• Tuberculosis and Respiratory Diseases
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• v.72 no.4
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• pp.386-389
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• 2012

Diffuse alveolar damage (DAD) is a histological change in lung tissue, and is generally caused by an acute lung injury, which is characterized by bilateral and widespread damages. Localized DAD occurs very rarely. The causes for DAD are numerous, but the chief cause is acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia, in cases of idiopathic manifestation. The 82-year-old patient, in this case study, showed a DAD lesion in only 1 lobe. The patient was otherwise healthy, with no previous symptoms of DAD. He was admitted to our medical center owing to localized infiltration, observed on his chest radiograph. Laboratory studies showed no signs of infections. DAD was confirmed by a surgical lung biopsy. The patient received corticosteroid treatment and had gradually improved. We report the case of a patient with localized, idiopathic DAD that cannot be classified as acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia.

• Tuberculosis and Respiratory Diseases
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• v.71 no.6
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• pp.470-475
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• 2011

So far more than 350 drugs have been reported to be the cause for lung injury and the incidence tends to increase. Although infiltrative lung disease is the most common pattern of drug-induced lung injury, it can appear in the form of alveolar changes, vasculitis and other injury. Herbal medicine also has been known as a cause for interstitial pneumonitis, but it is difficult to identify the key herbal medicine because of the complex components of the contents. Till date, there is no report of pneumonitis caused by golden thread. Here we report a case of a 54-year-old male who developed interstitial pneumonitis with acute liver injury caused by herbal medicine made from golden thread.

• Korean Journal of Veterinary Service
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• v.47 no.2
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• pp.95-100
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• 2024

An 11-year-old neutered male Dachshund dog weighing 7 kg presented with acute onset of respiratory distress after subcutaneous administration of cytosine arabinoside (CA). The patient previously diagnosed with meningoencephalitis of unknown origin and was being treated with oral prednisolone, levetiracetam, potassium bromide, gabapentin, and periodic subcutaneous CA administration (50 mg/m², q 12 h, subcutaneous, 4 times, every 3 weeks). The patient developed tachypnea with labored respiratory effort after 9th CA administration. Thoracic radiograph revealed bilateral diffuse interstitial to alveolar pulmonary opacities, and echocardiogram indicated no evidence of left-sided heart failure. Based on the onset coinciding with the administration of CA, low possibility of other pulmonary disease, remission of symptom showed after discontinuation of CA, we suspected CA-induced interstitial lung disease. The patient's pulmonary opacities on the radiograph improved to a similar degree as before the adverse event over time, but respiratory symptoms were not fully resolved. Sildenafil (2 mg/kg, per oral, q 12 h) was given as therapeutic trial to manage possible pulmonary hypertension, suspected a sequela of the lung disease, based on an echocardiographic evidence and clinical signs. The patient's respiratory symptom was well managed since, and achieved discontinuation of sildenafil.

• Tuberculosis and Respiratory Diseases
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• v.52 no.1
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• pp.62-69
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• 2002

Acute interstitial pneumonia (AIP) is a rare fulminant form of lung injury that presents acutely; usually in a previously healthy individual. It corresponds to a subset of cases of idiopathic adult respiratory distress syndrome (ARDS). Invasive pulmonary aspergillosis is a disease occuring predominantly with defects in immunity such as hematologic malignancy, influenza infection, postchemotherapy, long-term corticosteroid treatment. Invasive aspergillosis has worse prognosis and most cases are diagnosed at postmortem autopsies. We experienced a case of acute interstitial pneumonia with an invasive aspergillosis during corticosteroid treatment. Acute interstitial pneumonia with invasive aspergillosis was diagnosed by an open lung biopsy using thoracoscopy, showing fungal hyphae with sepsis and an acute angle branching invasion of the lung tissue and blood vessels. The patient was treated with IV amphotericin-B, but died due to septic shock.

