be common in [[Amish]], [[Mennonite]] and other populations where inbreeding is common.<ref name="paam">{{cite journal |vauthors =Kidd JR, Wolf B, Hsia E, Kidd KK |title=Genetics of propionic acidemia in a Mennonite-Amish kindred |journal=Am J Hum Genet. |volume=32 |issue=2 |pages=236–245 |year=1980 |pmid=7386459 |pmc=1686010 }}</ref>
==References==
{{reflist}}

Propionic acidemia epidemiology and demographics

2016-06-03T13:54:40Z

Donald Szlosek: Created page with "__NOTOC__ ==Overview== '''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|60..."

Propionic acidemia history and symptoms

2016-06-03T13:52:46Z

Donald Szlosek: Created page with "==History and Symptoms== Propionic acidemia is characterized almost immediately in newborns. Symptoms include poor feeding, vomiting, dehydration, acidosis, low [..."

==History and Symptoms==

Propionic acidemia is characterized almost immediately in newborns. Symptoms include poor feeding, [[vomiting]], [[dehydration]], [[acidosis]], low [[muscle]] tone ([[hypotonia]]), seizures, and [[lethargy]]. The effects of propionic acidemia quickly become life-threatening.

==References==
{{reflist}}

Propionic acidemia pathophysiology

2016-06-03T13:51:35Z

Donald Szlosek:

__NOTOC__
==Overview==
'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an [[autosomal]] [[recessive]]<ref>{{cite journal |pmid=10820128 |date=July 2000 |author1=Ravn K |author2=Chloupkova M |author3= Christensen E |author4=Brandt NJ |author5=Simonsen H |author6=Kraus JP |author7=Nielsen IM |author8=Skovby F |author9=Schwartz M |title=High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase |volume=67 |issue=1 |pages=203–206 |pmc=1287078 |doi=10.1086/302971 |journal=American Journal of Human Genetics}}</ref> [[metabolic disorder]], classified as a [[branched-chain amino acid|branched-chain]] [[organic acidemia]].<ref name="oad">{{cite journal |vauthors =Deodato F, Boenzi S, Santorelli FM, Dionisi-Vici C |title=Methylmalonic and propionic aciduria |journal=[[Am J Med Genet C Semin Med Genet]] |volume=142 |issue=2 |pages=104–112 |year=2006 |pmid=16602092 |doi=10.1002/ajmg.c.30090 }}</ref>

The disorder presents in the early [[neonatal]] period with progressive [[encephalopathy]]. Death can occur quickly, due to secondary [[hyperammonemia]], infection, cardiomyopathy, or basal ganglial stroke.<ref name="pbg">{{cite journal |vauthors =Hamilton RL, Haas RH, Nyhan WC, Powell HC, Grafe MR |title=Neuropathology of propionic acidemia: a report of two patients with basal ganglia lesions |journal=Journal of Child Neurology |volume=10 |issue=1 |pages=25–30 |year=1995 |pmid=7769173 |doi=10.1177/088307389501000107 }}</ref>

Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.

==Pathophysiology==

In healthy individuals, the enzyme propionyl CoA carboxylase converts propionyl CoA to methylmalonyl CoA. This is one step in the process of converting certain [[amino acids]] and fats into sugar for energy. Individuals with PA cannot perform this conversion because the enzyme propionyl CoA carboxylase is nonfunctional. The essential amino acids [[isoleucine]], [[valine]], [[threonine]], and [[methionine]], as well as odd-chain [[fatty acids]], are simply converted to propionyl CoA, before the process stops, leading to a buildup of propionyl CoA. Instead of being converted to methylmalonyl CoA, propionyl CoA is then converted into [[propionic acid]], which builds up in the bloodstream. This in turn causes an accumulation of dangerous acids and toxins, which can cause damage to the organs.

In many cases, PA can damage the brain, heart, and liver, cause seizures, and delays to normal development like walking and talking. During times of illness the affected person may need to be hospitalized to prevent breakdown of proteins within the body. Each meal presents a challenge to those with PA. If not constantly monitored, the effects would be devastating. Dietary needs must be closely managed by a metabolic [[geneticist]] or metabolic [[dietician]].

Mutations in both copies of the [[Propionyl-CoA carboxylase|PCCA]] or [[PCCB]] [[gene]]s cause propionic acidemia.<ref name="pamr">[http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm] Barry Lab - Vector and Virus Engineering. ''Gene therapy for Propionic Acidemia''</ref> These genes are responsible for the formation of the [[enzyme]] ''[[propionyl-CoA carboxylase]]'' ({{EC number|6.4.1.3}}), referred to as ''PCC''.

