Pub Date : 2021-12-24DOI: 10.15406/jlprr.2021.08.00268
Maaria Chaudhry, L. Didenko, K. Alekseyev, Mohammad Umar Farooq, B. Chaudhry
Upon examination, it was found that she was mildly tachypneic and had JVD (Jugular vein distention). Sem noted in tricuspid region. Abdominal fullness with shifting dullness was also noted. A chest radiograph was preformed in emergency room revealed a moderate right pleural effusion. Her BNP was mildly elevated at 1900 (1-200), and her creatinine was 2.5. She was subsequently admitted for lower extremity edema, abdominal ascites and right-sided pleural effusion related to her underlying cardiac disease. A CXR revealed minimal left effusion and moderate size right pleural effusion.
{"title":"A Case of hydropneumothorax","authors":"Maaria Chaudhry, L. Didenko, K. Alekseyev, Mohammad Umar Farooq, B. Chaudhry","doi":"10.15406/jlprr.2021.08.00268","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00268","url":null,"abstract":"Upon examination, it was found that she was mildly tachypneic and had JVD (Jugular vein distention). Sem noted in tricuspid region. Abdominal fullness with shifting dullness was also noted. A chest radiograph was preformed in emergency room revealed a moderate right pleural effusion. Her BNP was mildly elevated at 1900 (1-200), and her creatinine was 2.5. She was subsequently admitted for lower extremity edema, abdominal ascites and right-sided pleural effusion related to her underlying cardiac disease. A CXR revealed minimal left effusion and moderate size right pleural effusion.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"61 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79126237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-12-23DOI: 10.15406/jlprr.2021.08.00267
Gudisa Bereda
Medication-resistant tuberculosis is a considerable across-the-board public health challenge that menace’s the substantial advance made in tuberculosis heedfulness and precluding in current decades. Multidrug-resistant tuberculosis is caused by organisms that are resistant to the consummate effective anti-tuberculosis medications (isoniazid and rifampicin). Tuberculosis organisms resistant to the antibiotics used in its treatment are extendedly and happen in entire countries studied. Medication resistance noticed as a sequence of insufficient treatment and once tuberculosis organisms obtain resistance they can disseminate from person to person in the similar way as medication-sensitive tuberculosis. Multidrug-resistant tuberculosis sequences from either infection with organisms which are previously medication-resistant or perhaps advance in the program of a patient's treatment. Rifampicin-resistant tuberculosis is caused by bacteria that do not answered to rifampicin, one of the consummate influential anti- tuberculosis medications. These patients necessitated multidrug-resistant tuberculosis treatment. Extendedly medication-resistant tuberculosis is a figure of tuberculosis caused by organisms that are resistant to isoniazid and rifampicin (i.e. multidrug-resistant tuberculosis) as well as every fluoroquinolone and any of the second–line anti- tuberculosis injectable drugs (amikacin, kanamycin or capreomycin). Extendedly medication-resistant tuberculosis can elaborate when second-line medications are used incorrectly or wrongly managed and upon become ineffective.
