Analysis of growth factors in serum and induced sputum from patients with asthma.

Epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), the AA and BB isoforms of platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) are involved in the pathogenesis of airway inflammation in asthma. In the present study, the associations between asthmatic phenotypes and the expression levels of these mediators in induced sputum and serum were investigated. A total of 62 asthmatic patients were divided into eosinophilic or neutrophilic phenotypes by cytological classification of the induced sputum. In addition, patients were classified according to lung function (FEV1/FVC >70% or FEV1/FVC <70%) and asthma severity (mild, moderate or severe). The concentrations of EGF, bFGF, PDGF-AA, PDGF-BB and VEGF in the serum and induced sputum were measured using sandwich enzyme immunoassays. VEGF levels in the serum and induced sputum were higher in patients with an eosinophilic phenotype compared with those with a neutrophilic phenotype. In addition, VEGF expression was higher in patients with an FEV1/FVC value of <70% as compared with patients with an FEV1/FVC value of >70%. Furthermore, the levels of VEGF were higher in patients with severe asthma compared with the patients with mild and moderate asthma. There were no statistically significant differences observed with regard to EGF, bFGF, PDGF-AA and PDGF-BB levels among the various phenotypes. Therefore, the observations of the present study indicated that increased VEGF expression in the serum and induced sputum of patients may be associated with eosinophilic airway inflammation, severe airflow limitation and the severity of asthma.

Correlation between fungal sIgE and bronchial asthma severity.

Fungal sensitisation is closely associated with asthma; however, the correlation between fungi and asthma severity remains unclear. The aim of this study was to investigate the severity of asthma in 100 patients with asthma due to fungal and non-fungal allergens. A total of 100 outpatients and inpatients with asthma were selected from 2010 to 2011 and were divided into three groups (mild, moderate and severe) according to their clinical manifestations, lung function results and treatment situations. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of specific immunoglobulin E (sIgE) to five fungal allergens and seven non-fungal allergens in the serum of all patients. The levels of sIgE to Aspergillus, Penicillium and Candida albicans allergens in the severe group were significantly higher compared with those in the moderate and mild groups (P<0.001 and P<0.05, respectively); those of the moderate group were significantly higher compared with those of the mild group (P<0.05). No significant difference was observed for the levels of sIgE to Alternaria alternata among the three groups. sIgE to Cladosporium herbarum was not present for all three groups. No significant difference was observed for the levels of sIgE to non-fungal allergens among the three groups. Fungal allergens are closely correlated with the severity of asthma, whereas non-fungal allergens are not.

Attenuating effect of pretreatment with Yiqifumai on lipopolysaccharide-induced intestine injury and survival rate in rat.

BACKGROUND: Yiqifumai is a traditional Chinese medicine compound preparation used for treatment of microcirculatory disturbance-related diseases in China. We have previous reported that pretreatment with Yiqifumai could improve the lipopolysaccharide (LPS) -induced microcirculatory disturbance in rat mesentery. The present study intended to investigate the effect of pretreatment with Yiqifumai on intestine injury and survival rate of the rats subjected to LPS challenge. METHODS: Male Wistar rats were continuously infused with LPS (5 mg kg-1 body weight h-1) via the left jugular vein for 90 min. In some rats, Yiqifumai 80 (mg/kg) was administrated through the left jugular vein 10 min before LPS infusion. The mean arterial pressure (MAP), heart rate (HR), rectal temperature (RT), respiratory rate (RR) and survival rate were measured at 24 h, 48 h and 72 h after LPS infusion. At 72 h after exposure to LPS, the intestine morphology was observed under a stereomicroscope and the immunohistochemistry staining of intestine was conducted to evaluate the expression of intercellular adhesion molecule 1 (ICAM-1) and the number of myeloperoxidase (MPO) positive cells in tissue. After observation of intestine microcirculation, blood was collected from the abdominal aorta of each animal to analyze the level of inflammatory markers in plasma, including TNF-α and MCP-1. RESULTS: Compared to the control, LPS infusion significantly decreased MAP and the survival rate and increased the HR, RT and RR, as well as elicited leukocyte infiltration, intestine hemorrhage, enhanced expression of ICAM-1 and raised level of inflammatory markers. All of indicators, except for the RT, were significantly attenuated by Yiqifumai, in contrast to the LPS group. CONCLUSIONS: The results demonstrated the potential of pretreatment with Yiqifumai to ameliorate rat intestine injury, inflammatory response to LPS and the decrease in survival rate caused by LPS challenge.

