No abstract available.
Lung Neoplasms* ; Lung* ; Neoplasms, Squamous Cell*

Cutaneous metastases from internal malignancy are relatively rare. Three cases of cutaneous metastases, two from lung cancer and one from breast cancer are reported. Case 1-cutaneous metastasis from bronchioloalveolar carcinoma of the lung, where four erythematous to pinkish pea sized smooth surfaced nodules on the scalp were noticed for 2 years in a 48-year-old man. Case 2-cutaneous metastasis from adenocarcmoma of the lung, where two hard tender freely movable subcutaneous nodules, about 3 cm in diameter on the lateral chest wall were noticed for 6 months in a 61-year-old woman. Case 3-cutaneous metastasis from infiltrating ductal carcinoma of the right breast, where a hand, violaceous, non-tender plaque (8×6.5 cm) on the right areolar area was noticed for 4 months in a 47-year-old woman.
Adenocarcinoma, Bronchiolo-Alveolar ; Breast ; Breast Neoplasms ; Carcinoma, Ductal ; Female ; Hand ; Humans ; Lung ; Lung Neoplasms ; Middle Aged ; Neoplasm Metastasis ; Peas ; Scalp ; Thoracic Wall

Leser-Trelat sign is characterized by the sudden appearance and rapid increase in number and size of seborrheic keratoses associated with an internal malignancy. A 78-year-old woman showed multiple pea to bean sized dark brownish papules and plsques on the trunk. Skin lesions had appeared suddenly since 5 months ago and then rapidly increased in number and size. The histopathologic exsmination of the skin lesions revealed seborrheic keratoses. The chest roentgenogram revealed the mass shadow on the right hilar region and transbronchial lung biopsy revealed small cell carcinoma.
Aged ; Biopsy ; Carcinoma, Small Cell* ; Female ; Humans ; Keratosis, Seborrheic ; Lung* ; Peas ; Skin ; Thorax

BACKGROUND: Serum eosinophil cationic protein(ECP) level has been proposed as a indirect marker of eosinophilic inflammation of the airway in bronchial asthma. OBJECTIVE: To evaluate serum ECP against indirect clinical markers of disease, we compared bronchial obstruction, bronchial hyperresponsiveness and peripheral blood eosinophil counts, total IgE with serum ECP levels in patients with bronchial asthma and normal controls. METHOD: Fourty-two patients with bronchial asthma and twenty-six normal controls were enrolled. Measurement were made by spirometry, inhalation challenge with methacholine, peripheral blood eosinophil counts, total IgE and FEIA(fluoroenzymatic immunoassay) of serum ECP RESULT: Serum ECP levels were significantly higher in asthmatic patients than normal controls(p<0.0,5). Serum ECP levels were correlated with peripheral blood eosinophil counts(p<0.01, r=0.544) and bronchial hyperresponsiveness(PC,)(p<0.01, r=-0.456) in patients with bronchial asthma. Serum ECP levels were correlated with degree of bronchial obstruction(FEV, % to predicted value, FEV1/FVC%) in total subjects, but not in asthmatic patients. CONCLUSION: Serum ECP level may be used as indicator of disease activity in bronchial asthma and be helpful in differentiation between normal person and asthmatic patients on simple serological method. Further studies on the changes of serum ECP levels according to disease course and therapeutic responses are needed.
Asthma* ; Biomarkers ; Eosinophil Cationic Protein* ; Eosinophils ; Humans ; Immunoglobulin E ; Inflammation ; Inhalation ; Methacholine Chloride ; Spirometry

