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A low HDL cholesterol level on day 1 of severe sepsis is significantly associated with an increase in mortality and adverse clinical outcomes. In cultured macrophages, HDL can attenuate LPS-induced TNF-alpha production only if added concomitantly with, but not after, LPS exposure.

The angiotensin-converting enzyme I/D polymorphism is a significant prognostic factor for the outcome of ARDS. Patients with the II genotype have a significantly better chance of survival. This study did not show an increased risk for ARDS in Chinese patients with the D allele.

Mortality remains high among patients with pulmonary tuberculosis requiring mechanical ventilation (TBMV). This study was carried out to establish the mortality rates of TBMV and to identify factors that contribute to in-hospital mortality.From January 1996-April 2001, there were 825 patients with active pulmonary tuberculosis at the National Taiwan University Hospital, Taipei, Taiwan. Of these, 41 suffered acute respiratory failure and required mechanical ventilation in the intensive care unit (ICU). Of these 41 patients, 38 were followed up for 180 days. In-hospital deaths were documented in the medical records and all possible parameters contributing to mortality were collected.Of the 41 patients, 27 died in the hospital and 14 were discharged alive (in-hospital mortality rate 65.9%), with (mean¡SD) 40.7¡35.4 admission days before death. Of the 27 that died, 25 died during ICU admission and two died after being transferred to the ward. The mortality rate for the 180-day monitoring period was 79%. Factors contributing to in-hospital mortality included consolidations on chest radiographs and multiple organ failure.The mortality rate in the patients with pulmonary tuberculosis requiring mechanical ventilation is very high, with two factors affecting in-hospital mortality. These factors were multiple organ failure and consolidation on chest radiographs. In 2000, an estimated 8 million people were infected and 2 million people died of tuberculosis (TB) worldwide [1][2][3]. Despite advances in chemotherapy, cases of pulmonary TB and TB-related critical illness increased dramatically over the last few decades. In-hospital mortality rate remains high at y60%, for patients with active pulmonary TB and respiratory failure [4][5][6][7][8][9][10]. This is twice as high as the mortality rate of patients with pneumonia requiring mechanical ventilation [4,11,12].Delays in the diagnosis and treatment of pulmonary TB have been recognised as the main causes of death [2,4,8,[13][14][15][16]. Several studies have sought to reduce these delays by identifying factors that lead to a high index of suspicion [4,8,[13][14][15][17][18][19][20]. The reasons for delays in diagnosis include the failure to perform appropriate diagnostic investigation and the misinterpretation of radiological or clinical manifestations as malignancy, pneumonia or other conditions [4,8,[13][14][15][17][18][19][20][21][22].Reports of active pulmonary TB with acute respiratory failure are not scarce, but few focus on mechanically ventilated patients. Such patients have a higher mortality rate than patients who do not need mechanical ventilation [4-6, 8, 10]. However, w50% of the patients included in these previous studies were positive for human immunodeficiency virus (HIV) infection. Hence, conclusions derived from these studies may not apply to HIV-negative patients.Therefore, the authors conducted a retrospective study with three objectives in relation to active pulmonary TB patients requiring support by mechanical ventilation (TBMV). These object...

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We retrospectively studied the bacteriology and clinical features of empyema thoracis and lung abscess caused by viridans streptococci in 72 patients seen from January 1984 to September 1996. A total of 76 strains of viridans streptococci were isolated, of which the most common isolates were Streptococcus constellatus (21 strains), S. intermedius (17), and S. sanguis (10). Species belonging to the S. milleri group accounted for the majority (68%) of isolates. In 38 (53%) patients these organisms were recognized as the sole pathogens. Of the 72 patients, 53 had empyema, 14 had lung abscesses, and five had both empyema and lung abscess. Forty-six (64%) patients had underlying diseases. Of these, malignancies were the most common (17 patients), followed by diabetes mellitus (12 patients) and central nervous system diseases (10 patients). Of the 48 patients who underwent chest-tube drainage, 27 (56%) received further treatments, including intrapleural streptokinase (18 cases), surgery (9), and both intrapleural streptokinase and surgery (3). Two (14%) of the patients with lung abscess alone underwent surgical treatment. Although all viridans streptococcal isolates were susceptible to penicillin, the patients in the study had a high mortality (21%). Univariate and multivariate analysis of data for patients with empyema alone (n = 53) showed a significantly increased risk of death in those with underlying malignancy (OR = 16.0, p = 0.023) and those with non-S. milleri-group isolates (OR = 3.72, p = 0.030). These data imply a strong clinical significance of viridans streptococci in the pathogenesis of empyema and lung abscess, as well as the need for species identification of viridans streptococci in patients with pleuropulmonary diseases.

Background: Injurious mechanical ventilation can cause a pro-inflammatory reaction in the lungs. Recent evidence suggests an association of the renin-angiotensin system (RAS) with lung inflammation. A study was undertaken to investigate the pathogenic role of the RAS in ventilator-induced lung injury (VILI) and to determine whether VILI can be attenuated by angiotensin converting enzyme (ACE) inhibition. Methods: Male Sprague-Dawley rats were mechanically ventilated for 4 h with low (7 ml/kg) or high (40 ml/kg) tidal volumes; non-ventilated rats were used as controls. Lung injury and inflammation were measured by the lung injury score, protein leakage, myeloperoxidase activity, pro-inflammatory cytokine levels and nuclear factor (NF)-kB activity. Expression of the RAS components was also assessed. Some rats were pretreated with the ACE inhibitor captopril (10 mg/kg) for 3 days or received a concomitant infusion with losartan or PD123319 (type 1 or type 2 angiotensin II receptor antagonist) during mechanical ventilation to assess possible protective effects on VILI. Results: In the high-volume group (n = 6) the lung injury score, bronchoalveolar lavage fluid protein concentration, pro-inflammatory cytokines and NF-kB activities were significantly increased compared with controls (n = 6). Lung tissue angiotensin II levels and mRNA levels of angiotensinogen and type 1 and type 2 angiotensin II receptors were also significantly increased in the high-volume group. Pretreatment with captopril or concomitant infusion with losartan or PD123319 in the high-volume group attenuated the lung injury and inflammation (n = 6 for each group). Conclusions: The RAS is involved in the pathogenesis of ventilator-induced lung injury. ACE inhibitor or angiotensin receptor antagonists can attenuate VILI in this rat model.