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Background: Ventilation limitation has a significant adverse effects on cardiovascular function and tissue oxygenation during exercise in patients with chronic obstructive pulmonary disease (COPD). High flow nasal cannula (HFNC) improve ventilation by washing out the anatomical dead space and providing oxygen at constant concentration. This study aimed to examine the effects of HFNC on the exercise performance and hemodynamic status in COPD patients. Methods: Fifteen patients with COPD performed two constant load exercise tests (CLET) at the 70% of maximum workload achieved at a previous incremental exercise test on arm ergometer. The CLET were performed with HFNC and with nasal cannula (NC) in random order. The hemodynamics parameters of subjects during exercises were measured by a bioelectrical impedance device. The tissue oxygenation status (oxygenated hemoglobin, deoxygenated hemoglobin (hHb), total hemoglobin) was measured by a near infrared spectrophotometer. Results: The exercise duration was longer for HFNC test than NC test (962.9 ± 281.7 s, vs 823.9 ± 184.9 s, p < 0.05). At the end of CLET, the PetCO2 was lower for HFNC than NC (29.3 ± 5.1 mmHg vs 32.1 ± 5.5 mmHg, p 0.05), stroke volume (NC:73.5 ± 21.0 vs HFNC 67.5 ± 16.3 ml, p > 0.05). The changes of hHb in muscle tissues was significantly lower in HFNC test than that in NC test (p

Purpose: Recent studies reported that driving pressure has been associated with increased mortality in acute respiratory distress syndrome (ARDS) patients. We aimed to explore the association between 28-day mortality and driving pressure in patients with severe pneumonia without ARDS. Methods: In total, 207 non-ARDS patients with severe pneumonia were enrolled. Serial driving pressures were recorded daily for either 21 days or until ventilator support was no longer required. The relationships between all variables and 28-day mortality were analyzed using binary logistic regression analyses. Results: Non-survivors (56 patients) demonstrated high incidences of shock (55.4% vs. 24.5%, p

Acute respiratory distress syndrome (ARDS) is a heterogeneous syndrome caused by direct (local damage to lung parenchyma) or indirect lung injury (insults from extrapulmonary sites with acute systemic inflammatory response), the clinical and biological complexity can have a profound effect on clinical outcomes. We performed a retrospective analysis of 152 severe ARDS patients receiving extracorporeal membrane oxygenation (ECMO). Our objective was to assess the differences in clinical characteristics and outcomes of direct and indirect ARDS patients receiving ECMO. Overall hospital mortality was 53.3%. A total of 118 patients were assigned to the direct ARDS group, and 34 patients were assigned to the indirect ARDS group. The 28-, 60-, and 90-day hospital mortality rates were significantly higher among indirect ARDS patients (all p &lt, 0.05). Cox regression models demonstrated that among direct ARDS patients, diabetes mellitus, immunocompromised status, ARDS duration before ECMO, and SOFA score during the first 3 days of ECMO were independently associated with mortality. In indirect ARDS patients, SOFA score and dynamic compliance during the first 3 days of ECMO were independently associated with mortality. Our findings revealed that among patients receiving ECMO, direct and indirect subphenotypes of ARDS have distinct clinical outcomes and different predictors for mortality.

The high mortality rate of patients with severe acute respiratory distress syndrome (ARDS) warrants aggressive clinical intervention. Extracorporeal membrane oxygenation (ECMO) is a salvage therapy for life-threatening hypoxemia. Randomized controlled trials of ECMO for severe ARDS comprise a number of ethical and methodological issues. Therefore, indications and optimal timing for implementation of ECMO, and predictive risk factors for outcomes have not been adequately investigated. We performed propensity score matching to match ECMO-supported and non-ECMO-supported patients at 48 h after ARDS onset for comparisons based on clinical outcomes and hospital mortality. A total of 280 severe ARDS patients were included, and propensity score matching of 87 matched pairs revealed that the 90-d hospital mortality rate was 56.3% in the ECMO group and 74.7% in the non-ECMO group (p = 0.028). Subgroup analysis revealed that greater severity of ARDS, higher airway pressure, or a higher Sequential Organ Failure Assessment score tended to benefit from ECMO treatment in terms of survival. Multivariate logistic regression revealed that hospital mortality was significantly lower among patients who received ECMO than among those who did not. Our findings suggested that early initiation of ECMO (within 48 h) may increase the likelihood of survival for patients with severe ARDS.

