Sophia E. Schiza

Intrapleural urokinase in the treatment of complicated parapneumonic pleural effusions and empyema

Intrapleural urokinase has not been evaluated systemically in terms of efficacy, safety, and cost of treatment in a large series of patients with complicated (parapneumonic) pleural effusions (CPE) and pleural empyemas (PE). Furthermore, the optimal dose and duration of treatment is not known. Twenty consecutive patients with multiloculated parapneumonic effusions (13 with CPE and 7 with PE), in whom a single chest tube failed to drain the fluid, were studied prospectively. The age of the patients ranged 15-92 yrs (median 51 yrs). Urokinase was administered intrapleurally, in a low single daily dose of 50,000 U in 100 mL normal saline via the chest tube. Previous intrapleural instillation of 100 mL normal saline failed to promote drainage in all patients. Urokinase enhanced drainage in all patients. Clinical and radiological improvement was noted in all but one patient. The mean (SD) volume of fluid significantly increased in the first 24 h post-urokinase (p<0.001). The number of urokinase instillations ranged 3-7 (median 5). Radiological evaluation showed excellent improvement in 13 of the 20 (65%) patients. Urokinase was well-tolerated in all patients. The clinical course of patients was uneventful at a mean follow-up of 15 months (range 6-30 months) later. Mean total cost of treatment was

How common is sleep-disordered breathing in patients with idiopathic pulmonary fibrosis?

530 +/- 34.6. Our results show that intrapleural instillation of small doses of urokinase is a cost-effective and safe mode of treatment of complicated pleural effusions and pleural empyema and could be the fibrinolytic of choice.

Sleep patterns in patients with acute coronary syndromes

Background and aimThe frequency of obstructive sleep apnea–hypopnea syndrome (OSAHS) in patients with idiopathic pulmonary fibrosis (IPF) remains controversial. The aim of this study was to assess the frequency of OSAHS in newly diagnosed IPF patients and to identify possible correlations with body mass index and pulmonary function testing parameters.Materials and methodsThirty-four newly diagnosed IPF patients were included. All subjects underwent attended overnight PSG. None of the included subjects was under any of the currently available IPF treatments or nocturnal supplemental oxygen therapy.ResultsTotal apnea–hypopnea index (AHI) was <5, 5–15, and ≥15/h of sleep in 14 (41%), 15 (44%), and five patients (15%), respectively. REM AHI was statistically significant correlated with TLC [Total lung capacity] (p = 0.03, r = −0.38). Diffusing capacity of the lung for carbon monoxide was correlated with mean oxygen saturation during sleep (p = 0.02, r = 0.39).ConclusionsSleep-disordered breathing seems frequent, although remains usually under diagnosed in IPF patients. A decrease in TLC, reflecting the severity of pulmonary restriction, might predispose IPF patients in SDB, especially during the vulnerable REM sleep period.

Health-related quality of life in patients with obstructive sleep apnoea and chronic obstructive pulmonary disease (overlap syndrome).

BACKGROUND Little is known about sleep quality in patients with acute coronary syndromes (ACS) admitted to the coronary care unit (CCU). The aim of this study was to assess nocturnal sleep in these patients, away from the CCU environment, and to evaluate potential connections with the disease process. METHODS Twenty-two patients with first ever ACS, who were not on sedation or inotropes, underwent a full-night polysomnography (PSG) in our sleep disorders unit within 3 days of the ACS and follow-up PSGs 1 and 6 months later. RESULTS PSG parameters showed a progressive improvement over the study period. There was a statistically significant increase in total sleep time (TST), sleep efficiency, slow wave sleep (SWS), and rapid eye movement (REM) sleep, while arousal index, wake after sleep onset (WASO) and sleep latency decreased. Six months after the acute event, sleep architecture was within the normal range. CONCLUSIONS Patients with ACS have marked alterations in sleep macro- and micro-architecture, which have a negative influence on sleep quality. The changes tend to disappear over time, suggesting a relationship with the acute phase of the underlying disease.

Clinical presentation and management of empyema, lung abscess and pleural effusion.

The association of obstructive sleep apnoea (OSA) and chronic obstructive pulmonary disease (COPD) is not rare as COPD and OSA are both frequent diseases. The aim of this study was to determine the effect of OSA on quality of life (QOL) in patients with overlap syndrome (OVS). Thirty subjects with OVS and 15 control subjects participated. The St Georges Respiratory Questionnaire (SGRQ) was used to determine QOL. The control group included subjects with COPD and no evidence of OSA by overnight polysomnography. All subjects were habitual snorers with normal Epworth Sleepiness Scale scores. Significant differences were found between the groups for the total score and each of the three components of the SGRQ suggesting worse QOL in OVS patients (symptoms 54.9 ± 18.9 vs. 38.2 ± 19.3, p = 0.008; activity 59.2 ± 16.2 vs. 44.4 ± 11.3, p = 0.003; impacts 35.2 ± 23 vs. 20.8 ± 8.7, p = 0.025 and total 45.7 ± 17.7 vs. 30.9 ± 8.7, p = 0.004 in OVS patients and control group, respectively). Obstructive sleep apnoea has a major impact on QOL in patients with OVS and can exist in COPD patients with habitual snoring even in the absence of daytime sleepiness. Further studies are needed to determine the impact of OSA treatment on QOL and morbidity in this population.

