• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.823-834
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• 1998

Background: Chronic inhalation of silica induces the lung fiborsis. The alveolar macrophages ingest the inhaled silica; they liberate the pro-inflammatory cytokines such as IL-1$\beta$, IL-6, TNF-$\alpha$ and fibrogenic cytokines, TGF-$\beta$ and PDGF. Cytokines liberated from macrophage have pivotal role in pulmonary fibrosis. There is a complex cytokine network toward fibrosis. However, the exact roles and the interaction among the proinflammatory cytokines and TGF-$\beta$, a fibrogenic cytokine, have not been defined, yet. In this study, we investigated silica induced IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ production and the effect of IL-1$\beta$, IL-6, TNF-$\alpha$ on the production of TGF-$\beta$ from lung macrophages of Balb/C mice. Method: We extracted the lung of Balb/C mice and purified monocytes by Percoll gradient method. Macrphages were stimulated by silica ($SiO_2$) in the various concentration for 2, 4, 8, 12, and 24 hours. The supernatants were used for the measurement of protein levels by bioassay, and cells for the levels of mRNA by in situ hybridization. Results: The production of IL-6 was not observed till 4 hours, and reached the peak levels at 8 hours after stimulation of silica. The production of TNF-$\alpha$ increased from 2 hours and reached the peak levels at 4 hours after stimulation of silica. The spontaneous TGF-$\beta$ production reached the peak levels at 24 hours. TNF-$\alpha$ upregulated the silica induced TGF-$\beta$ production. Silica induced TGF-$\beta$ production was blocked by pretreated anti-TNF-$\alpha$ antibody. In situ hybridization revealed the increased positive signals at 4 hours in IL-6, at 4 hours TNF-$\alpha$ and 12 hours in TGF-$\beta$. Conclusion: The results above suggest that silica induced the sequential production of IL-6, 1NF-$\alpha$ and TGF-$\beta$ from macrophages and TNF-$\alpha$ upregultaes the production of TGF-$\beta$ from silica-induced macrophages.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.372-385
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• 1999

Background: The purpose of this study was to examine the causes and pathologic process of chronic non-productive cough as an isolated symptom with a normal spirometry and chest radiograph by investigating clinicopathologic findings. Method: We studied 25 adults with chronic non-productive cough over a 3-week period with a normal chest radiograph and pulmonary function tests without any other symptoms. Clinical assessment, cough score, chest and sinus radiograph, pulmonary function tests, methacholine challenge, allergic skin prick test, and bronchoscopy for bronchial biopsies were performed. Subjects were then treated with prednesolone 20 to 30 mg/day for 1 to 2 weeks. Results: The experimental group was divided into two subgroups-those infiltrated with eosinophils, and those infiltrated with lymphocytes depending on eosinophil and lymphocyte counts, both of which were respectively higher than those of the control group. Eosinophils infiltrated group had mean numbers of eosinophil of 89.8 $cells/mm^3$ while control group's mean was 0.4 $cells/mm^2$(p=0.005). Lymphocyte infiltrated group was 4 patients whose mean was 84.3 $cells/mm^2$ with 28.4 $cells/mm^2$ of control group(P=0.026). In addition, the mean thickness of the basement membrane of experimental group was $14.20{\pm}5.20{\mu}m$ in contrast of control group whose mean was $3.50{\pm}1.37{\mu}m$(P=0.001). With the methacholine challenge test, 7 of the 21 eosinophil infiltrated subjects were diagnosed with cough variant asthma ; the other 14 with eosinophilic bronchitis. Three subjects with eosinophilic bronchitis were atopic positive (21.4%) with the skin prick test In the lymphocyte dominant group, all four subjects were diagnosed with lymphocytic bronchitis. Cough score was improved after steroid treatment in 22 of 25 subjects in the experimental group (88.0%). Conclusion: These results suggest chronic non-productive cough as an isolated symptom with a normal spirometry and chest radiograph was associated with airway inflammation by eosinophil and lymphocyte infiltration. The causes for chronic non-productive cough were eosinophilic bronchitis, cough variant asthma, and lymphocytic bronchitis(written in frequency). They further suggest that therapeutic treatment with steroids can provide effective symptomatic relief.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.945-953
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• 1996

