• Title/Summary/Keyword: Pulmonary diseases

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A Case of Pulmonary Artery Sarcoma Presented as Cavitary Pulmonary Lesions

  • Min, Daniel;Lee, Ji-Hyun;Jeong, Hye-Cheol;Kim, Jung-Hyun;Shin, Suk-Pyo;Kim, Hong-Min;Han, Kyu Hyun;Jeong, Hye Yun;Kim, Eun-Kyung
    • Tuberculosis and Respiratory Diseases
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    • v.76 no.3
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    • pp.136-140
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    • 2014
  • Pulmonary artery sarcoma (PAS) is a rare, poorly differentiated malignancy arising from the intimal layer of the pulmonary artery. Contrast-enhanced chest computed tomography (CT) is a good diagnostic modality that shows a low-attenuation filling defect of the pulmonary artery in PAS patients. An 18-year-old man was referred to our hospital for the evaluation and management of cavitary pulmonary lesions that did not respond to treatment. A contrast-enhanced CT of the chest was performed, which showed a filling defect within the right interlobar pulmonary artery. The patient underwent a curative right pneumonectomy after confirmation of PAS. Although lung parenchymal lesions of PAS are generally nonspecific, it can be presented as cavities indicate pulmonary infarcts. Clinicians must consider the possibility of PAS as well as pulmonary thromboembolism in patients with pulmonary infarcts. So, we report the case with PAS that was diagnosed during the evaluation of cavitary pulmonary lesions and reviewed the literatures.

A Case of Pulmonary Thromboembolism Due to Congenital Antithrombin III Deficiency (선천성 Antithrombin III 결핍증에서 발생한 폐색전증 1 예)

  • Park, Hyeong-Kwan;Park, Chang-Min;Ko, Kyoung-Haeng;Rim, Myung-Soo;Kim, Yu-Il;Hwang, Jun-Hwa;Lim, Sung-Chul;Kim, Young-Chul;Park, Kyung-Ok
    • Tuberculosis and Respiratory Diseases
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    • v.47 no.3
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    • pp.394-399
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    • 1999
  • We report a case of congenital and familial antithrombin III deficiency developing massive pulmonary thromboembolism. A 44-year-old man was admitted to our hospital because of sudden chest pain and severe dyspnea. Five years ago, he was operated due to a mesenteric vein thrombosis of unknown cause. On admission, radioisotopic venogram showed deep vein thrombosis and lung scintigram showed multiple segmental perfusion defects. His plasma antithrombin III level was 10.5 mg/dL which was less than 50% of normal and those of a son and two daughters were also decreased. After treatment with tissue plasminogen activator, heparin and coumadin, his symptom and lung scintigram were significantly improved. As far as we reviewed, there were very rare reports with congenital antithrombin III deficiency presenting as pulmonary thromboembolism in Korea.

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Differences between Patients with TB-Destroyed Lung and Patients with COPD Admitted to the ICU

  • Seo, Young-Kyeong;Lee, Chae-Hun;Lee, Hyun-Kyung;Lee, Young-Min;Park, Hye-Kyeong;Choi, Sang-Bong;Kim, Hyun-Gook;Jang, Hang-Jea;Yum, Ho-Kee;Lee, Seung-Heon
    • Tuberculosis and Respiratory Diseases
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    • v.70 no.4
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    • pp.323-329
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    • 2011
  • Background: Although patients with tuberculous-destroyed lung (TDL) account for a significant proportion of those with chronic airflow obstruction, it is difficult to distinguish patients with airway obstruction due to TDL from patients with pure chronic obstructive pulmonary disease (COPD) on initial presentation with dyspnea. We investigated clinical features differing between (i) patients with TDL and airway obstruction and (ii) those with COPD admitted to the intensive care unit (ICU) due to dyspnea. Methods: We reviewed the medical records of patients with TDL who had a forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) of <70% on a pulmonary function test (PFT; best value closest to admission) and patients with COPD without a history of pulmonary tuberculosis (TB) who were admitted to the ICU. Ultimately, 16 patients with TDL and 16 with COPD were compared, excluding patients with co-morbidities. Results: The mean ages of the patients with TDL and COPD were 63.7 and 71.2 years, respectively. Mean FVC% (50.4% vs. 71.9%; p<0.01) and mean FEV1% (39.1% vs. 58.4%; p<0.01) were significantly lower in the TDL group than in the COPD group. More frequent consolidation with TB (68.8% vs. 31.3%; p=0.03) and more tracheostomies (50.0% vs. 0.0%; p=0.02) were observed in the TDL than in the COPD group. Conclusion: Upon ICU admission, patients with TDL had TB pneumonia more frequently, more diminished PFT results, and more tracheostomies than patients with COPD.

