OBJECTIVES: Our aims of this study is to analyze the clinical characteristics and the prognos is of the disease which develops in patient swith chronic liver disease as acutely exacerbated hepat it is accompanied by myosit is. Finally we try to identify and is olate the causative agent. METHODS: The patient swith chronic liver diseases, who developed muscle weakness and paralysis, were classified to group A or group B, according to the level of creatinine kinase ( CK) activity. The group A consists of patients with less than 3-fold increase of normal CK activity and the group B includes patients with over 3-fold increase of it. We evaluated clinical characteristics, blood chemistry, clinical course, and causes of deathin patients of study groups, compared with those of patients with chronic liver disease with normal CK activity as controls. The causative agent was suggested by conventional culture and RT-PCR analysis in two cases of group B. RESULTS: 1. There was no significant differences in age, sex, underlying disease, or liver function test bet ween control and study group ( control and group A or B) before entry. 2. The clinical symptoms and signs , such as drowsy mental state, generalized weakness/myalgia caused by hepatic encephalopathy and myositis , occurred frequently in the study group. 3. Significant elevation of aspartic acid transaminase (AST ) and alaninetr ans aminase ( ALT ) was noted in Group B. AST / ALT ratio is over 2 in group A or B. Synthetic function of the liver such as prothrombin time ( PT ) or serum albumin level is significantly decreased. Blood urea nitrogen ( BUN) and creatinine were increased as a result of impaired renal function. 4. Culture of coxs ackievirus was positive by immunofluor escence as say IFA) as a caus ative agent and also was positive in reverse transcription-polymerase chain reaction (RT-PCR) analys is using universal primer of enterovirus in two recent cases of group B. 5. Death rate increased significantly in study group, compared with that of control group ( 20.7% versus 5.6%). Major cause of death, 12 patients died of which, is hepatic failure. CONCLUSION: The patients with chronic liver disease abruptly developed a exacerbated hepaticdys function and muscle paralysis and/or weakness. This exacerbated hepatitis accompanied by myositis was suggested to be caused by coxsackie B viral infection. Furthermore, this infection increase deathrate and resulted in poor prognosis. Thus, further study should be continue to confirm the causative agent and classify the subtype.
Aspartic Acid ; Blood Urea Nitrogen ; Cause of Death ; Chemistry, Clinical ; Creatinine ; Enterovirus ; Hepatic Encephalopathy ; Hepatitis* ; Humans ; Liver Diseases* ; Liver Failure ; Liver Function Tests ; Liver* ; Mortality ; Muscle Weakness ; Myositis* ; Paralysis ; Phosphotransferases ; Prognosis ; Prothrombin Time ; Serum Albumin

Bleeding from esophageal or gastric varix is the most critical and life-threatening complication of portal hypertension and the most common cause of deaths in the patients with cirrhosis. In the management of variceal bleeding, the various therapeutic interventions including operation and nonoperative procedure were tried, but neither of management was successfully achieved. Between February 1992 and November 1994, we performed endoscopic injection sclerotherapy(EIS) in 35 cirrhotic patients who had recently bled from esophageal varices and had a past history of esophageal variceal bleeding in Chonbuk National Univesity Hospital. Among 35 patients, 32 were male and 3 were female. The underlying severity of liver disease was graded A, B or C according to modification of Child-Pugh classification. EIS was repeated every 1 week until the esophageal varices had been complete obliterated and removed. To investigate the effects of esophageal varix eradication by EIS on combined peri- cardial varix, endoscopic examinations were performed both before procedure and after complete EIS sessions and this study was performed to examine a changes of combined pericardial varices after EIS procedure for the treatment of esophageal varices bleeding secondary to portal hypertesion. We reviewed medical records and compared changes or sizes of pericardial varices before and after EIS procedure. Mean follow up peiod was 61 days. Total number of 162 EIS for variceal eradication were performed. Mean session for eradication of esophageal varices was 4.6 per person, mean amount of injected sclerosant was 8.3cc(1-18cc), mean duration of EIS was 39 days, and mean follow up was 62 days after complete EIS procedure. In total 162 EIS procedure, complications associated with EIS including substernal discomfort 53.7%(n=87), substernal chest pain 45.7%(n=74), fever 4.9%(n=8), dysphagia 14.2%(n=23) and pleural effusion 3.1%(n=5), were transient and not required specific management. During the follow-up period, complete disapperance of pericardial varix or reduction of size was appeared in l8 cases(51.4%) among total 35 patients. No significant changes of variceal size before and after procedure were l6 cases(45.7%) and only 1 case(2.9%) was more aggravated. So, these results suggest that EIS procedure of esophageal varix on pericardial varix seems either to improve or to maintain the severity of the pericardial gastric varix without aggravation.
Cause of Death ; Chest Pain ; Classification ; Deglutition Disorders ; Esophageal and Gastric Varices* ; Ethanolamine* ; Female ; Fever ; Fibrosis ; Follow-Up Studies ; Hemorrhage ; Humans ; Hypertension, Portal ; Jeollabuk-do ; Liver Diseases ; Male ; Medical Records ; Oleic Acid* ; Pleural Effusion ; Sclerotherapy* ; Varicose Veins