Background : Many acute and chronic lung diseases including pneumoconiosis are characterized by the presence of increased numbers of activated macrophages. These macrophages generate several inflammatory cell chemoattractants, by which neutrophil migrate from vascular compartment to the alveolar space. Recruited neutrophils secrete toxic oxygen radicals or proteolytic enzymes and induce inflammatory response. Continuing inflammatory response results in alteration of the pulmonary structure and irreversible fibrosis. Recently, a polypeptide with specific neutrophil chemotactic activity, interleukin-8(IL-8), has been cloned and isolated from a number of cells including : monocytes, macrophages and fibroblasts. IL-1 and/or TNF-${\alpha}$ preceded for the synthesis of IL-8, and we already observed high level of IL-1 and TNF-${\alpha}$ in the pneumoconioses. So we hypothesized that IL-8 may be a central role in the pathogenesis of pneumoconiosis. In order to evaluate the clinical utility of IL-8 as a biomarker in the early diagnosis of pneumoconiosis, we investigated the increase of IL-8 in the pneumoconiotic patient and the correlation between IL-8 level and progression of pneumoconiosis. Method : We measured IL-8 in the serum of 48 patients with pneumoconiosis and 16 persons without dust exposure history as a control group. Pneumoconiotic cases were divided into 3 groups according to ILO Classification : suspicious group(n=16), small opacity group(n=16) and large opacity group(n=16). IL-8 was measured by a sandwich enzytne immunoassay technique. All data were expressed as the $mean{\pm}standard$ deviation. Results: 1) The mean value of age was higher in the small opacity and large opacity group than comparison group, but smoking history was even. Duration of dust exposure was not different among 3 pneumoconiosis groups. 2) IL-8 level was $70.50{\pm}53.63pg/m{\ell}$ in the suspicious group, $107.50{\pm}45.88pg/m{\ell}$ in the small opacity group, $132.50{\pm}73.47pg/m{\ell}$ in the large opacity group and $17.85{\pm}33.85pg/m{\ell}$ in the comparison group. IL-8 concentration in all pneumoconiosis group was significant higher than that in the comparison group(p<0.001). 3) IL-8 level tended to increase with the progression of pneumoconiosis. Multiple comparison test using Anova/Scheffe analysis showed a significant difference between suspicious group and large opacity group(p<0.05). 4) The level of IL-8 was correlated with the progression of pneumoconiosis(r=0.4199, p<0.05). Conclusion : IL-8 is thought to be a good biomarker for the early diagnosis of pneumoconiosis.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.954-964
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• 1996

Background : The type of the infiltrating cells in al veolitis may be determined by the chemokines in the lesion. MIP-1 ${\alpha}$, a C-C type chemokine, stimulates proliferation and cytokine secretion from macrophages and induces early neutrophilic and later monocytic inflammation in vi vo. IL-8, a C-X-C type chemokine is known to attract neutrophils and T-lymphocytes. This study is performed to find out the relative role of two different chemokines in diffuse interstitial lung disease. Subject and Method : We measured the secretion of MIP- 1 ${\alpha}$ and IL-8 from alveolar macrophages(AM), and their level in BAL fluid of 26 patients with DILD (10 IPF, 4 collagen disease, 10 sarcoidosis, and 2 hypersensitivity pneumonitis) and 7 normal control. Result: IL-8 secretion was significantly increased in patients with DILD ($8.15{\pm}4.58$ ng/ml) than in normal ($1.10{\pm}0.93$ ng/ml, p=0.0003). Significant correlation was found between IL-8 secretion and total cell number in BAL fluid (r=0.484, p=0.0068), %(r=0.592, p=0.0004) and No. (r=0.516, p=0.0042) of lymphocyte, and % of AM (r=-0.505, 0.0032). MIP- 1 ${\alpha}$ secretion was also increased in DILD ($2.41{\pm}1.45$ ng/ml) compared to control ($0.63{\pm}0.30$ ng/ml, p=0.0031), and showed a tendency of correlation with total cell number (r=0.368, p=0.0456) and No. of alveolar macrophages (r=0.356, p=0.0579) in BAL fluid. The concentration of IL-8 in BAL fluid was significantly increased in the patients with DILD ($40.4{\pm}34.5$ pg/ml) compared to control ($3.90{\pm}2.47$ pg/ml, p=0.0094) and it showed a significant correlation with the total cell number (r=0.484, p=0.0068), %(r=-0.505, p=0.0032) of AM, and % (r=0.592, p=0.0004) and No. (r=0.516, p=0.0042) of lymphocyte in BAL fluid. But there was a no significant difference in MIP- 1 ${\alpha}$ concentration in BAL fluid between normal control group and the patients with DILD. Conclusion : From the above results, we concluded that AM of DILD releases increased amount of both IL-8 and MIP- 1 ${\alpha}$ but IL-8 has better correlation with the type of alveolitis.

