Background : Residual pleural thickening is frequently seen following treatment for tuberculous pleurisy, and pleural decortication is performed occasionally in patients with severe residual pleural thickening. However, predictive factors for the development of residual pleural thickening are uncertain at the initial diagnosis of the tuberculous pleurisy. Therefore, the purpose of this study was to identify the associated factors for residual pleural thickening at initial diagnosis. Methods : We separated 63 patients diagnosed as tuberculous pleurisy into two groups; group 1 consisted of patients without residual pleural thickening and group 2 comprised patients with residual pleural thickening at the end of tuberculous pleurisy treatment. We analyzed the clinical characteristics, radiological findings, pleural biopsy and characteristics of pleural fluid between group 1 and group 2. Results : The study population and clinical symptoms of the two groups were not significantly different and the duration of symptoms before treatment and the peripheral WBC were similar between the two groups. The presence of pulmonary tuberculosis, pleural fluid loculation or the amount of pleural effusion sid not differ significantly between the two groups. The incidence of positive AFB staining(group 1 : 8%, group 2 : 38%) and granuloma(group 1 : 30%, group 2: 62%)on pleural biopsy specimens was significantly higher in group 2 than in group 1. Pleural fluid WBC and differential count, adenosine deaminase level, pH, protein level or glucose level did not differ between the two groups. However, group 2 had higher LDH levels ($1370{\pm}208mg/dL$) than group 1 ($860{\pm}71mg/dL$, p<0.05). Conclusion : In tuberculous pleurisy, patients with residual pleural thickening following treatment demonstrated a higher incidence of positive AFB staining and granuloma on the pleural biopsy specimens or higher LDH level in the pleural fluid than patients without residual pleural thickening From these results, we speculate that the amount of tuberculous bacilli and granuloma are probably correlated with residual pleural thickening in the tuberculous pleurisy.
Background : Tuberculous pleurisy treatments improve symptoms such as fever, chest pain, cough, and prevents the progression to active pulmonary tuberculosis and the development of residual pleural thickening that decrease diaphragm and rib cage movement This study investigated how the degree of residual pleural thickening affects the pulmonary function. Methods : Fifty seven patients who were initially diagnosed as having tuberculous pleurisy, were treated with anti-tuberculous medication for 6 months and had residual pleural thickening between May 1998 and January 2000 at the Eulji university hospital were reviewed. A chest X-ray and pulmonary function test(PFT, Sensormedics 2200) were performed. The predicted value(%) of the forced vital capacity(FVC), forced inspiratory vital capacity(FNC) and total lung capacity(TLC) were measured. The residual pleural thickening was defined the average of the summation in the lateral chest at the level of the imaginary line intersecting from the cardiophrenic angle to the diaphragmatic dome and the lowest part of the costophrenic angle between them. The results were sorted into three grades according to pleural thickness ; <2mm(grade I), 2~10mm(grade II), 10mm(grade III). Results : 1. FVC(% pred) and FIVC(% pred) were statistically different between grade I and III, and II and III. However, there was no difference between the TLC(% pred) between each of the groups. 2. The pleural thickness that cause restrictive dysfunction(FVC<80%) and a statistically difference, is 3mm. Conclusion : The larger the extent of the residual pleural thickness after antituberculous medication, the greater the reduction in the FVC, FIVC, TLC. A pleural thickness of 3mm is recommended as a guideline for diagnosing a restrictive pulmonary dysfunction.
