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A total of 85 patients with alcoholic and viral cirrhosis were included in study to assess the prevalence of dysbiosis and its relationship with the severity of disease, and with development of dyspeptic disorders. Intestinal bacterial over-growth was measured by means of a lactulose breath test, fecal flora was cultured under aerobic and anaerobic conditions. Intestinal bacterial overgrowth and colon dysbiosis were determined in 82.4% of patients with equal prevalence in alcoholic and viral cirrhosis. Intestinal dysbiosis was found to be risk factor of increasing cirrhosis severity and liver dysfunction, as well as development of complications of portal hypertension. It was documented, that intestinal dyspepsia syndrome in cirrhotic patients is strongly associated with the presence of gut microflora disorders.

In developing countries diarrhea diseases take a big toll which can be prevented by adequate supply of safe drinking water. Thus a longitudinal study was taken up to determine the morbidity due to water borne diseases and bacteriological quality of water. 150 houses in two different areas, one supplied by bore well and other by tap water was selected by modified cluster sampling. Weekly morbidity details collected. Monthly water samples were assessed for bacteriological quality from main supply, household storage and morbidity reported houses. The difference in proportion of potable and non potable water at storage points was statistically significant. The overall incidence rate of target diseases was 3.58%,majority were diaarrhoel diseases with increased incidence in children less than five years.

We herein describe a case of secondary syphilis hepatitis in a liver transplant patient. This homosexual man presented 15 years after an orthotopic liver transplant with nonsquamous papillomacular rash, mild cytolysis, and anicteric cholestasis. Laboratory tests showed syphilis seroconversionwith a VDRL test titer of 1/256, a Treponema pallidum hemagglutination assay of 1/5120, and a positive immunoglobulin M fluorescent Treponemal antibody absorbance. A liver biopsy performed 13 months after the diagnosis showed low-grade hepatitis with a METAVIR score of A1F1; it also showed moderate, nonspecific portal inflammation consisting primarily of neutrophils, with no evidence of cholestasis. The patient was given benzathine-penicillin (2400000 IU) with a transient increase in prednisolone dosages. Cytolysis rapidly, and cholestasis progressively, disappeared. Results of an immunoglobulin M fluorescent Treponemal antibody absorbance test became negative, whereas the VDRL test and the Treponema pallidum hemagglutination assay titers decreased slightly over time.

Hepatitis of viral aetiology caused by hepatotropic virus (A, E, B, D and C) represents an important work load for the clinical virology laboratory. Most of the diagnostic is based upon detection in serum and plasma samples of different serological and virological markers, which correlates with different infection stages. In chronic infection by HBV and HCV is necessary to perform diagnostic by molecular methods as well as antigen detection in sequential samples along the course of the disease taking into account that a reliable storage must be provided for stability of structural components of the virus. Recent knowledge about mutations variants in some of the virus may alter the validity of particular markers.

Necrotizing fascitis (NF) is a rare disease with a mortality rate ranging from 24 to 60 percent. The infection may be mono- or polymicrobial and is characterized by extensive necrosis of the skin and muscle, as well as fascia and subcutaneous tissue. NF may develop at the site of injury, e.g. trauma, needle puncture, or surgical incision. The lower extremities, perineum, and abdominal wall are common sites of NF. The remaining 10 percent of cases occur in the upper extremities or neck, usually in patients with vascular disease or diabetes mellitus. The course is rapidly progressive and may be life-threatening if the diagnosis is not made promptly and appropriate surgical debridement is not carried out. We report on a 44-year-old man with necrotizing fascitis during interferon-alpha treatment for hepatitis C virus infection.

Hepatitis G virus (HGV) infection is often observed in patients with hepatitis B or C virus (HBV or HCV) infections. The aim of this study was an evaluation of the influence of HGV infection on the course of virus hepatitis B and C in children. 113 children aged 2-15 years old, with hepatitis B or C were enrolled to the study. In the study group children were examined for the presence of virus genetic material, e.g. HGV-RNA. The analysis of children records with respect to results of physical examination and additional tests (laboratory tests, abdomen ultrasonography) was carried out. On the basis of the analysis it was showed that HGV infection did not significantly change the course of basic liver disease.

