The use of flutamide in the management of hirsutism.

The aim of our study was to evaluate the clinical efficacy of flutamide (Flu), when used alone, on the course of hirsutism and to assess its effect on hormonal secretion. Thirty-six hirsute women [11 patients were affected by polycystic ovarian syndrome (PCOs), and 25 were classified as having idiopathic hirsutism (IH)] were treated with Flu, 375 mg daily for a 4-month period. We found a marked clinical improvement in the degree of hirsutism in all patients. Testosterone and free testosterone fell significantly in both groups, while SHBG concentrations showed an increase in PCOs. In these patients, a reduction in androstenedione levels was also evident. Basal DHEAS concentrations showed a significant decrease only in PCO women. No significant modifications in gonadotropin response to LHRH nor in adrenal steroid response to ACTH stimulation were observed in 12 of the IH women before therapy and after the first month. Although the main action of flutamide is attributed to its peripheral antiandrogenic properties, the decrease in circulating androgen levels observed during treatment suggests that it can also modulate androgen production and/or metabolism.

Atrial natriuretic peptide response is blunted in patients with acute myocardial infarction and mild left ventricular dysfunction.

Neurohumoral parameters in 45 asymptomatic patients with acute myocardial infarction were measured. In patients with mild left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mm Hg), atrial natriuretic peptide levels differed significantly from those in patients with normal left ventricular function (127 +/- 74 pg/ml vs. 79 +/- 71 pg/ml; p < 0.001). After stimulus an increase in atrial natriuretic peptide levels (79 +/- 71 to 118 +/- 86 pg/ml; p < 0.001) was found only in patients with normal hemodynamic parameters. These data show that in patients with left ventricular dysfunction, the atrial natriuretic system is activated; however, atrial natriuretic peptide response to stimulus is present only in patients with normal hemodynamics.

Selective activation of atrial natriuretic peptide in patients with myocardial infarction and mild left ventricular dysfunction.

The purpose of this study was to investigate whether neurohumoral activation occurs in asymptomatic patients with acute myocardial infarction (AMI) and without clinical signs of heart failure. During the early phase of AMI (mean 8 days), the neurohumoral profiles of 60 patients (mean age 59 range 37 to 70) were examined. Blood levels of the following humoral parameters were measured: atrial natriuretic peptide (ANP), plasma renin activity, aldosterone and vasopressin. All patients underwent cardiac catheterization during hospitalization. Baseline hemodynamic characteristics identified left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mmHg) in 32 patients; the remaining 28 patients had normal hemodynamic parameters. In patients with AMI, plasma ANP levels differed significantly from control subjects (111 +/- 74 pg/ml vs. 53 +/- 18 pg/ml; P < 0.001). In patients with AMI and mild left ventricular dysfunction ANP levels were significantly increased when compared to patients with AMI and normal left ventricular function (129 +/- 73 pg/ml vs. 82 +/- 69 pg/ml; P < 0.001). The hemodynamic data showed a significant correlation with ANP only in patients with AMI and left ventricular dysfunction (EF% r = 0.42; LVEDP r = 0.44; P < 0.001). These data show that in patients with myocardial infarction and without heart failure, the atrial natriuretic peptide is the only neurohumoral system activated out of all neurohumoral systems tested in this population and its circulating levels are strictly related to the degree of left ventricular dysfunction.