BACKGROUND: To evaluate airway responses and inflammation to antigen in Sprague-Dawley rat asthma model, we examined airway responses, serial histologic changes of the lung, and the relationship between airway responses and airway inflammation after antigen airway challenge. METHODS: Sprague-Dawley rats were sensitized with subcutaneous injection of 10 microgram ovalbumin(OA). Antigen airway challenges were done 14 ~16 days after sensitization and the sensitized rats were sacrificed 1h(AE), 6 ~8h(AL) and 1day(AD) after airway challenge, to examine the histologic changes of the lung. Airway responses were measured by body plethysmograph and recorded by enhanced pause(Penh) as an index of airway obstruction 6 ~8h after antigen challenges. Nonsensitized controls(10 rats) were also challenged with antigen and sacrificed 1 day later. Histopathologic examination of two trachea, large bronchi, small bronchi, and vessels was performed to evaluate the severity of inflammation and eosinophilic infiltration with H&E stain. RESULTS: In 17 of 20 rats(85%) in both groups, we observed airway responses. Among them, an early response(ER) in 15 rats(75%), an dual response in 5(25%), and an late response(LR) only in 2 rats(10%) displayed. There were no significant differences in the severity of inflammation among the trachea, large bronchi, small bronchi and vessels in all groups after antigen challenge(p>0.05) and between early and late responders. The significant eosinophil infiltration was observed in 5 rats(50%) of AL(p<0.05) compared with in AE and controls. Also, eosinophil infiltration was observed in higher trend in LR(57.1%) compared to ER(40%)(p>0.05). CONCLUSION: Sprague-Dawley rats sensitized with subcutaneous injection of OA showed a significant airway responses to antigen challenge. But antigen challenges caused a little eosinophil infiltration and no significant airway inflammation. Asthma model of Sprague-Dawley rats could be useful for antigen-induced airway responses, but this model has a limitation for the study of human asthma because of no significant pathologic change.
Airway Obstruction ; Animals ; Asthma* ; Bronchi ; Eosinophils ; Humans ; Inflammation* ; Injections, Subcutaneous ; Lung ; Ovalbumin* ; Rats ; Rats, Sprague-Dawley* ; Trachea

No abstract available.
Physiology* ; Prognosis* ; Pulmonary Disease, Chronic Obstructive* ; Respiratory Insufficiency*

Bronchial asthma is a chronic airway inflammation disorder involving lymphocyte activation and various cytokines secretion by lymphocyte. The inflammatory response results from a complex network of interactions between inflammatory cells (mast cells, eosinophils, macrophages) and resident cells belonging to the lung structure itself like EC, fibroblasts, or bronchial epithelial cells. IL-6 which is known to up-regulate the endothelial cell expression of adhesion molecules participating in the development of the inflammatory reaction in bronchial asthma is produced by alveolar macrophage. ICAM-1 is produced by bronchial epithelial cell and expression by endothelial cell, which is known to enhance of the influx of various cells. RANTES which is known to a potent chemoattractant for eosinophils, lymphocytes, and monocytes, a member of the CC chemokine family, is expressed by bronchial epithelial cell. To evaluate whether markers of lymphocyte activation are useful markers of disease activity in bronchial asthma, we measured sIL-6, sICAM-1, sRANTES in 42 patients with mild to moderate bronchial asthma and in 26 normal controls and compared the result with other disease activity markers in asthma (pulmonary function, blood eosinophil counts). The mean level of sIL-6 was higher than that of normal control and correlated significantly with sICAM-1, FEV1% to predicted value. The mean level of sICAM-1 was higher than that of normal control and correlated significantly with FEV1%, FEV1% to predicted value. The mean level of sRANTES showed the tendency to be higher than that of normal control, but not significant statistically, and did not correlated with sIL-6, sICAM-1, FEV1%, FEV1% to predicted value, blood eosinophil counts. It appeared that sIL-6 and sICAM-1 could be a disease marker in bronchial asthma. But, clinical application of the measurement of these markers needs to be studied further.
Asthma* ; Chemokine CCL5 ; Cytokines ; Endothelial Cells ; Eosinophils ; Epithelial Cells ; Fibroblasts ; Humans ; Inflammation ; Intercellular Adhesion Molecule-1 ; Interleukin-6 ; Lung ; Lymphocyte Activation ; Lymphocytes ; Macrophages, Alveolar ; Monocytes

PURPOSE: To evaluate changes in tuberculous cavities, one of the major factors used to determine the activityof tubereulosis, by high-resolution CT(HRCT) in active pulmonary tuberculosis patients after antituberculoustherapy. MATERIALS AND METHODS: The HRCT findings of 41 patients with active tuberculosis were analyzed withparticular emphasis on the appearance of tuberculous cavities before and after therapy. We measured the largestdiameter and maximal wall thickness of the cavities, as well as accompanying changes occurring during follow-up.The mean interval between initial and follow-up study was 8.7 months(minimum:4.1, maximum:33.2;S.D.: +/-5.0) andthe mean duration of antituberculous therapy was 7.5 months(minimum:4.7, maximum:14.8;S.D.: RESULTS: Among 41patients, 54 cavities were found on initial HRCT. Thirty one(57.4%) of these disappeared during follow up HRCTwith residual changes such as residual fibrotic scar(n=15), granuloma(10), paracicatrical emphysema(7),calcification(3), traction bronchiectasis(3), consolidation(3) and bullous emphysema(1). Twenty three of thecavities(42.6%) decreased in size and wall thickness, but did not disappear completely during follow-upexamination. Mean largest diameter and maximal thickness of 23 cavities were 32.0mm(+/-13.9) and 7.9mm(+/-4.8) oninitial HRCT, falling to 20.9mm(+/-12.5) and 4.1mm(+/-2.6), respectively, during follow-up HRCT. Among four patientswho underwent a second follow-up, the largest diameter and maximal thickness of the cavities decreasedcontinuously. In two patients, however, the cavities did not did not disappeas, though in the other two they haddisappeared by the time follow-up HRCT was performed a second time. CONCLUSION: During follow-up HRCT afterantituberculous therapy(mean duration of 7.5 months), 57.4%(31/54) of cavities were seen to have disappeared, withresidual changes such as fibrotic scars, granulomas, paracicatrical emphysema and calcification ; 42.6% of thecavitivies still remained, however, with retractive and fibrotic change. Such fibrotic and retractive changesshould not, therefore, be taken as indicative of active tuberculosis, especially in patients who have successfullycompleted their medication.
Cicatrix ; Emphysema ; Follow-Up Studies ; Granuloma ; Humans ; Lung ; Traction ; Tuberculosis ; Tuberculosis, Pulmonary