Background: A 2.5-year-old boy received a cadaveric orthotopic liver transplant for acute liver failure due to non-A, non-B, non-C hepatitis. After transplantation, he developed thrombocytopenia and neutropenia and subsequently severe aplastic anemia. The patient also suffered from recurrent cytomegalovirus (CMV) viremia, treated with foscarnet and ganciclovir., Methods: For treatment of his aplastic anemia, the patient underwent an allogeneic bone marrow transplantation from his HLA-identical sister after conditioning with cyclophosphamide at 200 mg/kg and antithymocyte globulin at 3 mg/kg for 5 days. Prophylactic acyclovir was given because of ongoing CMV viremia at the time of bone marrow transplantation., Results: The transplant course was uneventful, with rapid engraftment. There were no signs of liver dysfunction, graft-versus-host disease, or reactivation of CMV. The patient is in excellent health, with normal liver and bone marrow function 3 years after bone marrow transplantation., Conclusion: This case report shows that allogeneic bone marrow transplantation is feasible and well tolerated in a patient with severe aplastic anemia after liver transplantation for acute fulminant viral hepatitis.

The nucleotide sequences of the 5' noncoding region of the GB virus C/hepatitis G virus (GBV-C/HGV) were determined in 18 isolates from the United States. Two genotypes have been classified based on the sequence heterogeneity within the 5' noncoding region of GBV-C/HGV. The most distantly related isolates between the two genotypes were 84.6% identical. Sequence identity of the isolates within a genotype was 95-99%. The 5' noncoding region of this virus contains four highly conserved domains. These conserved elements would facilitate the selection of optimal primers for the sensitive detection of GBV-C/HGV RNA by PCR. In addition, they suggest a crucial role for this region in viral replication and/or gene expression. Detection of genotypic variation among GBV-C/HGV infected individuals may provide further insight into the possible pathogenicity and into the transmission of the virus.

Variants of hepatitis B virus (HBV), hepatitis C virus (HCV) and of the hepatitis Delta virus (HDV) have been identified in patients both with acute and chronic infections. In the HBV DNA genome, naturally occurring mutations have been found in all viral genes, most notably in the genes coding for the structural envelope and nucleocapsid proteins. In the HCV RNA genome, the regions coding for the structural envelope proteins 1 and 2 as well as the 3'-contiguous nonstructural region 1 were found to be hypervariable. Viral variants may be associated with a specific clinical course of the infection, e.g. acute-fulminant or chronic hepatitis. Specific mutations may reduce viral clearance by immune mechanisms ('immune escape') or response to antiviral therapy ('therapy escape'). Furthermore, mutations of envelope epitopes can lead to viral variants which are not recognized or neutralized by antibodies to wild-type virus, resulting in 'diagnosis escape' or 'vaccine escape'. The exact contribution, however, of specific mutations to the pathogenesis and natural course of HBV, HCV or HDV infection, including the development of hepatocellular carcinoma, remains to be established.

The authors give a short review of the recent data about the types of interferons and their biological activity. The role of interferons in the therapy of B, C and D chronic viral hepatitis is discussed. Interferon treatment means a substantial progress in the therapy of chronic viral hepatitis, however it represents a final recovery from chronic B or C hepatitis only in 25-40 percent or 40-45 percent of the cases, respectively. The authors refer to the combination therapy which seems to be promising in the future.

Varicella zoster virus is known to cause varicella in children and to reactivate years later as shingles. Both the primary disease and the reactivation can cause complications, both in the form of serious affection of organs by the virus itself, and through secondary bacterial infections owing to temporary immune deficiency. Relatively frequent complications include secondary bacterial skin infections, pneumonitis, complications affecting the central nervous system, and hepatitis. We describe a few typical cases seen recently in our department, and review important points connected to treatment and prophylaxis.