Choi, Youngkwon;An, Chang Hyeok;Kim, Yu Jin;Kyung, Sun Young;Lee, Sang Pyo;Park, Jeong Woong;Jeong, Sung Hwan
Tuberculosis and Respiratory Diseases
/
v.65
no.1
/
pp.7-14
/
2008
Background: Residual pleural thickening (RPT) is the most frequent complication of tuberculous pleurisy (TP), and this can happen despite of administering adequate anti-tuberculous (TB) therapy. Yet there was no definite relation between RPT and other variables. The aim of this study was to examine matrix metalloproteinases (MMPs) and the inhibitors of metalloproteinases (TIMPs) and to identify the factors that can predict the occurrence of RPT. Methods: The patients with newly-detected pleural effusions were prospectively enrolled in this study from January 2004 to June 2005. The levels of MMP-1, -2, -8 and -9, and TIMP-1 and -2 were determined in the serum and pleural fluid by ELISA. The residual pleural thickness was measured at the completion of treatment and at the point of the final follow-up with the chest X-ray films. Results: The study included 39 patients with pleural fluid (PF). Twenty-three had tuberculous effusion, 7 had parapneumonic effusion, 7 had malignant effusion and 2 had transudates. For the 17 patients who completed the anti-TB treatment among the 23 patients with TP, 7 (41%) had RPT and 10 (59%) did not. The level of PF TIMP-1 in the patients with RPT ($41,405.9{\pm}9,737.3ng/mL$) was significantly higher than that of those patients without RPT ($29,134.9{\pm}8,801.8$) at the completion of treatment (p=0.032). In 13 patients who were followed-up until a mean of $8{\pm}5$ months after treatment, 2 (15%) had RPT and 11 (85%) did not. The level of PF TIMP-2 in the patients with RPT ($34.4{\pm}6.5ng/mL$) was lower than that of those patients without RPT ($44.4{\pm}15.5$) at the point of the final follow-up (p=0.038). Conclusion: The residual pleural thickening in TP might be related to the TIMP-1 and TIMP-2 levels in the pleural fluid.
Background: Tuberculous pleural effusion responds well to the anti-tuberculosis agents in general, so no further aggressive therapeutic managements to drain the tuberculous effusion is necessary except in case of diagnostic thoracentesis. But in clinical practice, we often see some patients who later decortication need due to dyspnea caused by pleural thickening despite the completion of anti-tuberculosis therapy in the patients with tuberculous effusion. Especially, the patients with loculated tuberculous effusion might have increased chance of pleural thickening after treatment. The purpose of this study was that intrapleural urokinase instillation could reduce the pleural thickening in the treatment of loculated tuberculous pleural effusion. Methods: Thirty-seven patients initially diagnosed as having loculated tuberculous pleural effusion were randomly assigned to receive either the combined treatment of urokinase instillation and anti-tuberculosis agents(UK group) and anti-tuberculosis agents(Non-UK group) alone. The 16 patients in UK group received a single radiographically guided pig-tail catheter ranging in size from 10 to 12 French. 100,000 units of urokinase was dissolved in 150 ml of normal saline and instilled into the pleural cavity via pig-tail catheter every day, also this group was treated with anti-tuberculosis agents. While the 21 patients in Non-UK group were treated with anti-tuberculosis agents only except diagnostic thoracentesis. Then we evaluated the residual pleural thickening after treatment for their loculated tuberculous pleural effusion between the two groups. Also the duration of symptoms and the pleural fluid biochemistry like WBC counts, pH, lactic dehydrogenase(LDH), glucose, proteins, and adenosine deaminase(ADA) were compared. Results: 1) The residual pleural thickening(RPT)($5.08{\pm}6.77$ mm) of UK group was significantly lower than that($20.3222{\pm}26.37$ mm) of Non-UK group(P<0.05). 2) The duration of symptoms before anti-tuberculosis drug therapy of patients with RPT$\geq$10 mm($5.23{\pm}3.89$ wks) was significantly longer than the patients with RPT<10 mm($2.63{\pm}1.99$ wks)(P<0.05). 3) There were no significant differences in the pleural fluid findings like WBC count, glucose, LDH, proteins, pH, ADA between the patients with RPT$\geq$10 mm and the patients with RPT<10 mm. Conclusion : The treatment of loculated tuberculous pleural effusion with the urokinase instillation via percutaneous transthoraic catheter was effective to reduce the pleural thickening.