• Toxicological Research
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• v.18 no.2
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• pp.159-165
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• 2002

Recently, we reported (korean J. Biomed. Lab. Sci., 6(4): 245-251, 2000) that cyclohexane (l.56 g/kg of body wt., i.p.) administration led to lung injury in rats. However the detailed mechanism remain to be elucidated. This study was designed to clarify the mechanism of lung damage induced by cyclohexane in rats. First, lung damage was assessed by quantifying bronchoalveolar lavage fluid (BAL) protein content as well us by histopathological examination. Second, activities of serum xanthine oxidase (XO), pulmonary XO and oxygen free radical scavenging enzymes. XO tope conversion (O/D + O, %) ratio and content of reduced glutathione (GSH) were determined. In the histopathological findings, the vasodilation, local edema and hemorrhage were demonstrated in alveoli of lung. And vascular lumens filled with lipid droplets, increased macrophages in luminal margin and increased fibroblast-like interstitial cells in interstitial space were observed in electron micrographs. The introperitoneal treatment of cyclohexane dramatically increased BAL protein by 21-fold compared with control. Cyclohexane administration to rats led to a significant rise of serum and pulmonary XO activities and O/D + O ratio by 47%,30% and 24%, respectively, compared witれ control. Furthermore, activities of pulmonary oxygen free radical scavenging enzymes such as superoxide dismutase, glutathione peroxidase and glutathione S-transferase, and GSH content were not found to be statistically different between control and cyclohexane-treated rats. These results indicate that intraperitoneal injection of cyclohexane to rats may induce the lipid embolism in pulmonary blood vessel and lead to the hypoxia with the ensuing of oxygen free radical generation, and which may be responsible for the pulmonary injury.

• Clinical and Experimental Pediatrics
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• v.45 no.4
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• pp.529-534
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• 2002

Interstitial pneumonia is a heterogenous group of inflammatory and fibrosing lesions that manifest themselves as infiltrative lung disease. Of these, nonspecific interstitial pneumonia is characterized as a variable degree of interstitial inflammation with or without fibrosis and is distinguished from usual interstitial pneumonia and desquamative interstitial pneumonia, histologically. The influx of inflammatory cells and the responses of immune effector cells injury to the alveolar wall and these initial injuries results in alveolitis and fibrosis. Consequently, the gas exchange throughout the alveolar wall is impaired and the patients suffer from lung diseases of a restrictive pattern. The chief complaints represented are dyspnea and dry cough. We experienced a case of nonspecific interstitial pneumonia in a 10-year old girl. The patient had been healthy and had not been exposed to organic dusts or other toxic materials. The pathology of lung biopsy tissue showed that the alveoli were thickened by a mixture of chronic inflammatory cells and collagen type fibrosis. High resolution computed tomography(HRCT) found the patchy areas of ground-glass opacity with patchy consolidation and irregular reticular opacity, and diffuse distribution without zonal predominance. The forced vital capicity(FVC) was 31%, forced expiratory volume in one second ($FEV_1$) 29% and $FEV_1/FVC$ 90%, so a restrictive pulmonary insufficiency was found.

• Journal of Environmental Health Sciences
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• v.39 no.2
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• pp.105-116
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• 2013

Background: In Korea, there is low awareness of the respiratory health problems caused by the use of humidifiers, leading to a lack of governmental measures. Objectives: The objectives of this study were to review cases of varying degrees of humidifier lung and fever in connection with the use of humidifiers and to summarize the probable environmental agents causing these cases. Methods: We searched all articles reporting on humidifier lung, humidifier fever, and humidifier diseases caused by the use of a humidifier both at home and in the workplace. Results: We summarized a number of cases of varying degrees of respiratory diseases resulting from inhalation of water mist of humidifiers containing various species of bacteria and fungi and their toxins. Type of respiratory disease connected with humidifier lung includes interstitial pneumonitis, hypersensitivity pneumonitis, fever and several respiratory symptoms. Non-tuberculous mycobacteria (NTM), Actinomycetes, endotoxins and contaminated humidifier water were the most commonly suspected probable environmental agents causing humidifier lung. In Korea, the use of humidifier biocide is suspected as a likely cause of fatal lung injury including death and lung transplantation. Conclusion: Governmental policy should be devised and measures including a national surveillance system should be taken to prevent humidifier lung caused by the use of humidifiers.