The appearance of replication-competent variants of HBV with mutations in the envelope and precore/core and X proteins emphasizes that these proteins are the focus of immune selection pressures in the human host. The presence of an antibody response in the absence of a CTL response may create the ideal selection environment. This occurs in the early phase of passive/active immunization against HBV envelope proteins in neonates born to HBV-infected mothers and also during the emergence of HBeAg-negative variants during and after HBe antigen/antibody seroconversion in chronic HBV carriers with defective CTL responses. The sequence and speed of application of the multiple selection pressures (humoral and possibly cellular) determine the virologic and clinical outcome. When these variant viruses are passed to a new host, in the absence of the immune selection pressures or modified immune pressures that resulted in their selection, a picture clinically different from that seen in the original host may emerge.

A variety of viruses cause many of the disorders that are recognized as acute and chronic liver diseases. Remarkable scientific advances achieved during the past two decades have lead to readily available accurate diagnostic tests for hepatitis viruses designated A through E. Effective vaccines have been developed to prevent hepatitis B and, more recently, hepatitis A. Heightened understanding of the pathogenesis of chronic hepatitis caused by hepatitis B and C suggests several promising therapeutic approaches. Interferon is the sole drug yet proven to be effective in the treatment of some patients with chronic hepatitis B and C. Newer antiviral agents that will be used alone or in combination are under development.

The current literature fails to address the long-term course of hepatitis infection in the immunocompromised patient, in large part because of the characteristically slow progression of this disease. An overview of the literature available fails to demonstrate evidence that immunosuppression per se promotes progression of hepatitis. In fact, many studies document a relatively low incidence of chronic active hepatitis or cirrhosis in immunocompromised patients; however, properly designed, prospective studies of sufficient numbers of patients with long-term follow-up are not available. Thus, no reliable conclusions are possible at this time.

We studied eight patients who had orthotopic liver transplantation for fulminant hepatic failure in the course of acute non-A, non-B hepatitis. HBV DNA was searched for extensively in the liver tissue by PCR using several sets of primers in conventional and heminested reactions. All patients were negative for HBV DNA in liver tissue by all assays employed; furthermore, they were negative for HEV RNA, HCV RNA, and HBV DNA in serum. Although the causative role of HEV and HCV in fulminant non-A, non-B hepatitis cannot be excluded, our data do not support a causative association between this syndrome and HBV infection.

Recent advances have made available to the clinician multiple serologic tests for the diagnosis and evaluation of acute and chronic viral hepatitis. While the multiplicity of tests available can be confusing, selective use of these serologic tests tailored to the clinical situation can be of great value in identifying the agent causing the liver disease. I present a clinically oriented discussion of the serologic tests available to diagnose viral hepatitis.

Background/aims: It has been shown that hepatitis C virus (HCV) superinfection may suppress hepatitis B virus (HBV) leading to hepatitis B surface antigen (HBsAg) clearance and that hepatitis may persist after HBsAg clearance in a few patients. The role of HCV in continuing hepatitis after termination of chronic HBsAg antigenemia remains to be explored in a series of patients., Methods: HCV markers were studied using second generation enzyme immunoassay and polymerase chain reaction with reverse transcription and were compared between 41 patients with persistent alanine aminotransferase (ALT) elevation (hepatitis group) and 82 age/sex-matched patients with normal ALT (control group) after HBsAg clearance., Results: Twenty-six (63%) of the 41 hepatitis group patients were seropositive for antibodies to HCV (anti-HCV) compared with only 4 (5%) of 82 controls (P < 0.0001). Six patients of the hepatitis group and 1 control had an episode of acute hepatitis C with seroconversion of anti-HCV 1-68 months before HBsAg clearance. Of those seropositive for anti-HCV, serum HBV DNA was not detectable, and serum HCV RNA was detected in 23 (88.5%) of the 26 hepatitis patients but none of the 4 controls (P < 0.001). Liver biopsy in 6 anti-HCV positive patients with continuing hepatitis showed features compatible with chronic hepatitis C. HCV RNA, but not HBV DNA, was detected in liver tissues of these 6 patients., Conclusions: The results suggest that HCV may usurp the role of HBV in chronic hepatitis and act as the major cause of continuing hepatitis or ALT elevation after HBV/HBsAg clearance.

