21-Hydroxylase Antibodies, Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Chronic primary adrenal insufficiency (Addison disease) is most commonly caused by the insidious autoimmune destruction of the adrenal cortex and is characterized by the presence of adrenal cortex autoantibodies in the serum. It can occur sporadically or in combination with other autoimmune endocrine diseases, that together comprise Type I or Type II autoimmune polyglandular syndrome (APS).
The microsomal autoantigen 21-hydroxylase (55 kilodalton) has been shown to be the primary autoantigen associated with autoimmune Addison disease. 21-Hydroxylase antibodies are markers of autoimmune Addison disease, whether it presents alone, or as part of Type I or Type II (APS).
Investigation of adrenal insufficiency
Aid in the detection of those at risk of developing autoimmune adrenal failure in the future
Positive results (> or =1 U/mL) indicate the presence of adrenal autoantibodies consistent with Addison disease.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Lipemic or grossly hemolyzed serum should not be used in this assay. Interpretation of test results requires consideration of other factors such as the clinical status of the patient, other test results, etc.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Reference values apply to all ages.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
Tanaka H, Perez M, Powell M, et al: Steroid 21-hydroxylase autoantibodies: measurements with a new immunoprecipitation assay. J Clin Endocrinol Metab 1997;82:1440-1446