• Tuberculosis and Respiratory Diseases
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• v.42 no.6
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• pp.871-877
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• 1995

Background: The index which could predict the prognosis of critically ill patients is needed to find out high risk patients and to individualize their treatment. The APACHE III scoring system was established in 1991, but there has been only a few studies concerning its prognostic value. We wanted to know whether the APACHE III scores have prognostic value in discriminating survivors from nonsurvivors in sepsis. Methods: In 48 patients meeting the Bones criteria for sepsis, we retrospectively surveyed the day 1(D1), day 2(D2) and day 3(D3) scores of patients who were admitted to intensive care unit. The scores of the sepsis survivors and nonsurvivors were compared in respect to the D1 score, and also in respect to the changes of the updated D2 and D3 scores. Results: 1) Of the 48 sepsis patients, 21(43.5%) survived and 27(56.5%) died. The nonsurvivors were older($62.7{\pm}12.6$ vs $51.1{\pm}18.1$ yrs), presented with lower mean arterial pressure($56.9{\pm}26.2$ vs $67.7{\pm}14.2\;mmHg$) and showed greater number of multisystem organ failure($1.2{\pm}0.8$ vs $0.2{\pm}0.4$) than the survivors(p<0.05, respectively). There were no significant differences in sex and initial body temperature between the two groups. 2) The D1 score was lower in the survivors (n=21) than in the nonsurvivors ($44.1{\pm}14.6$, $78.5{\pm}18.6$, p=0.0001). The D2 and D3 scores significantly decreased in the survivors (D1 vs D2, $44.1{\pm}14.6$ : $37.9{\pm}15.0$, p=0.035; D2 vs D3, $37.9{\pm}15.0$ : $30.1{\pm}9.3$, p=0.0001) but showed a tendency to increase in the nonsurvivors (D1 vs D2 (n=21), $78.5{\pm}18.6$ : $81.3{\pm}23.0$, p=0.1337; D2 vs D3 (n=11), $68.2{\pm}19.3$ : $75.3{\pm}18.8$, p=0.0078). 3) The D1 scores of 12 survivors and 6 nonsurvivors were in the same range of 42~67 (mean D1 score, $53.8{\pm}10.0$ in the survivors, $55.3{\pm}10.3$ in the nonsurvivors). The age, sex, initial body temperature, and mean arterial pressure were not different between the two groups. In this group, however, D2 and D3 was significantly decreased in the survivors(D1 vs D2, $53.3{\pm}10.0$ : $43.6{\pm}16.4$, p=0.0278; D2 vs D3, $43.6{\pm}16.4$ : $31.2{\pm}10.3$, p=0.0005), but showed a tendency to increase in the nonsurvivors(D1 vs D2 (n=6), $55.3{\pm}10.3:66.7{\pm}13.9$, p=0.1562; D2 vs D3 (n=4), $64.0{\pm}16.4:74.3{\pm}18.6$, p=0.1250). Among the individual items of the first day APACHE III score, only the score of respiratory rate was capable of discriminating the nonsurvivors from the survivors ($5.5{\pm}2.9$ vs $1.9{\pm}3.7$, p=0.046) in this group. Conclusion: In sepsis, nonsurvivors had higher first day APACHE III score and their updated scores on the following days failed to decline but showed a tendency to increase. Survivors, on the other hand, had lower first day score and showed decline in the updated APACHE scores. These results suggest that the first day and daily updated APACHE III scores are useful in predicting the outcome and assessing the response to management in patients with sepsis.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.744-751
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• 1995