Viral hepatitis is a disease of antiquity, but evidence for more than one etiologic agent has been recognized only since the 1940s, when two viruses (hepatitis A virus and hepatitis B virus) were thought to account for all disease. In the past 20 years, three additional hepatitis agents (hepatitis C virus, hepatitis D virus, and hepatitis E virus) have been discovered, and there is evidence for at least one additional virus. Each of the five recognized hepatitis viruses belongs to a different virus family, and each has a unique epidemiology. The medical impact of these viruses on society has been strongly influenced by changes in human ecology. This has resulted in some cases in diminished disease and in others in increases in the incidence of disease.

Non-A, non-B hepatitis viruses have been implicated as the etiological agent(s) in up to 60% of patients with fulminant hepatitis. These agents are reported to induce a higher mortality than other causes of fulminant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV) at present constitute the major identifiable non-A, non-B hepatitis agents. Of these, HEV has been established as the sole cause of epidemic hepatitis in Afro-Asian countries, and fulminant hepatitis has been recorded during such epidemics. However, in sporadic cases, the etiological role of HEV in fulminant hepatitis has remained uncertain. The role of HCV in acute liver disease and fulminant hepatitis remains unclear. The present study was undertaken to investigate the association of HEV and HCV in patients with fulminant hepatitis by direct detection of the viral genome using reverse transcription-polymerase chain reaction (RT-PCR). Serum samples from 50 serologically identified non-A, non-B fulminant hepatitis cases negative for cryptic hepatitis B virus (HBV) infection examined via PCR were tested for HEV and HCV RNA using RT-PCR. For HEV primers from the nonstructural region (ORF-1) were used, and for HCV primers from the highly conserved 5' untranslated regions were used. The products were analysed using agarose gel electrophoresis and confirmed by hybridisation with radiolabelled internal oligonucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non-A, non-B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In 11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (40%) cases, HEV was detected alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Objectives: to define the roles of the hepatitis C and E viruses (HCV and HEV) in non-A, non-B (NANB) fulminant hepatitis., Methods: we utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANB fulminant hepatic failure (FHF) patients., Results: none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitis patients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA., Conclusions: we did not find evidence implicating HCV or HEV in presumed viral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with autoimmune hepatitis, drug-induced hepatotoxicity, or halothane hepatotoxicity.

Hepatitis due to herpes simplex virus (HSV) developed in a pregnant women at 38 weeks' gestation. She delivered a live-born infant who had serologically documented HSV 2 infection but did well with acyclovir therapy. The mother, however, died five days postpartum from fulminant hepatic failure despite antiviral treatment, and HSV was demonstrated in the liver. Twenty-three reported cases clearly establish pregnancy as a condition that can predispose to disseminated HSV infection. The majority of cases have been due to HSV 2, and primary infection in the latter part of pregnancy appears to constitute the greatest risk. The major disease manifestations appear to be hepatitis and encephalitis. Historically, maternal and fetal mortality rates have been high, but there is a trend toward improved survival in the acyclovir era.

Rubella was accompanied by hepatic dysfunction in a 28-year-old male. Serum aminotransferase levels were moderately elevated and LDH markedly increased, especially LDH isoenzyme 5, whereas total bilirubin and ALP remained almost normal. GOT, GPT and LDH levels were completely normalized by the 21st hospital day. Paired antibody titers of viruses which may cause hepatitis, other than rubella, were of no significance. Laparoscopy showed enlarged, red liver. Histologic and electron microscopic findings of the liver were consistent with acute hepatitis. Hepatic damage with rubella is rare, and it is possible that the hepatic dysfunction seen in adult rubella may be mediated by an immunopathologic mechanism.