PCC is required for the normal breakdown of the essential amino acids valine, isoleucine, threonine, and methionine, as well as certain odd-chained fatty-acids. Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized. As a result, [[propionyl-CoA]], propionic acid, [[ketones]], [[ammonia]], and other [[toxic]] compounds accumulate in the [[blood]], causing the signs and symptoms of propionic [[acidemia]].

==References==
{{reflist}}

Propionic acidemia pathophysiology

2016-06-03T13:50:56Z

Donald Szlosek: Created page with " __NOTOC__ ==Overview== '''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM..."

__NOTOC__
==Overview==
'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an [[autosomal]] [[recessive]]<ref>{{cite journal |pmid=10820128 |date=July 2000 |author1=Ravn K |author2=Chloupkova M |author3= Christensen E |author4=Brandt NJ |author5=Simonsen H |author6=Kraus JP |author7=Nielsen IM |author8=Skovby F |author9=Schwartz M |title=High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase |volume=67 |issue=1 |pages=203–206 |pmc=1287078 |doi=10.1086/302971 |journal=American Journal of Human Genetics}}</ref> [[metabolic disorder]], classified as a [[branched-chain amino acid|branched-chain]] [[organic acidemia]].<ref name="oad">{{cite journal |vauthors =Deodato F, Boenzi S, Santorelli FM, Dionisi-Vici C |title=Methylmalonic and propionic aciduria |journal=[[Am J Med Genet C Semin Med Genet]] |volume=142 |issue=2 |pages=104–112 |year=2006 |pmid=16602092 |doi=10.1002/ajmg.c.30090 }}</ref>

The disorder presents in the early [[neonatal]] period with progressive [[encephalopathy]]. Death can occur quickly, due to secondary [[hyperammonemia]], infection, cardiomyopathy, or basal ganglial stroke.<ref name="pbg">{{cite journal |vauthors =Hamilton RL, Haas RH, Nyhan WC, Powell HC, Grafe MR |title=Neuropathology of propionic acidemia: a report of two patients with basal ganglia lesions |journal=Journal of Child Neurology |volume=10 |issue=1 |pages=25–30 |year=1995 |pmid=7769173 |doi=10.1177/088307389501000107 }}</ref>

Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.

==Pathophysiology==
[[File:Odd-chain_FA_oxydation.png|thumb|right|Methylmalonic acidemia is caused by a defect in the vitamin B12-dependent enzyme methylmalonyl CoA mutase.]]

In healthy individuals, the enzyme propionyl CoA carboxylase converts propionyl CoA to methylmalonyl CoA. This is one step in the process of converting certain [[amino acids]] and fats into sugar for energy. Individuals with PA cannot perform this conversion because the enzyme propionyl CoA carboxylase is nonfunctional. The essential amino acids [[isoleucine]], [[valine]], [[threonine]], and [[methionine]], as well as odd-chain [[fatty acids]], are simply converted to propionyl CoA, before the process stops, leading to a buildup of propionyl CoA. Instead of being converted to methylmalonyl CoA, propionyl CoA is then converted into [[propionic acid]], which builds up in the bloodstream. This in turn causes an accumulation of dangerous acids and toxins, which can cause damage to the organs.

In many cases, PA can damage the brain, heart, and liver, cause seizures, and delays to normal development like walking and talking. During times of illness the affected person may need to be hospitalized to prevent breakdown of proteins within the body. Each meal presents a challenge to those with PA. If not constantly monitored, the effects would be devastating. Dietary needs must be closely managed by a metabolic [[geneticist]] or metabolic [[dietician]].

Mutations in both copies of the [[Propionyl-CoA carboxylase|PCCA]] or [[PCCB]] [[gene]]s cause propionic acidemia.<ref name="pamr">[http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm] Barry Lab - Vector and Virus Engineering. ''Gene therapy for Propionic Acidemia''</ref> These genes are responsible for the formation of the [[enzyme]] ''[[propionyl-CoA carboxylase]]'' ({{EC number|6.4.1.3}}), referred to as ''PCC''.

PCC is required for the normal breakdown of the essential amino acids valine, isoleucine, threonine, and methionine, as well as certain odd-chained fatty-acids. Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized. As a result, [[propionyl-CoA]], propionic acid, [[ketones]], [[ammonia]], and other [[toxic]] compounds accumulate in the [[blood]], causing the signs and symptoms of propionic [[acidemia]].

