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PubMed2003

A case of autoimmune hepatitis and autoimmune hemolytic anemia following hepatitis A infection.

UNLABELLED: Hepatitis A infection is known to induce autoimmune hepatitis and autoimmune hemolytic anemia. Here we present a case with autoimmune hepatitis type I and autoimmune hemolytic anemia following hepatitis A virus (HAV) infection. CASE: M.A., a male patient, was brought to the hospital with complaints of jaundice and malaise. Physical examination revealed paleness and icterus. The liver was palpable 5 cm below the costal margin in the midclavicular line; the spleen was palpable 2 cm from the costal margin. Laboratory examination revealed severe anemia, reticulocytosis and direct Coombs' IgG positivity. Liver enzymes, total and conjugated bilirubin and alkaline phosphates levels, total protein and immunglobulin levels were high and prothrombin time elongated. Hepatitis A IgM antibody was found positive, while other hepatitis serologic markers were negative. Anti-smooth muscle antibody (ASMA) was positive in 1/80 titer. With these laboratory findings, the case was diagnosed as autoimmune hepatitis and autoimmune hemolytic anemia induced by hepatitis A infection. Liver histology also supported the diagnosis. Steroid therapy resulted in clinical and laboratory remission. In conclusion, it is important to vaccinate children against hepatitis A infection to protect them from its complications and also from autoimmune diseases induced by this infection.

Anemia, Hemolytic, Autoimmune↗

PubMed1992

Current seroepidemiology of hepatitis D virus infection among hepatitis B surface antigen carriers of general and high-risk populations in Taiwan.

In order to assess the current seroepidemiology of hepatitis D virus (HDV) infection in Taiwan where hepatitis B virus (HBV) is hyperendemic, a total of 756 voluntary blood donors, 641 prostitutes, 1,014 patients with sexually transmitted diseases (STDs), and 628 drug abusers were studied. Radioimmunoassays were used for testing HBV infection markers and antibody against HDV (anti-HDV) among HBsAg carriers. The anti-HDV prevalence among HBsAg carriers was significantly higher in STD patients (9.6%), prostitutes (33.1%), and drug abusers (68.1%) than in blood donors from the general population (2.2%). The prevalence gradually increased with age in blood donors and STD patients, but reached a plateau at a young age in prostitutes and drug abusers. Males had a higher prevalence than females in blood donors (2.7% vs. 0), STD patients (8.2% vs. 7.5%), and drug abusers (69.0% vs. 57.1%), but the difference was not statistically significant. STD patients with syphilis had a higher prevalence (19.5%) than those affected with non-ulcerating STDs (5.3%). While unlicensed prostitutes had a lower prevalence (13.6%) than licensed prostitutes (44.9%), intravenous drug abusers had a higher prevalence (73.1%) than non-intravenous drug abusers (34.6%). There was a twofold increase in anti-HDV prevalence from 1986 to 1989 among prostitutes, but the prevalence remained unchanged in the general population and drug abusers. HDV infection remains limited to the high-risk groups and spread mainly by promiscuity and needle sharing in Taiwan.

Adult↗

PubMed1996

Effect of human immunodeficiency virus infection on hepatitis C virus infection in hemophiliacs.

