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Addison disease: blood chemistry

Addison’s disease, or primary adrenal insufficiency, is distinguished from other types of adrenal insufficiency in that the primary problem comes from the inability of the adrenal glands to produce sufficient levels of cortisol, and at times, aldosterone. Primary adrenal insufficiency is usually not apparent until 90% of the adrenal cortex has been destroyed. The most common cause of Addison’s disease is idiopathic adrenal insufficiency secondary to autoimmune destruction of the adrenal cortex. Symptoms include : chronic fatigue, muscle weakness, anorexia, wt loss, nausea, vomiting and diarrhea. Diffuse hyperpigmentation occurs secondary to a compensatory increase in ACTH and beta-lipotropin. Mineralocorticoids are usually deficient resulting in a reduction in urine sodium concentration (and can be accompanied by life threatening hyperkalemia). Laboratory investigation may thus show: hypercalcemia, hypoglycemia, hyperkalemia, and a metabolic acidosis.

Diagnosis involves an ACTH stimulation test during which the blood and/or urine cortisol levels are measured before and 30 minutes and 60 minutes after the IV administration of 250 micrograms of synthetic ACTH. A normal test reveals a rise in plasma cortisol of at least 7mg/dl sixty minutes after the ACTH injection. Patients with adrenal insufficiency demonstrate no or little adrenal response.

Patients on chronic steroids therapy can also develop an “Addisonian Crisis” upon abrupt discontinuation of the steroids or the failure to provide additional (or “stress dose steroids”) during periods of stress, such as surgery or critical illness. It is important to note that, unlike patients with primary Addison’s Disease, these patients have suppression of the hypothalamic—pituitary axis and will not have symptoms of ACTH excess (such as hyperpigmentation).

Hyponatremia occurs as a result of both the loss of sodium and volume caused by mineralocorticoid deficiency and increased vasopressin secretion due to cortisol deficiency. This at times results in significant salt craving. Hyperkalemia is often associated with a mild hyperchloremic acidosis due to a deficiency in mineralocorticoids.