Changing patterns of acute viral hepatitis at a major urban referral center in Egypt. (49/157)

BACKGROUND: Changes in the viral etiology of hospitalized patients can inform us of changes in the overall epidemiology of acute viral hepatitis infections. We hypothesized that improvements in health care and sanitation in the past 2 decades in Egypt have significantly impacted the viral causes of acute viral hepatitis in hospitalized patients. We compared the viral causes of acute viral hepatitis at a major urban referral center with results reported from the same center 20 years earlier. METHODS: Over a period of 10 months, 200 consecutive inpatients with clinical acute viral hepatitis were enrolled in the study, and serum samples were tested for hepatitis A through E, cytomegalovirus, and Epstein-Barr virus. RESULTS: The frequency of acute hepatitis B virus infection as a cause of symptomatic hepatitis decreased from 43.4% in 1983 to 28.5% in 2002 (P<.01), and acute hepatitis A virus infection increased from 2.1% in 1983 to 34% in 2002 (P<.01), and occurred at older ages. In 1983, non-A, non-B hepatitis virus infection caused acute viral hepatitis in 38.7% of cases, compared with 31% in the present study (P=.12). The mean alanine aminotransferase level was highest in patients with combined infections, and clinical presentation did not distinguish between different viral etiologies of hepatitis. CONCLUSIONS: A significant decrease in hepatitis B virus infection and an increase in hepatitis A virus infection have occurred since the earlier study was performed in 1983. The decrease in hepatitis B virus infection is attributable to the steep decrease in hepatitis B virus infection among children that resulted from the universal hepatitis B virus immunization of infants that was initiated in 1991. The increase in clinical hepatitis A virus infection occurred in older patients and could be attributed to improved sanitation that delayed individuals' initial exposures to the virus.  (+info)

Low prevalence of hepatitis B virus, hepatitis D virus and hepatitis C virus among patients with human immunodeficiency virus or acquired immunodeficiency syndrome in the Brazilian Amazon basin. (50/157)

Comorbidities in human immunodeficiency virus infection are of great interest due to their association with unfavorable outcomes and failure of antiretroviral therapy. This study evaluated the prevalence of coinfection by human immunodeficiency virus and viral hepatitis in an endemic area for hepatitis B in the Western Amazon basin. Serological markers for hepatitis B virus, hepatitis C virus and hepatitis D virus were tested in a consecutive sample of all patients referred for treatment of human immunodeficiency virus or acquired immunodeficiency syndrome. The variables sex, age, origin and exposure category were obtained from medical records and from the sexually transmitted diseases and acquired immunodeficiency syndrome surveillance database. Among 704 subjects, the prevalence of chronic hepatitis B carriage was 6.4% and past infection 40.2%. The presence of hepatitis B was associated with birth in hyperendemic areas of the Amazon basin, male sex and illegal drug use. The overall prevalence of hepatitis C was 5% and was associated with illegal drug use. The prevalence of hepatitis B and C among human immunodeficiency virus or acquired immunodeficiency syndrome patients in the Western Amazon basin was lower than seen elsewhere and is probably associated with the local epidemiology of these viruses and the degree of overlap of their shared risk factors. An opportunity presents itself to evaluate the prevention of hepatitis C through harm reduction policies and hepatitis B through vaccination programs among human immunodeficiency virus or acquired immunodeficiency syndrome patients.  (+info)

Immunoblot analysis demonstrates that the large and small forms of hepatitis delta virus antigen have different C-terminal amino acid sequences. (51/157)

Antisera to a peptide representing the extreme carboxy terminus of the hepatitis delta virus antigen (HDAg) open reading frame (residues 197 to 211) recognized only the large (p27 delta) and not the small (p24 delta) form of HDAg in immunoblots of infected liver extracts, thereby providing direct proof that p27 delta and p24 delta differ in their carboxyl-terminal sequence and that p27 delta results from mutation within the stop codon terminating translation of p24 delta. Reactions with other peptide antisera demonstrated that multiple smaller virus-specified proteins were carboxy-terminally truncated forms of HDAg, and immunoprecipitation studies suggested that different forms of HDAg were present as heterologous complexes within the liver extract.  (+info)