==References==
{{reflist}}

Propionic acidemia overview

2016-06-03T13:49:36Z

Donald Szlosek:

'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an [[autosomal]] [[recessive]]<ref>{{cite journal |pmid=10820128 |date=July 2000 |author1=Ravn K |author2=Chloupkova M |author3= Christensen E |author4=Brandt NJ |author5=Simonsen H |author6=Kraus JP |author7=Nielsen IM |author8=Skovby F |author9=Schwartz M |title=High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase |volume=67 |issue=1 |pages=203–206 |pmc=1287078 |doi=10.1086/302971 |journal=American Journal of Human Genetics}}</ref> [[metabolic disorder]], classified as a [[branched-chain amino acid|branched-chain]] [[organic acidemia]].<ref name="oad">{{cite journal |vauthors =Deodato F, Boenzi S, Santorelli FM, Dionisi-Vici C |title=Methylmalonic and propionic aciduria |journal=[[Am J Med Genet C Semin Med Genet]] |volume=142 |issue=2 |pages=104–112 |year=2006 |pmid=16602092 |doi=10.1002/ajmg.c.30090 }}</ref>

The disorder presents in the early [[neonatal]] period with progressive [[encephalopathy]]. Death can occur quickly, due to secondary [[hyperammonemia]], infection, cardiomyopathy, or basal ganglial stroke.<ref name="pbg">{{cite journal |vauthors =Hamilton RL, Haas RH, Nyhan WC, Powell HC, Grafe MR |title=Neuropathology of propionic acidemia: a report of two patients with basal ganglia lesions |journal=Journal of Child Neurology |volume=10 |issue=1 |pages=25–30 |year=1995 |pmid=7769173 |doi=10.1177/088307389501000107 }}</ref>

Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.

==References==
{{reflist}}

Propionic acidemia overview

2016-06-03T13:49:05Z

Donald Szlosek: Created page with "'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an au..."

Template:Propionic acidemia

2016-06-03T13:46:28Z

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'''Propionic acidemia Microchapters'''
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[[Propionic acidemia |Home]]
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[[Propionic acidemia (patient information)|Patient Information]]
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[[Propionic acidemia overview|Overview]]
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[[Propionic acidemia historical perspective|Historical Perspective]]
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[[Propionic acidemia classification|Classification]]
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[[Propionic acidemia pathophysiology|Pathophysiology]]
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[[Propionic acidemia causes|Causes]]
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[[Propionic acidemia differential diagnosis|Differentiating Propionic acidemia from other Diseases]]
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[[Propionic acidemia epidemiology and demographics|Epidemiology and Demographics]]
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[[Propionic acidemia risk factors|Risk Factors]]
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[[Propionic acidemia screening|Screening]]
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[[Propionic acidemia natural history, complications and prognosis|Natural History, Complications and Prognosis]]
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Diagnosis
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[[Propionic acidemia history and symptoms|History and Symptoms]]
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[[Propionic acidemia physical examination|Physical Examination]]
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[[Propionic acidemia laboratory findings|Laboratory Findings]]
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[[Propionic acidemia electrocardiogram|Electrocardiogram]]
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[[Propionic acidemia chest x ray|Chest X Ray]]
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[[Propionic acidemia CT|CT]]
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[[Propionic acidemia MRI|MRI]]
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[[Propionic acidemia echocardiography or ultrasound|Echocardiography or Ultrasound]]
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[[Propionic acidemia other imaging findings|Other Imaging Findings]]
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Treatment
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[[Propionic acidemia surgery|Surgery]]
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[[Propionic acidemia medical therapy|Medical Therapy]]
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[[Propionic acidemia Radiation therapy|Radiation therapy]]
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[[Propionic acidemia primary prevention|Primary Prevention]]
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[[Propionic acidemia secondary prevention|Secondary Prevention]]
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[[Propionic acidemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]]
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[[Propionic acidemia future or investigational therapies|Future or Investigational Therapies]]
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Case Studies
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[[Propionic acidemia case study one|Case #1]]
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Propionic acidemia

2016-06-03T13:45:57Z

Donald Szlosek:

__NOTOC__
{{ Propionic acidemia }}

{{CMG}}

==[[Propionic acidemia overview|Overview]]==

==[[Propionic acidemia historical perspective|Historical Perspective]]==

==[[Propionic acidemia classification|Classification]]==

==[[Propionic acidemia pathophysiology|Pathophysiology]]==

==[[Propionic acidemia causes|Causes]]==

==[[Propionic acidemia differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Propionic acidemia epidemiology and demographics|Epidemiology and Demographics]]==

==[[Propionic acidemia risk factors|Risk Factors]]==

==[[Propionic acidemia screening|Screening]]==

==[[Propionic acidemia natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Propionic acidemia history and symptoms|History and Symptoms]] | [[Propionic acidemia physical examination|Physical Examination]] | [[Propionic acidemia laboratory findings|Laboratory Findings]] | [[Propionic acidemia electrocardiogram|Electrocardiogram]] |[[Propionic acidemia chest x ray|Chest X Ray]] | [[Propionic acidemia CT|CT]] | [[Propionic acidemia MRI|MRI]] | | [[Propionic acidemia other imaging findings|Other Imaging Findings]] | [[Propionic acidemia other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Propionic acidemia medical therapy|Medical Therapy]] | [[Propionic acidemia surgery|Surgery]] | [[Propionic acidemia primary prevention|Primary Prevention]] | [[Propionic acidemia secondary prevention|Secondary Prevention]] | [[Propionic acidemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Propionic acidemia future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Propionic acidemia case study one|Case #1]]

