Specimen need not be refrigerated or frozen. Collect 2-3 ml of blood in a red top or serum separator tube. If possible, separate serum from clot and place into white tube provided with Immco Diagnostics’ collection kits. If separation facilities are not available, the blood can be sent in the tube used for collection.

Sample is stable at ambient temperature during shipment. If sample is stored prior to shipment, it is stable refrigerated (2-8˚C) up to five days and frozen (-20˚C or lower) up to one year.

Most cases of Addison’s disease are caused by the destruction of the adrenal cortex. About 70% of cases of Addison’s disease are autoimmune mediated, while tuberculosis accounts for 20%. 10% are due to less common causes such as chronic infections, amyloidosis, metastatic neoplasia, and surgical removal of the adrenal gland. Major clinical manifestations of Addison’s disease (anorexia, abdominal pain, wasting, apathy, weakness, fasting hypoglycemia, diminished ability to conserve sodium and excrete free water, hyponatremia, increased production of ACTH, and ß2 lipoprotein) are attributable to deficiencies of cortisol and aldosterone. The diagnosis of Addison’s disease is first made by biochemical methods to detect insufficient levels of cortisol followed by testing to establish the cause. Of such testing (which includes the ACTH stimulation test, insulin induced hypoglycemia test and x-ray exams) the autoantibody test for the presence of antibodies to adrenal cortex is of prime significance as over 70% of patients with Addison’s disease exhibit autoimmune etiology. Indirect immunofluorescence on human or primate adrenal cortex provides a simple, precise, and reliable method of detecting autoantibodies in Addison’s disease. Adrenal cortex antibodies (AAcAb) are present in greater than 90% of patients with recent onset autoimmune Addison’s disease. AAcAb are also markers of potential Addison’s disease. Clinical Relevance: Most cases of Addison’s disease are caused by the destruction of the adrenal cortex. About 70% of cases of Addison’s disease are autoimmune mediated, while tuberculosis accounts for 20%. 10% are due to less common causes such as chronic infections, amyloidosis, metastatic neoplasia, and surgical removal of the adrenal gland. Major clinical manifestations of Addison’s disease (anorexia, abdominal pain, wasting, apathy, weakness, fasting hypoglycemia, diminished ability to conserve sodium and excrete free water, hyponatremia, increased production of ACTH, and ß2 lipoprotein) are attributable to deficiencies of cortisol and aldosterone. The diagnosis of Addison’s disease is first made by biochemical methods to detect insufficient levels of cortisol followed by testing to establish the cause. Of such testing (which includes the ACTH stimulation test, insulin induced hypoglycemia test and x-ray exams) the autoantibody test for the presence of antibodies to adrenal cortex is of prime significance as over 70% of patients with Addison’s disease exhibit autoimmune etiology. Indirect immunofluorescence on human or primate adrenal cortex provides a simple, precise, and reliable method of detecting autoantibodies in Addison’s disease. Adrenal cortex antibodies (AAcAb) are present in greater than 90% of patients with recent onset autoimmune Addison’s disease. AAcAb are also markers of potential Addison’s disease.