Background: Recent studies reported that mechanical power (MP) has been associated with increased mortality in patients with acute respiratory distress syndrome (ARDS). We aimed to investigate the association between 28-day mortality and MP in patients with severe pneumonia. Methods: In total, 313 patients with severe pneumonia were enrolled. Serial MP was recorded daily for either 21 days or until ventilator support was no longer required. The associations between all variables and 28-day mortality were analyzed using binary logistic regression analyses. Results: The ARDS group (106 patients) demonstrated lower age, higher Acute Physiology and Chronic Health Evaluation II score, lower history of diabetes mellitus, high incidences of shock and jaundice, higher MP and driving pressure on Day 1, and higher death within 28 days than the non-ARDS group. Regression analysis revealed that MP was an independent factor associated with 28-day mortality (odds ratio, 1.041; 95% confidence interval, 1.013-1.071). MP persisted high in non-survivors and low in survivors among the ARDS group, the non-ARDS group and all patients.Conclusions: MP was associated with the 28-day mortality in ventilated patients with severe pneumonia both in the ARDS and non-ARDS groups. MP had better predicted value for 28-day mortality than driving pressure.

Obstructive sleep apnea (OSA) is a disease with great cardiovascular risk. Interleukin-8 (IL-8), an important chemokine for monocyte chemotactic migration, was studied under intermittent hypoxia condition and in OSA patients. Monocytic THP-1 cells were used to investigate the effect of intermittent hypoxia on the regulation of IL-8 by an intermittent hypoxic culture system. The secreted protein and mRNA levels were studied by means of enzyme-linked immunosorbent assay and RT/real-time PCR. The chemotactic migration of monocytes toward a conditioned medium containing IL-8 was performed by means of the transwell filter migration assay. Peripheral venous blood was collected from 31 adult OSA patients and RNA was extracted from the monocytes for the analysis of IL-8 expression. The result revealed that intermittent hypoxia enhanced the monocytic THP-1 cells to actively express IL-8 at both the secreted protein and mRNA levels, which subsequently increased the migration ability of monocytes toward IL-8. The ERK, PI3K and PKC pathways were demonstrated to contribute to the activation of IL-8 expression by intermittent hypoxia. In addition, increased monocytic IL-8 expression was found in OSA patients, with disease severity dependence and diurnal changes. This study concluded the monocytic IL-8 gene expression can be activated by intermittent hypoxia and increased in OSA patients.

Recent studies have reported that mechanical power (MP) is associated with increased mortality in patients with acute respiratory distress syndrome (ARDS). We aimed to investigate the association between 28-day mortality and MP in patients with severe pneumonia. In total, the data of 313 patients with severe pneumonia were used for analysis. Serial MP was calculated daily for either 21 days or until ventilator support was no longer required. Compared with the non-ARDS group, the ARDS group (106 patients) demonstrated lower age, a higher Acute Physiology and Chronic Health Evaluation II score, lower history of diabetes mellitus, elevated incidences of shock and jaundice, higher MP and driving pressure on Day 1, and more deaths within 28 days. Regression analysis revealed that MP was an independent factor associated with 28-day mortality (odds ratio, 1.048, 95% confidence interval, 1.020–1.077). MP was persistently high in non-survivors and low in survivors among the ARDS group, the non-ARDS group, and all patients. These findings indicate that MP is associated with the 28-day mortality in ventilated patients with severe pneumonia, both in the ARDS and non-ARDS groups. MP had a better predicted value for the 28-day mortality than the driving pressure.