[[Category:Projects]]
[[Category:Help]]

{{WH}}
{{WS}}

Sandbox/01

2016-06-03T13:44:31Z

Donald Szlosek:

{{Refimprove|date=August 2008}}
{{Infobox disease |
Name = Propionic acidemia |
ICD10 = {{ICD10|E|71|1|e|70}} |
ICD9 = {{ICD9|270.3}} |
ICDO = |
Image = Propionic acid structure.png |
Caption = [[Propionic acid]] |
OMIM = 606054 |
MedlinePlus = |
eMedicineSubj = ped |
eMedicineTopic = 1906 |
DiseasesDB = 29673 |
DiseasesDB_mult = {{DiseasesDB2|29904}} |
}}

'''Propionic acidemia''', also known as '''propionic aciduria''', '''propionyl-CoA carboxylase deficiency''' and '''ketotic glycinemia''',<ref>{{OMIM|606054}}</ref> is an [[autosomal]] [[recessive]]<ref>{{cite journal |pmid=10820128 |date=July 2000 |author1=Ravn K |author2=Chloupkova M |author3= Christensen E |author4=Brandt NJ |author5=Simonsen H |author6=Kraus JP |author7=Nielsen IM |author8=Skovby F |author9=Schwartz M |title=High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase |volume=67 |issue=1 |pages=203–206 |pmc=1287078 |doi=10.1086/302971 |journal=American Journal of Human Genetics}}</ref> [[metabolic disorder]], classified as a [[branched-chain amino acid|branched-chain]] [[organic acidemia]].<ref name="oad">{{cite journal |vauthors =Deodato F, Boenzi S, Santorelli FM, Dionisi-Vici C |title=Methylmalonic and propionic aciduria |journal=[[Am J Med Genet C Semin Med Genet]] |volume=142 |issue=2 |pages=104–112 |year=2006 |pmid=16602092 |doi=10.1002/ajmg.c.30090 }}</ref>

The disorder presents in the early [[neonatal]] period with progressive [[encephalopathy]]. Death can occur quickly, due to secondary [[hyperammonemia]], infection, cardiomyopathy, or basal ganglial stroke.<ref name="pbg">{{cite journal |vauthors =Hamilton RL, Haas RH, Nyhan WC, Powell HC, Grafe MR |title=Neuropathology of propionic acidemia: a report of two patients with basal ganglia lesions |journal=Journal of Child Neurology |volume=10 |issue=1 |pages=25–30 |year=1995 |pmid=7769173 |doi=10.1177/088307389501000107 }}</ref>

Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.

==Pathophysiology==
[[File:Odd-chain_FA_oxydation.png|thumb|right|Methylmalonic acidemia is caused by a defect in the vitamin B12-dependent enzyme methylmalonyl CoA mutase.]]

In healthy individuals, the enzyme propionyl CoA carboxylase converts propionyl CoA to methylmalonyl CoA. This is one step in the process of converting certain [[amino acids]] and fats into sugar for energy. Individuals with PA cannot perform this conversion because the enzyme propionyl CoA carboxylase is nonfunctional. The essential amino acids [[isoleucine]], [[valine]], [[threonine]], and [[methionine]], as well as odd-chain [[fatty acids]], are simply converted to propionyl CoA, before the process stops, leading to a buildup of propionyl CoA. Instead of being converted to methylmalonyl CoA, propionyl CoA is then converted into [[propionic acid]], which builds up in the bloodstream. This in turn causes an accumulation of dangerous acids and toxins, which can cause damage to the organs.

In many cases, PA can damage the brain, heart, and liver, cause seizures, and delays to normal development like walking and talking. During times of illness the affected person may need to be hospitalized to prevent breakdown of proteins within the body. Each meal presents a challenge to those with PA. If not constantly monitored, the effects would be devastating. Dietary needs must be closely managed by a metabolic [[geneticist]] or metabolic [[dietician]].

Mutations in both copies of the [[Propionyl-CoA carboxylase|PCCA]] or [[PCCB]] [[gene]]s cause propionic acidemia.<ref name="pamr">[http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm http://mayoresearch.mayo.edu/mayo/research/barry_lab/ropionic-Aciademia.cfm] Barry Lab - Vector and Virus Engineering. ''Gene therapy for Propionic Acidemia''</ref> These genes are responsible for the formation of the [[enzyme]] ''[[propionyl-CoA carboxylase]]'' ({{EC number|6.4.1.3}}), referred to as ''PCC''.