Background: Asthma is an inflammatory disease because there are many inflammatory changes in the asthmatic airways. Axon reflex mechanisms may be involved in the pathogenesis of asthma. Sensory neuropeptides are involved in this inflammation, which is defined as neurogenic inflammation. Substance p, neurokinin A, and neurokinin B may be main neuropeptides of neurogenic inflammation in airways. These tachykinins act on neurokinin receptors. Three types of neurokinin receptors, such as $NK_1$, $NK_2$, and $NK_3$, are currently recognized, at which substance p, neurokinin A, and neurokinin B may be the most relevant natural agonist of neurogenic inflammation in airways. The receptor subtypes present in several tissues have been characterized on the basis of differential sensitivity to substance p, neurokinin A, and neurokinin B. Plasma extravasation and vasodilation are induced by substance p more potently than by neurokinin A, indicating NK1 receptors on endothelial cells mediate the response. But airway contraction is induced by neurokinin A more potently than by substance P, indicating the $NK_2$ receptors in airway smooth muscles. These receptors are used to evaluate the pathogenesis of brochial asthma. FK224 was identified from the fermentation products of Streptomyces violaceoniger. FK224 is a dual antagonist of both $NK_1$ and $NK_2$ receptors. Purpose: For a study of pathogenesis of bronchial asthma, the effect of FK224 on plasma extravasation induced by vagal NANC electrical stimulation was evaluated in rat airway. Method: Male Sprague-Dawley rats weighing 180~450gm were anesthetized by i.p. injection of urethane. Plasma extravasation was induced by electrical stimulation of cervical vagus NANC nerves with 5Hz, 1mA, and 5V for 2 minutes(NANC2 group) and for sham operation without nerve stimulation(control group). To evaluate the effect of FK224 on plasma extravasation in neurogenic inflammation, FK224(1mg/kg, Fujisawa Pharmaceutical Co., dissolved in dimethylsulphoxide; DMSO, Sigma Co.) was injected 1 min before nerve stimulation(FK224 group). To assess plasma exudation, Evans blue dye(20mg/kg, dissolved in saline) was used as a plasma marker and was injected before nerve stimulation. After removal of intravascular dye, the evans blue dye in the tissue was extracted in formamide($37^{\circ}C$, 24h) and quantified spectrophotometrically by measuring dye absorbance at 629nm wavelength. Tissue dye content was expressed as ng of dye per mg of wet weight tissue. The amount of plasma extravasation was measured on the part of airways in each groups. Results: 1) Vagus nerve(NANC) stimulation significantly increased plasma leakage in trachea, main bronchus, and peripheral bronchus compared with control group, $14.1{\pm}1.6$ to $49.7{\pm}2.5$, $17.5{\pm}2.0$ to $38.7{\pm}2.8$, and $12.7{\pm}2.2$ to $19.1{\pm}1.6ng$ of dye per mg of tissue(mean ${\pm}$ SE), respectively(p<0.05). But there was not significantly changed in lung parenchyma(p>0.05) 2) FK224 had significant inhibitory effect upon vagal nerve stimulation-induced airway plasma leakage in any airway tissues of rat,such as trachea, main bronchus, and peripheral bronchus compared with vagus nerve stimulation group, 49%, 58%, and 70%, respectively(p<0.05). Inhibitory effect of FK224 on airway plasma leakage in neurogenic inflammation was revealed the more significant in peripheral bronchus, but no significant in lung parenchyma. Conclusion: These results suggest that FK224 is a selective NK receptor antagonist which effectively inhibits airway plasma leakage induced by the endogenous neurotransmitters relased by neurogenic inflammation in rat airway. Tachykinin receptor antagonists may be useful in the treatment of brochial asthma.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.646-653
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• 1995

Background: The confirmative diagnosis of pulmonary tuberculosis(Tb) can be made by the isolation of Mycobacterium Tuberculosis(MTb) in the culture of the sputum, respiratory secretions or tissues of the patients, but positive result could not always be obtained in pulmonary Tb cases. Although there are many indirect ways of the diagnosis of Tb, clinicians still experience the difficulty in the diagnosis of Tb because each method has its own limitation. Therefore development of a new diagnostic tool is clinically urgent. It was reported that silica cause some lysosomal enzymes to be released from macrophages in vitro and one of these enzymes is elevated in workers exposed to silica dust and in silicotic subjects. In pulmonary Tb, alveolar macrophages are known to be activated after ingestion of MTb. Activated macrophages can kill MTb through oxygen free radical species and digestive enzymes of lysosome. But if macrophages allow the bacilli to grow intracellularly, the macrophages will die finally and local lesion will enlarge. Then it is assumed that the lysosomal enzymes would be released from the dead macrophages. The goal of this investigation was to determine if there are differences in the plasma activities of lysosomal enzymes, ($\beta$-glucuronidase(GLU) and $\beta$-N-acetyl glucosaminidase(NAG), among the groups of active and inactive pulmonary Tb and healthy control, and to see if there is any possibility that the plasma activity of GLU and NAG can be used as diagnostic indicies of active pulmonary Tb. Methods: The plasma were obtained from 20 patients with bacteriologically proven active pulmonary Tb, 15 persons with inactive Tb and 20 normal controls. In 10 patients with active pulmonary Tb, serial samples after 2 months of anti-Tb medications were obtained. Plasma GLU and NAG activities were measured by the fluorometric methods using 4-methylumbelliferyl substrates. All data are expressed as the mean $\pm$ the standard error of the mean. Results: The activites of GLU and NAG in plasma of the patients with active Tb were $21.52{\pm}3.01$ and $325.4{\pm}23.37$(nmol product/h/ml of plasma), respectively. Those of inactive pulmonary Tb were $24.87{\pm}3.78$, $362.36{\pm}33.92$ and those of healthy control were $25.45{\pm}4.05$, $324.44{\pm}28.66$(nmol product/h/ml of plasma), respectively. There were no significant differences in the plasma activities of both enzymes among 3 groups. The plasma activities of GLU at 2 months after anti-Tb medications were increased($42.18{\pm}5.94$ nmol product/h/ml of plasma) in the patients with active pulmonary Tb compared with that at the diagnosis of Tb(P-value <0.05). Conclusion: The results of the present investigation suggest that the measurement of the plasma activities of GLU and NAG in the patients with active pulmonary Tb could not be a useful method for the diagnosis of active Tb. Further investigation is necessary to define the reasons why the plasma activities of the GLU was increased in the patients with active pulmonary Tb after Tb therapy.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.660-668
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• 1995