Background: Patients with severe sepsis frequently require intensive care unit (ICU) admission and different ICU care models may influence their outcomes. The mortality of severe septic patients between physician's high and low care volume remains unclear. Methods: We analyzed the data from a three-year prospective observation study, which was performed in an adult medical ICU of Chung Gung Memorial Hospital, Keelung. The data included initial bundle therapies based on the Surviving Sepsis Campaign (SSC) guidelines for patients with severe sepsis. Results: Clinical data of total 484 patients with severe sepsis were recorded. Cox regression model showed that physician's care volume was an independent factor for lowering mortality in ICU patients with severe sepsis (hazard ratio 0.708; 95% confidence interval 0.514–0.974; p = 0.034). Patients treated by high care volume physician had four out of nine bundle therapies that were significantly higher in percentage following the SSC guidelines. These four therapies were renal replacement therapy, administration of low-dose steroids for septic shock, prophylaxis of gastro-intestinal bleeding, and control of hyperglycemia. Conclusion: High care volume physician may decrease mortality in ICU patients with severe sepsis through fitting bundle therapies for sepsis.

Background Predicting acute renal failure in patients with severe sepsis is important, because patients may need renal replacement therapy (RRT). Neutrophil gelatinase-associated lipocalin (NGAL) has been evaluated for its ability to detect and predict acute kidney injury (AKI) in critically ill patients. This study aimed to assess the predictive value of plasma NGAL for acute renal failure in adult severely septic patients. Methods Thirty healthy adults and 85 adult patients admitted to the medical intensive care unit (ICU) were enrolled. Serum creatinine, plasma NGAL, and interleukin (IL)-6, IL-10, and IL-17 levels were evaluated. AKI was classified as Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease (RIFLE). Results RIFLE-Failure (RIFLE-F) developed in 30 of 76 (39.5%) patients with severe sepsis without chronic kidney disease within 7 days after ICU admission. Serum creatinine, plasma NGAL, IL-6, and IL-10 could predict RIFLE-F within 7 days after ICU admission. The discriminatory power of plasma NGAL was not significant for predicting hospital mortality. The area under the receiver operating characteristic curve of plasma NGAL was not higher than that of serum creatinine in predicting RIFLE-F within 7 days. Conclusion Plasma NGAL is a useful tool for predicting acute renal failure in adult patients with severe sepsis. Serum creatinine has a similar ability to detect RIFLE-F occurrence.

Acute respiratory distress syndrome (ARDS) has a high mortality rate in intensive care units (ICU). The elderly patients remain to be increased of ICU patients. The aim is to investigate the survival predictors of elderly patients with ARDS. We reported a prospective observational cohort research, including the patients with ARDS between October 2012 and May 2015. Demographic, comorbidities, severity, lung mechanics, laboratory data and survival outcomes were analyzed. A total of 463 patients with ARDS were ≥65 years old were enrolled and analyzed. Multivariate logistic regression analysis identified Charlson comorbidity index (CCI) [odds ratio (OR) 1.111, 95% CI 1.010–1.222, p = 0.031], Sequential Organ Failure Assessment (SOFA) score (OR 1.127, 95% CI 1.054–1.206, p

Background: Disease severity may change in the first week after acute respiratory distress syndrome (ARDS) onset. The aim of this study was to evaluate whether the reclassification of disease severity after 48 h (i.e. day 3) of ARDS onset could help in predicting mortality and determine factors associated with ARDS persistence and mortality. Methods: We performed a secondary analysis of a 3-year prospective, observational cohort study of ARDS in a tertiary care referral center. Disease severity was reclassified after 48 h of enrollment, and cases that still fulfilled the Berlin criteria were regarded as nonresolving ARDS. Results: A total of 1034 ARDS patients were analyzed. Overall hospital mortality was 57.7% (56.7%, 57.5%, and 58.6% for patients with initial mild, moderate, and severe ARDS, respectively, p = 0.189). On day 3 reclassification, the hospital mortality rates were as follows: resolved (42.1%), mild (47.9%), moderate (62.4%), and severe ARDS (76.1%) ( p 2/FiO2, or higher positive end-expiratory pressure on day 1 were significantly associated with nonresolving ARDS on day 3. A Cox regression model with ARDS severity as a time-dependent covariate and competing risk analysis demonstrated that ARDS severity was independently associated with hospital mortality, and nonresolving ARDS had significantly increased hazard of death than resolved ARDS ( p Conclusions: Reclassification of disease severity after 48 h of ARDS onset could help to divide patients into subgroups with greater separation in terms of mortality. The reviews of this paper are available via the supplemental material section.

