Does continuous positive airway pressure by face mask improve patients with acute cardiogenic pulmonary edema due to left ventricular diastolic dysfunction?

OBJECTIVE: Continuous positive airway pressure (CPAP) by face mask is an effective method of treating severe cardiogenic pulmonary edema (CPE). However, to our knowledge, no study has provided a precise evaluation of the effects of CPAP on cardiac function in patients presenting with CPE and preserved left ventricular (LV) function. DESIGN: Prospective observational clinical study. SETTING: A 14-bed, medical ICU at a university hospital. PATIENTS: Nine consecutive patients presenting with hypoxemic acute CPE. INTERVENTIONS: All patients were selected for 30 min of CPAP with 10 cm H(2)O by mask with fraction of inspired oxygen adjusted for a cutaneous saturation > 90%. Doppler echocardiography was performed before CPAP application and during the last 10 min of breathing with CPAP. Two-tailed, paired t-tests were used to compare data recorded at baseline (oxygen alone) and after CPAP. MEASUREMENTS AND RESULTS: Four patients presented CPE with preserved left ventricular (LV) function (a preserved LV ejection fraction [LVEF] > 45%, and/or aortic velocity time integral > 17 cm in the absence of aortic stenosis or hypertrophic cardiomyopathy). Oxygenation and ventilatory parameters were improved by CPAP in all patients. Hemodynamic monitoring and Doppler echocardiographic analysis demonstrated that in patients with preserved LV systolic function, mean arterial pressure and LV end-diastolic volume were decreased significantly by CPAP (p < 0.04). In patients with LV systolic dysfunction, CPAP improved LVEF (p < 0.05) and decreased LV end-diastolic volume (p = 0.001) significantly. CONCLUSION: CPAP improves oxygenation and ventilatory parameters in all kinds of CPE. In patients with preserved LV contractility, the hemodynamic benefit of CPAP results from a decrease in LV end-diastolic volume (preload).     

Laboratory and field trials at Ifakara (Kilombero District, Tanzania) on the plant molluscicide Swartzia madagascariensis

The molluscicidal activity of crushed seed pods of Swartzia madagascariensis was assessed by laboratory and field trials. Mature dry seed pods were ground and extracted in tap water for 24 h. Water extracts exerted a significant molluscicidal activity against Bulinus globosus up to dilutions of 100 mg of ground pods per litre. The chromatographically isolated saponin (1) responsible for the molluscicidal activity showed a toxicity of LC 100 at 3 mg/l after exposure of B. globosus and Biomphalaria glabrata for 24 h. Saponin (1) could be identified by FAB-MS and 13C-NMR-spectroscopy as oleanolic acid-3-O-beta-D-glucuronopyranosyl (1----3)-alpha-L-rhamnopyranoside. Two field trials with S. madagascariensis pod extracts in ponds (60 and 160 m3) harbouring dense populations of B. globosus compared well with the laboratory findings and showed the efficiency of the molluscicide in a natural habitat. A single application of the plant molluscicide significantly reduced the populations of B. globusus. The toxicity of S. madagascariensis pod extracts to non-target organisms remains an obstacle for its use in certain situations where schistosomiasis control is envisaged and where S. madagascariensis is found. However, S. madagascariensis is a valid candidate molluscicide which may be applied in selected epidemiological settings as part of integrated schistosomiasis control measures.     

PSA bounce after <Superscript>125</Superscript>I-brachytherapy for prostate cancer as a favorable prognosticator

Background

Permanent low-dose-rate brachytherapy (BT) with iodine 125 is an established curative treatment for localized prostate cancer. After treatment, prostate-specific antigen (PSA) kinetics may show a transient rise (PSA bounce). Our aim was to investigate the association of PSA bounce with biochemical control.

Patients and methods

Patients treated with BT in Switzerland were registered in a prospective database. Only patients with a follow-up of at least 2 years were included in our analysis. Clinical follow-up and PSA measurements were assessed after 1.5, 3, 6, and 12 months, and annually thereafter. If PSA increased, additional follow-up visits were scheduled. Cases of PSA bounce were defined as a rise of at least 0.2 ng/ml above the initial PSA nadir with a subsequent decline to or below the initial nadir without treatment. Biochemical failure was defined as a rise to nadir +?2 ng/ml.

Results

Between March 2001 and November 2010, 713 patients with prostate cancer undergoing BT with at least 2 years of follow-up were registered. Median follow-up time was 41 months. Biochemical failure occurred in 28 patients (3.9?%). PSA bounce occurred in 173 (24.3?%) patients; only three (1.7?%) patients with PSA bounce developed biochemical failure, in contrast to 25 (4.6?%) patients without previous bounce (p?<?0.05). The median time to bounce was 12 months, the median time to biochemical failure was 30 months. The median bounce increase was 0.78 ng/ml. Twenty-eight patients with bounce (16.5?%) had a transient PSA rise of +?2 ng/ml above the nadir.

