A 32-year-old woman presented with cough and hemoptysis. The radiologic findings showed increased interstitial markings in the right lung, a slightly decreased ling volume in the RLL and a hypoplastic right pulmonary arte ry with collaterals in the mediastinum and subpleural area. The pulmonary angiography showed an abrupt occlusion of the right lower pulmonary artery. The echocardiographic findings indicated pulmonary hypertension. A doppler leg ultrasonograph disclosed that the left politeal vein was occluded with collateral veins, not filling the defect in the venous lumen. The D-dimer increased 1.0 micro gram/ml. This condition was initially misdiagnosed as a congenital pulmonary artery agenesis. Finally, a chronic pulmonary thromboembolism with a deep vein thrombosis was confirmed.
Adult* ; Angiography ; Cough ; Echocardiography ; Female* ; Hemoptysis* ; Humans ; Hypertension, Pulmonary ; Leg ; Lung* ; Mediastinum ; Pulmonary Artery ; Pulmonary Embolism ; Veins ; Venous Thrombosis

BACKGROUND: Many clinicians are reluctant to prescribe systemic corticosteroids to manage and asthmatic attack because of many complications such as osteoporosis, cushing's syndrome, diabetes, hypertension and blee ding tendency. The use of nebulized budesonide may be of value in some infants, old men, and in particular adult asthmatic patients who complain of severe dyspnea. A clinical validation and steroid-sparing effect of nebulized budesonide in asthmatic adults and COPD were evaluated, and the short-term effects of budesonide use on the HPA axis were assessed. METHODS: Study A was propectively done with 41 patients diagnosed with pure asthma and 30 patients diagnosed wit COPD (including asthmatic component) in Soonchunhyang Hospital, Chunan from June. 2000 to Sep. 2001. They were treated with nebulized budesonide including sytemic steroids (Group 1), a budesonide tubuhaler including a sytemic steroid (Group 2), or only the systemic steroid (Group3). The peak flow rate, arterial blood gas in room air, pulmonary function test, symptom scoring, steroid amount and hospital stay were analyzed. Study B was conducted with 19 patients to evaluate the short-term effects on the HPA axis of treatment with nebulized budesonide 1mg twice daily and a budesonide turbuhaler 5 puffs twice daily. The adrenal function was assessed prior to budesonide inhalation and after 7 days of budesonide inhalation. RESULTS: In the pure asthmatic patients, the mean value of the symptoms (dyspnea, wheezing, cough, night asthma) or the arterial BGAs, total amounts of steroid or hospital stay and the difference in the results of the pulmonary function tests or peak expiratory flow rate were similar in the three groups. In COPD with an asthmatic component, there were no significant differences among the three groups. Although nebulized budesonide suppressed HPA function, (p=0.006) the HPA responses from the nebulized budesonide and turbuhaler budesonide were similar (p=0.288). CONCLUSION: This result suggests that systemic steroid should only be made available for acute asthmatic patients irrespective of the inhaled budesonides. Nebulized budesonide at the therapeutic dose has similar effects on the HPA axis compared to that of turbuhaler budesonide.
Adrenal Cortex Hormones ; Adult* ; Asthma ; Axis, Cervical Vertebra* ; Budesonide* ; Chungcheongnam-do ; Cough ; Cushing Syndrome ; Dyspnea ; Humans ; Hypertension ; Infant ; Inhalation ; Length of Stay ; Male ; Osteoporosis ; Peak Expiratory Flow Rate ; Pulmonary Disease, Chronic Obstructive ; Respiratory Function Tests ; Respiratory Sounds ; Steroids