Background: It is said that tuberculous pleuritis responds well to anti-tuberculous drug in general, so no further aggressive therapeutic management is unnecesarry except in case of diagnostic thoracentesis. But in clinical practice, we often see some patients who need later decortication due to dyspnea caused by pleural loculation or thickening despite several months of anti-tuberculous drug therapy. Therefore, we want to know the clinical difference between a group who received decortication due to complication of tuberculous pleuritis despite of anti-tuberculous drug and a group who improved after 9 months of anti-tuberculous drug only. Methods: We reviewed 20 tuberculous pleuritis patients(group 1) who underwent decortication due to dyspnea caused by pleural loculation or severe pleural thickening despite of anti-tuberculous drug therapy for 9 or more months, and 20 other tuberculous pleuritis patients(group 2) who improved by anti-tuberculous drug only and had similar degrees of initial pleural effusion and similar age, sex distribution. Then we compared between the two groups the duration of symptoms before anti-tuberculous drug treatment and pleural fluid biochemistry like glucose, LDH, protein and pleural fluid cell count and WBC differential count, and we also wanted to know whether there was any difference in preoperative PFT value and postoperative PFT value in the patients who underwent decortication, and obtained following results. Results: 1) Group 1 patients had lower glucose level{$63.3{\pm}30.8$(mg/dl)} than that of the group 2{$98.5{\pm}34.2$(mg/dl), p<0.05}, and higher LDH level{$776.3{\pm}266.0$(IU/L)} than the group 2 patients{$376.3{\pm}123.1$(IU/L), p<0.05}, and also longer duration of symptom before treatment{$2.0{\pm}1.7$(month)} than the group 2{$1.1{\pm}1.2$(month), p<0.05}, respectively. 2) In group 1, FVC changed from preoperative $2.55{\pm}0.80$(L) to postoperative $2.99{\pm}0.78$(L)(p<0.05), and FEV1 changed from preoperative $2.19{\pm}0.70$(L/sec) to postoperative $2.50{\pm}0.69$(L/sec)(p<0.05). 3) There was no difference in pleural fluid protein level($5.05{\pm}1.01$(gm/dL) and $5.15{\pm}0.77$(gm/dl), p>0.05) and WBC differential count between group 1 and group 2. Conclusion: It is probable that in tuberculous pleuritis there is a risk of complication in the case of showing relatively low pleural fluid glucose or high LDH level, or in the case of having long duraton of symptom before treatment. We thought prospective study should be performed to confirm this.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.559-573
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• 1997

