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Background: Statin-induced lung injury (SILI) is an uncommon but serious complication of statins. The clinical features and outcome of patients with SILI vary widely. Clinical data relevant to diagnosis and outcome of patients with SILI were investigated in this study., Method: Four cases of SILI diagnosed at our institute and 12 cases reported in the English literature from 1995 to 2010 were studied. The patients were further divided into favourable and unfavourable outcome groups and compared., Results: Compared with the 12 previously reported cases, fever (p=0.008) and consolidation (p=0.027) were more common and duration of statin treatment was significantly shorter (p=0.030) in our patients. Foamy alveolar macrophages in bronchoalveolar lavage fluid (BALF) were found in our four patients. Patients with cough (p=0.024), fever (p=0.026) and alveolar infiltrates (p=0.036), especially ground-glass opacity (GGO) (p=0.001) shown on thoracic high-resolution CT (HRCT), had a favourable outcome. Conversely, those with fibrosis shown on HRCT (p=0.008) had an unfavourable outcome. Stepwise logistic regression analysis demonstrated that cough (p=0.011), fever (p=0.005), and alveolar infiltrates (p=0.017), GGO (p<0.001) and fibrosis (p=0.002) shown on thoracic HRCT were independent factors affecting the outcome of SILI., Conclusions: For patients with SILI, pulmonary phospholipidosis, as shown by foamy alveolar macrophages in BALF, may be valuable in diagnosis, and clinical symptoms and thoracic HRCT findings are of value in predicting the outcome.

Introduction: The increased prevalence of erectile dysfunction (ED) has been reported in patients with chronic obstructive pulmonary disease, and sustained systemic inflammation seems to play a central role in this linkage. Asthma is also a chronic inflammatory airway disorder, eliciting a low-grade systemic inflammation; however, the influence of asthma on ED has not been investigated., Aim: Our study strived to explore the relationship of asthma and the subsequent development of ED using a nationwide, population-based database., Methods: From 2000 to 2007, we identified newly diagnosed asthma cases involving male patients 18-55 years old. A control cohort without asthma, which was matched for age and comorbidities, was selected for comparison., Main Outcome Measures: The two cohorts were followed up, and we observed the occurrence of ED by registry of ED diagnosis in the database., Results: Of the 17,302 sampled patients (3,466 asthma patients vs. 13,836 control), 114 (0.66%) experienced ED during a mean follow-up period of 4.56 years, including 34 (0.98% of the asthma patients) from the asthma cohort and 80 (0.58%) from the control group. Subjects with asthma experienced a 1.909-fold (95% confidence interval [CI], 1.276-2.856; P=0.002) increase in incident ED, which was independent of age, the number of clinical visits for urologist, and other comorbidities. Kaplan-Meier analysis also revealed the tendency of asthma patients for ED development (log rank test, P=0.002). The risk of ED was higher in cases with more frequent clinical visits for asthma (asthma patients with clinical visits with >24 times/year vs. <12 times/year: hazard ratio [HR]: 4.154 [95% CI:1.392-12.396], P=0.011; clinical visits with 12-24 times/year vs. <12 times/year HR: 3.534 [95% CI:1.245-10.032], P=0.018)., Conclusions: Asthma may be an independent risk factor for ED, and risk of ED probably increases in accordance with asthma severity., (© 2011 International Society for Sexual Medicine.)

Human decidual tissue consists of a heterogeneous population of cells, including stromal cells, lymphocytes, and macrophages. Lipopolysaccharides (LPS), which bind to specific cell surface receptors on macrophages, have been shown to increase prostaglandin production by the decidua and amnion. To determine whether LPS may also affect decidual hormone production, we have examined the effects of LPS on the synthesis and release of prolactin and renin. Dispersed cells from term decidual tissue exposed to LPS L2880 (Escherichia coli, 1 microgram/ml) released significantly less prolactin and renin than control cells after 24 h of exposure. Maximal inhibition of prolactin (31.6%) and renin (62.5%) release was noted at 72 and 96 h of exposure, respectively (p < or = 0.0002 in each instance). The inhibition of prolactin and renin release was dose-dependent, with half-maximal inhibition at a dose of approximately 10 ng/ml. LPS caused a decrease in prolactin synthesis as well as release. In addition, LPS inhibited the stimulation of prolactin release in response to insulin, a known secretagogue of prolactin release. After 24, 48, and 72 h of exposure, the magnitude of the stimulation of prolactin release by cells exposed to insulin (100 ng/ml) in the presence of LPS (1 microgram/ml) was 84.5, 57.5, and 35.2% less, respectively, than that of cells exposed to insulin alone (p = 0.0001 in each instance). LPS L6011 (Salmonella endotoxin) also inhibited prolactin and renin release. LPS had no effect on overall protein or DNA synthesis and did not cause release of alkaline phosphatase and lactate dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS)

