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.
Anoxia ; Child ; Classification ; Dilatation ; Esophageal and Gastric Varices ; Fibrosis ; Heart Failure ; Hepacivirus ; Hepatitis ; Hepatitis B virus ; Humans ; Hypertension, Portal ; Inhalation ; Liver Cirrhosis* ; Liver Cirrhosis, Alcoholic ; Liver*

BACKGROUND/AIMS: Transarterial chemoembolization (TACE) has been reported to be one of the useful palliative treatments in patients with unresectable hepatocelluar carcinoma. However, Bile duct injuries following TACE have been reported occasionally. In this study, we intended to clarify the incidence, pathogenic mechanisms and clinical implications of bile duct injuries following TACE. METHODS: A total of 950 consecutive patients with hepatocellular carcinoma (HCC) were subjected. 807 patients were treated with TACE. The remaining 143 were treated with transarterial chemoinfusion (TACI) of cisplatin. RESULTS: None of 143 HCC patients treated with TACI revealed to have any ischemic biliary injury radiologically. In contrast, out of 807 with TACE, 17 (2%) appeared to have biliary complications. Twelve out of 17 (71%) had bilomas at subcapsular area, three out of 17 (18%) had focal strictures at common hepatic duct or common bile duct with marked dilatation of intrahepatic bile ducts and two out of 17 (11%) had diffuse mild dilatation of intrahepatic bile ducts. Interestingly, two (17%) out of 12 bilomas were found at the lobe which was not embolized with Gelfoam. The median sessions of TACE to the occurrences of focal strictures tended to be longer compared with those of bilomas (median: 6 vs. 2.5; p=0.08). All three patients with focal strictures and four (33%) out of 12 patients with bilomas were associated with serious bacterial infections at presentation. CONCLUSIONS: Biloma seems to be caused by lipiodol rather than Gelfoam; focal strictures of large bile ducts by Gelfoam. It is suggested that adjustments of the amounts of lipiodol or Gelfoam and the sites or embolization may be required to reduce the ischemic biliary injuries following TACE.
Bacterial Infections ; Bile Ducts* ; Bile Ducts, Intrahepatic ; Bile* ; Carcinoma, Hepatocellular ; Cisplatin ; Common Bile Duct ; Constriction, Pathologic ; Dilatation ; Ethiodized Oil ; Gelatin Sponge, Absorbable ; Hepatic Duct, Common ; Humans ; Incidence ; Palliative Care