Sleep Disordered Breathing in Patients with Acute Coronary Syndromes

Purpose of review Pleural effusions, lung abscess and empyema remain a commonly encountered clinical problem and a significant source of morbidity. The aim of this review is to summarize recent developments with emphasis on controlled trials. Recent findings There is wide variation in the management of infectious pleural effusions, partly because of the relative lack of randomized controlled trials. The recent MRC/BTS UK controlled trial of interapleural streptokinase for pleural infection assessed the efficacy of intrapleural streptokinase compared with placebo in complicated parapneumonic effusions. The study showed no difference in the primary end point, mortality, or in the need for surgery or length of the hospital stay among patients with pleural infection. The first large report published for over a decade has suggested that the bacteriological characteristics of lung abscess have changed. Summary The major recent development in the management of pleural infections is the finding that we should dampen the ardor for the routine use of fibrinolytic agents in all patients with pleural infections. We strongly recommend the necessity for additional, well-designed trials to help determine optimal care for these seriously ill patients.

Deregulation of apoptosis mediators' p53 and bcl2 in lung tissue of COPD patients

STUDY OBJECTIVES Although the prevalence of obstructive sleep apnea/hypopnea syndrome (OSAHS) is high in patients with acute coronary syndromes (ACS), there is little knowledge about the persistence of OSAHS in ACS patients after the acute event. We aimed to assess the prevalence and time course of OSAHS in patients with ACS during and after the acute cardiac event. METHODS Fifty-two patients with first-ever ACS, underwent attended overnight polysomnography (PSG) in our sleep center on the third day after the acute event. In patients with an apnea hypopnea index (AHI) > 10/h, we performed a follow up PSG 1 and 6 months later. RESULTS Twenty-eight patients (54%) had an AHI > 10/h. There was a significant decrease in AHI 1 month after the acute event (13.9 vs. 19.7, p = 0.001), confirming the diagnosis of OSAHS in 22 of 28 patients (79%). At 6-month follow-up, the AHI had decreased further (7.5 vs. 19.7, p < 0.05), and at that time only 6 of the 28 patients (21%) were diagnosed as having OSAHS. Twelve of the 16 current smokers stopped smoking after the acute event. CONCLUSIONS We have demonstrated a high prevalence of OSAHS in ACS patients, which did not persist 6 months later, indicating that, to some degree, OSAHS may be transient and related with the acute phase of the underlying disease or the reduction in the deleterious smoking habit.

C-reactive protein evolution in obstructive sleep apnoea patients under CPAP therapy

Abnormal apoptotic events in chronic obstructive pulmonary disease (COPD) subvert cellular homeostasis and may play a primary role in its pathogenesis. However, studies in human subjects are limited.p53 and bcl2 protein expression was measured by western blot on lung tissue specimens from 43 subjects (23 COPD smokers and 20 non-COPD smokers), using beta-actin as internal control. Additionally, p53 and bcl2 expression patterns were evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same individuals.Western blot analysis showed statistically significant increased p53 protein levels in COPD smokers in comparison with non-COPD smokers (p = 0.038), while bcl2 protein levels were not statistically different between the two groups. Lung immunohistochemistry showed increased ratio of positive p53-stained type II pneumocytes/total type II pneumocytes in COPD smokers compared to non-COPD smokers (p = 0.01), whereas the p53 staining ratio in alveolar macrophages and in lymphocyte-like cells did not differ statistically between the two groups. On the other hand, bcl2 expression did not differ between the two groups in all three cell types.The increased expression of pro-apoptotic p53 in type II pneumocytes of COPD patients not counterbalanced by the anti-apoptotic bcl2 could reflect increased apoptosis in the alveolar epithelium of COPD patients. Our results confirm previous experiments and support the hypothesis of a disturbance in the balance between the pro- and anti-apoptotic mediators in COPD.

Altered Surfactant Protein-A Expression in Type II Pneumocytes in COPD

Eur J Clin Invest 2010; 40 (11): 968–975

Intensive versus standard follow-up to improve continuous positive airway pressure compliance

BACKGROUND Pulmonary surfactant protein A (SP-A) is a lectin, with multiple functions that contribute to innate host defense and the regulation of the inflammatory process in the lung. In normal conditions, SP-A seems to protect against the effects of smoking. However, studies in smokers with or without COPD are limited. METHODS Western blots on lung tissue specimens from 60 male subjects (32 patients with COPD, 18 smokers without COPD, and 10 control nonsmokers) for SP-A and the housekeeping protein actin were carried out. Additionally, the SP-A expression pattern was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same subjects. RESULTS Western blots revealed significantly higher SP-A levels in control nonsmokers (4.8 +/- 0.05) when compared with patients with COPD (0.6 +/- 0.7) and smokers without COPD (2.4 +/- 0.9), (P < .05). However, differences that were not statistically significant were observed in SP-A levels among the patients with COPD and the smokers without COPD (P = .12). The immunohistochemical examinations showed an increase in the overall number of type II pneumocytes per high-power field in patients with COPD, but a decreased ratio of SP-A positive type II pneumocytes to total type II pneumocytes, compared with smokers without COPD (P = .001). This ratio was also correlated with FEV(1) (percent predicted [% pred]), (r = 0.490, P = .001). The overall number of alveolar macrophages per high-power field was significantly higher in patients with COPD compared with smokers without COPD (P = .001). The ratio of SP-A positive alveolar macrophages was increased in patients with COPD when compared with smokers without COPD (P = .002), while this was correlated with airway obstruction (FEV(1), % pred) (r = 0.281, P = .04). CONCLUSIONS Our results indicate that altered SP-A expression could be another link to COPD pathogenesis and highlights the need for further studies on surfactant markers in COPD.