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Biomedical subjects

Y Tameda

Publications and source records attributed to Y Tameda.

At least 19 recordsLinked to original sources
PubMed2001

Prospective study of laparoscopic findings with regard to the development of hepatocellular carcinoma in patients with hepatitis C virus-associated cirrhosis.

BACKGROUND: The laparoscopic findings of hepatocarcinogenesis are not well defined. The purpose of this prospective study was to evaluate the predictive value of laparoscopic findings with regard to the development of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-associated cirrhosis. METHODS: One hundred nineteen patients with HCV-associated cirrhosis who underwent laparoscopy were enrolled in this study. Ten laparoscopic variables, including degree of development and size of regenerating nodules, irregularity of regenerating nodules, and size of both hepatic lobes, were measured. The predictive value of each finding for the development of HCC was investigated by using univariate and multivariate analyses. RESULTS: HCC developed in a total of 42 of the 119 patients (35.3%) during a mean follow-up period of 62.9 months. The degree of regenerating nodules, the presence of irregular regenerative nodules, and atrophic right lobe were significant predictive factors for HCC with univariate analysis. In particular, 67.1% of patients with irregular regenerative nodules had HCC develop within 5 years. Multivariate analysis revealed that irregular regenerative nodules (relative risk 6.32, p = 0.012), the degree of regenerative nodules (relative risk 4.78, p = 0.029), and atrophic right lobe (relative risk 3.87, p = 0.048) were independent predictive factors. CONCLUSIONS: Morphologic observation of the liver surface by laparoscopy is important and provides information on factors that are statistically significant early predictors of the development of HCC.

Adult↗
PubMed2000

Clinico-epidemiology of hepatitis B viral infection in Northeastern Thailand.

Hepatitis B viral (HBV) infection is a common disease world wide. A study of clinico-epidemiology of HBV infection was conducted in 381 patients who seropositive for hepatitis B surface antigen (HBsAg) in Srinagarind Hospital, Khon Kaen University, Northeastern Thailand, during August 1997 to December 1998. 293 males, 88 females and their mean age was 30.96 +/- 12.78 years with a range from 15 to 77 years. The clinical features of acute hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma (HCC) and asymptomatic carrier were 2.36, 34.12, 4.99, 1.05 and 57.48% of cases. Possible routes for HBV transmission were family history of hepatitis, tattooing, intravenous drug addict and blood transfusion in 20.3, 11.3, 8.2 and 6.9% of cases, respectively. Signs of chronic liver disease were common in liver cirrhosis and HCC. Acute fulminating hepatitis was not found in this study.

Adolescent↗
PubMed2000

Clinico-epidemiology of hepatitis C viral infection in northeastern Thailand.

Hepatitis C virus (HCV) is responsible for a large number of cases of chronic liver disease worldwide. A study of clinico-epidemiology of HCV infection was conducted in 214 patients who were seropositive for antibody to HCV (anti-HCV) in Srinagarind Hospital, Khon Kaen University, northeastern Thailand, during August 1997 to December 1998. There were 199 males, 15 females and their mean age was 34.96 +/- 9.75 years with a range from 16 to 72 years. The clinical features of acute hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma (HCC) and asymptomatic HCV infection were 2, 115, 15, 2 and 80 cases. Risk factors for HCV acquisition were intravenous drug use (IVDU), tattooing and blood transfusion in 46.7, 32.2 and 18.8% of cases, respectively. 23.36% had a history of multiple risk factors while 28.9% had no history of risk factor exposure.

Adolescent↗
PubMed1999

Expression of functional CD40 in human hepatocellular carcinoma.