Conclusion

In most cases, an early increase in PSA after BT indicates PSA bounce and is associated with a lower risk of biochemical failure.

     

Epidemiology, characteristics, and outcome of infective endocarditis in Italy: the Italian Study on Endocarditis

Background

The characteristics of patients with infective endocarditis (IE) vary significantly by region of the world. The aim of this study was to evaluate the contemporary epidemiology, characteristics, and outcome of IE in a large, nationwide cohort of Italian patients.

Methods

We conducted a prospective, observational study at 24 medical centers in Italy, including all the consecutive patients with a definite or possible diagnosis of IE (modified Duke criteria) admitted from January 2004 through December 2009. A number of clinical variables were collected through an electronic case report form and analyzed to comprehensively delineate the features of IE. We report the data on patients with definite IE.

Results

A total of 1,082 patients with definite IE were included. Of these, 753 (69.6?%) patients had infection on a native valve, 277 (25.6?%) on a prosthetic valve, and 52 (4.8?%) on an implantable electronic device. Overall, community-acquired (69.2?%) was more common than nosocomial (6.2?%) or non-nosocomial (24.6?%) health care-associated IE. Staphylococcus aureus was the most common pathogen (22.0?%). In-hospital mortality was 15.1?%. From the multivariate analysis, congestive heart failure (CHF), stroke, prosthetic valve infection, S. aureus, and health care-associated acquisition were independently associated with increased in-hospital mortality, while surgery was associated with decreased mortality.

Conclusions

The current mortality of IE remains high, and is mainly due to its complications, such as CHF and stroke.     

Comparison of the peripheral blood micronucleus test using flow cytometry in rat and mouse exposed to aneugens after single-dose applications

Detection of clastogenic compounds in the peripheral blood micronucleus test (MNT) in rats is a well-established methodology. However, the results obtained on the induction of micronuclei by aneugens in rat peripheral blood are controversial. Our aim was a comparative evaluation of the peripheral blood flow cytometry MNT in Wistar Han rat and CD1 mouse exposed to three aneugens (vinblastine, vincristine and colchicine) after single-dose applications. In addition, the same compounds were tested in the rat bone marrow MNT. The treatment with vinblastine (0.25, 0.5, 1, mg/kg), vincristine (0.025, 0.05, 0.1 mg/kg) or colchicine (0.7, 1, 1.3 mg/kg) induced no statistically significant increase in MN-PCEs (micronucleated polychromatic erythrocytes or reticulocytes) in rat peripheral blood. In rat bone marrow, a clear statistically significant increase in MN-PCE was found with vincristine and vinblastine. However, colchicine showed a clear increase in MN-PCE frequency without reaching statistically significant level only at 1 mg/kg. The positive effect in the bone marrow MNT shows that the target organ was exposed to the appropriate concentration levels of the respective aneugens. In mouse, the peripheral blood flow cytometry analysis after the treatment with vinblastine, vincristine and colchicine showed clear statistically significant increase in MN-PCE with all three compounds. The experiments with splenectomized rats treated with vincristine and colchicine were performed and statistically significant increases in MN-PCE were found with 0.05, 0.1, 0.15 mg/kg of vincristine and 0.7 and 1 mg/kg of colchicine. Our results demonstrate that micronucleated cells induced by aneugens are removed from rat peripheral blood by the spleen due to the large size of micronuclei. Based on our data, it is concluded that the flow cytometry peripheral blood MNT after single-dose applications is an appropriate test system for evaluating the genotoxic effects of aneugens in mice. However, in rats peripheral blood MNT aneugen detection might require multiple-dose applications to overwhelm the spleen effect.     

Proteolytic inactivation of alpha 1-proteinase inhibitor in infected bronchial secretions from patients with cystic fibrosis

The chronic, progressively destructive bronchitis of patients with cystic fibrosis (CF) is characterized by an important imbalance between tissue destroying granulocyte proteases such as granulocyte elastase (GE) and its physiological inhibitors in bronchial secretions. Recent in vitro studies suggest, that proteases derived from bacteria or endogenous proteases may contribute to inactivation of physiological inhibitors of GE. Since only trypsin-unreactive alpha 1-proteinase inhibitor (alpha 1-PI) was detected in CF bronchial secretions, we attempted to identify the mechanism of inactivation of alpha 1-PI. We found a heat stable, serine protease-like enzymatic activity capable of degrading 125I-labelled alpha 1-PI extensively in 22 infected but not in one non-infected CF bronchial secretion. In infected secretions, only degraded alpha 1-PI, which did not migrate like oxidized alpha 1-PI in tandem-crossed immunoelectrophoresis, was detectable. We conclude, that free GE in excess as well as GE bound to bronchial mucosal inhibitor may partly account for the alpha 1-PI-cleaving activity, but that other yet unknown bacterial or host serine proteases also contribute to alpha 1-PI inactivation.