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Biomedical subjects

M Yoshiba

Publications and source records attributed to M Yoshiba.

At least 19 recordsLinked to original sources
PubMed1998

Clinical and molecular virological differences between fulminant hepatic failures following acute and chronic infection with hepatitis B virus.

Clinical and molecular biological characteristics were compared between patients who presented with fulminant hepatic failure following acute infection with hepatitis B virus (HBV) and those who developed hepatic failure during they carried HBV. The 11 patients with acute HBV infection had higher levels of alanine aminotransferase (mean +/- SD: 4943 +/- 2867 vs 1157 +/- 678 IU/L, P < 0.01), more often with a single peak (91% vs. 0%, P < 0.001), and lower total bilirubin level (15.3 +/- 4.4 vs 28.1 +/- 14.3 mg/1000 ml, P < 0.01) than the 13 patients with chronic HBV infection. Hepatitis B surface antigen was detected less often (55% vs. 100%, P < 0.05) and viral DNA polymerase less frequently (0% vs. 46%, P < 0.05) in the patients with acute than chronic HBV infection. Hepatitis B e antigen was detected in one (9%) patient with acute infection, less frequently than in six (46%) patients with chronic infection (P < 0.05). Mutations in the precore region was detected in HBV DNA clones from ten (91%) patients with acute infection and only in those from eight (62%) patients with chronic infection. All HBV DNA clones from the five (38%) patients with chronic infection that did not have precore mutations, however, possessed mutations in the core promoter. These results indicate that HBV mutants incapable of translating hepatitis B e antigen would play a major role in fulminant hepatic failure occurring after acute HBV infection. In contrast, HBV variants with core promoter mutations for reducing the transcription of hepatitis B e antigen would play an additional role in fulminant hepatic failure developing during chronic infection.

Acute Disease↗
PubMed1998

[A close association of prognosis with effect of interferon in HBV carriers developing acute severe exacervation].

We have treated 19 HBV carriers who developed acute severe exacerbation using interferon and immunosuppressive agents. Of these 14 patients developed fulminant hepatic failure. Of 10 patients with positive result for serum HBV DNA polymerase before the start of te treatment, five patients in whom HBV DNA polymerase turned negative and one patient whose HBV DNA polymerase level fluctuated in a low abnormal range after the start of the treatment survived. While, four patients whose HBV DNA polymerase level remained high after the start of interferon treatment died. Thus, it is suggested that suppression of HBV virus replication is closely related to prognosis in HB carriers developing acute severe exacervation of hepatitis.

Acute Disease↗
PubMed1997

Case report: primary hepatic lymphoma associated with chronic liver disease.

We report on a case of primary hepatic lymphoma that developed in a patient with chronic hepatitis C. Given that Japan is an area endemic for both hepatitis B and C viruses, we reviewed 51 Japanese cases of primary hepatic lymphoma, addressing the question as to whether the Japanese cases have unique characteristics and whether there is a causal relationship to the presence of chronic liver disease. Primary hepatic lymphoma most commonly affected middle-aged males. Presenting symptoms and physical findings were non-specific. Aminotransferases tended to stay in the low range compared with marked increases in lactate dehydrogenase. Sixteen patients (31%) had chronic liver disease, eight had liver cirrhosis and eight had chronic hepatitis, suggesting that there is a possible aetiological link between chronic liver disease and primary hepatic lymphoma.

Adult↗
PubMed1997

Fulminant hepatic failure: observation with serial CT.

PURPOSE: To determine the imaging characteristics of fulminant hepatic failure at serial computed tomography (CT) and to assess if any CT findings have prognostic value. MATERIALS AND METHODS: In 40 patients, 207 CT scans were analyzed retrospectively. Thirty-four patients had fulminant hepatic failure (acute in seven and subacute in 27), and six had late-onset hepatic failure. Twenty-one patients died of hepatic failure. CT was performed soon after the onset of coma and repeated weekly. Liver volume was measured by tracing the hepatic contour and summing the areas to estimate whole-liver volume. RESULTS: Liver volumes in survivors (n = 19) and nonsurvivors (n = 21), respectively, were 1,090 cm3 +/- 300 and 830 cm3 +/- 240 at initial CT and 1,130 cm3 +/- 310 and 700 cm3 +/- 280 at last CT (P = .0001). III-defined hypoattenuating areas were noted in 20 patients and were distributed in a solitary (n = 13), multiple (n = 6), or diffuse (n = 1) pattern. At follow-up CT, the area of hypoattenuation increased in six patients (five nonsurvivors) and disappeared or markedly decreased in four survivors. An increase in or late occurrence of ascites was noted in 15 patients (14 nonsurvivors, P = .0001). CONCLUSION: Liver volumes at the initial and last CT examinations and an increase in or late occurrence of ascites are useful prognostic findings.

Adolescent↗
PubMed1997

[Causal relationship between GBV-C and fulminant hepatitis].

GBV-C is recently discovered RNA virus which appeared to be member of Flaviviridae. We previously reported the possible involvement of GBV-C in the etiology of fulminant hepatitis(FH). It is still controversial whether GBV-C cause FH. So far, the only reliable tool for the diagnosis of GBV-C is the detection of the viral genome using PCR. Detection of GBV-C in serum of patient with FH dose not necessarily mean that GBV-C is causal virus. Serial quantification of serum GBV-C RNA in patient with FH may reveal a pathogenetic role of GBV-C. Further study is needed to elucidate the relationship between FH and a specific strain of GBV-C.