Objectives: Echocardiography-guided pericardiocentesis has been the leading procedure for diagnosis and therapy of pericardial effusion. We aimed to identify risk factors for recurrence, complications, and mortality in pericardial effusion patients treated with pericardiocentesis. Methods: We identified and collected data from 8,101 patients receiving pericardiocentesis between 1997 and 2010 from the Taiwan National Health Insurance Research Database. A multivariate regression model was used to investigate risk factors for recurrence, complications, and death. Results: There were 8,565 admissions among 8,101 patients. The most common underlying condition was malignancy (41%), especially lung cancer (23%), tuberculosis (9.0%), and acute pericarditis (8.2%). Surgical drainage was required in 12.7% of cases. Recurrence was more likely in patients with malignancy (HR 2.20, p < 0.001), but complications were less likely (OR 0.52, p = 0.003). In-hospital death numbers and complication risks (OR 2.38, p < 0.001; OR 1.27, p = 0.01) were greater in the catheter-related cardiac procedure group than in the other groups. Conclusions: Malignant neoplasms and catheter-based cardiac procedures have become major risk factors for adverse events in patients receiving pericardiocentesis in Taiwan. Malignancy leads to an increase in recurrence and in-hospital mortality but is associated with a lower rate of acute complications. Cardiac catheterization procedures and surgery increase both complications and in-hospital mortality. i 2014 S. Karger AG, Basel

Background The survival predictors and optimal mechanical ventilator settings in patients with severe acute respiratory distress syndrome (ARDS) undergoing extracorporeal membrane oxygenation (ECMO) are uncertain. This study was designed to investigate the influences of clinical variables and mechanical ventilation settings on the outcomes for severe ARDS patients receiving ECMO. Methods We reviewed severe ARDS patients who received ECMO due to refractory hypoxemia from May 2006 to October 2015. Serial mechanical ventilator settings before and after ECMO and factors associated with survival were analyzed. Results A total of 158 severe ARDS patients received ECMO were finally analyzed. Overall intensive care unit (ICU) mortality was 55.1%. After ECMO initiation, tidal volume, peak inspiratory pressure and dynamic driving pressure were decreased, while positive end-expiratory pressure levels were relative maintained. After ECMO initiation, nonsurvivors had significantly higher dynamic driving pressure until day 7 than survivors. Cox proportional hazards regression model revealed that immunocompromised [hazard ratio 1.957; 95% confidence interval (CI) 1.216–3.147; p = 0.006], Acute Physiology and Chronic Health Evaluation (APACHE) II score (hazard ratio 1.039; 95% CI 1.005–1.073; p = 0.023), ARDS duration before ECMO (hazard ratio 1.002; 95% CI 1.000–1.003; p = 0.029) and mean dynamic driving pressure from day 1 to 3 on ECMO (hazard ratio 1.070; 95% CI 1.026–1.116; p = 0.002) were independently associated with ICU mortality. Conclusions For severe ARDS patients receiving ECMO, immunocompromised status, APACHE II score and the duration of ARDS before ECMO initiation were significantly associated with ICU survival. Higher dynamic driving pressure during first 3 days of ECMO support was also independently associated with increased ICU mortality.