Chronic liver disease due to hepatitis C virus (HCV) infection is a major problem in hemophiliacs. Recent reports suggested that hemophiliacs coinfected with hepatitis C virus and human immunodeficiency virus (HIV) have an increased incidence of liver failure but the mechanism of accelerated liver injury is not clear. We tested plasma from 100 hemophiliacs for anti-HCV by second generation ELISA, anti-HIV by EIA, and HCV RNA and HIV RNA by branched DNA and polymerase chain reaction assays to determine if hemophiliacs coinfected with HCV and HIV have higher HCV RNA levels and more active liver disease. Seventy-nine (79%) patients were anti-HCV positive, of whom 85% were HCV RNA positive. None of the anti-HCV-negative patients had detectable HCV RNA in plasma. Forty-two (42%) patients were anti-HIV positive, of whom 47% had detectable HIV RNA. All the anti-HIV-positive patients were also anti-HCV positive. The prevalence of both anti-HCV and anti-HIV increased significantly with age. There was no difference in HCV RNA levels between anti-HIV-positive and anti-HIV-negative patients (mean: 21 +/- 4 vs 18 +/- 5 Meq/ml), although HCV RNA levels were significantly higher in anti-HIV-positive patients with CD4 counts < 200/mm3 (P = 0.008). There was an inverse correlation between HCV RNA levels and CD4 counts but no correlation was found between HCV RNA and serum aminotransferase levels. We found a high prevalence of HCV and HIV coinfection in our hemophiliacs. Hepatitis C virus replication appears to be increased in patients with severe immunodeficiency secondary to progressive HIV infection. However, there was no correlation between HCV RNA and serum ALT level, suggesting that HCV is not directly cytopathic.

Adolescent↗

PubMed1993

Fulminant hepatic failure with massive necrosis as a result of hepatitis A infection.

Fulminant hepatic failure as a result of hepatitis A is a rarely diagnosed complication entity in developed countries. With the advent of specific serologic markers for acute hepatitis A virus infection, the incidence and pathology of fulminant hepatitis A can be more clearly defined. We describe four patients (one adult, three children; two males and two females, ages 2 1/2-58 years) referred to our institution for orthotopic liver transplantation subsequent to fulminant hepatic failure following hepatitis A infection. All of these patients had a history of residence in or travel to hepatitis A endemic areas. Hepatitis A infection was documented by the presence of serum IgM against hepatitis A virus prior to transplantation. Infection with hepatitis B virus, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus was excluded by clinical and specific serologic examinations. All patients presented with varying degrees of encephalopathy, progressing to coma. Coagulopathy in the form of prolonged prothrombin time and partial thromboplastin time was present in all patients. Peak liver parenchymal enzymes increased to greater than ten times the upper limit of the normal range. Total and direct bilirubin levels increased to > 20 and 10 mg/dl, respectively. Histologic evaluation of the explanted livers showed a spectrum of changes ranging from periportal hepatocellular necrosis with focal parenchymal collapse and prominent bile duct proliferation to massive necrosis with complete loss of hepatic architecture.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗

PubMed1999

Inactivated hepatitis A vaccine in Chinese patients with chronic hepatitis B infection.

BACKGROUND: Hepatitis B (HBV)-infected patients have a higher morbidity and mortality when super-infected by hepatitis A (HAV). AIM: To evaluate the immunogenicity and safety of a commercial inactivated HAV vaccine in Chinese patients with chronic HBV infection. METHODS: Sixty-five HBV-infected patients (30 carriers, 22 chronic hepatitis, 13 cirrhosis), who were seronegative for HAV, received a dose of 1440 ELISA units of HAV vaccine at weeks 0 and 24. Twenty-eight healthy individuals aged 18-57 years, who were seronegative for both HBV and HAV infection, also received the same vaccination regimen. Seroconversion was defined as an anti-HAV titre >/= 33 mIU/mL. RESULTS: The seroconversion rates for the HBV-infected patients at weeks 2, 4 and 24 were 72, 91 and 80%, respectively. The corresponding geometric mean titres (GMTs) were 103, 311 and 123 mIU/mL. In the healthy control group the seroconversion rates were 86, 93 and 89% at weeks 2, 4 and 24. The corresponding GMTs were 112, 158 and 250 mIU/mL. There was no difference in the seroconversion rates between the two groups, but healthy controls had a significantly higher GMT at week 24 (P=0.04). Side-effects were more common in HBV patients. CONCLUSION: The HAV vaccine is equally efficacious in patients with chronic HBV infection.

Adolescent↗

PubMed1998

[Extrahepatic manifestations of hepatitis C infection].

