Evaluation of glucocorticoid binding globulin levels and glucocorticoid reseptor polimorfizm fraquency in patients with adrenal masses and subclinical cushing syndrome

Number of patients with incidental adrenal masses are increasing due to frequent use of modern imaging methods. Subclinical Cushing' s Syndrome (sCS) is defined as adrenal gland-dependent glucocorticoid autonomy determined after hormonal tests with in patients presenting with adrenal masses without classic signs of Cushing' s Syndrome. The clinical signs of glucocorticoid excess of the (obesity, hypertension, glucose intolerance ...) has been shown in this patients, but not apparent as Cushing' s syndrome. Studies over the last 10 years shows that pateints with adrenal adenomas have worse metabolic and cardiovascular profile compared to patients without adenomas. This metabolic and cardiovascular profile though more pronounced in people with subclinical Cushing' s Syndrome not only in subclinical Cushing' s Syndrome but also in patient with nonfunctional adrenal masses have. This profile, supports a moderate glucocorticoid excess and a devious and continuous glucocorticoid autonomy. We thought, glucocorticoid autonomy of patients with nonfunctional adrenal masses and sCS, might be due to two reasons; the first of these, patients with nonfunctional adrenal masses and sCS have a lower CBG level according to individuals without adrenal masses, thus increase the functional free fraction of cortisol in blood levels; the second is GR polymorphism, causes an increased sensitivity and increased cellular effects of GC. In this study we examined the CBG levels in patients with adrenal masses and without adrenal masses. We found no difference between patients and controls. Fraquency of two single nucleotide polymorphisms associated with increased sensitivity of GR N363S and BcL I also been investigated in patients with non- adrenal adenoma and adrenal adenoma. BcL I polymorphism in patients and control group incidence are extremely close. The N363S polymorphism was found in a higher proportion of patients. The reasons for the increased cortisol load in patients with adrenal masses compared with healthy control groups may be the increased GR sensitivity with N363S polymorphism frequency, and increased cellular effects of GC's.