Autoimmune polyendocrine syndrome natural history, complications and prognosis
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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
If left untreated, patients with autoimmune polyendocrine syndrome (APS) may progress to involve other endocrine and non-endocrine organs. APS can be a life-threatening condition if vital hormone producing organs of the body are involved such as adrenal glands, thyroid, parathyroid glands. The complications of APS depend upon the subtype and organ system involved. Common complications of APS include those arising from hypoparathyroidism, Addison's disease and autoimmune thyroiditis. The prognosis of APS is variable and depends upon the duration and severity of endocrine/non-endocrine organ involved. Patients of APS with endocrine involvement generally require lifelong hormone replacement therapy.
Natural History, Complications, and Prognosis
Natural History
- If left untreated, patients with autoimmune polyendocrine syndrome (APS) may progress to involve other endocrine and nonendocrine organs.
- In APS, involvement of one organ is followed by autoimmune disorder of other endocrine-nonendocrine organs. Thus presentation of APS is highly variable and can lead to involvement of wide variety of organs.
- If untreated, APS can be life threatening condition since it may involve vital hormone producing endocrine glands such as adrenal glands, thyroid, parathyroid or pancreas.
Complications
The complications of autoimmune polyendocrine syndrome (APS) depends upon the subtype and endocrine/non-endocrine organ involved.
APS type 1
- Common complications of APS type 1 include those arising from hypoparathyroidism such as:[1][2][3][4]
- Renal complications (nephrolithiasis, nephrocalcinosis, impaired renal function, symptomatic hypocalcemia)
- Posterior subcapsular cataracts
- Basal ganglia calcifications[5]
- Complications of intravenous calcium extravasation
- Hypocalcemic seizure
- Dilated cardiomyopathy
- Pathological fractures
- Depression and other types of neuropsychiatric diseases
- Increased risk of infections
- Other common complications of the APS type 1 include Addison's disease
APS type 2
- Common complications of APS type 2 include those arising from Addison's disease such as:[6]
- Other common complications of the APS type 2 include autoimmune thyroiditis and type 1 diabetes mellitus
APS type 3
- Common complications of APS type 3 include those arising from autoimmune thyroiditis such as:[7][8][9][10][11]
- Other common complications of the APS type 3 include pernicious anemia
Prognosis
- The prognosis of autoimmune polyendocrine syndrome is variable and depends upon the duration and severity of endocrine/non-endocrine organ involved.
- Patients of APS with endocrine involvement generally require lifelong hormone(s) replacement therapy.
- Patients with family history of APS who are screened and diagnosed early have a good prognosis. In other patients, the prognosis depends upon the component diseases.
References
- ↑ Mitchell DM, Regan S, Cooley MR, Lauter KB, Vrla MC, Becker CB, Burnett-Bowie SA, Mannstadt M (2012). "Long-term follow-up of patients with hypoparathyroidism". J. Clin. Endocrinol. Metab. 97 (12): 4507–14. doi:10.1210/jc.2012-1808. PMC 3513540. PMID 23043192.
- ↑ Brandi ML, Bilezikian JP, Shoback D, Bouillon R, Clarke BL, Thakker RV, Khan AA, Potts JT (2016). "Management of Hypoparathyroidism: Summary Statement and Guidelines". J. Clin. Endocrinol. Metab. 101 (6): 2273–83. doi:10.1210/jc.2015-3907. PMID 26943719.
- ↑ Underbjerg L, Sikjaer T, Mosekilde L, Rejnmark L (2014). "Postsurgical hypoparathyroidism--risk of fractures, psychiatric diseases, cancer, cataract, and infections". J. Bone Miner. Res. 29 (11): 2504–10. doi:10.1002/jbmr.2273. PMID 24806578.
- ↑ Abate EG, Clarke BL (2016). "Review of Hypoparathyroidism". Front Endocrinol (Lausanne). 7: 172. doi:10.3389/fendo.2016.00172. PMC 5237638. PMID 28138323.
- ↑ Goswami R, Sharma R, Sreenivas V, Gupta N, Ganapathy A, Das S (2012). "Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism". Clin. Endocrinol. (Oxf). 77 (2): 200–6. doi:10.1111/j.1365-2265.2012.04353.x. PMID 22288727.
- ↑ Quinkler M (2012). "[Addison's disease]". Med Klin Intensivmed Notfmed (in German). 107 (6): 454–9. doi:10.1007/s00063-012-0112-3. PMID 22907517.
- ↑ Caturegli P, De Remigis A, Rose NR (2014). "Hashimoto thyroiditis: clinical and diagnostic criteria". Autoimmun Rev. 13 (4–5): 391–7. doi:10.1016/j.autrev.2014.01.007. PMID 24434360.
- ↑ Kirshner HS (2014). "Hashimoto's encephalopathy: a brief review". Curr Neurol Neurosci Rep. 14 (9): 476. doi:10.1007/s11910-014-0476-2. PMID 25027262.
- ↑ Lun Y, Wu X, Xia Q, Han Y, Zhang X, Liu Z, Wang F, Duan Z, Xin S, Zhang J (2013). "Hashimoto's thyroiditis as a risk factor of papillary thyroid cancer may improve cancer prognosis". Otolaryngol Head Neck Surg. 148 (3): 396–402. doi:10.1177/0194599812472426. PMID 23300224.
- ↑ Ahmed R, Al-Shaikh S, Akhtar M (2012). "Hashimoto thyroiditis: a century later". Adv Anat Pathol. 19 (3): 181–6. doi:10.1097/PAP.0b013e3182534868. PMID 22498583.
- ↑ Chiang B, Cheng S, Seow CJ (2016). "Commonly forgotten complication of Hashimoto's thyroiditis". BMJ Case Rep. 2016. doi:10.1136/bcr-2016-217568. PMID 27797845.