Autoimmune Addison’s disease (AAD)

 

 

Overview

AAD affects the function of the adrenal glands, which disrupts the production of several hormones including cortisol and aldosterone, which regulate stress response (fight or flight) and blood pressure.

Common Symptoms

Darkening of the skin (hyperpigmentation), extreme fatigue, salt cravings, weight loss, low blood sugar (hypoglycemia), gastrointestinal symptoms, fainting from low blood pressure, and abdominal pain.

Coexisting Diseases and Conditions

Autoimmune polyglandular syndromes, autoimmune thyroiditis (Hashimoto’s and atrophic hypothyroidism), vitiligo, premature ovarian failure, type 1 diabetes, and pernicious anemia.

Risk Factors

AAD affects males and females equally and is most common in ages 30-50. Research is ongoing to determine whether genetic factors can be a cause. In certain cases, non-immune causes such as tuberculosis can affect the adrenal glands and result in the emergence of AAD.

Sources

  1. Article Sources and Footnotes
    1. Addison’s Disease. (n.d.). NORD (National Organization for Rare Disorders). Retrieved July 12, 2021, from https://rarediseases.org/rare-diseases/addisons-disease/

    2. Adrenal Insufficiency & Addison’s Disease | NIDDK. (n.d.). National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved July 12, 2021, from https://www.niddk.nih.gov/health-information/endocrine-diseases/adrenal-insufficiency-addisons-disease

    3. Autoimmune Addison disease: MedlinePlus Genetics. (n.d.). Retrieved June 12, 2021, from https://medlineplus.gov/genetics/condition/autoimmune-addison-disease/

    4. Buonocore, F., & Achermann, J. C. (2020). Primary adrenal insufficiency: New genetic causes and their long‐term consequences. Clinical Endocrinology, 92(1), 11–20. https://doi.org/10.1111/cen.14109

    5. van Haren Noman, S., Visser, H., Muller, A. F., & Limonard, G. J. (2018). Addison’s Disease Caused by Tuberculosis: Diagnostic and Therapeutic Difficulties. European Journal of Case Reports in Internal Medicine, 5(8), 000911. https://doi.org/10.12890/2018_000911

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