{"title":"Medication resistant tuberculosis: multi drugresistant and extensively drug resistant","authors":"Gudisa Bereda","doi":"10.15406/jlprr.2021.08.00267","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00267","url":null,"abstract":"Medication-resistant tuberculosis is a considerable across-the-board public health challenge that menace’s the substantial advance made in tuberculosis heedfulness and precluding in current decades. Multidrug-resistant tuberculosis is caused by organisms that are resistant to the consummate effective anti-tuberculosis medications (isoniazid and rifampicin). Tuberculosis organisms resistant to the antibiotics used in its treatment are extendedly and happen in entire countries studied. Medication resistance noticed as a sequence of insufficient treatment and once tuberculosis organisms obtain resistance they can disseminate from person to person in the similar way as medication-sensitive tuberculosis. Multidrug-resistant tuberculosis sequences from either infection with organisms which are previously medication-resistant or perhaps advance in the program of a patient's treatment. Rifampicin-resistant tuberculosis is caused by bacteria that do not answered to rifampicin, one of the consummate influential anti- tuberculosis medications. These patients necessitated multidrug-resistant tuberculosis treatment. Extendedly medication-resistant tuberculosis is a figure of tuberculosis caused by organisms that are resistant to isoniazid and rifampicin (i.e. multidrug-resistant tuberculosis) as well as every fluoroquinolone and any of the second–line anti- tuberculosis injectable drugs (amikacin, kanamycin or capreomycin). Extendedly medication-resistant tuberculosis can elaborate when second-line medications are used incorrectly or wrongly managed and upon become ineffective.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"142 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77944998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-09-09DOI: 10.15406/jlprr.2021.08.00264
I. Klepikov
Despite the lack of scientific justification and objective arguments, the centuries-old experience of medicine allows us to note the general trend in the development of first aid methods for AP. Without being able to scientifically study the problem and test various procedures, ancient medicine was able to determine exclusively empirically the importance of reducing the load of blood on the pulmonary vessels in a critical situation. In fact, the only assessment of these efforts remained the results of treatment.
{"title":"First aid for acute lung inflammation","authors":"I. Klepikov","doi":"10.15406/jlprr.2021.08.00264","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00264","url":null,"abstract":"Despite the lack of scientific justification and objective arguments, the centuries-old experience of medicine allows us to note the general trend in the development of first aid methods for AP. Without being able to scientifically study the problem and test various procedures, ancient medicine was able to determine exclusively empirically the importance of reducing the load of blood on the pulmonary vessels in a critical situation. In fact, the only assessment of these efforts remained the results of treatment.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"53 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73030608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-09-03DOI: 10.15406/jlprr.2021.08.00263
R. Choron, Stephen Iacono, Karishma Maharaja, Christopher D. Adams, Christopher A. Butts, C. Bargoud, Amanda L. Teichman, Nicole Krumrei, M. Schroeder, M. B. Bover Manderski, M. Rodricks, M. Lissauer, Rajan Gupta
Background: Literature has well established COVID-19 associated coagulopathy with resulting thrombotic complications including microthrombi as an underlying mechanism leading to severe respiratory disease. Therapeutic anticoagulation (TAC) for COVID-19 patients has therefore been widely trialed to combat COVID-19’s coagulopathic effects. However, literature has yet to define which population of patients TAC benefits; the most current randomized controlled trials (RCTs) reveal TAC to be possibly beneficial to moderately-ill hospitalized COVID-19 patients, whereas benefits did not outweigh risks in critically-ill ICU patients. Importantly, these studies excluded patients who received prehospital TAC. We examined outcomes in critically ill COVID-19 ICU patients who received TAC vs prophylactic anticoagulation (PAC) and specifically whether prehospital TAC effected outcomes. Methods: Retrospective cohort study of 132 COVID-19 ICU patients admitted March-June, 2020. Initial clinical practice provided PAC, as literature demonstrating COVID-19 associated coagulopathy and increased thromboembolic complications emerged, a TAC protocol was initiated. Results: 130 patients were included in the study, 95 of whom received TAC and 35 PAC. There was 50.8% overall mortality, with lower mortality in the TAC vs PAC group (46.3% vs 62.9%, p=0.094). There were few thromboembolic and hemorrhagic complications, with no significant difference between TAC and PAC patients. Of 24 patients anticoagulated prior to and during hospitalization, only 1 (4.2%) died, whereas the mortality was 60.6% among patients therapeutically anticoagulated during hospitalization only (p<0.001). Multivariable analysis revealed patients who received prehospital and in hospital TAC had a 92% lower risk of death (p=0.008) compared to in hospital only TAC and PAC patients. Conclusions: Overall, therapeutic anticoagulation did not result in mortality benefit to COVID-19 ICU patients compared to prophylactic anticoagulation. However, a sub-population of patients who received TAC both prior to and during hospitalization had a 12-fold lower risk of death. This suggests a protective effect of TAC when it is continued before and during hospitalization. RCTs are needed to specifically examine this subset of COVID-19 patients.