The hepatitis C virus is associated with various extrahepatic manifestations. It is unequivocal that hepatitis C is associated with mixed cryoglobulinemia, membranoproliferative glomerulonephritis, and in Southern Europe to some extend also with porphyria cutanea tarda. The rare combination of hepatitis C and panarteriitis nodosa is still questionable. The Sicca syndrome also seems to be associated with hepatitis C virus, but this is not the typical Sjögren syndrome. It is still unclear whether the rare combination of hepatitis C with aplastic enemia has pathogenetic aspects. Although an epidemiological association of hepatitis C with lichen planus, lymphoma, neuropathies and other diseases has been observed, the etiological role and the pathogenetic involvement of the hepatitis C infection remains unclear. Furthermore, the question whether these extrahepatic diseases observed are autoimmune diseases remains open. Concerning the practical approach in a clinical setting, it has to be pointed out that with these diseases a hepatitis C infection has to be considered and testing for hepatitis C antibodies and, if positive, hepatitis C-RNA is indicated. If there will be any evidence of an etiological association of a replicative hepatitis C infection and the mentioned extrahepatic diseases antiviral medication should be discussed.

Autoimmune Diseases↗

PubMed2002

Genotype-specific mechanisms for hepatic steatosis in chronic hepatitis C infection.

BACKGROUND: Hepatic steatosis is common in hepatitis C, but the relative importance of host and viral factors is controversial. In the present prospective study, we examined metabolic factors associated with non-alcoholic fatty liver and viral genotype as predictors of steatosis and fibrosis in chronic hepatitis C infection. METHODS: In 124 chronic hepatitis C patients, the association between liver histology and the following was investigated: demographic and anthropometric data, alcohol intake, alanine aminotransferase (ALT), total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglyceride, transferrin saturation, ferritin, insulin, c-peptide, glucose and insulin resistance (homeostasis model). RESULTS: By multivariate analysis, genotype 3 was associated with increased steatosis grade (P = 0.02). There were significant pairwise interactions between genotype 3 status and total cholesterol (P = 0.01), current alcohol intake (P = 0.04) and serum ALT (P = 0.01). This showed that the etiology of steatosis was different in patients with genotype 3 and those with non-genotype 3 chronic hepatitis C infection. In genotype 3 patients, the degree of steatosis was inversely associated with serum cholesterol (P = 0.005) and positively associated with serum triglyceride (P = 0.02). There was no association between body mass index (BMI) and the extent of steatosis. Among patients with other genotypes, the steatosis grade was strongly influenced by BMI (P < 0.0001) and serum ALT (P < 0.01). Independent predictors of fibrosis were age (P = 0.001), past alcohol intake (P = 0.04), ALT (P = 0.002), serum insulin (P = 0.001) and portal inflammation (P < 0.001). CONCLUSIONS: Hepatitis C genotype 3 may interfere with pathways of hepatic lipid metabolism, whereas increased BMI appears to be a more important pathogenic factor in other genotypes. Although steatosis and BMI were not associated with hepatic fibrosis, their relationship with serum insulin suggests that metabolic factors related to insulin action could influence fibrogenesis in hepatitis C.

Adult↗

PubMed1996

The interaction of human immunodeficiency virus infection and hepatitis B virus infection in infected homosexual men.