No abstract available.
Adenocarcinoma*

BACKGROUND: It has long been suggested that neutrophils and their products are implicated as the central mediators of the acute lung injuries. Contrary to the dominant role of neutrophils in ARDS, many cases of ARDS has occurred in the setting of severe neutropenia without pufrnonary neutrophil infiltration. Therefore it is certain that effector cell(s) other than neutrophil play an important role in the pathogenesis of ARDS. This experiment was performed to define the mechanism of ARDS in the setting of neutiopenia, 1) by comparing the severity of endotoxin-induced lung injury, 2) by measurement of hydrogen peroxide production and cytokine concentration in the bronchoalveolar lavage cells and fluids obtained from different rats with and without cyclophosphamide-pretreatment. METHOD: The male Sprague-Dawleys were divided into the normal control (NC)-, endotoxin (ETX)-, and cyclophosphamide (CPA)-group in which neutropenia was induced by injecting cyclophosphamide intraperitoneally. Acute lung injury was evoked by injecting lipopolysaccharide (LPS) into a tail vein. The bronchoalveolar lavage (BAL) was performed at 3 and 6 hour after administration of LPS to measure the change of cell counts and concentrations of protein and cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Hydrogen peroxide (HPO) production from BAL cel]s was measured at 6 hour after LPS administration by phenol red microassay with and without zymosan stimulation. RESULTS: The results were as follows. A change of leukocyte counts in the peripheral blood after treatment with CPA More than 95% of total leukocytes and neutrophils were reduced after CPA administration, resulting in severe neutropenia. A change of BAL cells In the ETX-group, the number of total cells (p<0.01) and of macrophage and neutrophll (p<0.05) were increased at 3 and 6 hour after LPS administration compared to those of NC- group. In the CPA-group, the number of total leukocyte and macrophage were not changed after LPS administration, but neutrophil counts were significantly reduced and jt took part in less than 0.1% of total BAL cells (p<0.01 vs NC-group). BAL cells in this group were almost all macrophages (99.7%). A change of protein concentration in the BALF In the ETX-group, protein concentration was increased at 3 hour and was more increased at 6 hour after LPS administration (p<0.05 and <0.01 vs NC-group, respectively). In the CPA-group, it was also significantly elevated at 3 hour after LPS administration (p<0.05 vs NC-group) , but the value was statistically not different from that of ETh-group. The value measured at 6 hour after LPS administration in the CPA-group became lower than that of ETX-group (p<0.05), but showed still a higher value compared to that of NC-group (p<0.05). A change of cytokine concentration in the BALF TNF-alpha and IL-6 were elevated in the ETX- and CPA-group compared to those of NC-group at both time intervals. There was no statistical difference in the values of both cytokines between the ETX- and CPA-groups. Measurement of hydrogen peroxide production from BAL cells There was no intergroup difference of HPO production from resting cells. HPO production after incubation with opsonized zymosan was significantly elevated in all groups. The percent increment of HPO production was highest in the ETX-group (89.0%, p<0.0008 vs NC-group ), and was 42.85 in the CPA-group (p = 0.003 vs NC-group ). Conclusion Acute lung injury in the setting of neutropenia might be caused by functional activation of resident alveola r macrophages.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Cell Count ; Cyclophosphamide ; Cytokines ; Humans ; Hydrogen Peroxide ; Interleukin-6 ; Leukocyte Count ; Leukocytes ; Lung Injury ; Macrophages* ; Male ; Neutropenia ; Neutrophil Infiltration ; Neutrophils ; Phenolsulfonphthalein ; Rats* ; Tumor Necrosis Factor-alpha ; Veins ; Zymosan

