Response of ACTH to octreotide in a probable corticotropic adenoma associated with Addison's disease.

BACKGROUND: Our patient was a 65-year-old woman previously diagnosed with Addison's disease. She presented an empty sella turcica and, at the age of 47, was discovered to have autonomous hypersecretion of adrenocorticotropic hormone (ACTH), suggesting a corticotropic adenoma secondary to Addison's disease, with a lack of response to high levels of dexamethasone. She maintained high ACTH levels despite corticosteroid treatment.

METHODS: The patient underwent a CRH stimulation test using an intravenous bolus (100 microg) with samples every 30 minutes for 3 hours and, the day after, an octreotide infusion (0.1 mg/200 cc saline) for 2 hours with measurements every 30 minutes for 3 hours. The following month she received subcutaneous octreotide 0.1 mg tid., and samples were taken every week.

RESULTS: Thirty minutes after the corticotropic-releasing-hormone (CRH) stimulation test, baseline ACTH levels (1 063 pg/ml) increased to 1530, the other values lying between 1 020-862. After octreotide infusion, baseline ACTH (1 212 pg/ml) was 946-643-1 630-4 600-1 730 at 30-60-90-120-180 minutes. The following month, with octreotide treatment, serum ACTH levels were 454-768-1233-429 pg/ml each week.

DISCUSSION: Octreotide acts mainly on somatostatin type 2 receptors (SSTR2) and has no effect in Cushing's syndrome, although a suppressor effect in some ACTH ectopic hypersecretions and in Nelson's syndrome has been demonstrated. It has been observed that SSTR5 appear more frequently than SSTR2 in corticotropic adenomas and corticosteroids downregulate octreotide sensitivity.

CONCLUSIONS: Octreotide did not suppress secretion of ACTH in suspected corticotropic adenoma. Newer somatostatin analogues, acting mainly on SSTR5, may be able to control ACTH hypersecretion in cases such as this.