• Tuberculosis and Respiratory Diseases
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• v.49 no.2
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• pp.149-161
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• 2000

Background : Residual pleural thickening (RPT) develops in about 50% of tuberculous pleurisy ($PL_{TB}$). Some reports have suggested that elevated TNF-$\alpha$ and impaired fibrinolysis could be the cause of RPT, but until now, the mechanism and predictors of RPT have not been well known. TGF-$\beta$ has been known to promote fibrogenesis and is increased in tuberculous pleural fluid (PF). $PL_{TB}$ and malignant pleurisy ($PL_{MAL}$) manifest lymphocyte-dominant exudative pleural effusion, and it has clinical implications in the differentiation of the two diseases based on the findings of pleural effusion. We performed this study to compare pleural fluid TNF-$\alpha$ TGF-$\beta$, and fibrinolytic parameters between $PL_{TB}$ and $PL_{MAL}$, and to find the predictors of RPT in $PL_{TB}$. Methods : Thirty-five $PL_{TB}$ and 14 $PL_{MAL}$ patients who were admitted to the Asan Medical Center from February 1997 to August 1999 were enrolled. All $PL_{TB}$ patients were prescribed a primary, short-course, anti-tuberculosis regimen. INF-$\alpha$ tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), plasminogen, $\alpha$2-antiplasmin, and D-dimer were measured in both PF and PB. TGF-$\beta$was measured only in PF. Clinical characteristics, TNF-$\alpha$ TGF-$\beta$ and fibrinolytic parameters were compared between patients with RPT less than 2 mm and patients with more than 2 mm of the thirty patients who completed the anti-tuberculosis treatment. Results : The levels of TNF-$\alpha$ tPA, PAI-1, plasminogen, $\alpha$2-antiplasmin, and D-dimer in PF were higher than those in peripheral blood (PB) in $PL_{TB}$, whereas only plasminogen, $\alpha$2-antiplasmin, and D-dimer were higher in PF than in PB in $PL_{MAL}$. Pleural fluid TNF-$\alpha$ TGF-$\beta$, PAI-1, plasminogen, $\alpha$2-antiplasmin were increased in $PL_{TB}$ compared with $PL_{MAL}$, but these factors did not show any further advantages over ADA in differentiation between $PL_{TB}$ and $PL_{MAL}$. TNF-$\alpha$ TGF-$\beta$ and fibrinolytic parameters did not show any differences between patients with RPT less than 2 mm and patients with RPT more than 2 mm. Conclusion : Our data suggest that TNF-$\alpha$, TGF-$\beta$ and fibrinolytic parameters may play some role for the development of RPT in $PL_{TB}$, but they failed to predict the occurrence of RPT in $PL_{TB}$. Also these parameters did not seem to have any advantages over ADA in differentiating between two diseases.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.350-362
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• 1999

Background: Acute Respiratory failure which is developed after extubation in the weaning process from mechanical ventilation is an important cause of weaning failure. Once it was developed, endotracheal reintubation has been done for respiratory support. Noninvasive Positive Pressure Ventilation (NIPPV) has been used in the management of acute or chronic respiratory failure, as an alternative to endotracheal intubation, using via nasal or facial mask. In this study, we evaluated the usefulness of NIPPV as an alternative method of reintubation in patients who developed acute respiratory failure after extubation. Method: We retrospectively analyzed thirty one patients(eighteen males and thirteen females, mean ages $63\pm13.2$ years) who were developed acute respiratory failure within forty eight hours after extubation, or were extubated unintentionally at medical intensive care unit(MICU) of Asan Medical Center. NIPPV was applied to the patients. Ventilatory mode of NIPPV, level of ventilatory support and inspiratory oxygen concentration were adjusted according to the patient condition and results of blood gas analysis by the attending doctors at MICU. NIPPV was completely weaned when the patients maintained stable clinical condition under 8 $cmH_2O$ of pressure support level. Weaning success was defined as maintenance of stable spontaneous breathing more than forty eight hours after discontinuation of NIPPV. Respiratory rate, heart rate, arterial blood gas analysis, level of pressure support, and level of PEEP were monitored just before extubation, at thirty minutes, six hours, twenty four hours after initiation of NIPPV. They were also measured at just before weaning from NIPPV in success group, and just before reintubation in failure group. Results: NIPPV was successfully applied to thirty-one patients of thirty-two trials and one patient could not tolerated NIPPV longer than thirty minutes. Endotracheal reintubation was successfully obviated in fourteen patients (45%) among them. There was no difference in age, sex, APACHE III score on admission at MICU, duration of intubation, interval from extubation to initiation of NIPPV, baseline heart rate, respiratory rate, arterial blood gas, and $PaO_2/FiO_2$ between the success and the failure group. Heart rate and respiration rate were significantly decreased with increase $SaO_2$ after thirty minutes of NIPPV in both groups(p<0.05). However, in the patients of failure group, heart rate and respiratory rate were increased again with decrease in $SaO_2$ leading to endotracheal reintubation. The success rate of NIPPV treatment was significantly higher in the patients with COPD compared to other diseases(62% vs 39%) (p=0.007). The causes of failure were deterioration of arterial blood gas without aggravation of underlying disease(n=9), aggravation of undelying disease(n=5), mask intolerance(n=2), and retained airway secretion(n=l). Conclusion: NIPPV would be a useful therapeutic alternative which can avoid reintubation in patient who developed acute respiratory failure after extubation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.813-822
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• 1998