[The relationship between inflammatory mediators and pulmonary hypertension in patients with chronic obstructive pulmonary disease].

OBJECTIVE: The levels of C-reactive protein (CRP), tumor necrosis factor (TNF)-α, brain natriuretic peptide (BNP) and endothelin-1 (ET-1) were investigated to analyze the systemic inflammation in chronic obstructive pulmonary disease (COPD) patients with and without pulmonary hypertension. METHODS: From January 2006 to December 2010, 89 patients with COPD were enrolled in our hospital. There were 67 males and 22 females, with a mean age of (70 ± 7) and a mean FEV(1) of (47 ± 13)%. Pulmonary pressure was assessed by Doppler echocardiography. The levels of plasma BNP, TNF-α and ET-1 were measured by enzyme-linked immunosorbent assay kits. High-sensitivity plasma CRP level was assessed by chemiluminescent immunoassay. RESULTS: Forty-two patients were classified as COPD with pulmonary hypertension group and 47 patients as COPD without pulmonary hypertension group. The level of CRP [51.4 mg/L (20.1 - 92.0) mg/L], ET-1 [5.9 ng/L (3.7 - 10.4) ng/L] and BNP [303.2 ng/L (112.5 - 824.7) ng/L] in patients with pulmonary hypertension were significantly higher than in that in patients without hypertension, CRP [26.7 mg/L (11.5 - 62.9) mg/L], ET-1 [2.1 ng/L (1.3 - 4.7) ng/L] and BNP [143.7 ng/L (85.5 - 306.7) ng/L]. The level of TNF-α showed no difference between the 2 groups [8.5 ng/L (4.8 - 13.7) ng/L and 6.7 ng/L (3.2 - 10.3) ng/L], respectively. Multivariate analysis showed that PaO2 (P < 0.05), CRP (P < 0.05) and BNP (P < 0.05) could predict pulmonary hypertension independently. CONCLUSION: The level of CRP, ET-1 and BNP were related to pulmonary hypertension in COPD patients, suggesting that systemic inflammation play a role in the pathogenesis of pulmonary hypertension in COPD.

[The effect of spontaneous breathing trial on weaning from ventilators].

OBJECTIVE: To investigate whether spontaneous breathing trial is an essential process during weaning from ventilator in critically cared patients without chronic obstructive pulmonary disease (COPD). METHODS: The study was performed with a prospective, randomized, double-blinded method. A total of 67 adult patients, mechanically ventilated for at least 48 h in SICU of a teaching hospital, were enrolled. As soon as the patients were ready for weaning from ventilators, they were randomly assigned to 2 groups with target extubation without spontaneous breathing trial (SBT) (non-SBT group) and with SBT (SBT group). In the SBT group, the patient who tolerated the spontaneous breathing trial underwent immediate extubation. In the non-SBT group, as soon as a patient met weaning readiness criteria, he or she underwent extubation without SBT process. The primary outcome measure was successful extubation, defined as the ability to maintain spontaneous breathing for 48 hrs after extubation. Results were expressed as mean +/- SD. Mean values between the 2 groups were compared by student's t tests. The differences in proportions between the 2 groups were determined using chi(2)-test. RESULTS: There were no significant differences in demographic, respiratory, and hemodynamic characteristics between the 2 groups at the end of assessing weaning readiness criteria. Three (9.7%) patients in the SBT group and 3 (9.4%) patients in the non-SBT group needed reintubation (chi(2) = 0.013, P = 0.908). Five patients in the non-SBT group and 4 in the SBT group required noninvasive ventilation following extubation (chi(2) = 0.253, P = 0.727). There were no significant differences in in-hospital mortality between the 2 groups (chi(2) = 0.276, P = 0.600). CONCLUSION: The result suggests that spontaneous breathing trial may be not a necessary procedure preceding extubation in a general intensive care population.

[Acute fibrinous and organizing pneumonia: a case report and review of the literature].