Bleeding from esophageal or gastric varix is the most critical and life-threatening complication of portal hypertension and the most common cause of deaths in the patients with cirrhosis. In the management of variceal bleeding, the various therapeutic interventions including operation and nonoperative procedure were tried, but neither of management was successfully achieved. Between February 1992 and November 1994, we performed endoscopic injection sclerotherapy(EIS) in 35 cirrhotic patients who had recently bled from esophageal varices and had a past history of esophageal variceal bleeding in Chonbuk National Univesity Hospital. Among 35 patients, 32 were male and 3 were female. The underlying severity of liver disease was graded A, B or C according to modification of Child-Pugh classification. EIS was repeated every 1 week until the esophageal varices had been complete obliterated and removed. To investigate the effects of esophageal varix eradication by EIS on combined peri- cardial varix, endoscopic examinations were performed both before procedure and after complete EIS sessions and this study was performed to examine a changes of combined pericardial varices after EIS procedure for the treatment of esophageal varices bleeding secondary to portal hypertesion. We reviewed medical records and compared changes or sizes of pericardial varices before and after EIS procedure. Mean follow up peiod was 61 days. Total number of 162 EIS for variceal eradication were performed. Mean session for eradication of esophageal varices was 4.6 per person, mean amount of injected sclerosant was 8.3cc(1-18cc), mean duration of EIS was 39 days, and mean follow up was 62 days after complete EIS procedure. In total 162 EIS procedure, complications associated with EIS including substernal discomfort 53.7%(n=87), substernal chest pain 45.7%(n=74), fever 4.9%(n=8), dysphagia 14.2%(n=23) and pleural effusion 3.1%(n=5), were transient and not required specific management. During the follow-up period, complete disapperance of pericardial varix or reduction of size was appeared in l8 cases(51.4%) among total 35 patients. No significant changes of variceal size before and after procedure were l6 cases(45.7%) and only 1 case(2.9%) was more aggravated. So, these results suggest that EIS procedure of esophageal varix on pericardial varix seems either to improve or to maintain the severity of the pericardial gastric varix without aggravation.
Cause of Death ; Chest Pain ; Classification ; Deglutition Disorders ; Esophageal and Gastric Varices* ; Ethanolamine* ; Female ; Fever ; Fibrosis ; Follow-Up Studies ; Hemorrhage ; Humans ; Hypertension, Portal ; Jeollabuk-do ; Liver Diseases ; Male ; Medical Records ; Oleic Acid* ; Pleural Effusion ; Sclerotherapy* ; Varicose Veins