{"title":"Continuation of therapeutic anticoagulation before and during hospitalization is associated with reduced mortality in COVID-19 ICU patients","authors":"R. Choron, Stephen Iacono, Karishma Maharaja, Christopher D. Adams, Christopher A. Butts, C. Bargoud, Amanda L. Teichman, Nicole Krumrei, M. Schroeder, M. B. Bover Manderski, M. Rodricks, M. Lissauer, Rajan Gupta","doi":"10.15406/jlprr.2021.08.00263","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00263","url":null,"abstract":"Background: Literature has well established COVID-19 associated coagulopathy with resulting thrombotic complications including microthrombi as an underlying mechanism leading to severe respiratory disease. Therapeutic anticoagulation (TAC) for COVID-19 patients has therefore been widely trialed to combat COVID-19’s coagulopathic effects. However, literature has yet to define which population of patients TAC benefits; the most current randomized controlled trials (RCTs) reveal TAC to be possibly beneficial to moderately-ill hospitalized COVID-19 patients, whereas benefits did not outweigh risks in critically-ill ICU patients. Importantly, these studies excluded patients who received prehospital TAC. We examined outcomes in critically ill COVID-19 ICU patients who received TAC vs prophylactic anticoagulation (PAC) and specifically whether prehospital TAC effected outcomes. Methods: Retrospective cohort study of 132 COVID-19 ICU patients admitted March-June, 2020. Initial clinical practice provided PAC, as literature demonstrating COVID-19 associated coagulopathy and increased thromboembolic complications emerged, a TAC protocol was initiated. Results: 130 patients were included in the study, 95 of whom received TAC and 35 PAC. There was 50.8% overall mortality, with lower mortality in the TAC vs PAC group (46.3% vs 62.9%, p=0.094). There were few thromboembolic and hemorrhagic complications, with no significant difference between TAC and PAC patients. Of 24 patients anticoagulated prior to and during hospitalization, only 1 (4.2%) died, whereas the mortality was 60.6% among patients therapeutically anticoagulated during hospitalization only (p<0.001). Multivariable analysis revealed patients who received prehospital and in hospital TAC had a 92% lower risk of death (p=0.008) compared to in hospital only TAC and PAC patients. Conclusions: Overall, therapeutic anticoagulation did not result in mortality benefit to COVID-19 ICU patients compared to prophylactic anticoagulation. However, a sub-population of patients who received TAC both prior to and during hospitalization had a 12-fold lower risk of death. This suggests a protective effect of TAC when it is continued before and during hospitalization. RCTs are needed to specifically examine this subset of COVID-19 patients.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"66 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83720174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-09-03DOI: 10.15406/jlprr.2021.08.00262
N. Chokshi, A. Abdul-Hafez, B. Uhal
Purpose: Meconium pneumonitis occurs due to local lung injury and inflammation in newborn with meconium aspiration. The activation of Renin Angiotensin System (RAS) plays critical role in lung injury. Angiotensin converting enzyme-2 (ACE 2) functions as a negative regulator of the angiotensin system by converting pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. Our previous study has shown that meconium causes degradation of lung protective ACE-2 by proteolytic enzymes present in meconium. However, the specific proteases in meconium that degrade ACE-2 have not yet been identified. Objective: To begin characterizing ACE-2-degrading proteases in meconium through the use of different subtypes of protease inhibitors. Methods: Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium and meconium + specific protease inhibitors (PIs). Specific PIs used included chymostatin, AEBSF(Pefobloc) and leupeptin. At the end of incubation, cell lysates were collected for ACE-2 immunoblotting and enzyme activity. Results: Reduction of ACE-2 immunoreactive 100-115 kDa bands or enzymatic activity by meconium was attenuated by treatment with chymostatin, but not with the other the PIs. These data suggest the involvement of cysteine-like proteases in meconium in ACE-2 degradation, and suggest a potential therapeutic strategy of PI administration to babies aspirating meconium.
