Autoimmune polyendocrine syndrome primary prevention: Difference between revisions
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==Primary Prevention== | ==Primary Prevention== | ||
Effective measures for the primary prevention of autoimmune polyendocrine syndrome (APS) include: | 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. | *[[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 should be done for first degree relatives of patients with APS for auto-antibodies against 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]] against [[21-Hydroxylase|21- hydroxylase]], 17-hydroxylase, [[thyroid peroxidase]], [[parietal cell]], anti-intrinsic factor and [[islet cell]] antibodies. | ||
*Currently, there is not enough evidence to define optimal intervals for testing but data suggests that autoantibodies can develop at any age. Hence, we rescreen patients for autoantibodies even if their initial autoantibody tests are negative. Celiac disease, for instance, is usually asymptomatic and only detected after screening for transglutaminase autoantibodies. | *Currently, there is not enough evidence to define optimal intervals for testing but data suggests that [[autoantibodies]] can develop at any age. Hence, we rescreen patients for [[autoantibodies]] even if their initial [[autoantibody]] tests are negative. [[Celiac disease]], for instance, is usually [[asymptomatic]] and only detected after screening for [[transglutaminase]] [[autoantibodies]]. | ||
==References== | ==References== | ||
Revision as of 13:23, 28 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
There are no established measures for the primary prevention of [disease name].
OR
There are no available vaccines against [disease name].
OR
Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
OR
[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
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 against 21- hydroxylase, 17-hydroxylase, thyroid peroxidase, parietal cell, anti-intrinsic factor and islet cell antibodies.
- Currently, there is not enough evidence to define optimal intervals for testing but data suggests that autoantibodies can develop at any age. Hence, we rescreen patients for autoantibodies even if their initial autoantibody tests are negative. Celiac disease, for instance, is usually asymptomatic and only detected after screening for transglutaminase autoantibodies.