Background: For the diagnosis of pleural tuberculosis, polymerase chain reaction (PCR) of pleural effusion specimens has shown very low sensitivity, which might be due to the small number of bacilli in the samples. The purpose of this investigation is to determine whether the sensitivity of PCR testing can be improved when increasing the amount of pleural effusion specimens. Methods: We prospectively analyzed pleural effusion specimens obtained from 53 patients for whom the exclusion of the possibility of tuberculous pleural effusion was necessary. We performed Mycobacterium tuberculosis PCR testing using the Cobas Amplicor MTB test (Roche Diagnostic Systems) with three different amounts (10ml, 25ml, and 50ml) of pleural effusion specimen in each patient. Pleural tuberculosis was defined as having one of the following: culture-positive pleural fluid sample, histopathologic finding consistent with tuberculosis on pleural biopsy, culture-positive sputum specimen, and/or positive response to anti-tuberculous medication without other possible causes of pleural effusion. Results: Of the 53 patients, 26 received the diagnosis of pleural tuberculosis. The sensitivities of AFB smearing, Mycobacterium tuberculosis culture of pleural effusion specimen, pleural biopsy, and measurement of ADA were 3.8%, 15.4%, 84.6%, and 88.5%, respectively. The results of PCR testing were positive for 3 (11.5%), 4 (15.4%), and 3 (11.5%) of the 26 patients when using 10ml, 25ml, and 50ml of pleural effusion specimens, respectively. These results did not show a statistically significant difference in the sensitivity of PCR testing when increasing the amount of pleural effusion samples (p>0.05, symmetry exact test). Conclusion: For specimens such as pleural effusion, in which the bacillary load is very low, the clinical utility of PCR testing seems highly limited with the kits designed for the diagnosis of pulmonary tuberculosis. An increased amount of pleural effusion sample does not improve the sensitivity of PCR testing.
Jung, Jae Woo;Lee, Young Woo;Choi, Jae Cheol;Yoo, Seung Min;Lee, Hwa Yeon;Lim, Seoung Young;Shin, Jong Wook;Kim, Jae Yoel;Park, In Whn;Kim, Mi Kyung;Choi, Byoung Whui
Tuberculosis and Respiratory Diseases
/
v.60
no.5
/
pp.523-531
/
2006
Background : Cervical tuberculous lymphadenopathy is a very common disease with a similar incidence to pulmonary tuberculosis. Dendritic cells play a role of initial antigen presentation of this illness. Nevertheless, the precise role of these antigen-presenting cells according to the clinical features in unclear. The aim of this study was to determine the clinical implication of dendritic cell infiltration in the cervical lymph nodes. Methods : A review of the clinical characteristics was carried out retrospectively based on the clinical records and radiography. Immunohistochemical staining was performed on the available histology specimens of 72 cases using the S-100b polyclonal antibody for dendritic cells. The number of dendritic cells with tuberculous granuloma were determined. A $X^2$ test, unpaired T test and multiple logistic regression analysis were performed. Results : Thirty percent of subjects had previous or concurrent pulmonary TB. Twenty one percent of cases showed a positive reaction on the AFB stain. Within a granuloma, the number of infiltrated dendritic cells was $113.0{\pm}7.0$. The incidence of fever and cough decreased with increasing infiltration of dendritic cells Multivariate regression analysis showed that the infiltration of dendritic cells could significantly contribute to fever. Conclusion : Overall, dendritic cells can control a Mycobacterium tuberculosis infection and modulate the immune response, as well as resolve the clinical manifestations of TB lymphadenopathy.
Lee, Kye Young;Jee, Young Koo;Choi, Young Hi;Myong, Na Hye;Kim, Keun Youl
Tuberculosis and Respiratory Diseases
/
v.43
no.4
/
pp.613-622
/
1996
Constrictive bronchiolitis, one of small airway diseases, is very rare and occupies one of the two arms of bronchiolitis obliterans together with proliferative bronchiolitis. Proliferative bronchiolitis, presenting the prototype with bronchiolitis obliterans with organizing pneumonia(BOOP), can be easily taken into diagnostic consideration in terms of relatively rapid clinical course and radiologic presentation as if atypical pneumonia with interstitial and alveolar infiltrations. Meanwhile constrictive bronchiolitis is not only very Tare but also easily overlooked as chronic obstructive pulmonary diseases such as emphysema, because it usually shows normal chest radiographic finding and obstructive pattern in pulmonary function test. In the aspects of the response to treatment, proliferative bronchiolitis showed dramatic response to the corticosteroid while constrictive bronchiolitis is intractable, which is easily explained on the basis of the pathologic characteristics of cicartrical replacement of bronchiolar walls. The bronchiolitis, both proliferative and constrictive, can be associated with diverse conditions such as inhalational injury, postinfectious process, drug of chemical induced reactions, connective tissue diseases, and organ trasplantation. And there is idiopathic type which has no associated condition. There is one explanation that both types of bronchiolitis lie on the same disease spectrum because the different disease pattern can be evoked from the same etiology. In contrast, another explanation is suggested that both types of bronchiolitis are one of nonspecific tissue reaction rather than a disease specific histologic finding because the various types of causes can provoke the same histologic findings. These dilemma remains for further investigation. With literature investigation, the authors report a case of constrictive bronchiolitis proven by open lung biopsy in 47 year old female who was diagnosed as non-Hodgkin's lymphoma and simultaneously had relatively rapid progression of airflow obstruction and showed negative radiographic finding without the rise factors for the development of chronic obstructive lung disease. We consider it as idiopathic because we could not find any relationship between constrictive bronchiolitis and non-Hodgkin's lymphoma on the literature search and it requires further investigation.