OBJECTIVE: To better understand the clinical and pathological characteristics of acute fibrinous and organizing pneumonia (AFOP). METHODS: A case diagnosed with AFOP was reported and the related literature was reviewed. RESULTS: A 73 year-old man presenting with fever, cough with small amount of white sputum and gradually worsening dyspnea was admitted to this hospital. Chest CT scan showed bilateral multiple nodules and patchy infiltrates. Treatment including anti-bacterial and anti-fungal drugs was initiated, but no improvement was observed. The dyspnea deteriorated and repeated chest CT showed an increase of the nodules and the patchy infiltrates. Ultrasound guided percutaneous lung biopsy was performed and the pathological examination revealed slightly widened alveolar septa, lymphocyte and plasma cell infiltration and the presence of intra-alveolar fibrin in the form of fibrin "balls" (organization) within the alveolar spaces. No neutrophil and eosinophil infiltration was detected. The finding was consistent with AFOP. Corticosteroid therapy was started and the patient showed significant clinical and radiological improvement after a course of treatment. The patient was discharged and followed in the outpatient clinic. The chest CT became nearly normal after treatment with corticosteroids for 1.5 months. CONCLUSIONS: The main clinical manifestations of AFOP were similar to those of acute lung injury. Diagnosis was made by lung biopsy. The optimal treatment for AFOP had not been established. Therapy with corticosteroids could be attempted, but relapse may occur during the period of reducing the dosage of corticosteroids.

[Acute renal failure due to abdominal compartment syndrome].

OBJECTIVE: To observe the effect of intra-abdominal hypertension on renal function. METHODS: 30 intra-abdominal hypertension patients, 26 mals and 4 femals, age 42 +/- 17, were observed. Intra-abdominal pressure, mean arterial pressure, central venous pressure and serum creatinine were recorded and tested at the same time every day. RESULTS: When the intra-abdominal pressure increased, the urine output decreased (from 78 ml/h +/- 26 ml/h to 31 ml/h +/- 11 ml/h, P < 0.01), serum creatinine increased (from 110 mmol/L +/- 98 mmol/L to 224 mmol/L +/- 147 mmol/L, P < 0.01) with high central venous pressure (6.0 mm Hg +/- 2.1 mm Hg to 8.8 mm Hg +/- 2.5 mm Hg, 1 mm Hg = 0.133 kPa, P < 0.01) and high mean arterial pressure (from 79 mm Hg +/- 8 mm Hg to 86 mm Hg +/- 10 mm Hg, P < 0.01). There is a significant negative correlation between the intra-abdominal hypertension and urine output (r = -0.747, P < 0.01), and a significant positive correlation between the intra-abdominal hypertension and serum creatinine (r = 0.816, P < 0.01). During the ICU stay, 12 patients died, amoung which 8 died from multiple organ dysfunction due to septicemia and 4 died from abdominal hemorrhage. CONCLUSION: Intra-abdominal hypertension is correlated with lower urine output and increased blood creatinine significantly, and these results can be inversed when the intra-abdominal pressure decreases.

Aspiration of dead space in the management of chronic obstructive pulmonary disease patients with respiratory failure.

INTRODUCTION: Carbon dioxide clearance can be improved by reducing respiratory dead space or by increasing the clearance of carbon-dioxide-laden expiratory gas from the dead space. Aspiration of dead space (ASPIDS) improves carbon dioxide clearance by suctioning out (during expiration) the carbon-dioxide-rich expiratory gas while replacing the suctioned-out gas with oxygenated gas. We hypothesized that ASPIDS would allow lower tidal volume and thus reduce exposure to potentially injurious airway pressures. METHODS: With 8 hemodynamically stable, normothermic, ventilated patients suffering severe chronic obstructive pulmonary disease we tested the dead-space-clearance effects of ASPIDS. We compared ASPIDS to phasic tracheal gas insufflation (PTGI) during conventional mechanical ventilation and during permissive hypercapnia, which was induced by decreasing tidal volume by 30%. The mean P(aCO(2)) reductions with PTGI flows of 4.0 and 6.0 L/min and during ASPIDS (at 4.0 L/min) were 32.7%, 51.8%, and 53.5%, respectively. Peak, plateau, and mean airway pressure during permissive hypercapnia were significantly lower than during conventional mechanical ventilation but PTGI increased peak, plateau, and mean airway pressure. However, pressures were decreased during permissive hypercapnia while applying ASPIDS. Intrinsic positive end-expiratory pressure also increased with PTGI, but ASPIDS had no obvious influence on intrinsic positive end-expiratory pressure. ASPIDS had no effect on cardiovascular status. CONCLUSIONS: ASPIDS is a simple adjunct to mechanical ventilation that can decrease P(aCO(2)) during conventional mechanical ventilation and permissive hypercapnia.