Recent studies have shown that the basal release of PRL from anterior pituitary cells is inhibited by endothelin-1 (ET-1) and ET-3. To determine whether ET also regulates the synthesis and release of PRL by decidual cells, we examined the effects of ET on the synthesis and release of PRL from an enriched fraction of human decidual cells prepared by isopycnic centrifugation of enzymatically dispersed term decidual tissue. Exposure of decidual cells to ET-1 (10(-7) M) for 96 h caused a progressive decrease in basal PRL synthesis and release beginning 24 h after exposure with half-maximal inhibition occurring at an ET-1 concentration of 5 x 10(-9) M. Between 72-96 h of culture, ET-1-exposed cells synthesized 37.2 +/- 2.7% (SEM) and released 32.3 +/- 1.3% less PRL than control cells (P < 0.01). ET-1-exposed cells incubated with [35S]methionine between 72-96 h also released less [35S] PRL than control cells. Sarafotoxin S6C, an ETB receptor agonist, also inhibited basal PRL release, whereas BQ-123, an ETA receptor antagonist, had no effect on basal or on ET-1-mediated inhibition of PRL release. ET-1 also markedly inhibited the stimulation of PRL synthesis and release in response to insulin and insulin-like growth factor-1 (IGF-1). Cells exposed to insulin (100 ng/ml) and IGF-1 (50 ng/ml) alone released 61.2 +/- 3.6% and 40.0 +/- 3.8% more PRL, respectively, than control cells between 72-96 h of exposure. However, cells exposed simultaneously to insulin and ET-1 (10(-7) M) released only 17.1 +/- 3.5% more PRL than control cells during the same time period, and cells exposed simultaneously to IGF-1 and ET-1 released only 4.1 +/- 1.8% more PRL than controls during the same time interval (P vs. insulin or IGF-1 alone < 0.001 in each instance). Both basal and insulin- and IGF-1-stimulated PRL release were also inhibited by the ET isotypes ET-2 and ET-3, and by the ET-1 precursor, big ET. Since macrophages and decidual cells synthesize ET, and decidual tissue contains specific receptors for ET, the inhibitory action of ET on basal and stimulated PRL release may result from an autocrine and/or paracrine effect and appears to be mediated through the ETB receptor.

The factors that regulate the synthesis and release of renin by human decidua and other extrarenal tissues are poorly understood. Recent studies have demonstrated that the potent vasoconstrictive peptide endothelin (ET) inhibits the release of renin from renal juxtaglomerular cells, probably by a calcium-dependent mechanism. To determine whether ET also influences the release of renin from decidual tissue, we have examined the effects of ET on the synthesis and release of renin by primary cultures of human decidual cells. Decidual cells exposed continuously to ET (10(-7) mol/L) for 96 h released significantly more renin than control cells. At 48, 72, and 96 h, the ET-exposed cells released 284, 645, and 1300% more renin, respectively, than control cells. Greater than 95% of the renin released into the medium was in the form of prorenin, the precursor of renin. The stimulation by ET was dose-dependent, with half-maximal stimulation at a concentration of 7 x 10(-9) mol/L. ET-2 and ET-3, as well as the precursor to ET (big ET), also stimulated renin release. The total amount of renin in the media and cells of ET-exposed decidual cells was significantly greater than that of control cells, indicating that the increase in renin release was accompanied by an increase in synthesis. In addition, Northern blot analysis of total RNA from cells exposed for 96 h to ET-1 (10(-7) mol/L) indicated that the renin messenger RNA content of ET-1-exposed cells was approximately 100 times greater than that of control cells. These results indicate that ET is a potent stimulus to the synthesis and release of prorenin from human decidua and that the effect of ET on decidual renin expression is opposite to that observed for the expression of renal renin.