Background.Sepsis-induced immunosuppression may result in higher mortality rates in patients.Methods. We examined the relationship of cytokine responses from stimulated peripheral blood mononuclear cells (PBMCs) and monocyte human leukocyte antigen-DR (HLA-DR) expression (days 1 and 7) with low-dose steroid therapy in 29 septic patients. Patients were treated according to the guidelines. Thirty healthy controls were enrolled for validation.Results. Eighteen patients were prescribed low-dose steroids and 11 were not. Interleukin- (IL-) 12 responses in patients without low-dose steroid therapy on days 1 and 7 were higher than those with low-dose steroid therapy. Compared to day 1, IL-12 responses significantly increased on day 7 in patients without low-dose steroid therapy. After regression analysis, the change in the IL-12 response from day 7 to day 1 was found to be independently associated with the low-dose steroid therapy. There was no difference in monocyte HLA-DR expression between patients treated with and without low-dose steroid on day 1 or 7. No change in monocyte HLA-DR expression from day 7 to day 1 was observed in patients with or without low-dose steroid therapy.Conclusion. Decreased IL-12 response was associated with the low-dose steroid therapy in PBMCs of septic patients.

Sugar control is important in patients with sepsis. Interleukin (IL)-12 induces the polarization of CD4+ T cells to the T helper 1 (Th1) phenotype. Regulatory T (Treg) cells are important in immunity and disease. The aim of this work is to determine whether hyperglycemia or insulin alters IL-12 response in peripheral mononuclear cells (PBMCs). Methods The PBMCs from 15 type 2 diabetes mellitus (DM) patients and 13 healthy controls were used for cell analysis and culture with or without treatment by glucose and insulin or stimulation by lipopolysaccharide (LPS) for 1, 2, and 3 days. Results The IL-12 level in the supernatant of LPS-stimulated PBMCs in the DM patients was significantly higher than that of healthy controls from day 1 to day 3. Kinetic IL-12 responses of LPS-stimulated PBMCs in the DM patients from day 1 to day 3 were significantly higher than that in healthy controls. The LPS-stimulated PBMCs under glucose treatment produced more IL-12 in DM patients but this did not happen in healthy controls. In DM patients, insulin could suppress IL-12 production from stimulated PBMCs but not with additional glucose treatment. Conclusion The PBMCs of LPS-treated DM patients produced more IL-12 than that of LPS-treated healthy controls did. Hyperglycemia influenced IL-12 response from PBMCs in DM patients to some degree during infection.

The serial or dynamic changes of cytokine levels in severely septic patients, between shock and no shock, survivors and non-survivors are still unclear.Seventy-six patients with severe sepsis were enrolled to our study. Plasma levels of interferon-gamma, interleukin (IL)-6, IL-10, IL-12 and transforming growth factor-beta1 from day 1 to day 7 were determined.IL-6 level in non-survivors was higher than that in survivors on day 1. IL-10 level in non-survivors was higher than that in survivors on day 1, 2, and 3. IL-6 level in shock patients was higher than that in non-shock patients on day 1, 2, 6 and 7. IL-10 level in shock patients was higher than that in non-shock patients from day 1 to day 7. Plasma time-course curves of IL-6 and IL-10 were different between survivors and non-survivors. Plasma time-course curve of IL-6 was different between patients with shock and without shock. Regression analysis found that IL-6 was correlated with IL-10 and shock. IL-10 was correlated with IL-6 and mortality.IL-6 and IL-10 were the key cytokines in the pathogenesis of severe sepsis. IL-6 was comparatively more associated with septic shock and IL-10 was comparatively more associated with mortality.

Background/Purpose Pro- and anti-inflammatory cytokines, such as interferon (IFN)-γ, interleukin (IL)-6, IL-10, IL-12 and transforming growth factor (TGF)-β1, have been shown to be mediators associated with severe community-acquired pneumonia (CAP). It is unknown whether plasma TGF-β1 level can help physicians to judge disease severity. In this study, we investigated the value of predicting mortality in patients with severe CAP by the plasma levels of IFN-γ, IL-6, IL-10, IL-12 and TGF-β1 on admission day. Methods Patients who were admitted to the emergency department and soon transferred to the ICU because of severe CAP were enrolled in this study. Plasma levels of IFN-γ, IL-6, IL-10, IL-12 and TGF-β1 on the day of admission were determined in 49 survivors and 14 non-survivors within 28 days by ELISA. Clinical characteristics were also recorded. Results Plasma IL-6, IL-10 and TGF-β1 levels on admission were significantly different between survivors and non-survivors. Conversely, there was no significant difference in plasma IFN-γ and IL-12 levels between the survivors and non-survivors. Furthermore, the plasma TGF-β1 level was the only independent factor associated with mortality. The value of predicting mortality in patients with severe CAP was similar for IL-6, IL-10 and TGF-β1. Plasma IL-6 level was not related to the Acute Physiology and Chronic Health Evaluation (APACHE) II score. However, plasma IL-10 and TGF-β1 levels were correlated with APACHE II score. Conclusion A severity scoring system, including TGF-β1 level on admission, may be considered as a useful parameter to predict outcomes of patients with severe CAP.