BACKGROUND: The immediate host response to LPS is the production of proinflammatory cytokines that act as intercellular mediators in inflammatory reactions, including acute lung injury. These "early response" cytokines transmit signals from recognition cells to target or effector cells. This host response is futher amplified by the expression of leukocyte chemoattractants, growth factors, and adhesion molecules, resulting in an array of proinflammatory events. This experiment was performed to define the lung origin of proinflammatory cytokines, such as TNF-alpha IL 6 in early periods of endotoxin induced acute lung injury (ALl). METHOD: The healthy male Sprague-Dawley, weighted 150-250g, were divided into saline control (NC) and endotoxemia-induced ALl (ETX-), and leukopenic endotoxemia-induced ALl (CPA-ETX-Group) which was induced by cyclophosphamide, 70 mg/kg i.p. injection. Acute lung injury was evoked by LPS, 5 mg/kg, intravenously administered. Bronchoalveolar lavage was performed at 0, 3, 6 h after LPS-treated to estimate the influx of phagocytes and concentration of total protein, and cytokines as TNF-alpha and IL 6 by a bioassy using MTT method. We also examined the localization of TNF-alpha and IL 6 protein in endotoxemia-challenged lung tissue by immunohistochemical stain (IH). RESULTS: The total cell, macrophage and PMN count in BALF were elavated in ETX group compared to NC (p<0.05). In CPA-ETX group, total cell and macrophage count in BALF were not changed compared to NC, but PMN count was markedly reduced and it took part. in less than 0.1% of total BAL cells (p<0.01). The protein concentration in BALF were significantly increased in ETX and CPA-ETX group compared to NC (p<0.05), but there was signifcant difference between ETX- and CPA-ETX group only at 6 h (p<0.05). This observation suggested that even if PMNs are involved in the pathogenesis of acute lung injury, their role cannot be viewed as essential. The concentration of TNF-alpha and IL 6 in BALF was significantly increased in the ETX- and CPA-ETX group compared to NC. There was no difference between ETX- and CPA-ETX group. In IH, anti-TNF-alpha- and anti-IL 6 antibody was strongly localized at interstitial monocytes and alveolar macro-phages in endotoxemia-challenged lung tissue. From above point of view, activated alveolar macrophage/monocyte considered as a prominent source of proinflammatory cytokines in endotoxemia-challenged lung injury. CONCLUSION: The prominent source of proinflammatory cytokines in early periods of endotoxemia-induced lung injury will be the activated resident macrophages like an alveolar macrophage and interstitial monocytes. The pulmonary macrophage/monocyte will impact the initiation and continuance of lung injury without PMNs s certain inflammatory role, particularly in endotoxemia-induced acute lung injury.
Acute Lung Injury ; Bronchoalveolar Lavage ; Chemotactic Factors ; Cyclophosphamide ; Cytokines* ; Endotoxemia* ; Humans ; Intercellular Signaling Peptides and Proteins ; Interleukin-6* ; Interleukins* ; Leukocytes ; Lung Injury ; Lung* ; Macrophages ; Macrophages, Alveolar ; Male ; Monocytes ; Phagocytes ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha*

BACKGROUND: Bacterial infections in diabetic patients are an important cause of increased morbidity and mortality. It has been reported that bacterial infections in diabetics showed more impaired PMN functions such as reduced PMN respiratory burst and decreased microbicidal activity in inflammed tissues. Also, apoptosis(programmed cell death) is postulated to be a key mechanism for neutrophil elimination. It is very important that PMN apoptosis keeps the balance from an area of inflammation. Actuallly, as little was known about PMN apoptosis and respiratory burst in diabetes, we investigated PMN apoptosis and hydrogen peroxide production after endotoxin exposure. METHODS: Peripheral venous blood samples were collected by routine venipuncture from healthy volunteers and diabetics to harvest neutrophils. We respectively measured the PMN apoptosis, the production of hydrogen peroxide, and the cell viability. RESULTS: Normal neutrophils showed a tendency to decreased apoptosis after endotoxin treatment. In patients with diabetes, PMN apoptosis was significantly decreased compared with healthy controls. In addition, the LPS-induced neutrophils in diabetics demonstrated more decreased apoptosis. However, the production of hydrogen peroxide was not different between groups. CONCLUSION: These observations suggest that the decreased PMN apoptosis in diabetics with endotoxin exposure may also affect the increased susceptibility and severity of infections.
Apoptosis* ; Bacterial Infections ; Cell Survival ; Healthy Volunteers ; Humans ; Hydrogen Peroxide ; Inflammation ; Mortality ; Neutrophils* ; Phlebotomy ; Respiratory Burst

