ABSTRACT
BACKGROUND: This study investigates the prevalance of HBV precore mutant in chronic B hepatitis patients and whether HBV precore mutants affect hepatic inflammation and response to interferon alfa. METHODS: HBV DNA in liver tissue from 48 chronic hepatitis patients was amplified by polymerase chain reaction. The HBV precore mutants were detected by direct sequencing of amplified PCR products. Thirty-three HBeAg-positive patients (Group 1: wild- type, Group 2: mixed) were received 3-6 MU INF three times a week for 4-6 months. We did follow-ups for at least six months(mean : Group 1-11.3, Group 2- 13.7 months). A complete responder was defined as persistent(>6 months) normalization of transaminase and loss of HBeAg and/or seroconversion. RESULTS: The HBV precore mutants were found in 15 cases(31.2%) among 48 patients: 7 cases(21.2%) in 33 HBeAg-positive patients and 8 cases(53.3%) in 15 HBeAg-negative patients. The HBV precore mutants were more frequently found in HBeAg-negative patients(p= 0.043). Differences in severity of hepatic pathology were not observed in the wild-type versus mutant-type chronic hepatitis B patients(p =1.00). Initial response rate was not significantly different between two Groups(p= 0.228), but complete response rate had a lower tendency in Group 2 (p=0.073). CONCLUSION: There is a tendency for HBV precore mutants to be less responsive to INF therapy than wild type. Therefore the patients with chronic hepatitis B should be treated as early as possible in natural history of their liver disease before the emergence of HBV precore mutants.
Subject(s)
Humans , DNA , Follow-Up Studies , Hepatitis , Hepatitis B e Antigens , Hepatitis B, Chronic , Hepatitis, Chronic , Inflammation , Interferon-alpha , Interferons , Liver Diseases , Liver , Natural History , Pathology , Polymerase Chain ReactionABSTRACT
Endoscopic injection sclerotheraphy(EIS) was an effective method for treatment of bleeding esophageal varices. However, it might be associated with some undesirable complications. Endoscopic variceal ligation(EVL) is a recently developed method for control of active variceal bleeding and eradicating esophageal varices with similar efficacy and minimal risk of complications compare to EIS. We performed EVL in 40 patients who had recently bled from esophageal varices. Total 198 variceal ligations were performed during 64 separate EVL session. Control rate of acute bleeding was 90%(36 of 40patients) and 4 patients died after EVL because of failure of bleeding control. Rebleeding following initiation of EVL occured in 5 patients-three patients were successfully controlled by EVL, one patient was controlled but eradication was impossible and one patient died. Varices were eradicated or reduced to grade I in 31(86.1%) of 36 survivors by 1-9 ligation(mean 5.0) in l-4 EVL sessions(mean 1.6). After EVL, there were mild complications-mild substernal discomfort in 4 patients, mild dysphagia in 2 patients and fever in 2 patients. These results suggest that EVL is a safe and effective method for treatment of bleeding and eradication of esophageal varices with less complication.
Subject(s)
Humans , Deglutition Disorders , Esophageal and Gastric Varices , Fever , Hemorrhage , Ligation , Survivors , Varicose VeinsABSTRACT
Brunners gland adenoma is a benign epithelial tumor of the duodenum originating from submucosal Brunners gland. This is an extremely rare entity that account for only 10.6% of benign duodenal tumor, which are themselves relatively rare, representing 0.008% of all surgical and autopsy specimens. The clinical manifestation are nonspecific gastrointestinal complaints, such as bloating or epigastric pain, and the tumor gives rise to melena or anemia, due to the ulceration or erosion of the tumor. The diagnosis is usually made by radiologic studies and gastroduodenal endoscopy which can also provide definitive treatment. The aim of treatment is complete removal of the lesion and exclude malignancy. We report on 4 cases of Brunners gland adenoma which was confirmed by operation or endoscopic polypectomy.