Background.The risk factors forStaphylococcus aureus(S. aureus) pneumonia are not fully identified. The aim of this work was to find out the clinical characteristics associated withS. aureusinfection in patients with healthcare-associated pneumonia (HCAP) and hospital-acquired pneumonia (HAP), which may be applicable for more appropriate selection of empiric antibiotic therapy.Methods.From July 2007 to June 2010, patients who were admitted to the intensive care unit with severe HCAP/HAP and severe sepsis were enrolled in this study. Lower respiratory tract sample was semiquantitatively cultured. Initial broad-spectrum antibiotics were chosen by Taiwan or American guidelines for pneumonia management. Standard bundle therapies were provided to all patients according to the guidelines of the Surviving Sepsis Campaign.Results.The most frequently isolated pathogens werePseudomonas aeruginosa,S. aureus,Acinetobacter baumannii,Klebsiella pneumoniae, andEscherichia coli. Patients with positive isolation ofS. aureusin culture had significantly higher history of liver cirrhosis and diabetes mellitus, with odds ratios of 3.098 and 1.899, respectively. TheS. aureuspneumonia was not correlated with history of chronic obstructive pulmonary disease, hypertension, and hemodialysis.Conclusion.Liver cirrhosis and diabetes mellitus may be risk factors forS. aureusinfection in patients with severe HCAP or HAP.

Macrophages aided by interferon-gamma (IFN-gamma) are vital to controlling Mycobacterium tuberculosis (M. tuberculosis) infection. Although numerous studies have compared IFN-gamma response between tubercular patients and healthy controls, no studies have investigated IFN-gamma response in patients with pulmonary tuberculosis and non-tubercular pneumonia. The aim of this work was to examine the difference in IFN-gamma response between patients with tuberculosis and non-tubercular pneumonia.IFN-gamma production was detected based on the difference in supernatants between non-stimulated and stimulated peripheral blood mononuclear cells by phytohemagglutinin in 83 tubercular patients and 47 patients with pneumonia. Presence of a cavity on chest radiography and co-morbidities of pneumoconiosis, bronchiectasis, liver cirrhosis, renal failure on hemodialysis, diabetes mellitus (DM) and lung cancer were recorded for analysis.Interferon-gamma response, DM and a cavity on chest radiography were independent factors for predicting active pulmonary tuberculosis. Interferon-gamma response was decreased in patients with pulmonary tuberculosis compared with that in patients with non-tubercular pneumonia. Notably, M. tuberculosis infection was the principal factor correlated with IFN-gamma response.The IFN-gamma response was principally affected by M. tuberculosis infection and not by other co-morbidities. Further study is required to identify the mechanism of decreased IFN-gamma production.

Background: Lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMCs) of type 2 diabetes patients produce more interleukin (IL)-12 under glucose treatment. The aim of this study was to determine whether increased IL-12 response in hyperglycemic LPS-stimulated PBMCs is due to increased gene expression or osmolarity. Methods: LPS-stimulated PBMCs of 13 type 2 diabetes patients and 8 healthy controls were used for culture in the presence or absence of glucose or mannitol for 24 h. The IL-12 gene expressions of PBMCs and IL-12 protein levels in supernatants were evaluated. Results: After 24 h, the stimulated PBMCs of diabetes patients expressed more IL-12 mRNA and produced more IL-12 protein following glucose treatment than those without glucose treatment and with mannitol treatment. Stimulated PBMCs of controls did not express more IL-12 mRNA and produce more IL-12 protein following glucose treatment than those without glucose treatment and with mannitol treatment. Conclusions: Glucose increases the IL-12 production in stimulated PBMCs of diabetes patients through increased IL-12 gene expression.