BACKGROUND: It is known that airway inflammation is present in most patients with asthma, but the relationship between symptoms and the severity and nature of airway inflammation has not been established. Cough variant asthma is defined as an asthma in which the dominant symptom is cough and the condition can be successfully treated with inhaled steroids. This study was performed to evaluate the time coulee of bronchial responsiveness according to an inhaled anti-inflammatory therapy and the factors which affect the resolution of bronchial responsiveness, and an efficacy of nedocromil to cough asthma. METHOD: A prospective study for the investigation of bronchial responsiveness according to an inhaled anti-inflammatory treatment in sixty-one cough asthmatics was performed. Twenty-three entered budesonide (400microgram 2/day), twenty-two entered nedocromil (4mg2/day) and sixteen patients entered combined group. The bronchial hyperresponsiveness (BHR) was estimated by methacholine challenge test using counted breath method. The symptom was estimated by 'symptom score'. Reevaluation of BHR and symptom was performed at 2 month after treatment, and if BHR was not resoluted at this time, regarded as a non-responder, and then follow-up of BHR and symptom was performed at 4-and/or 6 month after treatment. RESULTS: The improvement of BHR and symptom was significant in 2 month (p < 0.05), but there was no change of them during follow-up period of 4-and/or 6 month in non-responders. In comparison of allergic markers such as serum total IgE, peripheral eosinophil count and skin test reactivity between responders and non-responders, there was no difference in each other. However, in comparison of other factors such as cumulative pack-years, symptom duration age, gender, and the initial degree of PC20, there was a significant difference in each other(p < 0.05). The percent of patients with the resolution of BHR in 2 month was not different in each group (p=0.95). There was no significant difference in the degree of improvement of BHR and symptom in each group. CONCLUSION: Bronchial responsiveness and symptom was not significantly improved in non-responders during follow-up period of 4-and/or 6 month. The effect of inhaled nedocromil was equivalent to that of inhaled steroid in cough asthmatics, and the response to combined treatment is not superior to that achieved by either of these agents used alone.
Asthma* ; Budesonide ; Cough* ; Eosinophils ; Follow-Up Studies ; Humans ; Immunoglobulin E ; Inflammation ; Methacholine Chloride ; Nedocromil ; Prospective Studies ; Skin Tests ; Steroids

BACKGROUND: The signal pathways and their precise roles for acute respiratory distress syndrome caused by endotoxin (ETX) has not been established. Since there has been several in vitro experiments suggesting that activation of protein kinase C (PKC) pathway may be responsible for endotoxin-induced inflammatory reaction, we performed in vivo experiments in the rats with the hypothesis that PKC-inhibition can effectively prevent endotoxin-induced acute lung injury. METHODS: We studied the role of PKC in ETX-induced ALl using PKC inhibitor (staurosporine, 5Th) in the rat. Specific pathogen free male Sprague-Dawley weighted from 165 to 270g were used for the study. Animals were divided into the normal control (NC)-, vehicle control (VC)-, ETX-, PMA (phorbolmyristateacetate)-, STP+PMA-, and STP+ETX-group. PMA (50mg/kg) or ETX (7mg/kg) was instilled through polyethylen catheter after aseptic tracheostomy with and without STP (0.2mg/kg) pretreatment. STP was injected via tail vein 30mm before intratracheal injection (IT) of PMA or ETX. Bronchoalveolar lavage (BAL) was done 3- or 6-hrs after IT of PMA or FTX respectively, to measure protein concentration, total and differential cell counts. RESULTS The results were as follows. The protein concentrations in BALF in the PMA- and ETX-group were very higher than that of VC-group (p<0.001). When animals were pretreated with STP, the %reduction of the protein concentration in BALF was 64.8 8.5 and 30.4 2.5% in the STP+PMA- and STP+ETX-group, respectively (p=0.028). There was no difference in the total cell counts between the PMA-and VC-group (p = 0.26). However the ETX-group showed markedly increased total cell counts as compared to the VC- (p=0.003) and PMA group (p=0.0027), respectively. The total cell counts in BALF were not changed after pretreatment with STP compared to the PMA- (p=0.22) and ETX-group (p=0.46). The percentage of PMN, but not alveolar macrophage, was significantly elevated in the PMA-, and ETX-group. Especially in the ETX-group, the percentage of PMN was 17 times higher than that of PMA (p<0.001). The differential cell counts was not different between the PMA and STP+PMA. On the contrary the STP+ETX-group showed decreased percentage of PMN (p = 0.016). There was no significant relationship between the protein concentration and the total or differential cell counts in each group. CONCLUSION: Pretreatment with PKC-inhibitor (staurosporine) partially but significantly inhibited ETX-in-duced ALI.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Catheters ; Cell Count ; Humans ; Macrophages, Alveolar ; Male ; Protein Kinase C* ; Protein Kinases* ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; Signal Transduction ; Specific Pathogen-Free Organisms ; Staurosporine ; Tracheostomy ; Veins