{"title":"Subtyping meconium protease activities which degrade lung protective angiotensin converting enzyme-2 in human lung cells","authors":"N. Chokshi, A. Abdul-Hafez, B. Uhal","doi":"10.15406/jlprr.2021.08.00262","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00262","url":null,"abstract":"Purpose: Meconium pneumonitis occurs due to local lung injury and inflammation in newborn with meconium aspiration. The activation of Renin Angiotensin System (RAS) plays critical role in lung injury. Angiotensin converting enzyme-2 (ACE 2) functions as a negative regulator of the angiotensin system by converting pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. Our previous study has shown that meconium causes degradation of lung protective ACE-2 by proteolytic enzymes present in meconium. However, the specific proteases in meconium that degrade ACE-2 have not yet been identified. Objective: To begin characterizing ACE-2-degrading proteases in meconium through the use of different subtypes of protease inhibitors. Methods: Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium and meconium + specific protease inhibitors (PIs). Specific PIs used included chymostatin, AEBSF(Pefobloc) and leupeptin. At the end of incubation, cell lysates were collected for ACE-2 immunoblotting and enzyme activity. Results: Reduction of ACE-2 immunoreactive 100-115 kDa bands or enzymatic activity by meconium was attenuated by treatment with chymostatin, but not with the other the PIs. These data suggest the involvement of cysteine-like proteases in meconium in ACE-2 degradation, and suggest a potential therapeutic strategy of PI administration to babies aspirating meconium.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84802344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-09-02DOI: 10.15406/jlprr.2021.08.00261
Fahad Alsulami, I. Dhaliwal, M. Mrkobrada, Michael Nicholson
Organizing pneumonia secondary to viral infection is well established entity in the literature. Here we describe 6 cases of organizing pneumonia secondary to COVID-19. All six cases were presented with respiratory symptoms after their initial COVID-19 infection, and they had CT changes compatible with organizing pneumonia. Steroid treatment was initiated in all cases empirically without the need for trans-bronchial biopsy. All presented cases showed significant improvement with steroid clinically and radiographically.
{"title":"Post Covid-19 organizing pneumonia: Case series for 6 patients with post-COVID interstitial lung disease","authors":"Fahad Alsulami, I. Dhaliwal, M. Mrkobrada, Michael Nicholson","doi":"10.15406/jlprr.2021.08.00261","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00261","url":null,"abstract":"Organizing pneumonia secondary to viral infection is well established entity in the literature. Here we describe 6 cases of organizing pneumonia secondary to COVID-19. All six cases were presented with respiratory symptoms after their initial COVID-19 infection, and they had CT changes compatible with organizing pneumonia. Steroid treatment was initiated in all cases empirically without the need for trans-bronchial biopsy. All presented cases showed significant improvement with steroid clinically and radiographically.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74922980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-08-31DOI: 10.21203/rs.3.rs-390496/v1
R. Choron, S. Iacono, Alexander Cong, C. Bargoud, Amanda L. Teichman, Nicole Krumrei, M. B. Manderski, M. Rodricks, Rajan Gupta, M. Lissauer