Korean journal of aerospace and environmental medicine
/
v.31
no.2
/
pp.57-59
/
2021
For nonsmall cell lung cancer (NSCLC), surgery is indicated only for stage 3 as a curative measure. Even so, there is a high risk of recurrence following stage 3 lung cancer surgery, a third (33.9%) of patients experienced a cancer recurrence mostly within 2 years after surgery. The median survival time for all stages reaches only 21.9 months. For people undergoing surgery for stage 3A NSCLC, a pre-operative course of (neoadjuvant chemotherapy) can improve survival times, by improving the resectability and lowering the risk of recurrence. Pleural metastases are frequently associated with tumors of the lung and breast. Chest radiographs and computed tomography scans of pleural metastases can present as an effusion or smooth or nodular pleural thickening. In the absence of irregular or nodular pleural thickening, it is difficult to distinguish a benign from a malignant pleural effusion. To treat lung cancer, tyrosine kinase inhibitors (TKIs) recently have been used to cope with genetic mutations, apart from cytotoxic anticancer drugs. Compared to cytotoxic drugs, they are effective, have fewer side effects, and are easy to administer. Airman must have no cancer disease to apply for Class-I medical certification. Specifically, if previously operated on cancer, the cancer should not remain in the body at present, and the disease free state should persist at least one year after all kinds of anti-cancer treatments including adjuvant chemotherapy are completed. Here, this case deals with a 41-year-old pilot who has ATP license who had stage 3A NSCLC. The pilot underwent curative lung cancer surgery (lobectomy) a year ago and showed suspicious pleural metastasis at the time of his application for certification and was still using an unauthorized TKI agent alectinib (Alecensa; Roche, Basel, Switzerland).
Background : Residual pleural thickening (RPT) is the most common complication of tuberculous pleurisy (TP), despite adequate anti-tuberculous chemotherapy. At the conclusion of treatment, 43-50% of patients present RPT, with its incidence varying according to the time of evaluation. To assess the spontaneous resolution of RPT, the RPT at the completion of treatment was compared with that at the final follow-up. The factors related to the development of RPT after the completion of treatment were also studied. Methods : The medical records of sixty four patients, diagnosed with TP between March 2001 and June 2003, were retrospectively. The RPT was measured at the completion of treatment and at the time of the final follow-up and the degree and frequency of RPT compared between the two measurements. Each time, the patients were divided into two groups: those with and without RPT. The clinical characteristics and the radiographic and pleural fluid findings of the two groups were compared. Results : Thirty six (56%) and 27 patients had RPT at the completion of treatment and at the time of the final follow-up, respectively (median follow up period: 8 months). Spontaneous resolution of the RPT was found in 9 patients (24%), and had decrease below 10mm in 15 (42%) during the follow-up period after treatment. The patients were initially divided into two groups: 36 and 27 patients with and without RPT, respectively. There was no predicting factor of RPT, with the exception of the presence of CRP, between the two groups. The patients were also separated into two groups at the time of final visit: 27 and 37 patients with and without RPT, respectively. The patients with RPT were found to have a lower total WBC count in pleural fluid. Conclusion : 57% of patients with RPT were found to have spontaneous resolution of the residual pleural thickening after completion of the chemotherapy. The time of evaluation for RPT and its predicting factors were decided after adequate follow-up, irrespective of the completion of treatment.
Park, Jae-Seuk;Chun, Yong;Choi, Eun-Kyung;Jee, Young-Koo;Lee, Kye-Young;Kim, Keum-Youl
Tuberculosis and Respiratory Diseases
/
v.46
no.1
/
pp.17-24
/
1999
Background : A sizable percentage of tuberculous pleurisy patients are known to have residual pleural thickening(RPT) despite adequate anti-tuberculous chemotherapy. But, the predictive factors related to the development of RPT is not well known. Therefore, we studied to determine which factors are related to the development of RPT after completion of therapy. Methods: By retrospective review of medical records, fifty-eight patients initially diagnosed as having tuberculous pleurisy between March 1995 and January 1998 were separated into two groups : 27 patients in group 1 had RPT on simple chest radiography, while 31 patients in group 2 had no RPT after 6 month of anti-tuberculous chemotherapy. The clinical characteristics, radiologic findings and pleural fluid findings of the two group were compared at the time of diagnosis and during the course of therapy. Results: 47% of patients had RPT after 6 month of chemotherapy, and RPT was more common in man than in women(54% vs 29%, p=0.092). In group 2 patients, complete resorption of pleural lesion occurred rather late stage of therapy(1-2 month: 26%, 3-4 month: 29%, 5-6 month: 45%). Group 1 patients had increased percentage of loculated pleural lesion(26 % vs 19%) and increased white blood cell and lymphocyte count, lactate dehydrogenase level in pleural fluid ($3527\pm5652$ vs $2467\pm2201$/ml, $2066\pm2022$ vs $1698\pm1835$/ml and $1636\pm1143$ vs $1441\pm923$IU/mL respectively) than group 2 at the time of diagnosis, but statistically insignificant. Duration of symptom prior to treatment, size of pleural effusion, presence of parenchymal lung lesion, level of total protein, glucose and adenosine deaminase(ADA)activity in pleural fluid were similar in both group. Conclusion: 53% of tuberculous pleurisy patients showed slow but complete resorption of pleural lesion after 6 month of chemotherapy. But, no clinical, radiological and pleural fluid findings are predictive for the development of RPT.