PCC is required for the normal breakdown of the essential amino acids valine, isoleucine, threonine, and methionine, as well as certain odd-chained fatty-acids. Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized. As a result, [[propionyl-CoA]], propionic acid, [[ketones]], [[ammonia]], and other [[toxic]] compounds accumulate in the [[blood]], causing the signs and symptoms of propionic [[acidemia]].

==Symptoms==
Propionic acidemia is characterized almost immediately in newborns. Symptoms include poor feeding, [[vomiting]], [[dehydration]], [[acidosis]], low [[muscle]] tone ([[hypotonia]]), seizures, and [[lethargy]]. The effects of propionic acidemia quickly become life-threatening.

==Genetic prevalence==

[[Image:autorecessive.svg|thumb|right|Propionic acidemia has an autosomal recessive pattern of [[inheritance]].]]

Propionic acidemia is inherited in an [[autosomal]] [[recessive]] pattern and is found in about 1 in 35,000<ref name="pamr" /> live births in the [[United States]]. The condition appears to be more common in [[Saudi Arabia]],<ref name="pasa">{{cite journal |vauthors =Al-Odaib AN, Abu-Amaro KK, Ozand PT, Al-Hellani AM |title=A new era for preventive genetic programs in the Arabian Peninsula |journal=Saudi Medical Journal |volume=24 |issue=11 |pages=1168–1175 |year=2003 |pmid=14647548 }}</ref> with a frequency of about 1 in 3,000.<ref name="pamr" /> The condition also appears to be common in [[Amish]], [[Mennonite]] and other populations where inbreeding is common.<ref name="paam">{{cite journal |vauthors =Kidd JR, Wolf B, Hsia E, Kidd KK |title=Genetics of propionic acidemia in a Mennonite-Amish kindred |journal=Am J Hum Genet. |volume=32 |issue=2 |pages=236–245 |year=1980 |pmid=7386459 |pmc=1686010 }}</ref>

==Management==
Patients with propionic acidemia should be started as early as possible on a low protein diet. In addition to a protein mixture that is devoid of methionine, threonine, valine, and isoleucine, the patient should also receive L-carnitine treatment and should be given antibiotics 10 days per month in order to remove the intestinal propiogenic flora. The patient should have diet protocols prepared for him with a “well day diet” with low protein content, a “half emergency diet” containing half of the protein requirements, and an “emergency diet” with no protein content. These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states.<ref>Saudubray JM, Van Der Bergh G, Walter J : Inborn Metabolic Diseases Diagnosis and Treatment (2012)</ref>

Liver transplant is gaining a role in the management of these patients, with small series showing improved quality of life.

==See also==
* [[Methylmalonic acidemia]]
* [[Isovaleric acidemia]]
* [[Maple syrup urine disease]]

==References==
{{Reflist}}

==External links==
*[http://www.pafoundation.com Propionic Acidemia Foundation]
*[http://www.oaanews.org Organic Acidemia Association]
*[http://www.paresearch.org Propionic Acidemia Research Network (PARnet)]
*[http://www.gwenforacure.com Gwen for a Cure]
* {{NLM|propionicacidemia}}
*{{RareDiseases|467|Propionic acidemia}}
*{{cite web |url=http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=EN&Expert=35 |title=Propionic acidemia |format= |work=Orphanet |accessdate=}}

{{Amino acid metabolic pathology}}
{{Fatty-acid metabolism disorders}}

{{DEFAULTSORT:Propionic Acidemia}}
[[Category:Amino acid metabolism disorders]]
[[Category:Autosomal recessive disorders]]
[[Category:Rare diseases]]
[[Category:Fatty-acid metabolism disorders]]

Porphyria cutanea tarda medical therapy

2016-06-03T13:42:11Z

Donald Szlosek:

==Medical Therapy==
[[Chloroquine]] and [[venesection]] can be part of a management strategy.<ref>{{cite journal | author=Sarkany RP | title=The management of porphyria cutanea tarda | journal=Clin Exp Dermatol | year=2001 | pages=225-32 | volume=26 | issue=3 | id=PMID 11422163}}</ref>

==References==
{{reflist}}

Porphyria cutanea tarda medical therapy

2016-06-03T13:41:27Z

Donald Szlosek: Created page with "==Medical Therapy== Chloroquine and venesection can be part of a management strategy.<ref>{{cite journal | author=Sarkany RP | title=The management of porphyria cutane..."