Objective and design T helper 17 (Th17) and regulatory T (Treg) lymphocytes might play important roles in patients with severe sepsis. The association of Th17 or Treg lymphocytes with survival is also unclear. Methods Eighty-seven patients with severe sepsis were enrolled from our intensive care units between August 2008 and July 2010. Leukocyte antigens and clinical data were determined on day 1 in all patients and on day 7 in first-year patients. Results The percentages in peripheral blood mononuclear cells (PBMCs) and circulatory counts of CD4+ and CD8+ lymphocytes in survivors were higher than those in non-survivors. Th1/CD4+ ratios and circulatory Th1 lymphocyte counts in survivors were higher than in non-survivors. Absolute counts of Th17 and Treg lymphocytes in survivors were higher than in non-survivors. The percentages of CD4+ and CD8+ in survivors’ PBMCs were increased after 6 days. Th17/CD4+ ratios and circulatory Th17 lymphocyte counts in survivors were increased after 6 days. Conclusions Higher Th1 differentiation and total CD4+ T lymphocyte counts were associated with higher survival. The association of circulatory Th17 and Treg lymphocytes with mortality in severe sepsis may be due to the change in total CD4+ T lymphocytes. In survivors, Th17 differentiation and counts were restored.

Intravenous hydrocortisone of 200-300 mg/day for 7 days is suggested for patients with septic shock who require vasopressors to maintain mean artery pressureor=65 mmHg, despite adequate fluid resuscitation. No study to date has compared the effects between physiologic doses of hydrocortisone and methylprednisolone in patients with septic shock.From July 2007 to June 2008, patients who were admitted to the intensive care unit at Chang Gung Memorial Hospital, Keelung, Taiwan, with low-dose steroid therapy due to septic shock were enrolled in this study. The typical steroid therapy included 7 days of intravenous hydrocortisone 50 mg every 6 hours. Methylprednisolone (20 mg every 12 hours) was replaced in these patients from January 2008 because no hydrocortisone could be prescribed.A total of 21 patients were prescribed hydrocortisone and 19 patients were prescribed methylprednisolone. The survival rates for patients receiving hydrocortisone were relatively higher compared with those receiving methylprednisolone, but the difference was not significant. There were no significant differences in the Kaplan-Meier curves for the time to reverse shock between patients who received hydrocortisone, or methylprednisolone. Further regression analysis showed no significant independent factors associated with the survival rates and the time to reverse shock among age, sex, Acute Physiology and Chronic Health Evaluation II (APACHE II) score, histories, and adverse events.Low-dose methylprednisolone and hydrocortisone might have a similar effect for the treatment of patients with septic shock.

Background and objective: It is unclear whether patients with liver cirrhosis and coal miners with pneumoconiosis are at increased risk of developing pulmonary tuberculosis (TB). Furthermore, little is known of the likelihood of pneumonia in patients with bronchiectasis, haemodialysis, diabetes mellitus or advanced lung cancer being due to TB. To answer these questions, patients with these clinical comorbidities were analysed. Methods: The study was retrospective and included 264 TB patients, 478 non-TB pneumonia patients, and as negative controls, 438 subjects without pneumonia. The parameters analysed were age, gender and the presence of pneumoconiosis, bronchiectasis, liver cirrhosis, haemodialysis, diabetes mellitus and advanced lung cancer. Results: Male gender was the only significant factor increasing the risk of pulmonary TB. When compared with non-TB pneumonia and control patients, the odds ratios were 1.862 and 2.182, respectively. Patients with liver cirrhosis did not show an increased risk of pulmonary TB after regression analysis. Pneumoconiosis resulted in a 2.260 (P = 0.003) odds ratio for pulmonary TB, compared with the controls. However, there was no difference in pneumoconiosis between TB and non-TB pneumonia patients. Patients with bronchiectasis, lung cancer and those receiving haemodialysis had a lower risk for pulmonary TB in lower respiratory tract infection, with odds ratios of 0.342, 0.311 and 0.182, respectively. Conclusion: Physicians should first consider non-TB bacterial infection rather than Mycobacterium tuberculosis infection in pneumonia in patients with bronchiectasis, lung cancer or those receiving haemodialysis.