A retrospective analysis of 99 hepatitis B-positive homosexual men with known human immunodeficiency virus (HIV) status was conducted to study the interaction of concurrent HIV infection on the course of their chronic hepatitis B virus (HBV) infection. All 99 subjects had chronic hepatitis B, 43 of whom were HIV antibody negative and 56 of whom were HIV antibody positive at the time of their initial presentation. Serial serum aminotransferase levels were used as an indirect estimate of the severity of hepatic inflammation. Factors that may influence the course of hepatitis B, HIV status, hepatitis B e antigen (HBeAg)/hepatitis B e antibody (HBeAb) status, alcohol intake, and zidovudine (AZT) therapy were correlated with aminotransferase values. Overall, there was no difference in mean serum alanine aminotransferase (ALT) levels between HIV antibody-negative and HIV antibody-positive patients. There is a higher prevalence rate of HBeAg in HIV antibody-positive patients (p < 0.05), and the seroconversion rate from HBeAg to HBeAb was lower in HIV antibody-positive patients compared with HIV antibody-negative patients (p < 0.05). However, reactivation rates from HBeAb to HBeAg were no different in the HIV antibody-positive and negative hepatitis B carriers. With mild, moderate, or heavy alcohol intake, we observed no statistically significant difference in mean serum alanine aminotransferase levels and no mean serum aspartate aminotransferase levels between HIV antibody-negative patients versus HIV antibody-positive patients. Similarly, there was no significant difference in the pattern of serum aminotransferase in those subjects treated with or without AZT. The mortality rates were higher in HIV antibody-positive patients (n = 8) compared with in HIV antibody-negative patients (n = 2). Seventy-five percent (n = 6) of the HIV antibody-positive patients died from acquired immunodeficiency syndrome (AIDS), and overall only two patients died of liver disease, one in each group. We conclude that there is no overt influence by HIV or the treatment thereof on the course of chronic HBV infection in a population of homosexual men. In HIV-infected patients, death from AIDS predominated; hence, the main target for therapy should be HIV rather than HBV.

Anti-HIV Agents↗

PubMed2004

Previous or occult hepatitis B virus infection in hepatitis B surface antigen-negative and anti-hepatitis C-negative patients with hepatocellular carcinoma.

PURPOSE: We investigated the clinical and virologic findings in hepatitis B surface antigen (HBsAg)-negative and anti-hepatitis C virus antibody (anti-HCV)-negative patients with hepatocellular carcinoma (HCC) to investigate the role of previous or occult hepatitis B virus (HBV) infections in the development of HCC. METHODS: We examined sera and HCC samples from 40 HBsAg-negative and anti-HCV-negative patients. Sera were tested for some viral markers, and genomic DNA was extracted from the HCC samples. HBx RNA was also extracted from the HCC and amplified by a polymerase chain reaction with reverse transcription (RT-PCR). RESULTS: Hepatocellular carcinomas from five patients with anti-HBc (group 1, 25 patients) and nine patients without anti-HBc (group 2, 15 patients) were examined for HBx RNA. HBx RNA was detected in four of the five HCC samples from group 1 and in four of the nine HCC samples from group 2. CONCLUSION: These findings suggested that previous or occult hepatitis B virus infection is common in HBsAg-negative and anti-HCV-negative patients with HCC.

Adult↗

PubMed2003

Viral hepatitis: new data on hepatitis C infection.

Viral hepatitis (VH) is almost as old as human beings, at least as old as known human history. However, the natural history and the epidemiology of the disease has undergone changes during the centuries and even recently we have been facing several new aspects. The estimated global prevalence is around 3-5%, which means that approximately 400 million patients are infected with hepatitis B virus and that there are 170 million infections with hepatitis C virus. The mortality figures are projected to show a 2- to 3-fold increase over the next two decades as hepatitis C virus-infected patients develop cirrhosis, which makes this the leading indication for liver transplantation. These data point to the importance of VH being a significant public health problem worldwide. The list of hepatotropic viruses is well known, including hepatitis A (HAV), B (HBV), C (HCV), D (HDV), E (HEV), G (HGV) and F (HFV). HGV and HFV are excluded from the present review, mainly because they are questionable in relation to the causation of liver disease. Our knowledge of HAV, HBV, HDV and HEV has accumulated over the last decade, so the present discussion is focused on HCV, which is currently generating considerable concern and controversy, and is the leading cause of chronic liver disease worldwide. The main questions to be discussed, are: the characterization of the agents' viral genotypes/subtypes, the viral-cell interaction, the pathogenesis of VH, the extrahepatic manifestations of viral infection and hepatocarcinogenesis.

Hepacivirus↗

PubMed2005

Prevention of hepatitis B virus infection from hepatitis B core antibody-positive donor graft using hepatitis B immune globulin and lamivudine in living donor liver transplantation.