BACKGROUND: Acute lung injury is an hypoxic respiratory failure resulting from damage to the alveolar-capillary membrane, which can be developed by a variety of systemic inflammatory diseases. In this study the therapeutic effects of intra-tracheal pulmonary surfactant instillation was evaluated in the intratracheal endotoxin induced acute lung injury model of a rat. METHODS: 20 Twenty Sprague-Dawley rats were divided into 4 groups, and normal saline (2 ml/kg, for group 1) or LPS (5 mg/kg, for group 2, 3, and 4) was instilled into the trachea respectively. Either normal saline (2 ml/kg, for group 1 & 2, 30 min later) or bovine surfactant (15 mg/kg, 30 min later for group 3, 5 hr later for group 5) was instilled into the trachea. The therapeutic effect of intratracheal surfactant therapy was evaluated with one chamber body plethysmography (respiratory frequency, tidal volume and enhanced pause), ABGA, BAL fluid analysis (cell count with differential, protein concentration) and pathologic examination of the lung. RESULTS: Intratracheal endotoxin instillation induced increase in increased the respiration rate, decrease in decreased the tidal volume and increase in increased the Penh in all group of rats. Intratracehal instillation of surfactant decreased Penh, increased arterial oxygen tension, decreased protein concentration of BAL fluid and decreased lung inflammation in at both time times of administration (30 minute and 5 hour after endotoxin instillation). CONCLUSION: Intratracheal instillation of surfactant would be can be a beneficial therapeutic modality as discovered in the acute lung injury model of rats induced by intratracheal LPS intillation. It deserves to be evaluated in the fortreatment of human acute lung injury.
Acute Lung Injury* ; Animals ; Humans ; Lung* ; Membranes ; Oxygen ; Plethysmography ; Pneumonia ; Pulmonary Surfactants ; Rats* ; Rats, Sprague-Dawley ; Respiratory Insufficiency ; Respiratory Rate ; Tidal Volume ; Trachea

BACKGROUND: Cough Coughing is the most common complaint for which patients seek medical service. When cough sustains caughing continues over 3 weeks in non-smokers who do not take cough-provoking drugs, they are classified as patients with chronic cough. As well-known, three Three well known main causes of chronic caugh are diseases - (delete) postnasal drip syndrome, bronchial asthma and gastroesophaseal reflux disease. - comprise the majority of the causes of chronic cough. Among them, postnasal drip syndrome is reported to be the most common cause of all in chronic cough diseases, and allergic inflammation plays an important role in the pathogenesis of postnasal drip syndrome. CD23 and CD25 which are low affinity receptor for IgE and IL-2 receptor alpha, respectively, are closely related to allergic inflammation and we evaluated the role of them in their roles were evaluated in chronic cough patients. METHODS: We evaluated 105 patients with chronic cough and selected 56 patients for measurement of serum CD23 & CD25 level levels. We selected 10 normal, medical students for comparison of serum CD23 & CD25 level. levels. RESULT: We found that postnasal drip syndrome was The postnasal drip syndrome was found to be the most common cause of chronic cough. Serum CD23 and CD25 level were did not increased increase in chronic cough patient compared to normal controls. However in bronchial asthma patient, serum CD23 level was increased relative to normal control (p<0.05). CONCLUSION: In bronchial asthma presented as chronic cough, lymphocyte mediated allergic inflammation might be may related with the pathogenesis of the disease.
Asthma ; Cough* ; Humans ; Immunoglobulin E ; Inflammation ; Lymphocytes ; Receptors, Interleukin-2 ; Students, Medical