Autoimmune polyendocrine syndrome primary prevention: Difference between revisions
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*[[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]] 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]] 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 have 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 family history of APS should be rescreened for [[autoantibodies]] even if their initial [[autoantibody]] tests are negative. | *Recent research have 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 family history of APS should be rescreened for [[autoantibodies]] at appropriate intervals even if their initial [[autoantibody]] tests are negative. | ||
==References== | ==References== | ||
Revision as of 18:29, 28 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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 relatives about presence of APS in family is necessary. In addition, screening should be done for first degree relatives of patients with APS for the presence of autoantibodies.
Primary Prevention
Effective measures for the primary prevention of autoimmune polyendocrine syndrome (APS) include:
- 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 with APS for auto-antibodies such as 21- hydroxylase, 17-hydroxylase, thyroid peroxidase, parietal cell, anti-intrinsic factor and islet cell antibodies.
- Recent research have 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 family history of APS should be rescreened for autoantibodies at appropriate intervals even if their initial autoantibody tests are negative.