Background: Extubation is recommended to be performed at minimum pressure support (PSmin) during the pressure support ventilation (PSV). In field, physicians sometimes perform additional 1 hr T-piece trial to the patient at PSmin to reduce re-intubation risk. Although it provides confirmation of patient's breathing reserve, weaning could be delayed due to increased airway resistance by endotracheal tube. Methods: To investigate the effect of additional 1 hr T-piece trial on weaning outcome, a prospective study was done in consecutive 44 patients who had received mechanical ventilation more than 3 days. Respiratory mechanics, hemodymic, and gas exchange measurements were done and the level of PSmin was calculated using the equation (PSmin=peak inspiratory flow rate $\times$ total ventilatory system resistance) at the 15cm $H_2O$ of pressure support. At PSmin, the patients were randomized into intervention (additional 1 hr T-piece trial) and control (extubation at PSmin). The measurements were repeated at PSmm, during weaning process (in cases of intervention), and after extubation. The weaning success was defined as spontaneous breathing more than 48hr after extubation. In intervention group, failure to continue weaning process was also considered as weaning failure. Results: Thirty-six patients with 42 times weaning trial were satisfied to the protocol. Mean PSmin level was 7.6 (${\pm}1.9$)cm $H_2O$. There were no differences in total ventilation times (TVT), APACHE III score, nutritional indices, and respiratory mechanics at PSmin between 2 groups. The weaning success rate and re-intubation rate were not different between intervention group (55% and 18% in each) and control group (70% and 20% in each) at first weaning trial. Work of breathing, pressure time product, and tidal volume were aggravated during 1 hr T-piece trial compared to those of PSmin in intervention group ($10.4{\pm}1.25$ and $1.66{\pm}1.08$ J/L in work of breathing) ($191{\pm}232$ and $287{\pm}217$cm $H_2O$ s/m in pressure time product) ($0.33{\pm}0.09$ and $0.29{\pm}0.09$ L in tidal volume) (P<0.05 in each). As in whole, TVT, and tidal volume at PSmin were significantly different between the patients with weaning success ($246{\pm}195$ hr, $0.43{\pm}0.11$ L) and the those with weaning failure ($407{\pm}248$ hr, $0.35{\pm}0.10$L) (P<0.05 in each). Conclusion : There were no advantage to weaning outcome by addition of 1 hr T-piece trial compared to prompt extubation to the patient at PS min.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.128-139
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• 1998

Background: It is well known that various cytokines and growth factors secreted mainly from alveolar macrophages do the key role in the pathogenesis of IPF. But recently it has been known that structural cells like fibroblast can also release cytokines. So the phenotypic changes in fibroblasts of IPF may do a role in continuous progression of fibrosis. The aim of this study is to find out whether there is a change in the biologic properties of the lung fibroblasts of IPF. Subjects and Method: The study was done on 13 patients with IPF diagnosed by open or thoracoscopic lung biopsy and 7 control patients who underwent resectional surgery for lung cancer. Lung fibroblast cell lines (FB) were established by explant culture technique from the biopsy or resected specimen Result: Basal proliferation of the fibroblast of IPF(IFB) measured by BrdU uptake tended to be highter than control fibroblast(NFB) (0.212 0.107 vs $0.319{\pm}0.143$, p=0.0922), also there was no significant difference in proliferation after the stimulation with PDGF or 10% serum. On the contrary, the degree of inhibition in proliferation by PGE2 was significantly lower($33.0{\pm}13.1%$) in IFB than control($46.7{\pm}10.0%$, p=0.0429). The IFB secreted significantly higher amount of MCP-l($l574{\pm}1283$ pg/ml) spontaneously than NFB($243{\pm}100$ pg/ml) and also after the stimulation with TGF-$\beta$($3.23{\pm}1.31$ ng/ml vs $0.552{\pm}0.236$ ng/ml, p=0.0012). Similarly IL-8 and IL-6 seretion of IFB was significantly higher than NFB at basal state and with TGF-$beta$ stimulation. But after the maximal stimulation with IL-1,8, no significant difference in cytokine secretion was found between IFB and NFB. Conclusion : Above data suggest that the fibroblasts of IPF were phenotypically changed and these change may do a role in the pathogenesis of IPF.

