Effect of Vitamin C on Airway Hyperresponsiveness in Heavy Smokers / 결핵

BACKGROUND: Vitamin C has been reported to have a role in the decrease of airway hyperresponsiveness in animal models. This data is based on some metabolic actions of vitamin C, such as promotion of histamine degradation, producing mote PGE2 than PGE2 alpha in cyclooxygenase pathway, decrease of smooth muscle contraction, and acting as reducing agent of oxidant. It has been also known that heavy smokers have lower blood levels of vitamin C than nonsmokers and this deficiency in heavy smokers have been explained by several mechanisms, such as increased oxidation by oxidants and free radicals, increased biosynthesis of catecholamine and serotorim released by nicotine, and inadequate dietary intake. In this study, We attempted to assess effect of vitamin C on bronchial hyperresponsiveness in heavy smokers who have bronchial hyerresponsiveness and role of vitamin C on bronchial hyperresponsiveness. METHOD: To assess acute effect of vitamin C on airway hyperresponsiveness, blood sample for vitamin C level and spirometry, methacholine challenge test were done in 17 smokers and 8 nonsmokers, and one hour after oral administration of vitamin C 3 g, blood sample for vitamin C level and spirometry, metliacholine challenge test were repeated. To assess chronic effect of vitamin C on airway hyperreeponsiveness after daily administration of vitamin C 1 g for one week in 17 smokers, blood sample for vitamin C level and spirometry, methacholirie challenge test were done. To assess role of vitamin C, after oral administration of vitamin C 3 g plus indomethacin 100 mg in 12 of 15 smokers who were reactive to methacholine challenge test, spirometry and methacholine challenge test were done and after oral intake of indomethacin 100 mg in 12 smokers who were reactive to methacholine challenge test, spirometry and metbachoine challenge test were repeated. RESULT: There were no significant differences in whole blood vitamin C levels between smokers(1.17+/-0.22mg/dL) and nonsinokers(1.14+/-0.19 mg/dL) (p>0.05). Fifteen of the 17 smokers(88.2%) were reactive to metbacholine chaflenge test amd 10 of the 15 smokers who were reactive to methacholine challenge test were less than 8 mg/dL in PC20FEV1, and 7 of the 8 nonsmokers(87.5%) were nonreactive to methacltoline challenge test There were significant decrease in bronchial responsiveness after oral administration of xitamin C 3 g in 13 of the 15 smokers who were reactive to methachoine challenge test. This significant decrease persisted with maintenance daily administration of 1 g for one week. PC20FEV1 were not correlated to vitamin C levels in smokers. After oral administration of indomethacin 100 mg, significant reduction of bronchial responsiveness that occured after oral administration of xdtamin C 3 g in smokers were attenuated. CONCLUISON: Although there were no significant differences in whole blood vitamin C levels between smokers and nonsmokers, heavy smokers have significant increase in bronchial responsiveness than nonsmokers. This bronchial hyperresponsiveness of heavy smokers can be attenuated by vitamin C supplement Disappearance of vitamin C effect by indcrnethaein supplement may suggest that vitamin C exert its effect via alteration of arachidonic acid metabolism.

A Case of Listeria Monocytogenes Endocarditis in Apparently Healthy Adult

About 50 cases of Listeria monocytogenes endocarditis were reported in worldwide literature in 1950-1995. Though clinical and laboratory data suggest a similarity with other types of bacterial endocarditis, the prognosis is more unfavorable and the mortality rate is higher. However, there has not been a report in Korean literature. We report a case of 55 year-old male with rapidly progressive native aortic endocarditis caused by L. monocytogenes. He had neither history of underlying cardiac disease nor definitive predisposing factor. He presented mild dyspnes, chest pain and febrile sensation for a week. Echocardiography showed large vegetation in aortic valve and severe aortic regurgitation. L. monocytogenes grew on blood culture. We underwent artificial aortic valve replacement due to rapidly progessive heart failure. A thromboembolism occured at right femoral artery on postoperative 2nd day was removed successfully. He discharged without any sequellae.

Bronchial Hyperresponsiveness in Liver Cirrhosis / 결핵

BACKGROUND: Arterial hypoxemia has been noted in patients with liver cirrhosis because of bronchial vessel dilatation. Cabenes et al. reported that bronchial hyperresponsiveness to the metacholine inhalation was observed in patients of left side heart failure, he suggested that one of the mechanism was bronchial vessel dilatation. We hypothesized that patients of liver cirrhosis might have bronchial hyperresponsiveness to metacholine inhalation due to portal hypertension. We evaluate the relationship between bronchial responsiveness and severity of liver cirrhosirs, severity of portal hypertension. METHODS: In the 22 patients of the liver cirrhosis with clinical portal hypertension metacholine provocation test was done and determined PC20 FEV1. We classified lifter cirrhosis according to Pugh- Child classification Esophagogastroscopies were performed for the evaluation of the relationship between bronchial hyperresponsiveness and severity of esophageal varix. RESULTS: In the 22 cases of the liver cirrhosis with clinical portal hypertension. The causes of liver cirrhosis, alcoholic hepatitis was 9 cases. hepatitis B virus was 12 cases, hepatitis C virus was 1 case. and 151 cases (68.18%) of total 22 cases were positive in metacholine provocation test. In positive cases There was no significant relationship between PC20FEV1 and severity of liver cirrhosis which were classified by Pugh-Child classification or severity of esophageal varix(p<0.05). CONCLUSION: we observed that bronchial responsiveness to metacholine increased in the patients of liver cirrhosis and there was no significant relationship between the severity of liver cirrhosis and the severity of esophageal varix.