BACKGROUND: Hepatic grafts from hepatitis B surface antigen-negative and anti-core antibody (HBcAb)-positive donors have been shown to transmit hepatitis B virus (HBV) infection. Recently, it has been reported that combined hepatitis B immune globulin (HBIG) and lamivudine therapy is effective in the prevention of hepatitis B recurrence after living donor liver transplantation (LDLT). In this report, we assessed the efficacy of combined HBIG and lamivudine therapy in preventing HBV transmission by graft with HBcAb-positive donors. METHODS: We studied 22 patients who had undergone LDLT with allografts from HBcAb-positive living donors at Gunma University Hospital and Kyushu University Hospital. Long-term combined HBIG and lamivudine therapy were administrated to all recipients. Serum samples from the donor and recipient were tested for HBcAb, HBV DNA, and hepatitis B surface antibody. Liver biopsies from grafts were tested for HBV DNA. RESULTS: All recipients were HBcAb negative before LDLT. All of the donor livers were HBV DNA positive at the time of LDLT. All of the recipients had HBsAb titers greater than 300 mIU/ml 4 weeks after LDLT, and remained 100 mIU/ml thereafter. None of the recipients have become infected with HBV with a follow-up of 25-86 months. CONCLUSIONS: Perioperative combined HBIG and lamivudine therapy can prevent HBV infection in recipients who receive liver grafts from HBcAb-positive donors.

Adolescent↗

PubMed2003

Hepatitis A virus infection in hepatitis C Brazilian patients.

OBJECTIVE: HAV infection in patients with pre-existing chronic liver disease has been associated with increased rate of fulminant hepatitis and mortality. The aim of this study was to investigate the presence of serological and molecular HAV markers in a population of HCV infected patients. PATIENTS AND METHODS: The presence of total and IgM anti-HAV antibodies was investigated in 197 patients (mean age 44.8+/-12.5 years) referred to the Brazilian Reference Center for Viral Hepatitis and who tested positive for anti-HCV antibodies and HCV RNA. HAV RNA was investigated by reverse transcription-nested PCR in these patients.Results. One hundred seventy patients (86%) had total, but not IgM anti-HAV antibodies, being therefore, immune to hepatitis A, while 27 (14%) were not. A high proportion (6/27, 22%) of the susceptible patients presented markers of recent HAV infection: One patient was IgM anti-HAV positive, three were HAV RNA positive, and two presented both markers. By nucleotide sequencing, it was demonstrated that the HAV isolates infecting these patients belonged to subgenotypes 1A and 1B. CONCLUSIONS: Superinfection with HAV was a common event in the group of HCV infected patients under study. Implementation of hepatitis A vaccination should be considered for this population.

Adult↗

PubMed1998

Clinical outcome of patients infected with hepatitis C virus infection on survival after primary liver transplantation under tacrolimus.

The outcome of hepatitis C virus (HCV) infection on patient and graft survival after orthotopic liver transplantation (OLT) has been controversial. An earlier experience with a higher dose of tacrolimus (>/=0.1 mg/kg/d intravenously and >/=0.2 mg/kg/d orally) was associated with a worse clinical outcome in patients infected with HCV. The clinical outcome of 183 liver transplant recipients with end-stage liver disease (ESLD) secondary to HCV infection (HCV group) was compared with a contemporary cohort of 556 patients with HCV infection who underwent transplantation for nonviral, nonmalignant ESLD (control group). All patients were prospectively screened for anti-HCV antibodies and HCV RNA by reverse-transcriptase polymerase chain reaction. All OLT patients were receiving low-dose tacrolimus immunosuppression. Cumulative patient survival rates for the HCV group were 80% after 1 year and 75% after 3 years compared with rates of 84% and 78%, respectively, in the control group (P = .452). Primary graft survival rates at the same time intervals for the HCV group and the control group were 72% and 77.5% at 1 year and 67% and 72% at 3 years, respectively (P = .144). The incidence of re-transplantation (re-OLT) in the HCV group and the control group was 12.6% and 10.4%, respectively (P = .42). Chronic HCV infection as an indication for OLT with a lower dose of tacrolimus immunosuppression (</=0.05 mg/kg/d intravenously and </=0.1 mg/kg/d orally) is associated with a similar patient and graft survival as those without HCV infection.

