[Detection of preclinical Cushing's syndrome in overweight type 2 diabetic patients]. / Detección de síndrome de Cushing preclínico en pacientes con sobrepeso y diabetes mellitus tipo 2.

Preclinical Cushing's syndrome (PCS) is a condition in which cortisol excess is not associated to clinical features of Cushing's syndrome. The aim of this study was to detect PCS in 48 ambulatory overweight type 2 diabetic patients (DM). Controls were 40 normoglycemic obese (Ob) and 36 normo-weight healthy subjects (N). In DM (47/48) total urinary cortisol (UF) levels were similar to those found in Ob and N. Evening urinary cortisol (Spot F) was significantly higher than either Ob (p: 0.0001) or N (p: 0.03), although values did not overcome the upper normal limit (44 ng/mg creatinine). False positive results to the overnight 1 mg dexamethasone suppression test were found in 31% and 22% of DM and Ob, respectively. In a DM female an elevated UF and Spot F associated to absence of cortisol inhibition to the overnight 1 mg dexamethasone suppression test was repeatedly detected. Diagnosis of PCS was performed. Remission of hypercorticism and glycemic control were achieved after pituitary surgery. It would be useful to screen DM patients with poor glycemic control for PCS.

Detección de síndrome de Cushing preclínico en pacientes con sobrepeso y diabetes mellitus tipo 2. / [Detection of preclinical Cushings syndrome in overweight type 2 diabetic patients]

Preclinical Cushings syndrome (PCS) is a condition in which cortisol excess is not associated to clinical features of Cushings syndrome. The aim of this study was to detect PCS in 48 ambulatory overweight type 2 diabetic patients (DM). Controls were 40 normoglycemic obese (Ob) and 36 normo-weight healthy subjects (N). In DM (47/48) total urinary cortisol (UF) levels were similar to those found in Ob and N. Evening urinary cortisol (Spot F) was significantly higher than either Ob (p: 0.0001) or N (p: 0.03), although values did not overcome the upper normal limit (44 ng/mg creatinine). False positive results to the overnight 1 mg dexamethasone suppression test were found in 31

and 22

of DM and Ob, respectively. In a DM female an elevated UF and Spot F associated to absence of cortisol inhibition to the overnight 1 mg dexamethasone suppression test was repeatedly detected. Diagnosis of PCS was performed. Remission of hypercorticism and glycemic control were achieved after pituitary surgery. It would be useful to screen DM patients with poor glycemic control for PCS.

Glucocorticoids: their role on gonadal function and LH secretion.

The aim of the study was to investigate gonadal function and LH reserve in patients on chronic therapy with supraphysiological doses of GC. We clinically evaluated 17 male subjects (aged 23-56 years-old) on chronic GC therapy. In four subjects (aged 23-39 years-old) randomly selected, three basal blood samples were drawn and pooled for measurement of SHBG, total, free and bioavailable testosterone. Following baseline samples, a GnRH stimulation test was performed. Starting with a priming of 5 micrograms, a bolus of 50 micrograms of GnRH was injected intravenously and samples obtained every 30 minutes for assessment of LH. Four healthy men (aged 24-28 years-old) were used as controls. Patients on steroids referred decreased libido (58%) and impotence (52%) and lower back pain (41%). Total, free and bioavailable serum testosterone were significantly lower than controls (p < 0.01, p < 0.05 and p < 0.05, respectively) while SHBG levels persisted unchanged. Baseline LH and its rise after GnRH was normal. This study shows that chronic GC administration involves gonadal function reducing sexual steroids without changes in baseline and stimulated LH secretion. In addition, the priming with physiological doses of GnRH optimizes the pituitary response to higher GnRH doses.

Long-term low-dose glucocorticoid therapy in hyperandrogenized women: utility and effects on bone mineral content and hypothalamic-pituitary-adrenocortical function.

The effect of chronic low-dose glucocorticoid administration on bone mineral content and corticotrope reserve was investigated in 12 hyperandrogenized women treated with 1-6 mg oral evening doses of 16 beta-methylprednisone for 12-58 months. The hypothalamic-pituitary-adrenal axis was evaluated in 9 patients by a standard metyrapone test after 45-75 days off steroid therapy. All the patients had a normal rise in serum 11-deoxycortisol after metyrapone. Bone densitometry was assessed at the end of therapy using dual photon absorptiometry. No significant differences between patients and age-matched hyperandrogenic controls were found either in spine (1.048 +/- 0.096 vs. 1.023 +/- 0.175 g/cm2) or femoral neck (0.863 +/- 0.115 vs. 0.899 +/- 0.216 g/cm2), respectively. In conclusion, absence of quantitative bone mass reduction and normal corticotrope reserve were observed even after 58 months of daily steroid administration.