Adult respiratory distress syndrome (ARDS) is of particular interest because of its severity of the associated lung injury and its high mortality. However, the pathophysiologies of ARDS in infant and childhood groups are still not well clarified inspite of many previous investigations. To investigate the time course of pathophysiology of ARDS in infant and childhood groups, this study was designed with experimental endotoxin-induced ARDS model using young rabbits (8 week-old). Material and Method: Rabbits were divided into the control group (n=8) and the endotoxin-treated group (n=32). The endotoxin group was subdivided into 4 groups by the sampling times as 3, 6, 12 and 24 hr-groups (G- $E_{3,6,12,24,}$ each n=8). The experimental ARDS was made by a bolus injection of endotoxin (Escherichia coli serotype 055 : B5, 0.50 mg/kg) via rabbit ear vein. For evaluation of the hematologic and inflammatory markers, and superoxide dismutase (SOD) concentrations, the blood samples were taken from the heart. The bronchoalveolar lavage fluid (BALF) were obtained for analysis of the leukocytes and protein concentration. With biopsy of the lung, histopathologic changes of the lung were also evaluated. Result: In the endotoxin groups, significant leukopenia (owing to pancytopenia) occurred in 3 and 6-hr groups, which was followed by significant leukocytosis (owing to neutrophilia) in the 12 and 24-hr groups (p<0.05). Serum levels of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-1 $\beta$ (IL-1 $\beta$) in the endotoxin groups were higher than those of control group (p<0.05). Serum levels of superoxide dismutase (SOD) of G- $E_{3}$ and G- $E_{6}$ were higher than those of control group, whereas those of G- $E_{12}$ were lower than those of control groups (p<0.05). Total leukocyte counts and protein con-centrations in BALF were significantly elevated in the endotoxin groups compared to the control group (p < 0.05). The hemorrhagic pattern of BALF showed occurred in the endotoxin groups. The endotoxin groups (in G- $E_{6}$) had severe infiltration of inflammatory cells (lymphocyte and monocyte) in the pulmonary interstitium and parenchyma, migrations of neutrophil and eosinophil into alveolar spaces and interstitial widening, which are the evidences of acute lung injury. In the endotoxin groups, there were significant positive correlations between the BALF findings and the immunologic markers (TNF-$\alpha$, IL-1$\beta$, SOD) (p<0.05). Conclusion: Severe acute lung injury occurred in all the endotoxin-treated rabbits. The pathophysiologic findings were so progressive until 6-hr by time dependant pattern, and then recovered slowly, Variable hematologic, immuno-logic, and pathologic factors were well correlated in the development and progression of endoxin-induced lung injury. The pathophysiologic responses were sensitive and rapid in young rabbit Young rabbit seemed to be a useful experimental animal model for infant and childhood groups.roups.
Hahn, Chang Hoon;Moon, Jin Wook;Chang, Jae Hyun;Choi, Byoung Wook;Shin, Dong Whan;Kim, Se Kyu;Chang, Joon;Kim, Sung Kyu;Kim, Young Sam
Tuberculosis and Respiratory Diseases
/
v.55
no.3
/
pp.311-316
/
2003
A 34-year-old man was admitted to our hospital due to fever and cough. He received the combination anti-cancer chemotherapy for testicular tumor, including bleomycin. The chest X-ray showed consolidation and ground glass opacity on the right upper lobe and subpleural areas of other lobes. This condition was initially misdiagnosed as a pneuomonia, but consolidation did not disappear after antibiotics treatment. We performed transbronchial lung biopsy and bleomycin induced pulmonary toxicity was confirmed. The bleomycin induced lung injury is the most common chemotherapeutically induced pulmonary disease. Bleomycin induced Bronchiolitis Obliterans Organizing Pneumonia(BOOP) is less common than interstitial pneumonitis and responds well to corticosteroid treatment.
Mostafa, Amira Ismail;Salem, Ayman Elsayed;Ahmed, Heba Allah Moussa;Bayoumi, Aml Ibrahim;Halim, Radwa M. Abdel;Samie, Rasha M. Abdel
Tuberculosis and Respiratory Diseases
/
v.84
no.3
/
pp.200-208
/
2021
Background: Hypersensitivity pneumonitis (HP) is an increasingly recognized form of diffuse parenchymal lung disease. Krebs von den Lungen-6 (KL-6) is now classified as a human MUC1 mucin protein, and regenerating type II pneumocytes are the primary cellular source of KL-6/MUC1 in the affected lungs of patients with interstitial lung diseases (ILD). Serum KL-6/MUC1 levels have been demonstrated to be useful for the evaluation of various ILD. To determine the role of circulating KL-6 in evaluating the disease activity and management of HP. Methods: An observational cross-sectional study was conducted on 51 patients with HP and 20 healthy controls. Serum KL-6 levels were measured in both groups. Patients were further assessed based on chest high-resolution computed tomography (HRCT), pulmonary function test, 6-minute walk test, echocardiography, bronchioalveolar lavage, and/or transbronchial biopsy. Patients were divided into the fibrotic and non-fibrotic groups according to the HRCT findings. Results: The median serum KL-6 levels were significantly higher in HP patients as compared to the control group. The median serum KL-6 levels were found to be higher in the non-fibrotic HP group (1,900 IU/mL) as compared to the fibrotic group (1,200 IU/mL). There was a significant inverse correlation between serum KL-6 serum level and the dose of steroids as well as the duration of steroid therapy. Conclusion: The presence of higher KL-6 levels in the non-fibrotic HP group implies its enhanced production by regenerating pneumocytes in response to alveolar injury. The significant association between serum KL-6 levels and the dose and the duration of steroid therapy emphasizes the significant role of steroids in the stabilization of the disease.
