Autoimmune polyendocrine syndrome primary prevention: Difference between revisions
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==Overview== | ==Overview== | ||
Effective measures for the [[primary prevention]] of autoimmune polyendocrine syndrome (APS) include [[patient education]] and [[Screening (medicine)|screening]]. Autoimmune polyendocrine syndrome may be [[inherited]] in [[autosomal recessive]] (APS type 1), [[autosomal dominant]] (APS type 2) or [[X linked inheritance|X linked]] fashion (APS type 3) and therefore educating the relatives about the importance of a positive family history is necessary. In addition, [[Screening (medicine)|screening]] should be done for '''first degree''' relatives of [[patients]] (parents, siblings or children) with APS for the presence of [[autoantibodies]]. | Effective measures for the [[primary prevention]] of autoimmune polyendocrine syndrome (APS) include [[patient education]] and [[Screening (medicine)|screening]]. Autoimmune polyendocrine syndrome may be [[inherited]] in [[autosomal recessive]] (APS type 1), [[autosomal dominant]] (APS type 2) or [[X linked inheritance|X linked]] fashion (APS type 3) and therefore educating the relatives about the importance of a positive [[family history]] is necessary. In addition, [[Screening (medicine)|screening]] should be done for '''first degree''' relatives of [[patients]] (parents, siblings or children) with APS for the presence of [[autoantibodies]]. | ||
==Primary Prevention== | ==Primary Prevention== | ||
Effective measures for the [[primary prevention]] of autoimmune polyendocrine syndrome (APS) include:<ref name="pmid15141045">{{cite journal |vauthors=Eisenbarth GS, Gottlieb PA |title=Autoimmune polyendocrine syndromes |journal=N. Engl. J. Med. |volume=350 |issue=20 |pages=2068–79 |year=2004 |pmid=15141045 |doi=10.1056/NEJMra030158 |url=}}</ref><ref name="pmid7608264">{{cite journal |vauthors=Badenhoop K, Walfish PG, Rau H, Fischer S, Nicolay A, Bogner U, Schleusener H, Usadel KH |title=Susceptibility and resistance alleles of human leukocyte antigen (HLA) DQA1 and HLA DQB1 are shared in endocrine autoimmune disease |journal=J. Clin. Endocrinol. Metab. |volume=80 |issue=7 |pages=2112–7 |year=1995 |pmid=7608264 |doi=10.1210/jcem.80.7.7608264 |url=}}</ref><ref name="pmid12092452">{{cite journal |vauthors=Perheentupa J |title=APS-I/APECED: the clinical disease and therapy |journal=Endocrinol. Metab. Clin. North Am. |volume=31 |issue=2 |pages=295–320, vi |year=2002 |pmid=12092452 |doi= |url=}}</ref><ref name="pmid14517510">{{cite journal |vauthors=Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas JE, Erlich H, Bugawan Tl Tl, Sokol RJ, Taki I, Norris JM, Rewers M |title=A prospective study of the incidence of childhood celiac disease |journal=J. Pediatr. |volume=143 |issue=3 |pages=308–14 |year=2003 |pmid=14517510 |doi= |url=}}</ref><ref name="pmid17873740">{{cite journal |vauthors=Liu E, Li M, Emery L, Taki I, Barriga K, Tiberti C, Eisenbarth GS, Rewers MJ, Hoffenberg EJ |title=Natural history of antibodies to deamidated gliadin peptides and transglutaminase in early childhood celiac disease |journal=J. Pediatr. Gastroenterol. Nutr. |volume=45 |issue=3 |pages=293–300 |year=2007 |pmid=17873740 |doi=10.1097/MPG.0b013e31806c7b34 |url=}}</ref> | Effective measures for the [[primary prevention]] of autoimmune polyendocrine syndrome (APS) include:<ref name="pmid15141045">{{cite journal |vauthors=Eisenbarth GS, Gottlieb PA |title=Autoimmune polyendocrine syndromes |journal=N. Engl. J. Med. |volume=350 |issue=20 |pages=2068–79 |year=2004 |pmid=15141045 |doi=10.1056/NEJMra030158 |url=}}</ref><ref name="pmid7608264">{{cite journal |vauthors=Badenhoop K, Walfish PG, Rau H, Fischer S, Nicolay A, Bogner U, Schleusener H, Usadel KH |title=Susceptibility and resistance alleles of human leukocyte antigen (HLA) DQA1 and HLA DQB1 are shared in endocrine autoimmune disease |journal=J. Clin. Endocrinol. Metab. |volume=80 |issue=7 |pages=2112–7 |year=1995 |pmid=7608264 |doi=10.1210/jcem.80.7.7608264 |url=}}</ref><ref name="pmid12092452">{{cite journal |vauthors=Perheentupa J |title=APS-I/APECED: the clinical disease and therapy |journal=Endocrinol. Metab. Clin. North Am. |volume=31 |issue=2 |pages=295–320, vi |year=2002 |pmid=12092452 |doi= |url=}}</ref><ref name="pmid14517510">{{cite journal |vauthors=Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas JE, Erlich H, Bugawan Tl Tl, Sokol RJ, Taki I, Norris JM, Rewers M |title=A prospective study of the incidence of childhood celiac disease |journal=J. Pediatr. |volume=143 |issue=3 |pages=308–14 |year=2003 |pmid=14517510 |doi= |url=}}</ref><ref name="pmid17873740">{{cite journal |vauthors=Liu E, Li M, Emery L, Taki I, Barriga K, Tiberti C, Eisenbarth GS, Rewers MJ, Hoffenberg EJ |title=Natural history of antibodies to deamidated gliadin peptides and transglutaminase in early childhood celiac disease |journal=J. Pediatr. Gastroenterol. Nutr. |volume=45 |issue=3 |pages=293–300 |year=2007 |pmid=17873740 |doi=10.1097/MPG.0b013e31806c7b34 |url=}}</ref> | ||