Medical Thoracoscopy in Pleural Disease: Experience from a One-Center Study

  • Kim, Soo Jung;Choi, Sun Mi;Lee, Jinwoo;Lee, Chang-Hoon;Lee, Sang-Min;Yim, Jae-Joon;Yoo, Chul-Gyu;Kim, Young Whan;Han, Sung Koo;Park, Young Sik
    • Tuberculosis and Respiratory Diseases
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    • v.80 no.2
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    • pp.194-200
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    • 2017
  • Background: Medical thoracoscopy (MT) is a minimally invasive, endoscopic procedure for exploration of the pleural cavity under conscious sedation and local anesthesia. MT has been performed at the Seoul National University Hospital since February 2014. This paper summarizes the findings and outcomes of MT cases at this hospital. Methods: Patients who had undergone MT were enrolled in the study. MT was performed by pulmonologists, using both rigid and semi-rigid thoracoscopes. During the procedure, patients were under conscious sedation with fentanyl and midazolam. Medical records were reviewed for clinical data. Results: From February 2014 to January 2016, 50 procedures (47 cases) were performed (diagnostic MT, 26 cases; therapeutic MT, 24 cases). The median age of patients was 66 years (59-73 years), and 38 patients (80.9%) were male. The median procedure duration from initial incision to insertion of the chest tube was 37 minutes. The median doses of fentanyl and midazolam were $50{\mu}g$ and 5 mg, respectively. All procedures were performed without unexpected events. Of the 26 cases of pleural disease with an unknown cause, 19 were successfully diagnosed using MT. Additionally, diagnostic MT provided clinically useful information in the other six patients. Therapeutic MT was very effective for treatment of malignant pleural effusion or empyema. The median number of days with chest tube drainage was 6 (3 days for diagnostic MT and 8 days for therapeutic MT). Conclusion: MT is a useful and necessary procedure for both diagnosis and treatment of pleural diseases.

Are Patients with Asthma and Chronic Obstructive Pulmonary Disease Preferred Targets of COVID-19?

  • Bouazza, Belaid;Hadj-Said, Dihia;Pescatore, Karen A.;Chahed, Rachid
    • Tuberculosis and Respiratory Diseases
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    • v.84 no.1
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    • pp.22-34
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    • 2021
  • The coronavirus pandemic, known as coronavirus disease 2019 (COVID-19), is an infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus first identified in patients from Wuhan, China. Since December 2019, SARS-CoV-2 has spread swiftly around the world, infected more than 25 million people, and caused more than 800,000 deaths in 188 countries. Chronic respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD) appear to be risk factors for COVID-19, however, their prevalence remains controversial. In fact, studies in China reported lower rates of chronic respiratory conditions in patients with COVID-19 than in the general population, while the trend is reversed in the United States and Europe. Although the underlying molecular mechanisms of a possible interaction between COVID-19 and chronic respiratory diseases remain unknown, some observations can help to elucidate them. Indeed, physiological changes, immune response, or medications used against SARS-CoV-2 may have a greater impact on patients with chronic respiratory conditions already debilitated by chronic inflammation, dyspnea, and the use of immunosuppressant drugs like corticosteroids. In this review, we discuss importance and the impact of COVID-19 on asthma and COPD patients, the possible available treatments, and patient management during the pandemic.

MR Imaging of Congenital Heart Diseases in Adolescents and Adults

  • Yeon Hyeon Choe;I-Seok Kang;Seung Woo Park;Heung Jae Lee
    • Korean Journal of Radiology
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    • v.2 no.3
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    • pp.121-131
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    • 2001
  • Echocardiography and catheterization angiography suffer certain limitations in the evaluation of congenital heart diseases in adults, though these are overcome by MRI, in which a wide field-of view, unlimited multiplanar imaging capability and three-dimensional contrast-enhanced MR angiography techniques are used. In adults, recently introduced fast imaging techniques provide cardiac MR images of sufficient quality and with less artifacts. Ventricular volume, ejection fraction, and vascular flow measurements, including pressure gradients and pulmonary-to-systemic flow ratio, can be calculated or obtained using fast cine MRI, phase-contrast MR flow-velocity mapping, and semiautomatic analysis software. MRI is superior to echocardiography in diagnosing partial anomalous pulmonary venous connection, unroofed coronary sinus, anomalies of the pulmonary arteries, aorta and systemic veins, complex heart diseases, and postsurgical sequelae. Biventricular function is reliably evaluated with cine MRI after repair of tetralogy of Fallot, and Senning's and Mustard's operations. MRI has an important and growing role in the morphologic and functional assessment of congenital heart diseases in adolescents and adults.

