• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.752-759
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• 1995

Background: Bronchial asthma is characterized by noctunal dyspnea, cough and wheezing because of airway hyperresponsiveness to nonspecific stimuli. These symptoms and signs are also observed in patients with congestive heart failure. Therefore, this is so called "cardiac asthma". There are lots of experimental and clinical datas to suggest that airway dysfunctions occur in acute and chronic congestive heart failure. However, it is still controversial whether bronchial hyperresponsiveness is present in patients with congestive heart failure. To assess whether bronchial hyperresponsiveness is present in patients with congestive heart failure and to demonstrate the relationship between bronchial responsiveness and vascular pressure, we performed methacholine provocation test in 11 patients with mitral valvular heart disease. Methods: All patients were in the New York Heart Association functional class II and treated continuously with digoxin and/or dichlozid and/or angiotensin converting enzyme inhibitor except one patient. All patients were undergone right and left side heart catheterization for hemodynamic measurements. A 20 percent fall of peak expiratory flow rate were considered as positive response to methacholine provocation test. Results: 1) Only one patient who has normal pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index was positive in methacholine provocation test. 2) Their mean pulmonary artery pressure, pulmonary capillary wedge pressure were $21.72{\pm}9.70mmHg$, $15.45{\pm}8.69mmHg$ respectively which were significantly higher. Conclusion: It is speculated that in stable congestive heart failure patients, bronchial responsiveness as assessed by methacholine provocation test may not be increased.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1256-1262
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• 1997

Background : Leukocyte-endothelial adhesion molecules have been implicated in the pathogenesis of inflammatory disease. ICAM-1, VCAM-1 and E-selectin are cell surface adhesion molecule on vascular endothelial cells. They are up-regulated by inflammatory cytokines and regulate the adhesion and migration of leukocytes across the endothelium. Tuberculosis, a granulomatous disorder is an infection caused by Mycobacterium tuberculosis. The clinical manifestations of tuberculosis are dependent on the cellular immune response to tubercule bacilli. Circulating adhesion molecules are probably formed by cleavage and release into the circulation of the extracellular domain of the membrane bound form. The elevated levels of circulating adhesion molecules have been reported in numerous disease state. To evaluate their role as markers of disease activity in tuberculosis, we measured a sE-selectin, sVCAM-1 and sICAM-1 levels in the serum with severities of mild, moderate and far advanced pulmonary tuberculosis. Methods : The control and test groups were divided as follows. Group I : control(n=5), Group II : patients with mild pulmonary tuberculosis(n=12), Group III : pateints with moderate pulmonary tuberculosis(n=20), Group IV : patients with far advanced pulmonary tuberculosis(n=19). Serum sICAM-1, sVCAM-1 and sE-selectin were measured by ELISA kit Results : Serum soluble adhesion molecules are elevated in patients with pulmonary tuberculosis, Circulating ICAM-1 levels were significantly elevated in patients with moderate and far advanced pulmonary tuberculosis when compared with control group. When compared with control group, serum sVCAM-1 levels showed significant elevation in patients with mild, moderate and far advanced pulmonary tuberculosis. Serum sE-selectin levels were significantly elevated in patients with far advanced pulmonary tuberculosis when compared with control group. Conclusion : These results suggest that sICAM-1, sVCAM-1, and sE-selectin may be invloved in the pathogenesis of tuberculosis. And, particularly, sICAM-1 and sVCAM-1 may be useful markers of the disease activity.

• The Korean Journal of Nuclear Medicine
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• v.36 no.6
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• pp.368-380
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• 2002

Purpose: Liver transplantation (LT), one of the therapeutic options of primary liver cancer has been suffering from recurrence caused by metastasis in 8-54% of patients. This study was performed to investigate whether FDG-PET is useful for detecting hidden metastasis in LT candidates. Materials and Methods: Twenty-six patients (male:female=23:3, mean age 55.7 years) underwent FDG-PET. Their previous conventional diagnostic studies (CDS) like abdomen US and CT, chest x-ray and CT, and bone scan were negative (n=22) or equivocal (n=4) for metastasis. Positive FDG-PET findings were confirmed by biopsy or clinical follow-up. Results: Among 4 patients with equivocal metastatic lesions on CDS, 3 had 6 hypermetabolic lesions on FDG-PET, which were confirmed as metastasis and subsequently LTs were cancelled. Of these, 5 lesions were initially negative on CDS. Remained 1 patient underwent LT with a negative FDG-PET result. Among 22 patients without metastasis on CDS, 5 had 7 hypermetabolic lesions on FDG-PET. One of these patients proved to have 2 metastatic lesions, and LT was cancelled. The other 4 patients had S hypermetabolic lesions on FDG-PET, which were confirmed as benign lesions, and 3 patients of them underwent LT. In summary, FDG-PET was useful in avoiding 4 unwarranted LT by detecting unsuspected metastatic lesions on CDS. A total of 17 patients underwent LT. In comparison with pathology, the sensitivity and specificity of FDG-PET for detecting viable primary liver cancer were 55.6% (5/9) and 87.5% (7/8), respectively. Conclusion: FDG-PET can detect additional hidden metastasis and contribute to reducing unwarranted LT in the patients with primary liver cancer.