452 32nd World Congress of Internal Medicine (October 24-28, 2014)
The Korean Academy of Tuberculosis and Respiratory Diseases
PS 1579 DILD
Incidence and Prevalence of Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis: A Population-Based Study
Hyun Jung Kim1, Hye In Jung1, Jin Wook Lee1, Won-Il Choi1 Keimyung University Dongsan Medical Center, Korea1
Background: Limited epidemiologic data are available regarding the occurrence of interstitial lung diseases (ILD) and idiopathic pulmonary fi brosis (IPF) in light of the launch of a new IPF statement.
We aimed to estimate the annual incidence and prevalence rate of ILD and IPF.
Methods: A retrospective cohort design utilizing the Korean Health Insurance Review and Assessment Service (HIRA) database, spanning the period from January 2008 to December 2012 was used. We analyzed data collected from approximately 37 million adult individuals. Patients with ILD and IPF were identifi ed based on the International Classifi cation of Disease-10 (ICD-10) diagnosis and procedure codes. Defi nition one is code J84. Defi nition two is code J84 and HRCT, broncho-alveolar lavage (BAL), or lung biopsy. Defi nition three is code J84.1. Defi nition four is code J 84.1and HRCT, BAL, or lung biopsy. Defi nition fi ve is code J84.1A and was specifi cally implemented for IPF.
Results: The incidence rate based on definition one, two, three, four, and five per 100,000 individuals were 48.5; 32.2; 16.2; 11.4 and 1.7, respectively. The prevalence rate based on defi nition one, two, three, four, and fi ve has been estimated to be 65.7;
39.7; 30.0; 18.6 and 7.9 per 100,000 individuals, respectively.
Conclusions: The incidence of ILD with fi brosis was approximately 23% of the ILD incidence (48.5 per 100,000 individuals). IPF incidence was approximately 10% of the incidence of ILD with fi brosis. The incidence rate of IPF was 1.7 per 100,000 individuals based on new ATS statements in 2011.
PS 1580 DILD
A Case of Isoniazid Induced Lung Fibrosis: Case Report
Chaeuk Chung1, Dong Il Park1, Sun Young Kim1, Ju Ock Kim1, Hee Sun Park1, Jae Young Moon1, Jeong Eun Lee1, Choong Sik Lee2, Sung Soo Jung1
Division of Pulmonology, Department of Internal Medicine, College of Medicine, Chungnam National University, Korea1, Department of Pathology, College of Medicine, Chungnam National University, Korea2
A 42-year-old man was diagnosed with tuberculous pleurisy. He was treated with iso- niazid (INH), rifampicin (RFP), ethmbutol (EB) and pyrazinamide (PZA). After two weeks of treatment, he developed dyspnea on exercise and symptom got worsened. His arterial O2 saturation was 87% and physical examination revealed velcro rale on both lower lung fi elds. A chest imaging showed newly developed bilateral lung infi ltrations including glass ground opacity (GGO), consolidation, and reticular opacity. Pulmonary function test showed severe restrictive pattern and markedly decreased diffusion lung capacity. Interstitial lung disease induced by anti-Tbc medication was mostly suspected, all drugs were discontinued. Open lung biopsy at right lower lobe revealed chronic interstitial inflammation with fibrosis. Among anti-Tbc medication, INH is most common cause of pneumonitis. At post-operation day 5, anti-Tbc medication except isoniazid was started with prednisolone (Pd) 60mg. After 2 weeks, Pd dose was decreased to 30mg and azathioprine 50mg was added. There are some case reports of INH induced pneumonitis. To our knowledge, this is the fi rst case of INH-induced lung fi brosis occurring in a month of anti-Tbc medication.
PS 1581 DILD
Idiopathic Pleuroparenchymal Fibroelastosis
Hyun-Young Kim1, Seung Yong Park1, Yeong Hun Choe1, So Ri Kim1, Gong Yong Jin2, Myung Ja Chung3, Yong Chul Lee1
Department of Internal Medicine, Research Center for Respiratory Disorders, Chonbuk National Uni- versity College of Medicine, Korea1, Department of Radiology, Chonbuk National University College of Medicine, Korea2, Department of Pathology, Chonbuk National University College of Medicine, Korea3
Pleuroparenchymal fi broelastosis (PPFE) is a rare type of fi brotic interstitial lung dis- ease usually occurred in subpleural areas with the predominance of both upper lungs.
In fact, PPFE was described as idiopathic upper lung fi brosis just about 20 years ago for the fi rst time. Due to this rarity and the shortage of information on this disease, there is no agreed definition regarding diagnostic criteria for PPFE. On radiologic images, it is characterized by progressive subpleural opacities with fi brotic changes, predominantly in upper lungs, and dense intra-alveolar fi brosis. In addition, the most important histologic fi nding is the intra-alveolar fi brosis with septal elastosis. To date, the clinical data is also very short to guide the physicians to the appropriate therapeu- tic management and to estimate the prognosis, although PPFE has been known to be link to recurrent pulmonary infections and to present with more diffuse involvement with different patterns of interstitial lung diseases. Herein, we describe an extremely rare case of PPFE in a 41-year-old man who presented asymptomatic radiologic ab- normalities of subpleural reticular pattern and nodular consolidation in upper lobes.a
PS 1582 DILD
Sulforaphane Attenuates TGF-ß-Induced Fibrosis and Alveolar Epithelial to Mesenchymal Transition
Sun Young Kyung1, Jin Young Yoon1, Sang Min Lee1, Shin Myung Kang1, Yu Jin Kim1, Sang Pyo Lee1, Jeong-Woong Park1, Sung Hwan Jeong1
Gachon University Gil Hospital, Korea1
Background: Sulforaphane(SF) is a isothiocyanate that has anti-infl ammatory effect via induction of antioxidant/phase II enzymes. We evaluated the effects of SF on pul- monary fi brosis and alveolar epithelial to mesenchymal transition (EMT).
Methods: Western blotting for fi bronectin, collagen, total/phosphorylated smad2/3, 7 was evaluated in TGF-ß-treated pulmonary fi broblast cells (MRC-5 cells) with or without SF. In alveolar epithelial cells (A549 cells), morphological changes induced by TGF-ß was observed with or without SF. And then Western blotting for E-cadherin, vi- mentin, a-Smooth muscle actin (SMA) and quantitative real-time PCR were evaluated for transcriptional factors: Slug, Snail, and Twist.
Results: SF attenuates TGF-ß-induced fi bronectin and collagen protein production in pulmonary fi broblasts. Furthermore, SF showed relation to smad 2/3 and smad 7 phosphorylation. In A549 cells, we observed TGF-ß-induced alveolar EMT by morpho- logical changes, decreased E-cadherin expression, increased expression of vimentin and a-SMA. These alveolar EMT was inhibited by SF treatment related to inhibiting Snail, Slug, and Twist.
Conclusions: SF has anti-fi brotic potential in pulmonary fi brosis which attenuates the expression of fi brogenic proteins via TGF-ß-smad signaling and inhibits alveolar EMT.
