Autoimmune polyendocrine syndrome secondary prevention: Difference between revisions

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{{Autoimmune polyendocrine syndrome}}
{{Autoimmune polyendocrine syndrome}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}}{{Akshun}}


==Overview==
==Overview==
There are no established measures for the secondary prevention of [disease name].
Effective measures for the [[secondary prevention]] of autoimmune polyendocrine syndrome (APS) include [[patient education]] and periodic screening. In APS the time interval between involvement of one [[endocrine organ]] to other [[endocrine]]/nonendocrine [[Organ (anatomy)|organ]] may take years. Thus, patient should be informed about signs and symptoms of commonly associated conditions/disorders with APS. In addition, periodic screening at an interval of 6-12 months should be done to detect the presence of any autoantibody such as [[antibodies]] against [[21-Hydroxylase|21-hydroxylase]] or [[Islet cell|islet cells]].
 
OR
 
Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].


==Secondary Prevention==
==Secondary Prevention==
Secondary prevention: Annual measurement of the corticotropin level and the level of cortisol both before and after cosyntropin stimulation (at 8 a.m.) in those with autoantibodies against 21-hydroxylase seems prudent to detect adrenal damage before a hypotensive crisis.
Effective measures for the [[secondary 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="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="pmid8805992">{{cite journal |vauthors=Corazza GR, Di Sario A, Cecchetti L, Jorizzo RA, Di Stefano M, Minguzzi L, Brusco G, Bernardi M, Gasbarrini G |title=Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease |journal=Bone |volume=18 |issue=6 |pages=525–30 |year=1996 |pmid=8805992 |doi= |url=}}</ref><ref name="pmid10969260">{{cite journal |vauthors=Hoffenberg EJ, Bao F, Eisenbarth GS, Uhlhorn C, Haas JE, Sokol RJ, Rewers M |title=Transglutaminase antibodies in children with a genetic risk for celiac disease |journal=J. Pediatr. |volume=137 |issue=3 |pages=356–60 |year=2000 |pmid=10969260 |doi=10.1067/mpd.2000.107582 |url=}}</ref>
*There are no established measures for the secondary prevention of [disease name].
*[[Patient education]]: [[Patient education]] is an important aspect in early [[diagnosis]] and management of APS. In APS the time interval between involvement of one [[endocrine organ]] to another [[endocrine]]/nonendocrine [[Organ (anatomy)|organ]] may take years. For example, patients with APS type 1 develops mucocutaneous [[candidiasis]] in [[infancy]] and it may take upto five years for them to develop [[hypoparathyroidism]]. [[Patient|Patients]] should also be informed about [[symptoms]] of other [[disorders]] for which they are at high risk such as [[Addison's disease]] or [[diabetes mellitus]].
OR
*[[Patients]] with type 1 and type 2 APS should be screened at an interval of 6 to 12 months for development of other [[endocrine]]/non-endocrine disorders. If [[autoantibodies]] (such as antibodies against [[21-Hydroxylase|21-hydroxylase]] or [[islet cell]]) are present without the associated disease, functional testing is indicated:
*Effective measures for the secondary prevention of [disease name] include:
**[[Patients]] with [[antibodies]] against [[21-Hydroxylase|21-hydroxylase]] who are [[asymptomatic]] should be monitored annually for [[Adrenocorticotropic hormone|ACTH]] levels, morning (8 am) [[Cortisol level|cortisol levels]], and [[cosyntropin]] stimulation testing. The time interval between testing may vary depending upon the [[Signs and Symptoms|signs and symptoms]] of the [[disease]].
**[Strategy 1]
**[[Patients]] with [[antibodies]] against [[islet cell]] who are [[asymptomatic]] should be tested for serum glucose level. This can help in early detection of [[diabetes]] before overt clinical [[symptoms]] sets in. Educating these patients about the importance of [[diet]] and [[glucose]] home monitoring can help prevent progression and [[complications]] of the [[disease]].
**[Strategy 2]
**[Strategy 3]


==References==
==References==

Latest revision as of 15:39, 3 October 2017

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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 secondary prevention of autoimmune polyendocrine syndrome (APS) include patient education and periodic screening. In APS the time interval between involvement of one endocrine organ to other endocrine/nonendocrine organ may take years. Thus, patient should be informed about signs and symptoms of commonly associated conditions/disorders with APS. In addition, periodic screening at an interval of 6-12 months should be done to detect the presence of any autoantibody such as antibodies against 21-hydroxylase or islet cells.

Secondary Prevention

Effective measures for the secondary prevention of autoimmune polyendocrine syndrome (APS) include:[1][2][3][4][5]

References

  1. Eisenbarth GS, Gottlieb PA (2004). "Autoimmune polyendocrine syndromes". N. Engl. J. Med. 350 (20): 2068–79. doi:10.1056/NEJMra030158. PMID 15141045.
  2. 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.
  3. 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)
  4. Corazza GR, Di Sario A, Cecchetti L, Jorizzo RA, Di Stefano M, Minguzzi L, Brusco G, Bernardi M, Gasbarrini G (1996). "Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease". Bone. 18 (6): 525–30. PMID 8805992.
  5. Hoffenberg EJ, Bao F, Eisenbarth GS, Uhlhorn C, Haas JE, Sokol RJ, Rewers M (2000). "Transglutaminase antibodies in children with a genetic risk for celiac disease". J. Pediatr. 137 (3): 356–60. doi:10.1067/mpd.2000.107582. PMID 10969260.

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