Impact of hepatitis D virus infection on the long-term outcomes of patients with hepatitis B virus and HIV coinfection in the era of highly active antiretroviral therapy: a matched cohort study. (52/157)

BACKGROUND: Triple infection with human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis D virus (HDV) is rare. The influence of HDV infection on the responses to highly active antiretroviral therapy and hepatic complications in patients with HBV-HIV coinfection remains uncertain. METHODS: Twenty-six HDV-infected case patients and 78 HDV-uninfected matched control subjects were identified between 1 January 1995 and 30 June 2003. Clinical and immunologic outcomes were noted, and HBV and HIV loads and genotypic resistance of HBV to lamivudine were determined. RESULTS: Case patients had a higher rate of injection drug use (7.7% vs. 1.3%; P=.05) and lower serum levels of HBV DNA (median level, 4.04 vs. 5.75 log10 copies/mL; P=.07) than control subjects. During a median observation period of 54.7 months, HDV infection did not have an adverse impact on clinical, virological, or immunologic responses to highly active antiretroviral therapy. However, case patients had higher rates of hepatitis flares (57.7% vs. 23.1%; P=.002), hyperbilirubinemia (34.6% vs. 14.1%; P=.04), liver cirrhosis (26.9% vs. 5.1%; P=.009), hepatic decompensation (23.1% vs. 5.1%; P=.007), and death (adjusted hazard ratio, 5.41; 95% confidence interval, 1.39-23.85; P=.02), although these patients had a lower risk of genotypic resistance to lamivudine (0% vs. 57.1%; P=.003). CONCLUSIONS: HDV infection did not affect clinical, virological, or immunologic responses to highly active antiretroviral therapy in patients with HBV-HIV coinfection. HDV infection increased risk of hepatitis flares, liver cirrhosis, hepatic decompensation, and death in patients with HBV-HIV coinfection.  (+info)

Seroprevalence of hepatitis B virus and its co-infection with hepatitis D virus and hepatitis C virus in Iranian adult population. (53/157)

CONTEXT: Hepatitis B virus (HBV) infection is one of the most prevalent public health problems worldwide (especially in developing countries). AIMS: This study was carried out to determine the seroprevalence of HBV and its co-infection with hepatitis D (HDV) and C (HCV) viruses in the northeastern part of Iran. SETTING AND DESIGN: A population-based cross-sectional study in Iran. MATERIALS AND METHODS: As many as 1,850 subjects were explored for HBsAg. Anti-HDV and anti-HCV antibodies were assessed in HBsAg-positive cases. STATISTICAL ANALYSIS USED: Proportions were compared by Chi-square and Fisher's exact tests. RESULTS: The mean age of subjects was 43.86 +/- 11.2 years. The age- and sex-standardized prevalence for HBsAg positivity was 9.7%. It was higher in males than in females (OR: 1.28; 95% CI: 0.9-1.7). The risk of infection in singles was significantly higher than in married cases (OR: 2.13). Eight (5.8%) of HBsAg-positive cases were infected with HDV and 17 (12.3%) were positive for anti-HCV antibody. CONCLUSION: This study demonstrates that the prevalence of HBsAg seropositivity in Golestan province of Iran is higher than the levels reported by WHO and previous studies from Iran. It is very important, especially for health providers and policy makers, to recognize the risk factors of HBV infection and its co-infection with HDV and HCV in this area and design effective preventive programs.  (+info)

Clinical presentation and genotype of hepatitis delta in Karachi. (54/157)