Previous findings in liver transplantation patients have raised the concept that HLA plays a dualistic role. HLA matching will reduce rejection but may augment MHC restricted cellular immune mechanisms of liver allograft injury. To evaluate this concept, we studied CMV hepatitis in 399 FK506-treated liver transplant patients, including 355 cases for which complete HLA-A,B,DR,DQ typing information was available. CMV hepatitis developed in 25 patients, and 17 of them (or 68%) showed a one or two HLA-DR antigen match with the donor. In contrast, HLA-DR matches were found in only 35% of 330 patients without CMV hepatitis (P = 0.005). No significant associations were seen for HLA-A, HLA-B, and HLA-DQ antigens. In pretransplant CMV-seronegative patients with seropositive grafts (n = 39), the frequency of CMV hepatitis was 44% for HLA-DR-matched livers but 14% for HLA-DR-unmatched livers. In seropositive recipients (n = 187), these frequencies were 12% and 2% for HLA-DR-matched and unmatched liver grafts. Chronic rejection developed in 29 patients (or 8%) during a follow-up between 10 and 24 months after transplantation. Its incidence was higher in the CMV hepatitis group (24% vs. 6%) (P = 0.007). Although no associations were found between HLA matching and the incidence of chronic rejection, there was an earlier onset of chronic rejection of HLA-DR-matched livers irrespective of CMV hepatitis. These findings suggest that an HLA-DR match between donor and recipient increases the incidence of CMV hepatitis in both primary and secondary CMV infections. Although HLA compatibility leads to less acute cellular rejection, it is suggested that DR matching may accelerate chronic rejection of liver transplants, perhaps through HLA-DR-restricted immunological mechanisms toward viral antigens, including CMV.

The frequency and histological pattern of multiple hepatitis virus infection was studied in 161 Italian patients who had consecutively undergone liver biopsy from 1989 to 1991. The histological features were compared with that of infection with a single virus. Thirty-nine per cent of patients had evidence of past or present multiple infection, the commonest of which was hepatitis C virus (HCV) in patients with evidence of previous infection with hepatitis B virus (HBV). In general, the severity of the histological pattern of each viral infection was maintained even when more than one virus was involved; there was neither exacerbation nor diminution of the histological changes. The delta-virus (HDV) was not associated with severe necro-inflammatory lesions, but HDV-positive patients were few in this cohort. Lymphoid follicle formation (a putative histological marker of HCV infection) was also found in a high proportion of HCV-negative patients but expressing much HBcAg or HDAg in liver tissue. Possible explanations for this finding are that follicles are relatively non-specific for HCV infection, or that these cases represent HCV infection with false-negative serology. The results of this study suggest that multiple hepatitis virus infection is common in the population investigated and that HBV and HCV co-infection cannot be reliably diagnosed histologically. Whether double infection with these viruses influences the cirrhotic evolution of the liver lesion remains unclear.

The authors report an unusual case of herpes simplex type 2 (HSV) hepatitis which presented as part of a systemic HSV infection accompanied by disseminated intravascular coagulation (DIC). The patient was a 49-year-old Japanese male who three months prior to admission underwent surgical resection of his thymus for an invasive thymoma. Postoperatively, he received a course of chemotherapy which included prednisone, cyclophosphamide, vincristine, and pinorubicin. After discharge from the hospital, he was put on a maintenance dosage of prednisone and cyclophosphamide. Two weeks prior to this admission, the patient developed rhinorrhea, chills and general fatigue. Routine follow-up laboratory tests revealed markedly elevated liver enzymes which led to his immediate hospitalization. The tentative diagnosis on admission was fulminant hepatitis with DIC. The patient's condition steadily worsened during his hospitalization and acyclovir was initiated on the 4th hospital day due to the possibility of HSV hepatitis. He died on the same day. Histopathology performed on the liver at autopsy revealed hepatic inclusion bodies of HSV with positive immunohistochemical detection of the HSV type 2 antigen. Our case is the first report of HSV hepatitis associated with the removal of the thymus secondary to thymoma. It supports previous observations of disseminated HSV infection being prevalent in those patients with disorders of cell mediated immunity.