Park, Sang Sun;Kim, Eun Joung;Son, Chang Young;Wi, Jeong Ook;Park, Kyung Hwa;Cho, Gye Jung;Ju, Jin Young;Kim, Kyu Sik;Kim, Yu II;Lim, Sung Chul;Kim, Young Chul;Park, Kyung Ok;Na, Kook Joo
Tuberculosis and Respiratory Diseases
/
v.55
no.1
/
pp.88-97
/
2003
Background : Although smoking is a major cause of chronic obstructive pulmonary disease (COPD), only 10-20% of cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in the activities of the enzyme that detoxify hazardous chemical products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase M1 subunit (GSTM1) genes. Methods : The genotypes of 58 patients with COPD, and 79 age matched control subjects, were determined by a polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX, and multiplex PCR for the GSTM1. Results : GSTM1 was deleted in 53.3% of the subjects. There was no difference in GSTM1 deletion rates between the COPD patients (32/58, 55.2%) and the control subjects (41/79, 51.9%). The combination patterns of two polymorphisms of mEPHX showed slow enzyme activity in 29(21.2%), normal in 73(53.3%) and fast in 32(23.4%). The COPD group (7/57, 12.3%) showed a significantly lower incidence of slow enzyme activity compared to the control subjects (22/77, 28.6%, p<0.05). However, when the COPD and control groups were compared with smokers only, there were no significant differences in the genotypes of GSTM1 and mEPHX. Conclusion : The genotypes of GSTM1 and mEPHX were not significant risk factors of COPD in this cohort of study.
Background : Aquaporins (AQPs) may play a role in the pathogenesis of pulmonary inflammation and edema. This study investigated the role ofAQPs in acute lung injury following bleomycin inhalation in rats. Methods : Sprague-Dawley rats were treated via inhalation with 10 U/kg bleomycin hydrochloride dissolved in 5 ml of normal saline. The control rats were treated with 5 ml normal saline. The animals (n = 6-8 rats per group) were sacrificed at 4, 7, and 14 d. The changes in AQP1, AQP4, and AQP5 expression levels over time were analyzed by Western blotting. The nitrate and nitrite concentrations in the bronchoalveolar lavage fluid (BALF) were measured using a modified Griess reaction. ELISA was used to check cytokines. Results : The respiration rates were significantly higher 4 and 7 days after the bleomycin treatment compared with those of the control rats. The tidal volume was lower in rats at 4 days after the bleomycin treatment, and the wet/dry weights of the lung were significantly higher than those of the control group. The nitrite and nitrate concentrations in the BALF from the rats at 4 days after exposure to bleomycin were greater than those from the saline-treated rats. Immunoblotting studies demonstrated that the AQP1 and AQP4 expression levels were lower in the rats at 4 days. However, the AQP4 expression level was higher at 7 days. The AQP5 expression level increased at 4, 7 and 14 days after the bleomycin treatment. Conclusion : This study demonstrates that AQPs are expressed differently in bleomycin-induced pulmonary edema.
Shin, Jong Wook;Kim, Kae-Young;Lee, Young Woo;Jung, Jae Woo;Lee, Byoung Jun;Kim, Jae-Yeol;Jo, Inho;Park, In Won;Choi, Byoung Whui
Tuberculosis and Respiratory Diseases
/
v.57
no.1
/
pp.37-46
/
2004
Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$$CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.
Backgrounds: This study investigated whether or not a polymorphism in the gene encoding the surfactant protein A(SP-A) has any bearing on the individual susceptibility to the development of chronic obstructive pulmonary disease(COPD) in a genetically homogenous Korean population. Methods: The genotypes of 19 COPD patients and 20 healthy neonates as controls were tested using a polymerase chain reaction followed by restriction fragment length polymorphism analysis for the SP-A gene. Results: The specific frequencies of the 6A2 and 6A18 alleles of SP-A1 and the 1A2 allele of SP-A2 were much higher in the COPD group than control group (p<0.05). However, the frequencies of the 6A3 and 6A4 alleles of SP-A1 and the 1A0 allele of SP-A2 in the COPD group were significantly lower than the control group. In the COPD group, the frequencies of the +50 locus genotypes GG of SP-A1 and the +9 locus genotypes CC of SP-A2 were 85.0% and 60.6%, respectively, and 19.7% and 24.8% in the control group, respectively. The frequencies of the polymorphic genotypes or alleles showed a statistically significant difference between the COPD group and the control group (P<0.05). Conclusion: A genetic polymorphism in SP-A is associated with the development of COPD in the Korean population.