Seungho Lee;Yoon-Ji Kim;Youngki Kim;Dongmug Kang;Seung Chan Kim;Se-Yeong Kim
Annals of Occupational and Environmental Medicine
/
v.35
/
pp.26.1-26.15
/
2023
Background: The objective of this study is to investigate the differences in incidence rates of targeted diseases by classification of occupations among construction workers in Korea. Methods: In a subject-based cohort of the Korean Construction Worker's Cohort, we surveyed a total of 1,027 construction workers. As occupational exposure, the classification of occupations was developed using two axes: construction business and job type. To analyze disease incidence, we linked survey data with National Health Insurance Service data. Eleven target disease categories with high prevalence or estimated work-relatedness among construction workers were evaluated in our study. The average incidence rates were calculated as cases per 1,000 person-years (PY). Results: Injury, poisoning, and certain other consequences of external causes had the highest incidence rate of 344.08 per 1,000 PY, followed by disease of the musculoskeletal system and connective tissue for 208.64 and diseases of the skin and subcutaneous tissue for 197.87 in our cohort. We especially found that chronic obstructive pulmonary disease was more common in construction painters, civil engineering welders, and civil engineering frame mold carpenters, asthma in construction painters, landscape, and construction water proofers, interstitial lung diseases in construction water proofers. Conclusions: This is the first study to systematically classify complex construction occupations in order to analyze occupational diseases in Korean construction workers. There were differences in disease incidences among construction workers based on the classification of occupations. It is necessary to develop customized occupational safety and health policies for high-risk occupations for each disease in the construction industry.
Background: Video-Assisted Thoracic Surgery can be performed with the lung collapsed. During the procedure, pleural adhesion may result in lung injury, bleeding, and thoracotomy conversion. Identifying the presence of pleural adhesion before surgery can make it easy to plan trocar introduction and perform the procedure. Material and Method: Between June 2009 and November 2009, we performed ultrasound in 24 patients to detect pleural adhesion before surgery and compared the results with the operative findings. We primarily examined the lateral chest, where the trocar would be inserted, and, occasionally, the anterior or posterior chest. Result: Patient diseases were: 6 hyperhidroses, 8 interstitial lung diseases, 5 lung cancers, 2 mediastinal tumors, 1 peripheral pulmonary embolism, 1 metastatic lung cancer, and 1 sarcoidosis. Of the 22 patients who did not have pleural adhesions on ultrasound, four revealed mild adhesions not related to the trocar insertion sites. However, ultrasound showed pleural adhesions in two patients, consistent with the operative findings. There was no air leak or thoracotomy conversion related with trocar insertion. Conclusion: Ultrasound requires only a few minutes to detect the presence of the pleural adhesion and was very useful in identifying the pleural adhesion before VATS.
Park, Chul-Yun;Chung, Jung-Seok;Chung, Jin-Wook;Lee, Choong-Ki;Hyun, Dae-Sung;Choe, Jung-Yoon
Journal of Yeungnam Medical Science
/
v.25
no.2
/
pp.117-123
/
2008
Dermatomyositis is characterized by progressive, symmetric, proximal muscle weakness and a nonsuppurative inflammatory myopathy of unknown etiology involving predominantly skeletal muscles. It is also characterized by typical skin lesions. Interstitial lung disease has a poor prognosis when it is associated with dermatomyositis. Organizing pneumonia is a disease in which granulation tissue fills the lumina of terminal and respiratory bronchioles and extends into the distal airspaces. The cryptogenic nature of the process is appreciated in that organizing pneumonia patterns of injury can be seen in secondary forms of the disease (secondary organizing pneumonia). Organizing pneumonia has been reported to occur in 5~10% in dermatomyositis-polymyositis patients. Anti-histidyl tRNA synthetase antibody (anti-Jo-1) is a predictive disease marker that is reported to occur in up to 70% of patients. We describe a 49-year-old male dermatomyositis patient who presented with organizing pneumonia and was found to have negative anti-Jo-1 antibody.
