• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.358-360
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• 2022

• Journal of Yeungnam Medical Science
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• v.37 no.4
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• pp.269-276
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• 2020

Fibrosis is characterized by excessive accumulation of extracellular matrix components. The fibrotic process ultimately leads to organ dysfunction and failure in chronic inflammatory and metabolic diseases such as pulmonary fibrosis, advanced kidney disease, and liver cirrhosis. Idiopathic pulmonary fibrosis (IPF) is a common form of progressive and chronic interstitial lung disease of unknown etiology. Pathophysiologically, the parenchyma of the lung alveoli, interstitium, and capillary endothelium becomes scarred and stiff, which makes breathing difficult because the lungs have to work harder to transfer oxygen and carbon dioxide between the alveolar space and bloodstream. The transforming growth factor beta (TGF-β) signaling pathway plays an important role in the pathogenesis of pulmonary fibrosis and scarring of the lung tissue. Recent clinical trials focused on the development of pharmacological agents that either directly or indirectly target kinases for the treatment of IPF. Therefore, to develop therapeutic targets for pulmonary fibrosis, it is essential to understand the key factors involved in the pathogenesis of pulmonary fibrosis and the underlying signaling pathway. The objective of this review is to discuss the role of kinase signaling cascades in the regulation of either TGF-β-dependent or other signaling pathways, including Rho-associated coiled-coil kinase, c-jun N-terminal kinase, extracellular signal-regulated kinase 5, and p90 ribosomal S6 kinase pathways, and potential therapeutic targets in IPF.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.548-554
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• 1995

Background: Cardiogenic pulmonary edema increases nonspecific airway responsiveness in humans and animals. Increased extravascular lung water from overt pulmonary edema to subclinical interstitial edema is a common finding in patients with chronic renal failure. Several studies carried out to assess pulmonary function disturbances in this condition have documented a reduction in forced expiratory volume that usually reverses after hemodialysis, suggesting airway edema as the underlying mechanism. This interstitial edema may also lead to nonspecific bronchial hyperresponsiveness. We hypothesized that patients with chronic renal failure may present nonspecific bronchial hyperresponsiveness due to subclinical interstitial pulmonary edema. Methods: We studied 18 chronic renal failure undergoing regular hemodialysis 3 times a week(New York Heart Association Class II) without concomittent disease. These patients were checked pulmonary function test and metacholine provocation test before hemodialysis and same procedure was repeated if responsive, after hemodialysis. Results: 1) 12 out of 18 patients before hemodialysis were reactive in metacholine provocation test(66.7%) before hemodialysis. This airway hyperresponsiveness were decreased after hemodialysis. 2) Pulmonary function was improved after hemodialysis and change in $FEV_1$ was correlated with change in weight(r=-0.62, p<0.01). 3) There was a close correlation between log $PD_{20}$ and $FEF_{25}$, which is one of the variables of the peripheral airways(r=0.58, p<0.05). Conclusion: We speculated interstitial pulmonary edema may play a significant role in bronchial hyperresponsiveness and lung function impaired in patients with chronic renal failure.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1426-1432
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• 1997

Sj$\ddot{o}$gren's syndrome(SS) is a chronic inflammatory disorder characterized by lymphocytic infiltration of lacrimal and sailvary glands, which results in dry eyes and dry mouth. SS may exist as a primary condition or as a secondary condition in association with connective tissue disease such as rheumatoid arthritis, systemic lupus erythematosus, or progressive systemic sclerosis. We experienced a patient with primary SS who developed multiple bullae, nodular type of pulmonary amyloidosis and lymphocytic interstitial peumonitis. We believe this to be the first reported case of SS acompanied by these three types pulmonary manifestations at the same time.