CD40, a member of the tumor necrosis factor receptor (TNFR) family, plays a crucial role in the survival, proliferation, and differentiation in B cells. However, the expression of CD40 other than in B cells has not been well studied. Therefore, we investigated the expression and function of CD40 in hepatocellular carcinomas (HCCs). Expression of CD40 mRNA in 6 established HCC cell lines was analyzed by reverse-transcription polymerase chain reaction (RT-PCR) and CD40 expression on cell surface was examined by flow cytometrical analysis. We also examined the expression of CD40 in human HCC tissues (45 cases) and nontumor liver tissues (30 cases) by immunohistochemistry. To examine the function of CD40 in HCC cells, we investigated the effect of CD40 signaling on anti-Fas antibody and TNF-alpha-induced apoptosis in HepG2 cells. In addition, intracellular levels of cysteine protease P32 (CPP32) protein in HepG2 cells were also determined by Western blotting. We have shown that 6 HCC cell lines constitutively expressed CD40 mRNA and membrane-bound CD40 antigen, which was slightly up-regulated by interferon gamma (IFN-gamma). In addition, 60% of human HCC tissues demonstrated positive staining for CD40, whereas nontumor tissues showed little detectable staining. In HepG2 cells, CD40 stimulation does not affect cell viability, but significantly inhibited Fas and TNFR-mediated apoptosis in a dose-dependent manner by blocking the activation of CPP32. From these results, we conclude that CD40 expression in HCCs plays an important role in tumor biology, especially the resistance against Fas and TNFR-mediated apoptosis.

Apoptosis↗
PubMed1998

Flow cytometric analysis of IL-6 receptors on peripheral lymphocytes in patients with primary biliary cirrhosis.

Interleukin-6 receptors (IL-6R) and interleukin-1 receptors (IL-1R) on lymphocyte surfaces were analyzed, using flow cytometry and dye-labeled IL-6 and IL-1 beta, to examine the clinical and immunological significance of these receptors. Incubation of peripheral blood mononuclear cells in the presence of mitogen resulted in a remarkable increase of lymphocytes expressing the IL-6 and IL-1 beta receptors on the cell surface. The increase in lymphocytes bearing these cytokine receptors may reflect an increase in stimulated lymphocytes. When peripheral blood from patients with primary biliary cirrhosis (PBC) was examined for these receptors, the percentage of IL-6R positive cells was significantly higher in the patients than in healthy controls (P < 0.01). The increase in IL-6R positive cells was only significant for the T lymphocyte fraction (P < 0.01). No significant change in IL-1R was observed. There was a significant positive correlation between the percentage of IL-6R positive T lymphocytes and the titer of antimitochondrial antibody in patients with PBC. These findings concerning IL-6R may be noteworthy elucidating autoimmune etiological features of PBC.

Adult↗
PubMed1997

Asymptomatic primary pulmonary hypertension associated with liver cirrhosis.

We report a case of asymptomatic primary pulmonary hypertension associated with liver cirrhosis (type B) and portal hypertension found by chance during a preoperative Swan-Gantz catheterization study. Our experience suggests that the actual prevalence of primary pulmonary hypertension associated with liver cirrhosis may be greater than that previously reported. During the follow-up of liver cirrhosis with portal hypertension, we should consider primary pulmonary hypertension, even if the patient is free of symptoms, and a chest X-ray check may be necessary.

Catheterization, Swan-Ganz↗
PubMed1997

Liver cirrhosis with synchronous gas gangrene and spontaneous bacterial peritonitis due to E. coli.

We report a case of synchronous gas gangrene and spontaneous bacterial peritonitis associated with liver cirrhosis. The patient was a 52-year-old man who was being followed for decompensated liver cirrhosis. He experienced sudden onset lower abdominal pain with distension and pain in the left leg. A bullous lesion, with crepitation, later appeared in the thigh and showed air-bubbles on X-ray. Eschericia coli was cultured from ascites and the bullous lesions; there was associated gas gangrene. The patient died of bacteremia with disseminated intravascular coagulopathy 26 h after admission, despite receiving intensive care. We discuss the route of bacteria causing the spontaneous bacterial peritonitis and simultaneous gas gangrene.

Bacteremia↗
PubMed1996

Osteodystrophy in patients with chronic hepatitis and liver cirrhosis.