BACKGROUND: Patients with established ARDS have a mortality rate that exceeds 50 percent despite of intensive care including artificial ventilation modality. Mortality has been associated with sepsis and organ failure preceding or following ARDS ; APACHE ll score ; old age and predisposing factors. Revised ventilator strategy over last 10 years especially at ARDS appeared to improve the mortality of it. We retrospectively investigated 40 ARDS patients of respiratory-care unit to examine how these factors influence outcome. METHODS: A retrospective investigation of 40 ARDS patients in respiratory-care unit with ventilator management over 46 months was performed. We investigated the clinical characteristics such as a risk factor, cause of death and mortality, and also parameters such as APACHE ll score, number of organ dysfunction and hypoxia score (HS, PaO2/FIO2) at day 1, 3, 7 of severe acute lung injury, and simultaneously the PEEP level and tidal volume. RESULTS: Clinical conditions associated with ARDS were sepsis 50%, pneumonia 30%, aspiration pneumonia 20%, and mortality rate based on the etiology of ARDS was sepsis 50%, pneumonia 67% (p<0.01 vs sepsis), aspiration pneumonia 38%. Overall mortality rate was 60%. In 28 day-nonsurvivors, leading cause of death was severe sepsis (42.9%) followed by MOF (28.6%), respiratory failure (19.1%), and others (9.5%). There were no differences in variables of age, sex, APACHE ll score, HS, and numbers of organ dysfunction at day 1 of ARDS between 28-days survivor and nonsurvivors. In view of categorized variables of age( > 70), APACHE ll score( > 26), HS(< 150) at day 1 of ARDS, there were significant differences between 28-days survivor and nonsurvivors(p<0.05). After day 1 of ARDS, the survivors have improved their APACHE ll score, HS, numbers of organ dysfunction over the first 3d to 7d, but nonsurvivors did not improve over a seven-day course. There were significant differences in APACHE II score and numbers of organ dysfunction of day 3, 7 of ARDS, and HS of day 7 of ARDS between survivors and nonsurvivors(p<0.05). Fatality rate of ARDS has been declined from 68% to less than 40% between 1995 and 1998. There were no differences in APACHE ll score, HS, numbers of organ dysfunction, old age at presentation of ARDS. In last years, mean PEEP level was significantly higher and mean tidal volume was significantly lower than previous years during seven days of ARDS(p<0.01). CONCLUSIONS: Improvement of HS, APACHE ll score, organ dysfunction over the first 3d to 7d is associated with increased survival. Decline in ARDS fatality rates between 1995 and 1998 seems that this trend must be attributed to improved supportive therapy including at least high PEEP instead of conventional-least PEEP approach in ventilator management of acute respiratory distress syndrome.
Acute Lung Injury ; Anoxia ; APACHE ; Causality ; Cause of Death ; Humans ; Intensive Care Units* ; Critical Care* ; Mortality ; Organ Dysfunction Scores ; Pneumonia ; Pneumonia, Aspiration ; Respiratory Distress Syndrome, Adult* ; Respiratory Insufficiency ; Retrospective Studies ; Risk Factors ; Sepsis ; Survivors ; Tidal Volume ; Ventilation ; Ventilators, Mechanical

BACKGROUND: Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. METHODS: After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. alpha and beta IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. RESULTS: 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-2Ralpha on eosinophils, instead of no effect on the expression of IL-2Rbeta. CONCLUSION: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.
Animals ; Antibodies, Neutralizing ; Asthma ; Eosinophilia ; Eosinophils* ; Humans ; Interleukin-2 ; Interleukin-2 Receptor alpha Subunit ; Interleukin-5 ; Lymphocytes ; Mucous Membrane ; Receptors, Interleukin-2 ; Survival Rate ; Trypan Blue