Hong, Koo Hyun;Lim, Sang Soo;Shin, Jae Min;Park, Jae Seuk
Tuberculosis and Respiratory Diseases
/
v.61
no.6
/
pp.526-532
/
2006
Backgroud: Traditionally, tuberculous pleurisy has been known to largely develop as primary tuberculosis. However, as the incidence of tuberculosis decrease, recent studies have shown reactivation tuberculosis has become the main cause of tuberculous pleurisy. Methods: 141 cases of tuberculous pleurisy, between January 2003 and February 2006, at the Dankook university hospital. were retrospectively studied. The patients were divided into primary and reactivation tuberculosis. based on the history and radiological characteristics, and the clinical, radiological characteristics at the time of diagnosis and residual pleural thickening after 6 month of chemotherapy were compared between the two groups. Results: 1. Of the 141 tuberculous pleurisy cases, in 135 it was possible to differentiate between primary and reactivation tuberculosis. 2. Of the 135 tuberculous pleurisy cases, 38 (28%) showed a primary tuberculosis pattern, and 98 (72%) showed a reactivation tuberculosis pattern. 3. There were no significant differences between primary and reactivation tuberculosis in relation to age, sex, duration of symptom, amount of pleural effusion, pleural fluid WBC, lymphocyte count, and level of protein, LDH and ADA at the time of diagnosis 4. 124 patients were followed for 6 months after diagnosis of tuberculous pleurisy, and there was no significant difference in the residual pleural thickening between primary and reactivation tuberculosis. Conclusion: In South Korea, a reactivation disease is currently a more common cause of tuberculous pleurisy than a primary disease. There was no difference in the clinical characteristics between primary and reactivation tuberculosis.
Background: The routine application of the combined regimen of corticosteroid-antituberculosis therapy to the tuberculous pleurisy remains controversial. Steroid therapy to tuberculous pleurisy could be effective on the acceleration of absorption of pleural effusion and symptom improvement, but there has been debate about the effect of prednisolone on the prevention of pleural adhesion. So we studied the efficacy of combined regimen of prednisolone-antituberculosis therapy on the absorption of pleural effusion and prevention of pleural adhesion. Method: A prospective, randomized study was performed in 82 patients, 50 patients(non-steroid group) were treated with only antituberculosis regimen for 6 months and in 32 patients(steroid group) prednisolone(30mg/day) were administered in addition to antituberculosis regimen for one months and tapered for another month. The amount of pleural effusion was compared at the beginning of treatment, 2nd month, 6th month and final visit with chest X-ray findings which were graded from grade 0(complete absorption) to grade 6(near total haziness). Results: The amount of pleural effusion of steroid group at 2nd month, 6th month and final visit was lesser than that of non-steroid group(P<0.05). The incidence of the complete absorption of the pleural effusion was 3/32(9.4%) in steroid group, 1/50(2%) in non-steroid group at 2nd month after treatment; and 12/32(37.5%) in steroid group, 6/50(12%) in non-steroid group at 6th month after treatment(P<0.05). At final observation, the incidence of residual pleural thickening was 15/32(47%) in steroid group and 37/50(74%) in non-steroid group(P<0.05). No serious side effects were noted during the treatment with prednisolone. Conclusion: The administration of prednisolone in conjunction with antituberculosis chemotherapy improved the absorption of pleural effusion and decreased the residual pleural thickening.
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.
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