Autoimmune polyendocrine syndrome secondary 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
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
Secondary Prevention
Effective measures for the secondary prevention of autoimmune polyendocrine syndrome (APS) include:[1][2][3][4][5]
- 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 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. 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.
- 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 or islet cell) are present without the associated disease, functional testing is indicated:
- Patients with antibodies against 21-hydroxylase who are asymptomatic should be monitored annually for ACTH levels, morning (8 am) cortisol levels, and cosyntropin stimulation testing. The time interval between testing may vary depending upon the signs and symptoms of the disease.
- 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.
References
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.
- ↑ 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)
- ↑ 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.
- ↑ 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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