Background: Recent literature suggests respiratory system compliance (Crs) based phenotypes exist among COVID-19 ARDS patients. We sought to determine whether these phenotypes exist and whether Crs predicts mortality. Methods: A retrospective observational cohort study of 111 COVID-19 ARDS patients admitted March 11-July 8, 2020. Crs was averaged for the first 72-hours of mechanical ventilation. Crs < 30ml/cmH2O was defined as poor Crs(phenotype-H) whereas Crs ≥ 30ml/cmH2O as preserved Crs(phenotype-L). Results: 111 COVID-19 ARDS patients were included, 40 phenotype-H and 71 phenotype-L. Both the mean PaO2/FiO2 ratio for the first 72-hours of mechanical ventilation and the PaO2/FiO2 ratio hospital nadir were lower in phenotype-H than L(115[IQR87] vs 165[87], p = 0.016), (63[32] vs 75[59], p = 0.026). There were no difference in characteristics, diagnostic studies, or complications between groups. Twenty-seven (67.5%) phenotype-H patients died vs 37(52.1%) phenotype-L(p = 0.115). Multivariable regression did not reveal a mortality difference between phenotypes; however, a 2-fold mortality increase was noted in Crs < 20 vs > 50ml/cmH2O when analyzing ordinal Crs groups. Moving up one group level (ex. Crs30-39.9ml/cmH2O to 40-49.9ml/cmH2O), was marginally associated with 14% lower risk of death(RR = 0.86, 95%CI 0.72, 1.01, p = 0.065). This attenuated(RR = 0.94, 95%CI 0.80, 1.11) when adjusting for pH nadir and PaO2/FiO2 ratio nadir. Conclusion: We identified a spectrum of Crs in COVID-19 ARDS similar to Crs distribution in non-COVID-19 ARDS. While we identified increasing mortality as Crs decreased, there was no specific threshold marking significantly different mortality based on phenotype. We therefore would not define COVID-19 ARDS patients by phenotypes-H or L and would not stray from traditional ARDS ventilator management strategies.
{"title":"The Correlation of Respiratory System Compliance and Mortality in COVID-19 Acute Respiratory Distress Syndrome: Do Phenotypes Really Exist?","authors":"R. Choron, S. Iacono, Alexander Cong, C. Bargoud, Amanda L. Teichman, Nicole Krumrei, M. B. Manderski, M. Rodricks, Rajan Gupta, M. Lissauer","doi":"10.21203/rs.3.rs-390496/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-390496/v1","url":null,"abstract":"\u0000 Background:\u0000\u0000Recent literature suggests respiratory system compliance (Crs) based phenotypes exist among COVID-19 ARDS patients. We sought to determine whether these phenotypes exist and whether Crs predicts mortality.\u0000Methods:\u0000\u0000A retrospective observational cohort study of 111 COVID-19 ARDS patients admitted March 11-July 8, 2020. Crs was averaged for the first 72-hours of mechanical ventilation. Crs < 30ml/cmH2O was defined as poor Crs(phenotype-H) whereas Crs ≥ 30ml/cmH2O as preserved Crs(phenotype-L).\u0000Results:\u0000\u0000111 COVID-19 ARDS patients were included, 40 phenotype-H and 71 phenotype-L. Both the mean PaO2/FiO2 ratio for the first 72-hours of mechanical ventilation and the PaO2/FiO2 ratio hospital nadir were lower in phenotype-H than L(115[IQR87] vs 165[87], p = 0.016), (63[32] vs 75[59], p = 0.026). There were no difference in characteristics, diagnostic studies, or complications between groups. Twenty-seven (67.5%) phenotype-H patients died vs 37(52.1%) phenotype-L(p = 0.115). Multivariable regression did not reveal a mortality difference between phenotypes; however, a 2-fold mortality increase was noted in Crs < 20 vs > 50ml/cmH2O when analyzing ordinal Crs groups. Moving up one group level (ex. Crs30-39.9ml/cmH2O to 40-49.9ml/cmH2O), was marginally associated with 14% lower risk of death(RR = 0.86, 95%CI 0.72, 1.01, p = 0.065). This attenuated(RR = 0.94, 95%CI 0.80, 1.11) when adjusting for pH nadir and PaO2/FiO2 ratio nadir.\u0000Conclusion:\u0000\u0000We identified a spectrum of Crs in COVID-19 ARDS similar to Crs distribution in non-COVID-19 ARDS. While we identified increasing mortality as Crs decreased, there was no specific threshold marking significantly different mortality based on phenotype. We therefore would not define COVID-19 ARDS patients by phenotypes-H or L and would not stray from traditional ARDS ventilator management strategies.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78274744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-08-09DOI: 10.15406/jlprr.2021.08.00260
Najat Id el haj, Sara Hafidi, Ibtissam Rezouki, S. Boubia, Mehdi Karkour, M. Ridai