• Tuberculosis and Respiratory Diseases
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• v.78 no.3
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• pp.281-285
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• 2015

Statins lower the hyperlipidemia and reduce the incidence of cardiovascular events and related mortality. A 60-year-old man who was diagnosed with a transient ischemic attack was started on acetyl-L-carnitine, cilostazol, and rosuvastatin. After rosuvastatin treatment for 4 weeks, the patient presented with sudden onset fever, cough, and dyspnea. His symptoms were aggravated despite empirical antibiotic treatment. All infectious pathogens were excluded based on results of culture and polymerase chain reaction of the bronchoscopic wash specimens. Chest radiography showed diffuse ground-glass opacities in both lungs, along with several subpleural ground-glass opacity nodules; and a foamy alveolar macrophage appearance was confirmed on bronchoalveolar lavage. We suspected rosuvastatin-induced lung injury, discontinued rosuvastatin and initiated prednisolone 1 mg/kg tapered over 2weeks. After initiating steroid therapy, his symptoms and radiologic findings significantly improved. We suggest that clinicians should be aware of the potential for rosuvastatin-induced lung injury.

• Tuberculosis and Respiratory Diseases
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• v.77 no.3
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• pp.145-148
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• 2014

Valproic acid is one of the most common antiepileptic drugs used for the treatment of several seizure disorders. A 20-year-old man presented with a sudden decline of consciousness. He had a neurosurgery operation for intracranial and intraventricular hemorrhage. Following surgery, antiepileptic medication was administered to the patient in order to control his seizure events. On valproic acid treatment, he began to complain of fever and dyspnea. His symptoms persisted despite receiving empirical antibiotic treatment. All diagnostic tests for infectious causes were negative. A high-resolution computed tomography scan of the chest revealed predominantly dependent consolidation and ground-glass opacities in both lower lobes. The primary differential was drug associated with interstitial lung disease. Therefore, we discontinued valproic acid treatment and began methylprednisolone treatment. His symptoms and radiologic findings had significantly improved after receiving steroid therapy. We propose that clinicians should be made aware of the potential for valproic acid to induce lung injury.

• Journal of Chest Surgery
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• v.32 no.11
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• pp.978-983
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• 1999

Background: Complement activation with transpulmonary leukocyte sequestration is considered a main mediator leading to ischemia-reperfusion lung(I-R) injury. We studied the role of leukocytes in the formation of I-R injury in ovine cardiopulmonary bypass(CPB) model with a membrane oxygenator. Material and Method: Five sheep were used. CPB circuitry consisted of a roller pump(American Optical Corp., Greenwich, CT, USA) and a membrane oxygenator(UNIVOX-IC, Bentley, Baxter Health Corp, Irvine, CA, USA). The CPB time was fixed at 120 min. Ten minutes after the start of CPB, total CPB was established. Thereafter a total CPB of 100 min was performed, followed by another 10 min of partial CPB. The CPB was discontinued and the animals were fully recovered. For measuring left and right atrial leukocyte counts, blood samples were taken before thoracotomy, 5 min and 109 in after the start of CPB, and 30 min and 120 min after weaning. C3a was measured before thoracotomy, 109 min after the start of CPB, and 30 min and 120 min after weaning. Plasma malondialdehyde(MDA) was checked before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. One to two grams of lung tissue were taken for water content measurement before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. Lung biopsy specimens were examined by light and electron microscopy. Result: Of 5 animals, 4 survived the experimental procedures. Of these, 3 animals survived on a long-term basis. No significant differences in transpulmonary gradients of leukocyte were found and no significant complement activation was expressed by C3a levels. MDA level did not show significant changes related to lung reperfusion despite an increase after the start of CPB. On both light and electron microscopic examinations, mild to moderate acute lung change was observed. Interstitial edema, leakage of erythrocytes into the alveolar space and endothelial cell swelling were the main findings. Water content of the lung showed a slight increase after the start of CPB, but there was no statistical significance. Conclusion: These findings indicate that ischemia-repersusion lung injury may not be from complement activation-leukocyte sequestration but from another source of oxygen free radicals related to CPB.