• 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.4
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• pp.569-583
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• 1995

Background: The expression of the adhesion molecules on the cell surface is important in the movement of cells and the modulation of immune response. DILD starts as an alveolitis and progresses to pulmonary fibrosis. So adhesion molecules in these patients is expected to be increased. There are several reports about adhesion molecules in DILD in terms of the percentage of positive cells in immuno-stain, in which the interpretation is subjective and the data were variable. Methods: So we measured the relative median fluorescence intensity(RMFI) which is the ratio of the FI emitted by bound primary monoclonal antibody to FI emitted by isotypic control antibody of the cells in BALF of 28 patients with DILD(IPF:10, collagen disease:7, sarcoidosis:9, hypersensitivity pneumonitis:2) and 9 healthy control. Results: RMFI of the ICAM-1 on AM($3.30{\pm}1.16$) and lymphocyte($5.39{\pm}.70$) of DILD were increased significantly than normal control($0.93{\pm}0.18$, $1.06{\pm}0.21$, respectively, p=0.001, P=0.003). RMFI of the CD18 on lymphocyte was also higher($24.9{\pm}14.9$) than normal($4.59{\pm}3.77$, p=0.0023). And there was a correlation between RMFI of ICAM on AM and the % of AM(r=-0.66, p=0.0001) and lymphocyte(r=0.447, p=0.0116) in BALF. Also RMFI of ICAM on lymphocyte had a significant (r=0.593, p=0.075) correlation with the % of IL-2R(+) lymphocyte in BALF. The soluble ICAM(sICAM) in serum was also significantly elevated in DILD($499.7{\pm}222.2\;ng/ml$) compred to normal($199.0{\pm}38.9$) (p=0.00097) and sICAM in BAL fluid was also significantly higher than normal control group($41.8{\pm}23.0\;ng/ml$ vs $20.1{\pm}13.6\;ng/ml$). There was a Significant correlation between sICAM level in serum and the expression of ICAM-l on AM(r=0.554, p=0.0259).Conclusion: These data suggest that in DILD the expression of adhesion molecules is increased in the AM and BAL lymphocytes with elevated serum sICAM, and these parameter may be useful in determining disease activity.

• 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.44 no.3
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• pp.592-600
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• 1997

Background : The level of imposed work of breathing (WOB) is important for patient-ventilator synchrony and during weaning from mechanical ventilation. Triggering methods and the sensitivity of demand system are important determining factors of the imposed WOB. Flow triggering method is available on several modern ventilator and is believed to impose less work to a patient-triggered breath than pressure triggering method. We intended to compare the level of imposed WOB on two different methods of triggering and also at different levels of sensitivities on each triggering method (0.7 L/min vs 2.0 L/min on flow triggering ; $-1\;cmH_2O$ vs $-2cm\;H_2O$ on pressure triggering). Methods : The subjects were 12 patients ($64.8{\pm}4.2\;yrs$) on mechanical ventilation and were stable in respiratory pattern on CPAP $3\;cmH_2O$. Four different triggering sensitivities were applied at random order. For determination of imposed WOB, tracheal end pressure was measured through the monitoring lumen of Hi-Lo Jet tracheal tube (Mallincrodt, New York, USA) using pneumotachograph/pressure transducer (CP-100 pulmonary monitor, Bicore, Irvine, CA, USA). Other data of respiratory mechanics were also obtained by CP-100 pulmonary monitor. Results : The imposed WOB was decreased by 37.5% during 0.7 L/min on flow triggering compared to $-2\;cmH_2O$ on pressure triggering and also decreased by 14% during $-1\;cmH_2O$ compared to $-2\;cmH_2O$ on pressure triggering (p < 0.05 in each). The PTP(Pressure Time Product) was also decreased significantly during 0.7 L/min on flow triggering and $-1\;cmH_2O$ on pressure triggering compared to $-2\;cmH_2O$ on pressure triggering (p < 0.05 in each). The proportions of imposed WOB in total WOB were ranged from 37% to 85% and no significant changes among different methods and sensitivities. The physiologic WOB showed no significant changes among different triggering methods and sensitivities. Conclusion : To reduce the imposed WOB, flow triggering with sensitivity of 0.7 L/min would be better method than pressure triggering with sensitivity of $-2\;cm\;H_2O$.