Bronchogenic cysts are rare unusual congenital cysts, resulting from abnormal budding of the primary tracheobronchial tube and can be located either in the mediastinum or in the pulmonary parenchyma. They remain asymptomatic in most adults unless they are large to compress adjacent structures or infected. We report a case of a 43-year-old woman, who presented recurrent episodes of hemoptysis low abundance 4 months ago revealing a huge mediastinal cystic formation, initially taken as a hydatid cyst, the chest CT showed a voluminous cystic formation of 11,4x10, 9x8, 8 cm exerting a mass effect on the posterior mediastinal structures: the superior vena cava, the azygos vein, and the trachea. The diagnosis as a bronchogenic cyst is done after resected by uniportal video-assisted surgery (VATS), and histological confirmation. The patient does not present any complications or reoffending during the follow-up. The rarity of this entity and even more a rare association of this lesion with symptoms of hemoptysis led to the report of this case. This case illustrates the interest of uniportal VATS for the extirpation of the bronchogenic cyst. We recommend a complete exeresis in most cases to confirm the diagnosis, relieve symptoms, and prevent complications.
{"title":"Huge mediastinal bronchogenic cyst revealed by hemoptysis and resected by uniportal VATS: A case report","authors":"Najat Id el haj, Sara Hafidi, Ibtissam Rezouki, S. Boubia, Mehdi Karkour, M. Ridai","doi":"10.15406/jlprr.2021.08.00260","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00260","url":null,"abstract":"Bronchogenic cysts are rare unusual congenital cysts, resulting from abnormal budding of the primary tracheobronchial tube and can be located either in the mediastinum or in the pulmonary parenchyma. They remain asymptomatic in most adults unless they are large to compress adjacent structures or infected. We report a case of a 43-year-old woman, who presented recurrent episodes of hemoptysis low abundance 4 months ago revealing a huge mediastinal cystic formation, initially taken as a hydatid cyst, the chest CT showed a voluminous cystic formation of 11,4x10, 9x8, 8 cm exerting a mass effect on the posterior mediastinal structures: the superior vena cava, the azygos vein, and the trachea. The diagnosis as a bronchogenic cyst is done after resected by uniportal video-assisted surgery (VATS), and histological confirmation. The patient does not present any complications or reoffending during the follow-up. The rarity of this entity and even more a rare association of this lesion with symptoms of hemoptysis led to the report of this case. This case illustrates the interest of uniportal VATS for the extirpation of the bronchogenic cyst. We recommend a complete exeresis in most cases to confirm the diagnosis, relieve symptoms, and prevent complications.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85129037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-22DOI: 10.15406/jlprr.2021.08.00259
N. Syabbalo
Chronic obstructive pulmonary disease (COPD) is currently considered the third leading cause of death in the world. COPD represents an important public health challenge and a socio-economical problem that is preventable and treatable. The main cause of COPD is chronic inhalation of cigarette smoke, and other harmful constituents of air pollution, which cause epithelial injury, chronic inflammation and airway remodeling. Airway remodeling is most prominent in small airways. It is due to infiltration of the airways by inflammatory cells, such as neutrophils, eosinophils, macrophages, and immune cells, including CD8+ T-cells, Th1, Th17 lymphocytes, and innate lymphoid cells group 3. Fibroblasts, myofibroblasts, and airway smooth muscle (ASM) cells also contribute to airway remodeling by depositing extracellular matrix (ECM) proteins, which increase the thickness of the airway wall. Activated inflammatory cells, and structural cells secrete cytokines, chemokines, growth factors, and enzymes which propagate airway remodeling. Airway remodeling is an active process which leads to thickness of the reticular basement membrane, subepithelial fibrosis, peribronchiolar fibrosis, and ASM cells hyperplasia and hypertrophy. It is also accompanied by submucosal