AIM: To assess the clinical presentation and genotypes of delta hepatitis in local population. METHODS: In this prospective study, 39 consecutive patients who were positive for HBsAg and hepatitis D virus (HDV) antibody were included. The patients were divided in two groups on the basis of presence or absence of HDV RNA and a comparative study was done. Genotype of HDV was determined in PCR positive patients. RESULTS: Overall there is male dominance, in which 34 patients out of 39 (87.2%) were male. Twenty (51%) patients were from the adjacent areas of three provinces; Sindh, Punjab and Balochistan indicating the higher prevalence of delta hepatitis in this mid region of Pakistan. Patients of all age groups were affected with delta hepatitis (median 31.5 years, range 12-75). HDV RNA was detectable in 23 patients (59%). All the HDV strains belonged to genotype I. HBV DNA was detectable only in 3 cases who were also HBeAg and HDV RNA positive. Patients with detectable HDV RNA were younger than patients with undetectable RNA; mean age 29.7 +/- 12.8 years vs 36.8 +/- 15.2. There were no statistically significant differences in the clinical presentation and routine biochemical profile of patients with detectable or undetectable HDV RNA. Clinical cirrhosis was present in 19 (49%) patients; 12 with detectable RNA and 7 with undetectable HDV RNA (P = 0.748). Decompensated disease was seen in eight patients; five and three respectively from each group. Four patients with undetectable RNA and two patients with detectable RNA had normal ALT and ultrasound abdomen. CONCLUSION: HDV may infect at any age, usually young adult males. Genotype I is prevalent. With time some of the patients become HDV RNA negative or asymptomatic carrier. Most of the patients have suppressed HBV DNA replication. Significant numbers of patients have cirrhosis.  (+info)

Spontaneous rupture of the liver in a patient with chronic hepatitis B and D. (55/157)

Spontaneous rupture of the liver is a rare condition with serious consequences, if not recognized and treated in time. It has been reported as a complication of several disorders, including benign or malignant liver tumors, connective tissue disease, infiltrating liver disease, preeclampsia, and post anticoagulant therapy. We report a case of spontaneous rupture of liver in a non-cirrhotic, chronic hepatitis B and D patient presenting with acute hemoperitoneum and shock. The subcapsular hematoma and rupture of liver were documented by image studies. The patients' condition gradually stabilized after fluid resuscitation. The reported case and literature review suggest that spontaneous rupture of liver must be considered in a differential diagnosis of acute hemoperitoneum. A high index of suspicion and early diagnosis with imaging are critically important.  (+info)

Evaluation of commercial enzyme immunoassays for detection of hepatitis delta antigen and anti-hepatitis delta virus (HDV) and immunoglobulin M anti-HDV antibodies. (56/157)

Panels of hepatitis B virus surface antigen-positive sera from drug abusers were used to evaluate 14 commercial enzyme immunoassays from six companies for detecting hepatitis delta virus (HDV) markers. For detecting hepatitis delta virus antigen (HDAg), the Wellcome, Pasteur and Noctech assays had 100% sensitivity for all 42 HDAg-positive serum specimens that were confirmed in-house; the Organon reagents gave 59.5% sensitivity without detergent and 64.3% sensitivity with detergent, but there were 14 discrepant results with and without detergent. The Sorin assay detected HDAg in only 10 of the positive samples (23.8% sensitivity). For the detection of antibody to HDV (anti-HDV) all six commercial enzyme immunoassays were reactive with all 36 anti-HDV-positive specimens that were confirmed in-house. There were no false-positive results with the Wellcome, Noctech, or Sorin assay, but one specimen was false positive by the Organon assay. One HDAg-positive specimen gave a false anti-HDV-positive result in the Abbott assay and an equivocal result in the Pasteur assay (97.8% specificity). For the detection of immunoglobulin M anti-HDV, the Wellcome, Noctech, and Sorin assays agreed for the 38 positives confirmed in-house, except for one false negative with the Sorin test. We conclude that there has been a substantial improvement over previously evaluated assays in sensitivity and specificity of commercial assays for anti-HDV detection, and the sensitivities of immunoglobulin M anti-HDV assays are also comparable. However, there are still major differences in sensitivity among some assays for HDAg detection.  (+info)