Porphyria cutanea tarda causes

2016-06-03T13:40:34Z

Donald Szlosek:

__NOTOC__
==Overview==
'''Porphyria cutanea tarda''' (PCT) is the most common subtype of [[porphyria]]. The disorder results from low levels of the [[enzyme]] responsible for the [[uroporphyrinogen III decarboxylase|fifth step]] in [[heme]] production. Heme is a vital molecule for all of the body's organs. It is a component of [[hemoglobin]], the molecule that carries [[oxygen]] in the blood.
==Causes==
*In the acquired form, the signs and symptoms of this condition are triggered by non genetic factors such as alcohol abuse, excess iron, certain hormones, and viral infections. However, in the inherited form of the disease, which affects up to 20% of PCT patients, the condition arises from a mutation in the uroporphyrinogen decarboxylase gene, although environmental and chemical factors may trigger or exacerbate symptoms.
*Drug side effect: [[Chlorpropamide]], [[Tolbutamide]], [[Tolazamide]]

==Genetics==

Inherited mutations in the ''[[UROD]]'' [[gene]] cause about 20 % of cases (the other 80 % of cases do not have [[mutation]]s in UROD, and are classified as sporadic). UROD makes an enzyme called [[uroporphyrinogen III decarboxylase]], which is critical to the chemical process that leads to heme production. The activity of this enzyme is usually reduced by 50 % in all tissues in people with the inherited form of the condition.

Nongenetic factors such as [[alcohol abuse]], excess [[iron]], and others listed above can increase the demand for heme and the enzymes required to make heme. The combination of this increased demand and reduced activity of uroporphyrinogen decarboxylase disrupts heme production and allows byproducts of the process to accumulate in the body, triggering the signs and symptoms of porphyria cutanea tarda.

The ''[[HFE]]'' gene makes a protein that helps cells regulate the absorption of iron from the digestive tract and into the cells of the body. Certain mutations in the ''HFE'' gene cause [[hemochromatosis]] (an [[iron overload disorder]]). People who have these mutations are also at an increased risk of developing porphyria cutanea tarda.

In the 20% of cases where porphyria cutanea tarda is inherited, it is inherited in an [[autosomal dominant]] pattern, which means one copy of the altered gene is sufficient to decrease enzyme activity and cause the signs and symptoms of the disorder.

[[Image:autodominant.jpg|thumb|center|20% of cases of porphyria cutanea tarda are inherited in an [[autosomal dominant]] pattern.]]

==References==
{{reflist}}

Porphyria cutanea tarda causes

2016-06-03T13:39:58Z

Donald Szlosek: Created page with "__NOTOC__ ==Overview== '''Porphyria cutanea tarda''' (PCT) is the most common subtype of porphyria. The disorder results from low levels of the enzyme responsible for..."

Porphyria cutanea tarda history and symptoms

2016-06-03T13:39:13Z

Donald Szlosek: Created page with " ==History and Symptoms== When signs and symptoms occur, they usually begin in adulthood and result from the skin becoming overly sensitive to sunlight. Areas of skin exposed..."

==History and Symptoms==
When signs and symptoms occur, they usually begin in adulthood and result from the skin becoming overly sensitive to sunlight. Areas of skin exposed to the sun develop severe blistering, scarring, changes in pigmentation, and increased hair growth. Exposed skin becomes fragile and is easily damaged. People with porphyria cutanea tarda also have increased iron levels in the liver. They face a higher risk of developing abnormal liver function and liver cancer.<ref>{{cite journal | author=Fracanzani AL, Taioli E, Sampietro M, Fatta E, Bertelli C, Fiorelli G, Fargion S | title=Liver cancer risk is increased in patients with porphyria cutanea tarda in comparison to matched control patients with chronic liver disease | journal=J Hepatol | year=2001 | pages=498-503 | volume=35 | issue=4 | id=PMID 11682034}}</ref>

==References==
{{reflist}}

Porphyria cutanea tarda epidemiology and demographics

2016-06-03T13:37:08Z

Donald Szlosek: Created page with " __NOTOC__ ==Overview== '''Porphyria cutanea tarda''' (PCT) is the most common subtype of porphyria. The disorder results from low levels of the enzyme responsible f..."

Porphyria cutanea tarda physical examination

2016-06-03T13:35:47Z

Donald Szlosek:

__NOTOC__

==Physical Examination==
====Skin====
=====Extremities=====
<gallery>

Image:Porphyria cutanea tarda01.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>
Image:Porphyria cutanea tarda02.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda03.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda04.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda05.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda06.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda07.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda08.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda09.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda11.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda12.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda13.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda14.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

=====Face=====
<gallery>

Image:Porphyria cutanea tarda10.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

==References==
{{reflist}}

Porphyria cutanea tarda physical examination

2016-06-03T13:35:05Z

Donald Szlosek: Created page with "==Physical Examination== ====Skin==== =====Extremities===== <gallery> Image:Porphyria cutanea tarda01.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatolog..."