Cho, Joo Yeon;Lee, Hyun Kyung;Lee, Sung Soon;Lee, Hye Kyung;Lee, Young Min;Lee, Hyuk Pyo;Kim, Joo In;Choi, Soo Jeon;Yum, Ho-Kee
Tuberculosis and Respiratory Diseases
/
v.61
no.5
/
pp.479-483
/
2006
Acute fibrinous and organizing pneumonia (AFOP) is a histological pattern consisting of prominent intra-alveolar fibrin and organizing pneumonia, with out hyaline membranes or prominent eosinophilia. The clinical manifestations of AFOP resemble those of acute lung injury such as acute interstitial pneumonia (AIP). However, the classic histological patterns of AFOP differ from diffuse alveolar damage (DAD), bronchiolitis obliterans with organizing pneumonia (BOOP) or acute eosinophilic pneumonia (AEP). The characteristic intra-alveolar fibrin ball and lack of classic hyaline membrane are the predominant histological features of AFOP. Although some reports suggest that its clinical course is less catastrophic than DAD, the clinical entity that distinguishes AFOP from DAD has not been established. We present a case of pathologically demonstrated AFOP in a 79-year-old man. The radiological findings of our case were similar to those of DAD, presented with diffuse bilateral lung infiltrations. However, despite the rapid development of respiratory failure, the patient had a better response and outcome to steroid therapy than what would be expected for DAD.
Background: Effect of sulfur dioxide($SO_2$) exposure on airway is well known but little about the effect of $SO_2$ exposure on lung parenchyme. This study is to determine if short tenn exposure to $SO_2$ in concentration commonly found in industrialized environment cause potentially harmful effect on the lung parenchyme, and to evaluate the exposure time-response relationship between short tenn exposure to $SO_2$ and the inflammatory response in mouse lung. Method: 5ppm $SO_2$ gas was used and 48 mice were grouped into control(10), 30(9), 60(11), and 120 minute exposure(18) group. In each group, bronchoalveolar lavage(BAL) was done immediately after and at 1,2,3 days after exposure. Histological examination was performed in control and 120 minute exposure group. Results: 1) Cell response in bronchoalveolar lavage fluid. In 30 and 60 minute exposure group, compared to the control group, lymphocyte count has significantly increased(p<0.05) at 1 day after exposure but did not differ at 2 days after exposure. In 120 minute exposure group, also compared to the control group, there was significant increase in total cell, macrophage, and lymphocyte count at 1 day after exposure, (p<0.05) which lasted for 2 days but did not significantly differ at 3 days after exposure. 2) Histological findings in 120 minute exposure group. In the airway, mild epithelial cell damage and ciliary loss were noted but there was no evidence of inflammatory cell infiltration. Interstitial inflammatory infiltration was noted at 1 day after exposure, which lasted for 3 days after exposure and there was no evidence of edema or fibrosis in the interstitium Conclusions: These data indicate potentially noxious effect of $SO_2$ on the lung parenchyme as well as the airway at exposure level that are regarded as relatively safe, and the duration of injury depends on the exposure time.
Background : Acute pulmonary injury by paraquat are caused by multiple mechanisms including direct injury with oxygen free radicals and several mediators released from inflammatory cells. In order to clarify whether vitamin E could reduce tissue damages induced by intraperitoneal administration of paraquat and to investigate the pathogenetic mechanisms of paraquat-induced pulmonary injury, vitamin E as a free radical scavenger was administered. Method : Rats were divided into three groups (group 1 : control, group 2 : paraquat treated group, group 3 : paraquat and vitamin E treated group). Animals were sacrificed on day 1, day 2, day 3, and day 8 after the administration of saline, paraquat, or paraquat/vitamin E. Results : Treatment with vitamin E decreased the death rate of rats treated with paraquat. Comparing with control group ($1.37{\times}10^6/ml$), mean total cell counts recovered from the lavage fluid from animals treated with paraquat($1.65{\times}10^6/ml$) were increased(p=0.06). Magnitudes of increment of the total cell counts on the Day 8 in the vitamin E treated group were smaller than those of the animals treated with paraquat alone. The neutrophils began to appear in significant amounts in the lavage fluid on Day 8 after the administration of paraquat(37.0+12.7%). A significant decreasing neutrophil concentration at Day 8 was observed in the paraquat/vitamin E treated group(20.6+13.4%). Histologically the degree of pulmonary fibrosis was most prominent in the paraquat treated group while diffuse alveolar damage was continuously observed in the paraquat/vitamin E treated group and extensive interstitial lymphocytic infiltration was seen in the paraquat/vitamin E treated group. The paraquat/vitamin E treated group showed the less histologic changes. Conclusion : In this study vitamin E acting as a scavenger of neutrophil-derived free radicals and suppressant of lipid peroxidation, seemed to be the effective antioxidant in the inhibition of paraquat-induced pulmonary injury.
Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.
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