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Clinical Year-in-Review of Chronic Obstructive Pulmonary Disease in Korea (호흡기내과 의사를 위한 COPD 리뷰)

  • Shin, Kyeong-Cheol
    • Tuberculosis and Respiratory Diseases
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    • v.71 no.1
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    • pp.1-7
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    • 2011
  • Many findings suggest that chronic obstructive pulmonary disease (COPD) imposes an enormous burden on patients, health-care professionals and society. COPD contributes to morbidity and mortality and to a significant use of health-care resources. In spite of a higher prevalence of COPD in Korea, the result of COPD treatment is not effective. The purpose of this article was to review recent advances in the study of COPD in Korea with the aim of improving effective management. This review highlights articles pertaining to the following topics; prevalence, assessment of COPD, risk factors for hospitalization, co-morbid diseases, phenotypes, and treatment issues.

The Relationship between Airway Inflammation and Exacerbation in Chronic Obstructive Pulmonary Disease

  • Perng, Diahn-Warng;Chen, Pei-Ku
    • Tuberculosis and Respiratory Diseases
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    • v.80 no.4
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    • pp.325-335
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    • 2017
  • Chronic obstructive pulmonary disease (COPD) is associated with abnormal inflammatory response and airflow limitation. Acute exacerbation involves increased inflammatory burden leading to worsening respiratory symptoms, including dyspnea and sputum production. Some COPD patients have frequent exacerbations (two or more exacerbations per year). A substantial proportion of COPD patients may remain stable without exacerbation. Bacterial and viral infections are the most common causative factors that breach airway stability and lead to exacerbation. The increasing prevalence of exacerbation is associated with deteriorating lung function, hospitalization, and risk of death. In this review, we summarize the mechanisms of airway inflammation in COPD and discuss how bacterial or viral infection, temperature, air pollution, eosinophilic inflammation, and concomitant chronic diseases increase airway inflammation and the risk of exacerbation.

Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension

  • Zhou, Tong;Tang, Haiyang;Han, Ying;Fraidenburg, Dustin;Kim, Young-Won;Lee, Donghee;Choi, Jeongyoon;Bang, Hyoweon;Ko, Jae-Hong
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.3
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    • pp.353-360
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    • 2017
  • Several human diseases have been associated with mitochondrial voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology. First, we identified the genes differentially expressed between wild-type and Vdac1 knockout mouse embryonic fibroblasts in hypoxic conditions. These genes were deemed to be influenced by VDAC1 deficiency. Gene ontology analysis indicates that the VDAC1 influenced genes are significantly associated with PAH pathobiology. Second, a molecular signature derived from the VDAC1 influenced genes was developed. We suggest that, VDAC1 has a protective role in PAH and the gene expression signature of VDAC1 influenced genes can be used to i) predict severity of pulmonary hypertension secondary to pulmonary diseases, ii) differentiate idiopathic pulmonary artery hypertension (IPAH) patients from controls, and iii) differentiate IPAH from connective tissue disease associated PAH.

Progressive Pulmonary Fibrosis: Where Are We Now?

  • Hyung Koo Kang;Jin Woo Song
    • Tuberculosis and Respiratory Diseases
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    • v.87 no.2
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    • pp.123-133
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    • 2024
  • Interstitial lung diseases (ILDs) are a diverse collection of lung disorders sharing similar features, such as inflammation and fibrosis. The diagnosis and management of ILD require a multidisciplinary approach using clinical, radiological, and pathological evaluation. Progressive pulmonary fibrosis (PPF) is a distinct form of progressive and fibrotic disease, occurring in ILD cases other than in idiopathic pulmonary fibrosis (IPF). It is defined based on clinical symptoms, lung function, and chest imaging, regardless of the underlying condition. The progression to PPF must be monitored through a combination of pulmonary function tests (forced vital capacity [FVC] and diffusing capacity of the lung for carbon monoxide), an assessment of symptoms, and computed tomography scans, with regular follow-up. Although the precise mechanisms of PPF remain unclear, there is evidence of shared pathogenetic mechanisms with IPF, contributing to similar disease behavior and worse prognosis compared to non-PPF ILD. Pharmacological treatment of PPF includes immunomodulatory agents to reduce inflammation and the use of antifibrotics to target progressive fibrosis. Nintedanib, a known antifibrotic agent, was found to be effective in slowing IPF progression and reducing the annual rate of decline in FVC among patients with PPF compared to placebos. Nonpharmacological treatment, including pulmonary rehabilitation, supplemental oxygen therapy, and vaccination, also play important roles in the management of PPF, leading to comprehensive care for patients with ILD. Although there is currently no cure for PPF, there are treatments that can help slow the progression of the disease and improve quality of life.