Molecular biology techniques are now a vital part of hepatitis virology, with a central role in studies of diagnosis, epidemiology, virology, pathogenesis, and natural history of infection. Cloning of the genome of hepatitis E virus has allowed its tentative classification as a calici- or related virus, and is the first step toward the development of a vaccine. Long-term implications of hepatitis C for groups such as children with hemophilia, thalassemia, and even leukemia can be better understood by comparison of virus load measured by molecular amplification of the plasma viral RNA with the serologic and clinical status of the respective cohorts of children. A new vaccine for hepatitis A has been licensed in several European countries, and recent experience with severe hepatitis in infants after unexpected transmission of hepatitis B from anti-hepatitis B e positive mothers reemphasizes the value of universal hepatitis B immunization programs. Mother-to-infant transmission of hepatitis C virus has now been well documented, but there are still insufficient data on the dynamics of this, particularly in the absence of passive immunoprophylaxis or a vaccine, to permit recommendations regarding the management of individual pregnancies or deliveries. There is especially too little information to suggest whether breast feeding may be an important mechanism for transmission.

One hundred and seven patients with acute viral hepatitis (AVH) were studied prospectively regarding the viral aetiological agent HAV, HBV and NANB (by exclusion) using radioimmunoassay. Acute HAV infection occurred in 43 patients, and acute HBV infection in 34 patients, while HDS occurred in two patients only. Acute, presumably NANB, infection occurred in 28 patients. Ten out of 28 sera of patients with AHBV infection were positive for smooth muscle antibody by immunofluorescence. Important findings include: (1) presence of delta superinfection in the absence of HBsAg; (2) HBsAg as the only marker in two patients with AHBV infection; (3) concurrent presence of HBsAg and anti-HBsAg in three patients with AHBV infection.

The prevalence of serum antibodies to hepatitis C virus was assessed by an enzyme-linked immunosorbent assay in patients with epidemic non-A, non-B hepatitis (14), sporadic non-A, non-B hepatitis (42), chronic hepatitis (14) and cirrhosis (26). None of the patients with epidemic non-A, non-B hepatitis (14) and acute self-limiting sporadic non-A, non-B hepatitis without prior parenteral exposure (38) tested positive for hepatitis C virus antibody. Based on epidemiologic features, hepatitis E virus is presumably the etiologic agent for both these entities. Hepatitis C virus (HCV) antibody was positive in none of the patients with cryptogenic chronic hepatitis (11) and in 2(8%) patients with cryptogenic cirrhosis (25). It was concluded that cryptogenic chronic hepatitis and cirrhosis in India may be caused by alternative viral agents of the non-A, non-B type or by hepatotoxins to which the population may be exposed. Of 8 patients with prior parenteral exposure (transfusions 6, needle pricks 2) 5 (62.5%) patients tested positive for HCV antibody. HCV antibody was detected in 1 (25%) patient with acute self-limiting, parenterally transmitted non-A, non-B hepatitis and in 4 (100%) patients with chronic parenterally transmitted non-A, non-B hepatitis.

Through a series of 76 cases of jaundice observed in pregnant women, the authors emphasize on the biggest frequency of viral hepatitis among the all of etiology. In fact that one represents the 2/3 of cases. They insist on the graves forms of the diseases which are responsible of a high maternal mortality and big foetal complications.

Five viruses are the major causes of hepatitis. These viruses are totally unrelated to each other in structure and mode of replication despite the similarity in the acute syndrome produced by each virus. HAV is a single-stranded RNA virus that has a very stable capsid and whose proteins are derived from a single polyprotein. HBV is a DNA virus that replicates through an RNA intermediate. HCV is a labile single-stranded RNA virus whose proteins are derived from a polyprotein. HDV is a defective RNA virus related to viroids that encodes a capsid antigen, delta antigen, and requires the envelope protein of HBV (HBsAg) for its propagation. HEV is a labile RNA virus that is unrelated to other known viruses. Hepatitis B, C, and D can cause chronic hepatitis. Both chronic hepatitis B and C virus infections are associated with primary hepatocellular carcinoma. The most likely mechanism for hepatitis B and C promotion of primary hepatocellular carcinoma in that these viruses cause chronic inflammation and increased mitotic activity of the pluripotent oval cells of the liver. Most likely, primary hepatocellular carcinoma arises out of synergy between chronic viral infection and some other carcinogenic stimulus such as exposure to a hepatotoxin.