*[[Patient education]]: Autoimmune polyendocrine syndrome may be [[inherited]] in [[autosomal recessive]] (APS type 1), [[autosomal dominant]] (APS type 2) or [[X linked inheritance|X linked]] fashion (APS type 3) and therefore educating relatives about presence of APS in [[family]] is necessary. | *[[Patient education]]: Autoimmune polyendocrine syndrome may be [[inherited]] in [[autosomal recessive]] (APS type 1), [[autosomal dominant]] (APS type 2) or [[X linked inheritance|X linked]] fashion (APS type 3) and therefore educating relatives about presence of APS in [[family]] is necessary. | ||
*[[Screening (medicine)|Screening]] should be done for '''first degree''' relatives of [[patients]] (parents, siblings or children) with APS for [[Autoantibodies|auto-antibodies]] such as [[21-Hydroxylase|21- hydroxylase]], 17-hydroxylase, [[thyroid peroxidase]], [[parietal cell]], anti-intrinsic factor and [[islet cell]] antibodies. | *[[Screening (medicine)|Screening]] should be done for '''first degree''' relatives of [[patients]] (parents, siblings or children) with APS for [[Autoantibodies|auto-antibodies]] such as [[21-Hydroxylase|21- hydroxylase]], 17-hydroxylase, [[thyroid peroxidase]], [[parietal cell]], anti-[[intrinsic factor]] and [[islet cell]] antibodies. | ||
*Recent research | *Recent research has shown that in APS, [[autoantibodies]] can develop at any age and there is insufficient evidence to suggest optimum interval between testing. For example, patients of [[celiac disease]] are often [[asymptomatic]] and are detected only after [[Screening (medicine)|screening]] for [[transglutaminase]] [[autoantibodies]]. Thus, individuals with a [[family history]] of APS should be re-[[Screening (medicine)|screened]] for [[autoantibodies]] at appropriate intervals even if their initial [[autoantibody]] tests are negative. | ||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
Effective measures for the primary prevention of autoimmune polyendocrine syndrome (APS) include patient education and screening. Autoimmune polyendocrine syndrome may be inherited in autosomal recessive (APS type 1), autosomal dominant (APS type 2) or X linked fashion (APS type 3) and therefore educating the relatives about the importance of a positive family history is necessary. In addition, screening should be done for first degree relatives of patients (parents, siblings or children) with APS for the presence of autoantibodies.
Primary Prevention
Effective measures for the primary prevention of autoimmune polyendocrine syndrome (APS) include:[1][2][3][4][5]
- Patient education: Autoimmune polyendocrine syndrome may be inherited in autosomal recessive (APS type 1), autosomal dominant (APS type 2) or X linked fashion (APS type 3) and therefore educating relatives about presence of APS in family is necessary.
- Screening should be done for first degree relatives of patients (parents, siblings or children) with APS for auto-antibodies such as 21- hydroxylase, 17-hydroxylase, thyroid peroxidase, parietal cell, anti-intrinsic factor and islet cell antibodies.
- Recent research has shown that in APS, autoantibodies can develop at any age and there is insufficient evidence to suggest optimum interval between testing. For example, patients of celiac disease are often asymptomatic and are detected only after screening for transglutaminase autoantibodies. Thus, individuals with a family history of APS should be re-screened for autoantibodies at appropriate intervals even if their initial autoantibody tests are negative.
References
- ↑ Eisenbarth GS, Gottlieb PA (2004). "Autoimmune polyendocrine syndromes". N. Engl. J. Med. 350 (20): 2068–79. doi:10.1056/NEJMra030158. PMID 15141045.
- ↑ Badenhoop K, Walfish PG, Rau H, Fischer S, Nicolay A, Bogner U, Schleusener H, Usadel KH (1995). "Susceptibility and resistance alleles of human leukocyte antigen (HLA) DQA1 and HLA DQB1 are shared in endocrine autoimmune disease". J. Clin. Endocrinol. Metab. 80 (7): 2112–7. doi:10.1210/jcem.80.7.7608264. PMID 7608264.
- ↑ Perheentupa J (2002). "APS-I/APECED: the clinical disease and therapy". Endocrinol. Metab. Clin. North Am. 31 (2): 295–320, vi. PMID 12092452.
- ↑ Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas JE, Erlich H, Bugawan Tl T, Sokol RJ, Taki I, Norris JM, Rewers M (2003). "A prospective study of the incidence of childhood celiac disease". J. Pediatr. 143 (3): 308–14. PMID 14517510. Vancouver style error: initials (help)
- ↑ Liu E, Li M, Emery L, Taki I, Barriga K, Tiberti C, Eisenbarth GS, Rewers MJ, Hoffenberg EJ (2007). "Natural history of antibodies to deamidated gliadin peptides and transglutaminase in early childhood celiac disease". J. Pediatr. Gastroenterol. Nutr. 45 (3): 293–300. doi:10.1097/MPG.0b013e31806c7b34. PMID 17873740.