Bone mineral density (BMD) of the lumber vertebrae and factors related to bone metabolism were determined in patients with chronic viral hepatitis and patients with liver cirrhosis to clarify correlations between hepatic dysfunction, considered to be one of the causes of hepatic osteodystrophy, and decrease in bone mass. BMD of the second to fourth lumbar vertebrae was determined with a Lunar (Madison, WI, USA) DPX, a dual-energy X-ray absorptiometry diagnostic system. BMD was significantly lowest in patients with liver cirrhosis, followed by patients with chronic hepatitis, and healthy subjects, in this order. There was a significantly positive but weak correlation between albumin and BMD. Levels of 25(OH)D and 1,25(OH)2D were significantly lower in patients with liver cirrhosis than in those with chronic hepatitis. BMD and vitamin D were decreased in all patients whose cholinesterase (ChE) was below 0.3 delta pH. Urinary pyridinoline (Upyr) was significantly higher in the patients with liver cirrhosis, in whom bone mass was decreased, than in the patients with chronic hepatitis, whereas serum osteocalcin levels were distributed in the upper normal range in patients with chronic hepatitis and those with liver cirrhosis. There was a positive correlation between 25(OH)D and serum osteocalcin levels in patients with liver cirrhosis. These results indicate that osteogenesis is decreased and suggest that the decrease in BMD which occurs in viral liver cirrhosis, probably related to decreased, bone formation and slight promotion of bone resorption, reflects deranged hepatic function. This is the first report of Upyr and urinary deoxypyridinoline (UDpyr) determination in patients with liver cirrhosis and patients with chronic hepatitis. The negative correlation of Upyr and UDpyr with ChE is a novel finding.

Adult↗
PubMed1996

Pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis.

We report a 58-year-old woman with pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis. She was receiving treatment for liver cirrhosis and hepatic failure when sudden severe right upper abdominal pain and fever developed. Abdominal radiograph disclosed pneumatosis intestinalis, involving the ascending colon, and small collections of free air along the right hemidiaphragm. The pneumatosis intestinalis appeared in both cystic and linear form. Autopsy revealed necrosis and multiple gas-filled mural cysts in the ascending colon. To our knowledge, this is the first case to be reported of pneumatosis intestinalis and necrotizing enterocolitis associated with liver cirrhosis.

Colon↗
PubMed1996

Infection with GB virus C (GBV-C) in patients with fulminant hepatitis.

BACKGROUND/METHODS: There appear to be hepatitis viruses other than hepatitis A, B, C, D and E. One of these has been proposed with a designation of GB virus C. Sera from 44 patients with fulminant hepatitis were tested for RNA of GB virus C by reverse-transcription polymerase chain reaction with nested primers deduced from the putative non-structural 3 (helicase) region. RESULTS: RNA of GB virus C was detected in three (20%) of 15 patients with hepatitis B virus infection and three (12%) of 25 patients without markers of hepatitis A-E virus infection. Overall, GB virus C RNA was detected in six (14%) of the 44 patients with fulminant hepatitis, at a frequency significantly higher (p < 0.001) than that in three (0.9%) of 326 blood donors matched for age with the patients. CONCLUSIONS: These results indicate a role of GB virus C in inducing fulminant hepatitis either by itself or in concert with the other hepatitis viruses.

Acute Disease↗
PubMed1996

Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative).

The cause of fulminant hepatic failure is reported to be unknown in more than half the cases in Japan. We recently reviewed 23 cases of fulminant hepatic failure that had been treated at our hospital. The cause of disease had been regarded as unknown before this study. It was found that seven of these patients had been under ecarazine hydrochloride therapy when they developed fulminant hepatic failure. We examined the reasons why fulminant hepatic failure in these seven patients had not been previously attributed to ecarazine, and found that it could be explained by the following factors: (1) the time from the start of ecarazine therapy to the onset of hepatic failure was long; (2) in all cases, hepatic failure developed more than 10 days after the clinical recognition of hepatitis; and (3) characteristic signs of drug-induced hepatic failure such as a skin rash and positive lymphocytes stimulation test with the drug were absent in all cases. Fulminant hepatic failure in these cases could be characterized by: (1) rapid decrease in serum alanine transaminase (ALT) level after discontinuation of ecarazine, (2) prolonged jaundice despite discontinuation of ecarazine, (3) high incidence of anti-nuclear antibody (ANA) (57%), and (4) histological findings of extensive hepatocellular necrosis ranging from bridging necrosis to massive necrosis. Of the seven patients, four died of fulminant hepatic failure. These four patients had received high doses of ecarazine hydrochloride for prolonged periods. Our data suggest that there may be many cases in which the cause of fulminant hepatic failure or acute hepatitis was not previously determined that can be attributed to long-term drug therapy for chronic diseases.

Adult↗