==Physical Examination==
====Skin====
=====Extremities=====
<gallery>

Image:Porphyria cutanea tarda01.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>
Image:Porphyria cutanea tarda02.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda03.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda04.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda05.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda06.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda07.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda08.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda09.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda11.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda12.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda13.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda14.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

=====Face=====
<gallery>

Image:Porphyria cutanea tarda10.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

==References==
{{reflist}}

Porphyria cutanea tarda classification

2016-06-03T13:33:57Z

Porphyria cutanea tarda overview

2016-06-03T13:31:15Z

Donald Szlosek:

Porphyria cutanea tarda overview

2016-06-03T13:30:50Z

Donald Szlosek: Created page with " __NOTOC__ ==Overview== '''Porphyria cutanea tarda''' (PCT) is the most common subtype of porphyria. The disorder results from low levels of the enzyme responsible..."

Template:Porphyria cutanea tarda

2016-06-03T13:29:30Z

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Porphyria cutanea tarda

2016-06-03T13:27:03Z

Donald Szlosek:

__NOTOC__
{{ Porphyria cutanea tarda }}

{{CMG}}

==[[Porphyria cutanea tarda overview|Overview]]==

==[[Porphyria cutanea tarda historical perspective|Historical Perspective]]==

==[[Porphyria cutanea tarda classification|Classification]]==

==[[Porphyria cutanea tarda pathophysiology|Pathophysiology]]==

==[[Porphyria cutanea tarda causes|Causes]]==

==[[Porphyria cutanea tarda differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Porphyria cutanea tarda epidemiology and demographics|Epidemiology and Demographics]]==

==[[Porphyria cutanea tarda risk factors|Risk Factors]]==

==[[Porphyria cutanea tarda screening|Screening]]==

==[[Porphyria cutanea tarda natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Porphyria cutanea tarda history and symptoms|History and Symptoms]] | [[Porphyria cutanea tarda physical examination|Physical Examination]] | [[Porphyria cutanea tarda laboratory findings|Laboratory Findings]] | [[Porphyria cutanea tarda electrocardiogram|Electrocardiogram]] |[[Porphyria cutanea tarda chest x ray|Chest X Ray]] | [[Porphyria cutanea tarda CT|CT]] | [[Porphyria cutanea tarda MRI|MRI]] | | [[Porphyria cutanea tarda other imaging findings|Other Imaging Findings]] | [[Porphyria cutanea tarda other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Porphyria cutanea tarda medical therapy|Medical Therapy]] | [[Porphyria cutanea tarda surgery|Surgery]] | [[Porphyria cutanea tarda primary prevention|Primary Prevention]] | [[Porphyria cutanea tarda secondary prevention|Secondary Prevention]] | [[Porphyria cutanea tarda cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Porphyria cutanea tarda future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Porphyria cutanea tarda case study one|Case #1]]

[[Category:Projects]]
[[Category:Help]]

{{WH}}
{{WS}}

Sandbox/01

2016-06-03T13:25:12Z

Donald Szlosek:

{{DiseaseDisorder infobox |
Name = Porphyria cutanea tarda |
ICD10 = {{ICD10|E|80|1|e|70}} |
ICD9 = {{ICD9|277.1}} |
}}
{{SI}}

{{CMG}}; {{AE}} {{KS}}

==Overview==
'''Porphyria cutanea tarda''' (PCT) is the most common subtype of [[porphyria]]. The disorder results from low levels of the [[enzyme]] responsible for the [[uroporphyrinogen III decarboxylase|fifth step]] in [[heme]] production. Heme is a vital molecule for all of the body's organs. It is a component of [[hemoglobin]], the molecule that carries [[oxygen]] in the blood.

==Presentation==
When signs and symptoms occur, they usually begin in adulthood and result from the skin becoming overly sensitive to sunlight. Areas of skin exposed to the sun develop severe blistering, scarring, changes in pigmentation, and increased hair growth. Exposed skin becomes fragile and is easily damaged. People with porphyria cutanea tarda also have increased iron levels in the liver. They face a higher risk of developing abnormal liver function and liver cancer.<ref>{{cite journal | author=Fracanzani AL, Taioli E, Sampietro M, Fatta E, Bertelli C, Fiorelli G, Fargion S | title=Liver cancer risk is increased in patients with porphyria cutanea tarda in comparison to matched control patients with chronic liver disease | journal=J Hepatol | year=2001 | pages=498-503 | volume=35 | issue=4 | id=PMID 11682034}}</ref>