• Journal of Veterinary Clinics
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• v.39 no.5
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• pp.240-245
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• 2022

A 15-year-old, neutered male, Shih-Tzu, was presented at the Chonnam National Veterinary Medical Teaching Hospital for evaluation of acute onset of persistent coughing, exercise intolerance, and abnormal heart sound. On thoracic auscultation, a split-second heart sound and a wheezing sound were detected on both sides of the chest walls. On physical examination, the dog's body condition score (BCS) was 7/9, and had stenotic nares. Thoracic radiographs revealed right-sided enlargement of the cardiac silhouette (vertebral heart score (VHS) 11.2; reference interval = 8.9-10.1), mild main pulmonary artery (MPA) bulging, mild interstitial infiltration, and hepatomegaly. The electrocardiogram showed right axis deviation, suggesting right ventricular hypertrophy. The echocardiographic study showed moderate pulmonary hypertension and moderate tricuspid regurgitation. There were no findings of a tracheobronchial disease, pulmonary thromboembolism, congenital shunt, left heart disease, or parasitic disease. Based on clinical signs and diagnostic findings, the dog was diagnosed with pulmonary hypertension secondary to brachycephalic syndrome. To rectify respiratory exacerbating factors, the dog was recommended weight control by restricting dietary intake and managing concurrent Cushing's syndrome. Treatments included sildenafil, pimobendan, furosemide, and ramipril. After five months of taking medications and weight control, the severity of pulmonary hypertension improved from moderate to mild. The clinical signs of the patient, including coughing and exercise intolerance, improved a lot. For 5 months of follow-up, the patient has not reported further recurrence of respiratory distress.

• Tuberculosis and Respiratory Diseases
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• v.51 no.1
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• pp.59-64
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• 2001

Nonspecific interstitial pneumonia (NSIP) was first described as a new category of idiopathic interstitial pneumonia in 1994. This is a disease with a more insidious onset and has a chronic course. The histological findings are unusual for other idiopathic interstitial pneumonia cases (usual interstitial pneumonia, diffuse interstitial pneumonia, and acute interstitial pneumonia). In contrast to NSIP, acute interstitial pneumonia (AIP) has an acute onset and a fulminant course with the rapid development of respiratory failure. A pathological examination demonstrated characteristic diffuse interstitial fibrosis, hyaline membranes, thrombi, and architectural derangement. Here we report a 48-year-old woman who was diagnosed pathologically NSIP, but with a rapid progressive course similar to AIP.

• Tuberculosis and Respiratory Diseases
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• v.40 no.2
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• pp.197-202
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• 1993

Polymyositis (PM) is a inflammatory connective tissue disease involving predominantly skeletal muscles, characterized by symmetrical, proximal muscle weakness, inflammation, and frequently, degeneration. Interstitial lung disease in association with PM occurs in 5~10% of cases and carries an especially grave prognosis. Although the cause of lung involvement in PM is not known, the underlying pathologic process in the lung is an immune mediated inflammation of alveolar structures, alveolitis. It is of interest, therefore, that cyclophosphamide, an immune modulating agent, has been reported to be effective in the treatment of PM. We report a case of corticosteroid resistant PM associated with interstitial lung disease, successfully treated with cyclophosphamide. A 37-year-old female was presented with 8 months duration of cough, exertional dyspnea, and muscle weakness. She had typical symptoms, physical findings, and elevated muscle enzyme levels in serum with characteristic findings of muscle biopsy. She also had typical interstitial lung disease pattern on chest X-ray and high resolution CT with restrictive pattern on pulmonary function test. The findings of transbronchial lung biopsy was compatible with interstitial lung disease. She failed to respond to corticosteroid initially. Subsequently steroids and cyclophosphamide were given with excellent clinical improvement.

• Korean Journal of Veterinary Research
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• v.41 no.2
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• pp.233-241
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• 2001

Dirofilaria immitis, the causative agent of canine heartworm disease, inhabits mainly in the pulmonary arteries and the heart of dogs and cats, causing circulatory and respiratory disorders. Although diagnosis of the disease is based on the presence of microfilaria in the peripheral blood or of specific antigens released from the adult worms into the peripheral blood, the severity of the infection and the assessment of disease progression are based on the clinical signs and radiographic image analysis. We analysed 12 mixed-bred Jindo dogs naturally infected with Dirofilaria immitis without any clinical signs and compared the radiographic images of the heart and the lung with the number of adult worms at necropsy. The dorsoventral radiographs of 12 infected dogs revealed that the right caudal lobar pulmonary arteries (RCaLPA) were dialated in 66.7% of dogs, whereas the main pulmonary artery segment was enlarged in 50.3% of dogs. The cranial lobar pulmonary arteries (RCrLPA) were dilated or pruned in 33.3% of dogs. All dogs displayed the interstitial lung pattern, while the vertebral heart size (VHS) was of normal range. Although a range of 9 to 166 adult worms (av. 45.6) was found in the pulmonary arteries, in the heart or in the vena cava, no correlation with the radiographic findings and/or with the clinical signs was observed.