• 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.43 no.2
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• pp.201-209
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• 1996

Background : Auto-PEEP which develops when expiratory lung emptying is not finished until the beginning of next inspiration is frequently found in patients on mechanical ventilation. Its presence imposes increased risk of barotrauma and hypotension, as well as increased work of breathing (WOB) by adding inspiratory threshold load and/or adversely affecting to inspiratory trigger sensitivity. The aim of this study is to evaluate the relationship of auto-PEEP with WOB and to evaluate the effect of PEEP applied by ventilator (external PEEP) on WOB in patients with auto-PEEP. Method : 15 patients, who required mechanical ventilation for management of acute respiratory failure, were studied. First, the differences in WOB and other indices of respiratory mechanics were examined between 7 patients with auto-PEEP and 8 patients without auto-PEEP. Then, we applied the 3 cm $H_2O$ of external PEEP to patients with auto-PEEP and evaluated its effects on lung mechanics as well as WOB. Indices of respiratory mechanics including tidal volume ($V_T$), repiratory rate, minute ventilation ($V_E$), peak inspiratory flow rate (PIFR), peak expiratory flow rate (PEFR), peak inspiratory pressure (PIP), $T_I/T_{TOT}$, auto-PEEP, dynamic compliance of lung (Cdyn), expiratory airway resistance (RAWe), mean airway resistance (RAWm), $p_{0.1}$, work of breathing performed by patient (WOB), and pressure-time product (PTP) were obtained by CP-100 Pulmonary Monitor (Bicore, USA). The values were expressed as mean $\pm$ SEM (standard error of mean). Results : 1) Comparison of WOB and other indices of respiratory mechanics in patients with and without auto-PEEP : There was significant increase in WOB ($l.71{\pm}0.24$ vs $0.50{\pm}0.19\;J/L$, p=0.007), PTP ($317{\pm}70$ vs $98{\pm}36\;cm$ $H_2O{\cdot}sec/min$, p=0.023), RAWe ($35.6{\pm}5.7$ vs $18.2{\pm}2.3\;cm$ H2O/L/sec, p=0.023), RAWm ($28.8{\pm}2.5$ vs $11.9{\pm}2.0cm$ H2O/L/sec, p=0.001) and $P_{0.1}$ ($6.2{\pm}1.0$ vs 2.9+0.6 cm H2O, p=0.021) in patients with auto-PEEP compared to patients without auto-PEEP. The differences of other indices including $V_T$, PEFR, $V_E$ and $T_I/T_{TOT}$ showed no significance. 2) Effect of 3 cm $H_2O$ external PEEP on respiratory mechanics in patients with auto-PEEP : When 3 cm $H_2O$ of external PEEP was applied, there were significant decrease in WOB ($1.71{\pm}0.24$ vs $1.20{\pm}0.21\;J/L$, p=0.021) and PTP ($317{\pm}70$ vs $231{\pm}55\;cm$ $H_2O{\cdot}sec/min$, p=0.038). RAWm showed a tendency to decrease ($28.8{\pm}2.5$ vs $23.9{\pm}2.1\;cm$ $H_2O$, p=0.051). But PIP was increased with application of 3 cm $H_2O$ of external PEEP ($16{\pm}2$ vs $22{\pm}3\;cm$ $H_2O$, p=0.008). $V_T$, $V_E$, PEFR, $T_I/T_{TOT}$ and Cdyn did not change significantly. Conclusion : The presence of auto-PEEP in mechanically ventilated patients was accompanied with increased WOB performed by patient, and this WOB was decreased by 3 cm $H_2O$ of externally applied PEEP. But, with 3 cm $H_2O$ of external PEEP, increased PIP was noted, implying the importance of close monitoring of the airway pressure during application of external PEEP.