Adult↗

PubMed2001

The management of chronic hepatitis B infection.

Chronic hepatitis B infection is frequently diagnosed within the genitourinary clinic setting with sexual transmission the commonest route of acquisition in the United Kingdom. Only 3--5% of adults who contract acute hepatitis B will progress to chronic infection, and these individuals can be identified by the presence of hepatitis B surface antigen (HBsAg) in the bloodstream 6 months after infection. Individuals at highest risk of long-term complications such as cirrhosis and hepatocellular carcinoma, carry HBeAg and have high levels of circulating hepatitis B virus (HBV) deoxyribonucleic acid (DNA). Therapy should be targeted towards this group of patients. Two forms of therapy are now licensed for use in chronic hepatitis B infection: interferon-alpha and lamivudine. Seroconversion occurs in 30--40% of patients treated with interferon and treatment is often limited by toxicity. Lamivudine is well tolerated with seroconversion rates of 15--20% at one year, rising with increasing duration of therapy. Long-term monotherapy is limited however by the development of resistance mutations and combination nucleoside therapy is likely to become the treatment of choice in the future. Patients with chronic hepatitis B should be counselled regarding transmission, partner vaccination and alcohol intake and co-infection with other hepatitis viruses should be excluded.

Antiviral Agents↗

PubMed2000

Treatment of autoimmune and extra-hepatic manifestations of HCV infection.

Hepatitis C virus (HCV) infects mononuclear cells and may, like other viruses, cause immunological disorders. Immunological abnormalities observed in HCV infections are usually nonspecific (e.g. cryoglobulinemia, immune complex deposits, autoantibodies). There is a clear association between cryoglobulinemia and hepatitis C and cryoglobulinemia related symptoms are usually improved by treatment with interferon alpha, although patients usually relapse after treatment end. The relationships between hepatitis C and other immunological abnormalities are unclear. The association between chronic hepatitis C and anti-smooth muscle or anti-nuclear antibodies does not appear to be significantly different from that in other hepatic disorders, particularly hepatitis B. Conversely, patients with hepatitis C have significantly more often anti-liver kidney microsomal (LKM1) antibodies than patients with other causes of liver diseases. When clinical, histological and biological findings are indicative of HCV infection with chronic hepatitis, interferon alpha or combination therapy with ribavirin are treatments options. Conversely, when clinical context and results of laboratory tests are in favor of an autoimmune disorder or of overlap-syndromes (i.e. both autoimmune and viral hepatitis), interferon should not be given in first intention, since revelation or exacerbation of autoimmune hepatitis have been reported under interferon. An important prevalence of anti-HCV antibodies has also been reported in patients with sialadenitis, lichen planus and thyroiditis. It has been clearly demonstrated that interferon may induce or worsen such immunological diseases, but there are very few studies showing improvement of these manifestations under interferon. In conclusion, interferon may be appropriate in patients with HCV infection and extrahepatic manifestations linked to immune complex deposition, whereas, in other cases, careful assessment of patients with autoimmune processes is necessary before choosing any treatment strategy.

Antiviral Agents↗

PubMed1983

Prevention of perinatally transmitted hepatitis B virus infections with hepatitis B immune globulin and hepatitis B vaccine.

A randomised blind controlled trial of hepatitis B immune globulin (HBIG) plus hepatitis B vaccine for the prevention of the perinatally transmitted HBsAg carrier state was conducted in Taipei. Infants of e-antigen-positive HBsAg carrier mothers were given HBIG immediately after birth, and then one of three schedules of vaccination. There was no difference in efficacy between the three schedules; the combined efficacy was 94%, compared with that of HBIG alone (71%) or of vaccination alone (75%). Persistent HBs antigenaemia developed in only 9 (6%) of the 159 infants receiving prophylaxis, but in 88% of the controls. Antibodies developed in all those who did not become antigenaemic and presumably will provide long-term protection from hepatitis B virus infection. HBIG should be given as soon as possible after birth and need not be given again if the infant is subsequently vaccinated. With HBIG coverage from birth, the timing of the start of vaccination does not seem to be of importance within the first month of life, but to maximise compliance and minimise costs hepatitis B vaccination should be initiated during the confinement.