glands and goblet cells hypertrophy and mucus hypersecretion, and angiogenesis. Epithelial mesenchymal transmission (EMT) plays a key role in airway remodeling. In patients with COPD and smokers, cellular reprograming in epithelial cells leads to EMT, whereby epithelial cells assume a mesencymal phenotype. Additionally, COPD is associated with increased parasympathetic cholinergic activity, which leads to ASM cells hypercontractility, increased mucus secretion, and vasodilatation. Treatment of COPD is intricate because of the heterogeneous nature of the disease, which requires specific treatment of the pathophysiological pathways, such as airway inflammation, ASM cell hypercontractility, and parasympathetic cholinergic hyperreactivity. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020 strategy report recommends personalized approach for the treatment of COPD. However, some patients with COPD are unresponsive to the standards of care. They may require a triple combination of LABA/LAMA/ICS. Single-inhaler triple therapy (SITT), such as fluticasone fuorate/vilanterol/umeclidinium has been shown to significantly improve symptoms and asthma control, reduce moderate and severe exacerbations, and to improve lung function.
{"title":"The role of airway remodeling in the pathogenesis and treatment of chronic obstructive pulmonary disease","authors":"N. Syabbalo","doi":"10.15406/jlprr.2021.08.00259","DOIUrl":"https://doi.org/10.15406/jlprr.2021.08.00259","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is currently considered the third leading cause of death in the world. COPD represents an important public health challenge and a socio-economical problem that is preventable and treatable. The main cause of COPD is chronic inhalation of cigarette smoke, and other harmful constituents of air pollution, which cause epithelial injury, chronic inflammation and airway remodeling. Airway remodeling is most prominent in small airways. It is due to infiltration of the airways by inflammatory cells, such as neutrophils, eosinophils, macrophages, and immune cells, including CD8+ T-cells, Th1, Th17 lymphocytes, and innate lymphoid cells group 3. Fibroblasts, myofibroblasts, and airway smooth muscle (ASM) cells also contribute to airway remodeling by depositing extracellular matrix (ECM) proteins, which increase the thickness of the airway wall. Activated inflammatory cells, and structural cells secrete cytokines, chemokines, growth factors, and enzymes which propagate airway remodeling. Airway remodeling is an active process which leads to thickness of the reticular basement membrane, subepithelial fibrosis, peribronchiolar fibrosis, and ASM cells hyperplasia and hypertrophy. It is also accompanied by submucosal glands and goblet cells hypertrophy and mucus hypersecretion, and angiogenesis. Epithelial mesenchymal transmission (EMT) plays a key role in airway remodeling. In patients with COPD and smokers, cellular reprograming in epithelial cells leads to EMT, whereby epithelial cells assume a mesencymal phenotype. Additionally, COPD is associated with increased parasympathetic cholinergic activity, which leads to ASM cells hypercontractility, increased mucus secretion, and vasodilatation. Treatment of COPD is intricate because of the heterogeneous nature of the disease, which requires specific treatment of the pathophysiological pathways, such as airway inflammation, ASM cell hypercontractility, and parasympathetic cholinergic hyperreactivity. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020 strategy report recommends personalized approach for the treatment of COPD. However, some patients with COPD are unresponsive to the standards of care. They may require a triple combination of LABA/LAMA/ICS. Single-inhaler triple therapy (SITT), such as fluticasone fuorate/vilanterol/umeclidinium has been shown to significantly improve symptoms and asthma control, reduce moderate and severe exacerbations, and to improve lung function.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78500462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：