==Causes==
*In the acquired form, the signs and symptoms of this condition are triggered by non genetic factors such as alcohol abuse, excess iron, certain hormones, and viral infections. However, in the inherited form of the disease, which affects up to 20% of PCT patients, the condition arises from a mutation in the uroporphyrinogen decarboxylase gene, although environmental and chemical factors may trigger or exacerbate symptoms.
*Drug side effect: [[Chlorpropamide]], [[Tolbutamide]], [[Tolazamide]]

==Diagnosis==
===Physical Examination===
====Skin====
=====Extremities=====
<gallery>

Image:Porphyria cutanea tarda01.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>
Image:Porphyria cutanea tarda02.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda03.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda04.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda05.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda06.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda07.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda08.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda09.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda11.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda12.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda13.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

Image:Porphyria cutanea tarda14.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

=====Face=====
<gallery>

Image:Porphyria cutanea tarda10.jpg|Porphyria cutanea tarda. ''[http://www.atlasdermatologico.com.br/ With permission from Dermatology Atlas.]''<ref name="Dermatology Atlas">{{Cite web | title = Dermatology Atlas | url = http://www.atlasdermatologico.com.br/}}</ref>

</gallery>

==Epidemiology==
This type of porphyria occurs in an estimated 1 in 25,000 people, including both inherited and sporadic (noninherited) cases. An estimated 80 % of porphyria cutanea tarda cases are sporadic. The exact frequency is not clear because many people with the condition never experience symptoms.

==Genetics==

Inherited mutations in the ''[[UROD]]'' [[gene]] cause about 20 % of cases (the other 80 % of cases do not have [[mutation]]s in UROD, and are classified as sporadic). UROD makes an enzyme called [[uroporphyrinogen III decarboxylase]], which is critical to the chemical process that leads to heme production. The activity of this enzyme is usually reduced by 50 % in all tissues in people with the inherited form of the condition.

Nongenetic factors such as [[alcohol abuse]], excess [[iron]], and others listed above can increase the demand for heme and the enzymes required to make heme. The combination of this increased demand and reduced activity of uroporphyrinogen decarboxylase disrupts heme production and allows byproducts of the process to accumulate in the body, triggering the signs and symptoms of porphyria cutanea tarda.

The ''[[HFE]]'' gene makes a protein that helps cells regulate the absorption of iron from the digestive tract and into the cells of the body. Certain mutations in the ''HFE'' gene cause [[hemochromatosis]] (an [[iron overload disorder]]). People who have these mutations are also at an increased risk of developing porphyria cutanea tarda.

In the 20% of cases where porphyria cutanea tarda is inherited, it is inherited in an [[autosomal dominant]] pattern, which means one copy of the altered gene is sufficient to decrease enzyme activity and cause the signs and symptoms of the disorder.

[[Image:autodominant.jpg|thumb|center|20% of cases of porphyria cutanea tarda are inherited in an [[autosomal dominant]] pattern.]]

==Treatment==
[[Chloroquine]] and [[venesection]] can be part of a management strategy.<ref>{{cite journal | author=Sarkany RP | title=The management of porphyria cutanea tarda | journal=Clin Exp Dermatol | year=2001 | pages=225-32 | volume=26 | issue=3 | id=PMID 11422163}}</ref>

==Cultural references==
Porphyria Cutanea Tarda is also the name of a song by the punk band AFI on their album Black Sails in the Sunset.

==References==
<references/>

==Additional Resources==
* {{cite journal | author=Kauppinen R | title=Porphyrias | journal=Lancet | year=2005 | pages=241-52 | volume=365 | issue=9455 | id=PMID 15652607}}
* {{cite journal | author=Lecha M, Herrero C, Ozalla D | title=Diagnosis and treatment of the hepatic porphyrias | journal=Dermatol Ther | year=2003 | pages=65-72 | volume=16 | issue=1 | id=PMID 12919129}}
* {{cite journal | author=Nordmann Y, Puy H | title=Human hereditary hepatic porphyrias | journal=Clin Chim Acta | year=2002 | pages=17-37 | volume=325 | issue=1-2 | id=PMID 12367763}}
* {{cite journal | author=Sassa S | title=The porphyrias | journal=Photodermatol Photoimmunol Photomed | year=2002 | pages=56-67 | volume=18 | issue=2 | id=PMID 12147038}}
* [http://web.uct.ac.za/depts/porphyria/professional/prof-pct.htm "Porphyria Cutanea Tarda"] Porphyria South Africa, University of Cape Town/Groote Schurr Hospital

{{Vesiculobullous disease}}
{{Endocrine, nutritional and metabolic pathology}}
{{SIB}}

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[[Category:Porphyrias]]
[[Category:Genetic disorders]]
[[Category:Dermatology]]
[[Category:Genetic Disease]]
[[Category:Inborn errors of metabolism]]

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