Background : Asthma causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough. These symptoms are usually associated with widespread but variable airflow limitation that is partly reversible either spontaneously or with treatment. The inflammation also causes an associated increase in airway responsiveness to a variety of stimuli. Method : Of the 403 adult bronchial asthma patients enrolled from March 1992 to March 1994 in Allergy Clinics of Severance Hospital in Yonsei University, this study reviewed the 97 cases to evaluate the treatment effects and to analyse prognostic factors. The patients were classified to five groups according to treatment responses ; group 1 (non control group) : patients who were not controlled during following up, group 2 (high step treatment group) : patients who were controlled longer than 3 months by step 3 or 4 treatment of "Global initiative for asthma, Global strategy for asthma management and prevention" (NHLBI/WHO) with PFR(%) larger than 80%, group 3 (short term control group) : patients who were controlled less than 1 year by step 1 or 2 treatment of NHLBI/WHO, group 4 (intermediate term control group) : patients who were controlled for more than 1 year but less than 2 years by step 1 or 2 treatment of NHLBI/WHO, group 5 (long term control group) : patients who were controlled for more than 2 years by step 1 or 2 treatment of NHLBI/WHO. Especially the patients who were controlled more than 1 year with negatively converted methacholine test and no eosinophil in sputum were classified to methacholine negative conversion group. We reviewed patients' history, atopy score, total IgE, specific IgE, methacholine PC20 and peripheral blood eosinophil count, pulmonary function test, steroid doses and aggrevation numbers after treatment. Results : On analysis of 98 patients, 20 cases(20.6%) were classified to group 1, 26 cases(26.8%) to group 2, 23 cases(23.7%) to group 3, 15 cases(15.5%) to group 4, and 13 cases(13.4%) to groups 5. There were no differences of sex, asthma type, family history, smoking history, allergic rhinitis and aspirin allergy among the groups. In long term control group, asthma onset age was younger, symptom duration was shorter, and initial pulmonary function was better. The long term control group required lower amounts of oral steroid. had less aggrevation during first 3months after starting treatment and shorter duration from enrollment to control Atopy, allergic skin test, sputum and blood eosinophil, total IgE, nonspecific bronchial responsiveness was not significantly different among the groups. Seven out of 28 patients who were controlled more than 1 years showed negatively converted methachloine test and no eosinophils in the sputum. The mean control duration was $20.3{\pm}9.7$ months and relapse did not occur. Conclusion : Patients who had asthma of onset age younger, shorter symptom duration, better PFT, lower treatment initial steps, lower amounts of steroid needs and less aggravation numbers after starting treatment were classified in the long term control groups compared to the others.

• Journal of Chest Surgery
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• v.34 no.12
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• pp.917-923
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• 2001

Background : Bronchial sleeve resection for centrally located primary lung cancer is a lung-parenchyma-sparing operation in patients whose predicted postoperative lung function is expected to diminished markedly. Because of its potential bronchial anastomotic complications, it is considered to be an alternative to pneumonectomy. However, since sleeve lobectomy yielded survival results equal to at least those of pneumonectomy, as well as better functional results, it became and accepted standard procedure for patients with lung cancer who have anatomically suitable tumors, regardless of lung function. In this study, from analyzing of occurrence rate of postoperative complication and survival rate, we wish to investigate the validity of sleeve resection for primary lung cancer. Material and Method : From January 1989 to December 1998, 45 bronchial sleeve resections were carried out in the Department of Thoracic Surgery of Seoul National University Hospital. We included 40 men and 5 women, whose ages ranged from 23 to 72 years with mean age of 57 years. Histologic type was squamous cell carcinoma in 35 patients, adenocarcinoma in 7, and adenosquamous cell carcinoma in 1 patients. Right upper lobectomy was peformed in 24 patients, left upper lobectomy in 11, left lower lobectomy in 3, right lower lobectomy in 1, right middle lobecomy and right lower lobectomy in 3, right upper lobectomy and right middle lobecomy in 2, and left pneumonectomy in 1 patient. Postoperative stage was Ib in 11, IIa in 3, IIb in 16, IIIa in 13, and IIIb in 2 patients. Result: Postoperative complications were as follows; atelectasis in 9, persistent air leakage for more than 7 days was in 7 patients, prolonged pleural effusion for more than 2 weeks in 7, pneumonia in 2, chylothorax in 1, and disruption of anastomosis in 1. Hospital mortality was in 3 patients. During follow-up period, bronchial stricture at anastomotic site were found in 7 patients under bronchoscopy, Average follow-up duration of survivals(n=42) was 35.5$\pm$29 months. All of stage I patients were survived, and 3 year survival rate of stage II and III patients were 63%, 21%, respectively. According to Nstage, all of N0 patients were survived and 3 year survival rates of Nl and N2 were 63% and 28% respectively. Conclusion: We suggest that this sleeve resection, which is technically demanding, should be considered in patients with centrally located lung cancer, because ttlis lung-saving operation is safer than pneumonectomy and is equally curative.