Base Sequence↗
PubMed1996

Chronic hepatitis A with persistent viral replication.

Hepatitis A virus (HAV) usually causes an acute self-limited illness. This report describes a patient with hepatitis A whose serum aminotransferase activities remained above normal and whose serum was persistently positive for immunoglobulin (Ig) M class anti-hepatitis A 31 months after the onset of hepatitis. Liver biopsy carried out 11 months after the onset of hepatitis showed histological changes consistent with chronic hepatitis of moderate severity. HAV RNA was detected by polymerase chain reaction (PCR) in feces collected at the time of the liver biopsy. Furthermore, the patient developed esophageal varices 25 months after the onset of hepatitis. We believe this to be the first reported case in which persistent replication of HAV is implicated in chronic hepatitis with the potential to develop into liver cirrhosis.

Hepatitis A↗
PubMed1996

Favorable effect of new artificial liver support on survival of patients with fulminant hepatic failure.

The two most serious symptoms of fulminant hepatic failure are bleeding and hepatic coma. To overcome these problems, we developed an artificial liver support system comprising a combination of plasma exchange and hemodiafiltration using a high performance membrane. We treated 67 patients with fulminant hepatic failure. Of these, 65 patients (97.0%) regained normal consciousness, and 55 patients (80.9%) were kept alert as long as we continued to apply this system. All 7 patients (100%) with fulminant hepatitis caused by hepatitis A virus infection and 9 of 12 patients (75%) with fulminant hepatitis caused by acute hepatitis B (HB) virus infection survived. In addition, 7 of 15 HB virus carriers (46.7%) who developed fulminant hepatitis and 11 of 29 patients (37.9%) with fulminant hepatitis caused by non-A, non-B hepatitis viruses survived. The overall survival rate was 37 of 67 patients (55.2%). Our artificial liver support system allows as high a survival rate as liver transplantation.

Aged↗
PubMed1995

Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology.

Hepatitis viruses A, B, C, D, and E have not accounted for all cases of hepatitis, hence "non A-E" agent(s) might be implicated. A set of new viruses (GBV-A, -B, and -C) whose genomes have been sequenced, are being investigated as possible causes of non A-E hepatitis. We investigated six cases of fulminant hepatitis of unknown aetiology for the presence of GBV-C genome in their serum, and three showed positive signals by semi-nested PCR using primers derived from the NS3/helicase region. Nucleotide sequence analyses confirmed these signals to be derived from a GBV-C sequence. The results suggest the importance of GBV-C in the aetiology of fulminant hepatitis.

Adolescent↗
PubMed1995

Interferon and cyclosporin A in the treatment of fulminant viral hepatitis.

The prognosis of fulminant hepatitis due to non-A, non-B virus infection and acute reactivation of hepatitis B virus in HB carriers is generally poor, and the treatment of choice in Western countries is recognized as liver transplantation. In countries such as Japan where liver transplantation is not readily available, however, these intractable types of fulminant hepatitis have to be treated medically. Based on the assumption that persistent replication of causal viruses and enhanced host immune responses, especially cellular immunity, to eradicate the viruses are the key mechanism in progressive liver cell destruction and the poor prognosis, we attempted a combination treatment with interferon and cyclosporin A for these types of fulminant viral hepatitis. Subjects in the present study consisted of 1 patient with acute severe hepatitis without coma and 13 patients with coma (13 with fulminant hepatic failure) due to non-A, non-B virus and acute reactivation of hepatitis B virus. The patients were given interferon-beta, 300 x 10(4) U daily, and cyclosporin A, at an initial dose of 3 mg/kg, with tapering. Fourteen patients with coma received artificial liver support that we devised. The patient with acute severe hepatitis survived, showing histologically remarkable liver regeneration. Eight of the 14 patients with hepatic coma, all of whom were indications for liver transplantation according to the criteria of the King's College group, survived. Decreased transaminase level, increased liver volume, and histological liver regeneration were observed in all the survivors. The combination of interferon and cyclosporin A is worth attempting in fulminant hepatitis caused by non-A, non-B virus and acute reactivation of hepatitis B virus in HB carriers.

Acute Disease↗
PubMed1995

A common-source outbreak of fulminant hepatitis B in hemodialysis patients induced by precore mutant.

From September 9 to October 3, 1994, five patients on maintenance hemodialysis in a dialysis unit in Tokyo contracted hepatitis B virus (HBV) infection successively, and four of them died of fulminant hepatitis. The unit treated 181 patients three times a week on eight shifts, and all five afflicted patients were on the same shift along with 27 other patients. HBV DNA clones from the hepatitis patients had a point mutation converting codon 28 in the precore region to a stop codon, which aborts the synthesis and secretion of hepatitis B e antigen, and showed a sequence similarity of > 99.5% within 645 base pairs covering the X gene and precore region. There were two HBV carriers with antibody to hepatitis B e antigen who were receiving hemodialysis on the same shift. HBV DNA clones from one of them had the stop codon 28 in the precore region, and a sequence similarity of > 99.7% to those from the five patients. Based on these results, it was deduced that the fulminant HBV strain was transmitted from the carrier to five patients, and resulted in the death of four. The outbreak indicates that immunocompromised hosts like hemodialysis patients can develop fulminant hepatitis B if and when they are infected with extremely virulent HBV strains.

Acute Disease↗