In the early stage of Mycobacterium tuberculosis infection, macrophages, in cooperation with interferon-gamma, a Th1 effector, are the first line of defense. Interleukin (IL)-4, a Th2 effector, is known to downregulate interferon-gamma. It is believed that the expression levels of IL-4 and its splicing variant-IL-4delta2 might be associated with Mycobacterium tuberculosis infection and chest radiographic patterns. The IL-4 and IL-4delta2 expressions in stimulated peripheral blood mononuclear cells of 76 tuberculosis patients, 48 pneumonic patients. and 36 healthy control subjects were evaluated by nested reverse transcriptase-polymerase chain reaction, and the expression of glyceraldehydes-3-phosphate dehydrogenase was used as an internal reference. The results showed that IL-4 mRNA expression was significantly decreased in patients with tuberculosis and nontubercular pneumonia compared with that in controls. The IL-4delta2 mRNA expression was positively correlated with IL-4 mRNA expression in all cases. The ratio of IL-4delta2 to IL-4 mRNA expression in tubercular patients with a cavity on chest radiography was significantly lower than that in patients without a chest cavity. In conclusion, the ratio of IL-4delta2 to IL-4 mRNA expression may play a key role in disease severity for patients with pulmonary tuberculosis. From our observations, the IL-4 mRNA expression efficiency was attenuated in patients with pulmonary infection, either tuberculosis or pneumonia.

We read the letter from Antonio et al. They think humidification may be beneficial in selected obstructive sleep apnea patients during continuous positive airway pressure (CPAP) titration such as patients with mouth breathing and patients requiring high positive airway pressure to eliminate airway obstruction. The role of humidification during CPAP titration cannot be discarded. Our study is not to discard the role of humidification. Our results just showed that routine use of humidification during CPAP titration did not yield significant benefits regardless of initial nasal symptoms or diseases. Therefore, we emphasize that the routine humidification may be not necessary, but it does not mean that humidification is useless for specific patents. We hope the readers do not misunderstand this point. Antonio et al. point out a very important and interesting issue in this part. We agree that humidification may be beneficial in patients with mouth breathing and patients needing high CPAP pressure to maintain airway. But there are no clinical parameters that can early find out which patients are mouth breathers or those who required high CPAP pressure. Otherwise, there is no clear definition about mouth breathing and what level of pressure can be classified as high CPAP pressure. The severity of mouth breathing may be variable and which degree of mouth breathing will interrupt the normal humidity level is not known. In our points of view, the best way to evaluate this issue is to monitor mouth leak and CPAP flow together with humidification level in real time. Further study is needed to clarify this point, but there are some technical problems that should be overcome.

Interferon (IFN)-gamma expression is altered in pulmonary lesions, such as cavities and granulomas. However, the exact association between patterns on chest radiography and IFN-gamma responses are unclear. The purpose of this study was to determine the IFN-gamma response in patients with tuberculosis and to correlate the pulmonary lesions with the IFN-gamma responses. We enrolled 78 patients with tuberculosis, as diagnosed with initial positive results for acid-fast bacilli in the sputum and final positive cultures for Mycobacterium tuberculosis. Cell cultures of stimulated peripheral blood mononuclear cells were performed. The supernatants were analyzed for the IFN-gamma response and the results statistically analyzed. The patients' chest radiographs were examined for fibronodules, masses, pleural effusion, cavities, and the severity of parenchymal involvement. IFN-gamma responses were lower in patients with cavities on chest radiography than in those without cavities (403.306+/-397.048 vs 698.154+/-593.436 pg/ml, P