Carrier State↗

PubMed1997

The natural history of chronic hepatitis B infection.

Chronic hepatitis B infection is a global health problem that affects about 300 million people. Of these, 75% are Chinese. Most Chinese who become chronic carriers, contract the virus during the perinatal period. The natural history of these chronic hepatitis B carriers includes an initial immune tolerance phase, followed by immune clearance and an inactive hepatitis B non-replicative phase with the development of cirrhosis that may be complicated by hepatocellular carcinoma. The classification of hepato-cellular carcinoma has recently been revised. Based on immunohistochemical studies, it has been found that patients with hepatocellular carcinoma and biliary markers have a poorer survival than patients with hepatocellular carcinoma but who have negative biliary markers. Sometimes, a fourth phase, a hepatitis B envelope-negative hepatitis B virus replicative phase, reflecting the emergence of a pre-core mutant strain, may follow. Our improved understanding of the natural history of chronic hepatitis B infection has led to more effective approaches towards the control of this viral infection and its sequelae. Most importantly, immunisation against hepatitis B virus in the perinatal setting has been shown to prevent chronic infection.

Journal Article↗

PubMed2005

HBsAg-negative hepatitis B virus infections in hepatitis C virus-associated hepatocellular carcinoma.

This study was conducted to evaluate reports that hepatitis B virus (HBV) DNA sequences can be found in the serum and/or tumour tissue from some hepatocellular carcinoma (HCC) patients who have no detectable hepatitis B surface antigen (HBsAg) in their sera. Such HBV infections would be highly atypical, because prospective studies have shown a clear succession of specific serologic markers during and after most HBV infections. As most HBsAg-negative HCC patients in Japan have hepatitis C virus (HCV) infections, the present study was conducted to determine whether some of these patients actually have unrecognized HBV infections. Thirty newly diagnosed HCC patients from Kurume, Japan, with antibody to the hepatitis C virus (anti-HCV) were studied. None of the 30 had HBsAg detectable in their serum. Of 22 for whom test results for antibodies to the hepatitis B core antigen (anti-HBc) and antibodies to HBsAg (anti-HBs) were available, 14 (64%) had anti-HBc and anti-HBs, four (18%) had anti-HBc alone, and four (18%) had no HBV markers. Nested polymerase chain reaction was used to detect the HBV surface (S), core (C), polymerase (P) and core promoter gene sequences in the HCC tissues and in the adjacent nontumorous liver tissues. HBV DNA was detected in HCC and/or adjacent nontumorous liver in 22 of 30 (73%) patients [detected in both HCC and nontumorous liver in 19/30 patients (63%)]. Among the 22 patients with detectable HBV DNA, more than one HBV gene was detected in 10 (46%). Among the four patients whose sera were negative for all HBV markers, three had HBV DNA in either HCC and nontumorous liver (two cases) or only in the nontumorous liver (one case); HBV DNA could not be detected in tissues from the fourth patient. In 18 of 21 (86%) patients with detectable HBV core promoter sequences, mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found. No deletions were detected in the core promoter gene region of the type reported to be associated with some cases of HBsAg-negative HBV infection. Thus, HBV DNA was detectable in 22 (73%) HBsAg-negative, anti-HCV-positive HCCs, including three (10%) who were also negative for anti-HBc and anti-HBs. HBV mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found in the majority of cases, mutations that have previously been reported in HBV that is integrated in HCC DNA. In serologic surveys to determine etiologic associations of HCC, patients such as those in this study would have been incorrectly designated as having 'HCV-associated HCC,' whereas the data in this study suggest that HBV could have played a role in the development of their HCCs.

Adult↗