Objective: To explore whether or not statins have any impact on the progression of components of benign prostatic hyperplasia (lower urinary tract symptoms severity, prostate volume and serum prostate specific antigen (PSA) when combined with other agents inhibiting growth of prostate cells. Materials and Methods:This was a preliminary, clinical study. Eligible patients were aged > 50 yrs, with International Prostate Symptom Score (IPSS) between 9 and 19, total prostate volume (TPV) > 40 mL, and serum PSA > 1.5 ng/mL. Patients were divided in two groups: those with and those without lipidemia. After selection, eligible BPH patients with lipidemia (n = 18) were prescribed lovastatin 80 mg daily and finasteride 5 mg daily, while eligible patients without lipidemia (n = 15) were prescribed only finasteride 5 mg daily. IPSS, TPV and serum PSA were evaluated at end point (4 months).Results: There was no difference between the two groups on the primary end point of mean change from baseline in IPSS (p = 0.69), TPV (p = 0.90) and PSA (p = 0.16) after 4 months of treatment. Conclusions: Short-term lovastatin treatment does not seem to have any effect on IPSS, TPV and PSA in men with prostatic enlargement due to presumed BPH.

Pulmonary hypertension may occur after pneumonectomy with its known adverse effects. Patients with late postoperative pulmonary artery systolic pressure > 35.5 mm Hg are at higher risk of a suboptimal clinical outcome.

Studies on head injury-induced pituitary dysfunction are limited in number and conflicting results have been reported. To further clarify this issue, 29 consecutive patients (24 males), with severe (n = 21) or moderate (n = 8) head trauma, having a mean age of 37 ± 17 years were investigated in the immediate post-trauma period. All patients required mechanical ventilatory support for 8-55 days and were enrolled in the study within a few days before ICU discharge. Basal hormonal assessment included measurement of cortisol, corticotropin, free thyroxine (fT4), thyrotropin (TSH), testosterone (T) in men, estradiol (E2) in women, prolactin (PRL), and growth hormone (GH). Cortisol and GH levels were measured also after stimulation with 100 µg human corticotropin releasing hormone (hCRH) and 100 µg growth hormone releasing hormone (GHRH), respectively. Cortisol hyporesponsiveness was considered when peak cortisol concentration was less than 20 µg/dl following hCRH. TSH deficiency was diagnosed when a subnormal serum fT4 level was associated with a normal or low TSH. Hypogonadism was considered when T (males) or E2 (women) were below the local reference ranges, in the presence of normal PRL levels. Severe or partial GH deficiencies were defined as a peak GH below 3 µg/l or between 3 and 5 µg/l, respectively, after stimulation with GHRH. Twenty-one subnormal responses were found in 15 of the 29 patients (52%) tested; seven (24%) had hypogonadism, seven (24%) had cortisol hyporesponsiveness, five (17%) had hypothyroidism, and two patients (7%) had partial GH deficiency.These preliminary results suggest that a certain degree of hypopituitarism occurs in more than 50% of patients with moderate or severe head injury in the immediate post-trauma period, with cortisol hyporesponsiveness and hypogonadism being most common. Further studies are required to elucidate the pathogenesis of these abnormalities and to investigate whether they affect long-term morbidity. P2Cortisol reserve in head trauma victims: evaluation with the low-dose (1 µ µg) corticotropin (ACTH) stimulation test To investigate cortisol reserve in head trauma, 35 consecutive patients (30 men) with a mean age of 36 ± 16 years were studied 5-60 days after physical injury. Patients were enrolled in the study within a few days before ICU discharge. First, a morning blood sample was obtained to measure baseline cortisol, and ACTH plasma levels. Subsequently, 1 µg synthetic ACTH was injected intravenously and, 30 min later, a second blood sample was drawn to determine stimulated plasma cortisol. Patients having stimulated cortisol levels below 18 µg/dl were defined as nonresponders to the low-dose stimulation test (LDST). Mean (± SD) values for ACTH, baseline, and stimulated cortisol concentrations were 49 ± 27 pg/ml, 19.7 ± 5.5 µg/dl and 23.6 ± 6.7 µg/dl, respectively. Six of the 35 patients (17%) failed the LDST. Nonresponders were similar to responders with regard to age, gender, and severity of head injury. However, nonresponders more frequently required vasopres...