• Tuberculosis and Respiratory Diseases
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• v.42 no.1
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• pp.58-66
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• 1995

Background: Acute interstitial pneumonia is a relatively rare form of interstitial pneumonia, since the vast majority of interstitial pneumonia have a more chronic course. It corresponds to the lesion described by Hamman and Rich, as Hamman-Rich disease in 1944. Another name in the clinical literature is accelerated interstitial pneumonia, idiopathic acute respiratory distress syndrome (idiopathic ARDS), and the organizing stage of diffuse alveolar damage. Acute interstitial pneumonia differs from chronic interstitial pneumonia by clinical and pathologic features. Clinically, this disease is characterized by a sudden onset and a rapid course, and reversible disease. Method and Purpose: Five cases of pathologically proven acute interstitial pneumonia were retrospectively studied to define the clinical, radiologic, and pathologic features. Results: 1) The five cases ranged in age from 31 to 77 years old. The onset of illness was acute in all patients, it began with viral-like prodrome 6~40 days prior to shortness of breath, and respiratory failure eventually developed in all patients. In 2 cases, generalized skin rash was accompanied with flu-like symptoms. Etiologic agent could not be identified in any case. 2) All patients had leukocytosis and severe hypoxemia. Pulmonary function test of 3 available cases shows restrictive ventilatory defect, and one survived patient(case 5) has a complete improvement of pulmonary function after dismissal. 3) Diffuse bilateral chest infiltrates were present radiologically. Theses were the ground-glass, consolidation, and reticular densities without honeycomb fibrosis in all patients. The pathologic abnormalities were the presence of increased numbers of macrophages and the formation of hyaline membranes within alveolar spaces. There was also interstitial thickening with edema, proliferation of immature fibroblast, and hyperplasia of type II pneumocyte. In the survived patient(case5), pathologic findings were relatively early stage of acute interstitial pneumonia, such as hyaline membrane with mild interstitial fibrosis. 4) Of the 5 patients, four patients died of respiratory failure 14~90 days after onset of first symptom, and one survived and recovered in symptoms, chest X ray, and pulmonary function test Conclusion: These results emphasize that acute interstitial pneumonia is clinically, radiologically, and pathologically distinct form of interstitial pneumonia and should be separated from the group of chronic interstitial pneumonia. Further studies will be needed to evaluate the pathogenesis and the treatment of acute interstitial pneumonia.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.597-602
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• 2001

A 47-years-old woman presented with a 2-month history of a dry mouth and dry cough. The patient had been taking medication for Sj$\ddot{o}$gren's syndrome for approximately 7 years. The chest radiography showed multiple cystic lesions and a hazy density in both lower lung fields. The HRCT showed a diffuse ground glass like appearance and multiple variable sized cystic lesions in both lung fields. After medication, the symptoms were aggravated. Bronchoscopy was preformed with a transbronchial lung biopsy. The biopsies showed an infiltration of lymphocytes, neutrophils, monocytes and histiocytes through the interstitial space of the alveola and a widening of the alveolar septa. However, the histological findings of the cysts were not obtained. Sj$\ddot{o}$gren's syndrome is a slowly progressive inflammatory autoimmune disease, which is characterized by lymphocyte mediated destruction of the exocrine glands, with pulmonary involvement in approximately 19-65%, High-resolution CT is a sensitive technique for assessing the pulmonary involvement in patients with Sj$\ddot{o}$gren's syndrome. Although a lung biopsy is not always necessary for establishing a diagnosis of an interstitial lung disease in Sj$\ddot{o}$gren's syndrome. A lung biopsy may reveal a wide spectrum of changes ranging from a mild inflammatory response to end stage fibrosis with honeycombing. Because of the predominantly peribronchiolar inflammatory infiltration and inspissated secretions the cysts were suspected to have been formed by the ball-valve phenomen. However, no definite evidence was obtained.