Autoimmune polyendocrine syndrome primary prevention: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(17 intermediate revisions by 3 users not shown)
Line 2: Line 2:
{{Autoimmune polyendocrine syndrome}}
{{Autoimmune polyendocrine syndrome}}


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


==Overview==
==Overview==
There are no established measures for the primary prevention of [disease name].
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]].
 
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==
==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:<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]] with APS for [[Autoantibodies|auto-antibodies]] against [[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]].
*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]].
*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==

Latest revision as of 14:01, 31 October 2017

Autoimmune polyendocrine syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Autoimmune polyendocrine syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Autoimmune polyendocrine syndrome primary prevention On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Autoimmune polyendocrine syndrome primary prevention

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Autoimmune polyendocrine syndrome primary prevention

CDC on Autoimmune polyendocrine syndrome primary prevention

Autoimmune polyendocrine syndrome primary prevention in the news

Blogs on Autoimmune polyendocrine syndrome primary prevention

Directions to Hospitals Treating Autoimmune polyendocrine syndrome

Risk calculators and risk factors for Autoimmune polyendocrine syndrome primary prevention

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]

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. Perheentupa J (2002). "APS-I/APECED: the clinical disease and therapy". Endocrinol. Metab. Clin. North Am. 31 (2): 295–320, vi. PMID 12092452.
  4. 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)
  5. 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.

Template:WH Template:WS