Clinical characteristics of patients with chronic obstructive pulmonary disease overlapped with bronchial asthma.

BACKGROUND: The clinical characteristics of patients with chronic obstructive pulmonary disease overlapped with bronchial asthma (COPD-BA) have not been discussed thoroughly. OBJECTIVE: To reveal the clinical features of patients with COPD-BA, to evaluate the risk factors of COPD-BA, and to provide suggestions for COPD individualized therapy. METHODS: A retrospective observational study was performed. A total of 182 patients with COPD (90 with COPD-BA and 92 with pure COPD) were recruited in the study. Information on the following items was collected: demographics, clinical manifestations, complications, laboratory findings, other histories, and inpatient treatments during exacerbation. RESULTS: A total of 182 patients were diagnosed with COPD, with 90 (49.45%) being classified as having COPD-BA. Patients with COPD-BA were more likely to be female (P = .004) and experienced more severe respiratory exacerbations (P = .04) despite being younger (P = .008). Those patients at onset of recurrent cough and sputum production were younger (P = .001). Significantly, a positive asthmatic family history (P = .03) was observed. Patients with COPD-BA usually had higher level of total serum IgE (although no differences were observed), had higher positive rates of the serum specific IgE (P = .004), and were more like to have an allergic history (P = .003). Allergic factor was the risk factor of COPD-BA (odds ratio, 4.477). During hospitalization, patients with COPD-BA tended to be treated with systemic corticosteroids (P = .008). CONCLUSION: Patients with COPD-BA were characterized by persistent airflow limitation with unique clinical features. Allergic factor was associated with the presence of asthmatic characteristics in patients with COPD. When hospitalized for exacerbation, the individualized therapy for COPD-BA might include the use of corticosteroids systemically.

Attenuating effect of Ginsenoside Rb1 on LPS-induced lung injury in rats.

BACKGROUND: Sepsis causes neutrophil sequestration in the lung which leads to acute lung injury (ALI). Radix Ginseng (RG), a traditional herb used as herbal remedy in eastern Asia for thousands of years, which has been traditionally used in China to improve blood circulation and ameliorate pathological hemostasis. This study investigated whether Ginsenoside Rb1, the main components of RG, can attenuate ALI induced by LPS. METHODS: In vivo, 30 male Wistar rats were divided into three groups (n = 10 each groups) on the basis of the reagent used, which were subjected to LPS injection with or without Ginsenoside Rb1 (5 mg/kg) treatments to induce ALI model. Lung injury was assessed by pulmonary histology, lung wet-weight to dry-weight (W/D) ratio, the number of myeloperoxidase (MPO) positive cells, immunohistochemical analysis of intercellular adhesion molecule-1 (ICAM-1), gene expression of ICAM-1, ultrastructure changes of pulmonary microvasculature, concentration of inflammatory markers and in plasma. In vitro, pulmonary microvascular endothelial cells (PMVECs) were stimulated with LPS in the presence and absence of Ginsenoside Rb1 (50 mM), nuclear factor-κB (NF-κB) p65 was measured by immunocytochemistry staining and western blotting. RESULTS: Infusion of LPS induced lung injury, in vivo, as demonstrated by pulmonary edema with infiltration of neutrophils and hemorrhage, the increase in lung W/D ratio, the number of MPO positive cells, the level of inflammatory markers such as TNF-α, MCP-1 and IL-8, enhanced expression of ICAM-1 and ICAM-1 gene. Moreover, resulted in the changes of intercellular junctions in the endothelial cells of pulmonary microvasculature. In vitro, the significant increased release of NF-κB p65 and its subsequent translocation into the nucleus in PMVECs were observed. In contrast, Ginsenoside Rb1 treatment significantly ameliorated the LPS-induced lung injury, as judged by the marked improvement in all these indices. CONCLUSIONS: These results indicate that Ginsenoside Rb1 attenuated LPS-induced lung injury through an inhibition of the inflammatory signaling pathway, besides the direct inhibitory effect on proinflammatory molecules.

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.

Improving effect of Sivelestat on lipopolysaccharide-induced lung injury in rats.

Sepsis causes neutrophil sequestration in the lung, which leads to acute lung injury (ALI). Neutrophil elastase (NE) is thought to play an important role in the pathogenesis of ALI. This study investigated whether Sivelestat, a specific NE inhibitor, can attenuate ALI induced by lipopolysaccharide (LPS). In vivo, 30 male Wistar rats were divided into three groups (n = 10 each groups) on the basis of the reagent used, which were subjected to LPS injection with or without Sivelestat treatments to induce ALI model. Lung injury was assessed by pulmonary histology, lung wet-weight to dry-weight (W/D) ratio, immunohistochemical analysis of intercellular adhesion molecule-1 (ICAM-1), the number of myeloperoxidase (MPO)-positive cells, and gene expression of ICAM-1. In vitro, pulmonary microvascular endothelial cells (PMVECs) were stimulated with LPS in the presence and absence of Sivelestat; nuclear factor-κB (NF-κB) p65 was measured by immunocytochemistry staining and Western blotting. Infusion of LPS induced lung injury, in vivo, as demonstrated by pulmonary edema with infiltration of neutrophils, the increase in lung W/D ratio, the number of MPO-positive cells and enhanced expression of ICAM-1 and ICAM-1 gene. In vitro, the significant increased release of NF-κB p65 and its subsequent translocation into the nucleus in PMVECs. In contrast, Sivelestat treatment significantly ameliorated the LPS-induced lung injury, as judged by the marked improvement in all these indices. These results indicated that inhibition of NE attenuated LPS-induced lung injury through an inhibition of the inflammatory signaling pathway, besides the direct inhibitory effect on NE.

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.

Multiple dimensions of cardiopulmonary dyspnea.

BACKGROUND: The current theory of dyspnea perception presumes a multidimensional conception of dyspnea. However, its validity in patients with cardiopulmonary dyspnea has not been investigated. METHODS: A respiratory symptom checklist incorporating spontaneously reported descriptors of sensory experiences of breathing discomfort, affective aspects, and behavioral items was administered to 396 patients with asthma, chronic obstructive pulmonary disease (COPD), diffuse parenchymal lung disease, pulmonary vascular disease, chronic heart failure, and medically unexplained dyspnea. Symptom factors measuring different qualitative components of dyspnea were derived by a principal component analysis. The separation of patient groups was achieved by a variance analysis on symptom factors. RESULTS: Seven factors appeared to measure three dimensions of dyspnea: sensory (difficulty breathing and phase of respiration, depth and frequency of breathing, urge to breathe, wheeze), affective (chest tightness, anxiety), and behavioral (refraining from physical activity) dimensions. Difficulty breathing and phase of respiration occurred more often in COPD, followed by asthma (R(2) = 0.12). Urge to breathe was unique for patients with medically unexplained dyspnea (R(2) = 0.12). Wheeze occurred most frequently in asthma, followed by COPD and heart failure (R(2) = 0.17). Chest tightness was specifically linked to medically unexplained dyspnea and asthma (R(2) = 0.04). Anxiety characterized medically unexplained dyspnea (R(2) = 0.08). Refraining from physical activity appeared more often in heart failure, pulmonary vascular disease, and COPD (R(2) = 0.15). CONCLUSIONS: Three dimensions with seven qualitative components of dyspnea appeared in cardiopulmonary disease and the components under each dimension allowed separation of different patient groups. These findings may serve as a validation on the multiple dimensions of cardiopulmonary dyspnea.

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.

[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.