Background: It has been recognized that systemic inflammatory reaction and oxygen free radical formed by activated leukocyte in the procedure of cardiopulmonary bypass(CPB) frequently produce postoperative cardiac and pulmonary dysfunction. The purpose of this study was to evaluate the efficacy of leukocyte-depleting filters in the cardiopulmonary bypass circuit for patients undergoing open heart surgery(OHS). Material and method: The study involved 15 patients who underwent OHS with a Leukoguard-6 leukocyte filter placed in the arterial limbs of the bypass circuit(filter group, n=15) and 15 patients who did not have the filter(control group, n=15). We analyzed the differences between the groups in intraoperative changes of peripheral blood leukocyte and platelet counts, pre- and postbypass changes of malondialdehyde(MDA), troponin-T(TnT), 5'-nucleotidase(5'-NT) in coronary sinus blood, spontaneous recovery rate of heart beat after CPB, pre-and postoperative cardiac index(Cl) and pulmonary vascular resistance(PVR), and the amounts of postoperative bleeding and sternal wound complication. Result: During CPB, total leukocyte count of the filter group(9,567$\pm$ 842/㎣) was significantly less than that of the control group(13,573+1,167/㎣) (p<0.01), but there was no significant difference in platelet count between the groups. Postoperative levels of MDA(3.78+0.32 $\mu$mol/L vs 5.86+0.65 $\mu$mo1/L, p<0.01), TnT(0.40$\pm$0.04 ng/mL vs 0.59$\pm$0.08 ng/mL, p<0.05) and 5'-NT(3.88$\pm$0.61 U/L vs 5.80$\pm$0.90 U/L, p<0.05) were all significantly lower in the filter group than the control group. Postoperative Cl was higher in the filter group than the control group(3.26$\pm$0.18 L/$m^2$min vs 2.75$\pm$0.17 L/$m^2$/min, p=0.05). PVR of the filter group was lower than that of the control group(65.87$\pm$7.59 dyne/sec/cm$^{5}$ vs 110.80+12.22 dyne/sec/cm$^{5}$ , p<0.01). Spontaneous recovery rate of heart beat in the filter group was higher than that in the control group(12 patients vs 8 patients, p<0.05). Postoperative wound infection occurred in one case in the filter group and 4 case in the control group(p<0.05). Postoperative 24 hour blood loss of the filter group was more than that of the control group (614$\pm$107 mL vs 380+71 mL, p=0.05).
Epidemiological studies have demonstrated an association between exposure to diesel exhaust particles (DEP) and adverse cardiopulmonary effects. Despite the epidemiological proof, the pathogenesis of DEP-related pulmonary diseases remain poorly understood. So, comprehensive in vivo and in vitro researches are required to know the effects of DEP on diverse lung diseases. Alveolar macrophages (AM) and airway epithelial cells are known as important cellular targets in DEP-induced lung diseases. Other studies have shown that nitric oxide (NO) is involved in particle matter induced lung injury. The present study was undertaken to determine whether DEP has an synergistic effects on lipopolysaccharide (LPS)-induced NO formation and inducible nitric oxide synthase (iNOS) with nitrotyrosilated-protein formation in cultured primary alveolar macrophages. The formation of NO was determined through the Griess reaction in the cultured medium and iNOS with nitrotyrosilated-proteins are analyzed by immunohistochemical staining and Western analysis. The results indicate that DEP exposure does not induce NO formation by itself, however DEP showed significant synergistic effects on LPS-induced NO formation. So, our results suggest that DEP inhalation could aggravate inflammatory lung disease through NO formation.
A total of 1,192 patients, who complained a continued chronic cough, suptum or occasional hemoptysis, in spite of successful completion of antituberculous chemotherapy or had some suspected fungal infection, were included. Serum specimens were collected from all the patients studied and sputum or other specimens collected and cultured from the most of the patients. 405(34.0%) cases of the total patients studied showed a positive precipitin reaction to the one or more of the fungal antigens on immunodiffusion tests and 303 cases of them were found to have been infected with Aspergilli, of which Aspergillus fumigatus was involved in 287 cases, followed by Aspergillus flavus(1.7%), Aspergillus nidulans(0.3%), Aspergillus niger(0.3%) and Aspergillus nidulans var. latus(0.1%). pricipitin antibodies were produced to Candida albicans(8.1%) and Pseudallerscheria boydii(0.8%). In the chest radiographs of 186 precipitin positive patients, distinct fungus ball shadows were seen in 47 cases and 45 cases of them were formed by A. fumigatus. The isolates from sputum specimens of 724 patients were aspergilli which were consisted of the 46.4% of the total fungal isolates. Identification of 137 yeast like fungi from the sputum specimens of 413 patients revealed that C. albicans(64.2%) was a commonest yeast flora.
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