Different ligands can lead to the activation of epidermal growth factor receptor, and the subsequent signal transduction leads to an increase in cellular motility, proliferation, invasion, and blocking of apoptosis, and all of this contributes to the development and progression of cancer. Our studies clarified; 1) The EGFR expression level is reduced during tumor progression or during ligand-induced EGFR activation. 2) ANXA8 and its regulatory pathway may well be alternative, strategic targets for inhibiting tumor metastasis. 3) The molecular pathway of EphA2 signaling and provide insight into the mechanisms that control cancer progression and metastatic spread in cholangiocarcinoma (CC). Therefore, therapeutic strategies that target EphA2 and its downstream effectors may be useful to control CC.
Apoptosis ; Cholangiocarcinoma* ; Ligands ; Neoplasm Metastasis* ; Receptor, Epidermal Growth Factor ; Signal Transduction

No abstract available.
Focal Nodular Hyperplasia*

No abstract available.
Cell Culture Techniques ; Cell Line, Tumor ; Cells, Cultured ; Cells, Immobilized ; Hepacivirus/isolation & purification/*physiology ; Hepatocytes/physiology/*virology ; Humans ; Models, Biological ; RNA, Viral/analysis ; *Virus Replication

A Case of double pylorus, in 56 year old man, was diagnosed by fiberoptic gastroscopy and upper gastrointestinal series. Two ovoid large openings of pyloric canal divided by smooth thickened septum were observed endoscopically And the relevant literatures on tihe subject were reviewed.
Gastroscopy ; Humans ; Middle Aged ; Pylorus*

Focal nodular hyperplasia (FNH) is a rare, benign hepatic tumor which was usually discovered incidentally by imaging procedure performed for some other reasons. FNH is typically asymptomatic and, it seldom bleeds. There is no evidence to support any relation with primary liver cancer. Accordingly, the preferred management is conservative, and excision is reserved for large symptomatic and complicated lesion, or when the diagnosis remains uncertain. Although many cases of FNH has been described to date in the other countries, only four cases of FNH has been reported in Korean literature. In the present report we describe a 7 cm sized asymptomatic lesion of FNH in a 23-year-old woman, that was disclosed by various kinds of imaging procedure. The left lateral segmentectomy was performed. The mass was firm and showed areas of localized growth of mature hepatocytes and septal fibrosis accompanied with marginal ductal proliferation, consistent with FNH. It also displayed an incomplete stellate architectual configration consisted of a central fibrous scar.
Cicatrix ; Diagnosis ; Female ; Fibrosis ; Focal Nodular Hyperplasia* ; Hepatocytes ; Humans ; Liver Neoplasms ; Liver* ; Mastectomy, Segmental ; Young Adult

The analysis of recurring chromosome aberrations has become an integral part of the diagnostic and prognostic workup of many human cancers, and their molecular analyses have facilitated the identification of genes related to the pathogenesis of cancer. Cholangiocarcinoma (CC), a malignant neoplasm of the biliary epithelium, is usually fatal because of the difficulty in early diagnosis and unavailability of effective therapy. Furthermore, little is known about the genetics and biology of CC. Only few reports concerning cytogenetic studies of CC have been published and few cell lines have been established. We recently established CC cell line, designated as PCK1. The purpose of this study is to establish in detail karyotype of PCK1 cell line. The origins of the unidentified marker chromosomes were analyzed by G-banding, cross species color banding (RxFISH), and human chromosome-specific painting. In PCK1 cell line, gains involved chromosomes and chromosome regions, 4, 5, 9, 12, 16, 21, 1q, 7q11-q22, 8q, 12p, 14q11-q22, 15q21-qter, 17p11-qter, and 18p. Losses involved Y, 7q31-qter, 8p, 14q23-qter, 17p12-pter, and 18q. Established PCK1 cell line will be able to use the basic research of cholangiocarcinoma and the abnormal chromo-somes may be the candidate regions for isolation of the genes related to CC.
Biology ; Cell Line* ; Cholangiocarcinoma ; Chromosome Aberrations* ; Cytogenetics ; Early Diagnosis ; Epithelium ; Genetics ; Humans ; Karyotype ; Paint ; Paintings

No abstract available.
Bromodeoxyuridine* ; Hep G2 Cells* ; Kinetics* ; Tretinoin*