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Query: UMLS:C0239946 (
liver fibrosis
)
8,268
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We report on a 26-year-old man who presented with severe jaundice and elevated serum liver enzyme activities after having received a dose of Twinrix. In his past medical history, jaundice or abnormal liver function tests were never recorded. Following admission, an elevated immunoglobulin G level and antinuclear antibodies at a titer of 320 with a homogenous pattern were found. Histology of a liver biopsy showed marked bridging
liver fibrosis
and a chronic inflammation, compatible with autoimmune hepatitis. Treatment was started with budesonide and ursodeoxycholic acid, and led to complete normalization of the pathological liver function tests. We believe that Twinrix led to an acute exacerbation of an unrecognized autoimmune hepatitis in our patient. The pathogenesis remains to be clarified. It is tempting to speculate that inactivated hepatitis A virus and/or recombinant
surface antigen
of the hepatitis B virus -as seen in patients with chronic hepatitis C and unrecognized autoimmune hepatitis who were treated with interferon alpha-might have been responsible for disease exacerbation.
...
PMID:Acute exacerbation of autoimmune hepatitis induced by Twinrix. 1599 42
The persistence of hepatitis B virus (HBV) genomes in HBV
surface antigen
(HBsAg) negative individuals is termed occult HBV infection. Occult HBV status is associated in some cases with mutant viruses undetectable by HBsAg assays, but more frequently it is due to a strong suppression of viral replication and gene expression. Occult HBV infection is an entity with world-wide diffusion, although the available data of prevalence in various categories of individuals are often contrasting because of the different sensitivity and specificity of the methods used for its detection in many studies. Occult HBV may impact in several different clinical contexts, including the transmission of the infection by blood transfusion or organ transplantation and its acute reactivation when an immunosuppressive status occurs. Moreover, much evidence suggests that it can favour the progression of
liver fibrosis
and above all the development of hepatocellular carcinoma.
...
PMID:Occult hepatitis B virus infection. 1711 22
The co-existence of hepatitis B
surface antigen
(HBsAg) and anti-HBs antibodies (HBsAb) in serum of hepatitis B virus (HBV)-chronic carriers has been previously associated with HBsAg-amino acid (aa) substitutions. However, the aa pattern of HBV-reverse transcriptase (RT) and the clinical settings associated with this serological profile remain largely unknown. We studied thirteen HBsAg-positive/HBsAb-positive patients. Newly diagnosed HBsAg-positive/HBsAb-negative patients (n=51) served as controls. HBsAg/RT sequences were obtained using in-house protocols. HBsAg-positive/HBsAb-positive patients were predominantly immunosuppressed (69%). Five presented advanced
liver fibrosis
. HBV DNA >5.0 log(10) copies/ml was significantly more frequent than in controls. A significantly higher aa variability was observed versus controls within HBsAg major hydrophilic region (MHR), especially the a-determinant, and within RT for regions overlapping the MHR, the a-determinant, and HBsAg C terminal region where drug resistance mutations occur. Further studies are needed to determine whether this higher HBsAg/HBV-RT variability might favor dissemination of anti-HBsAb escape HBV mutants and concomitantly alter nucleos(t)ide analogs efficacy.
...
PMID:Clinical and virological significance of the co-existence of HBsAg and anti-HBs antibodies in hepatitis B chronic carriers. 1757 90
The prevalence of antibodies to hepatitis C virus (anti-HCV) has been measured in 113 Saudi patients with chronic liver diseases. Twenty-five percent of 20 patients with hepatocellular carcinoma (HCC) were positive for anti-HCV and 29.7% of 38 patients with cirrhosis and 27.3% of 33 patients with
liver fibrosis
, respectively, also tested positive. The positivity rate for a miscellany of liver diseases (22) was 13.6%. The differences between these prevalence rates were not statistically significant. By comparison, 45% of HCC tested positive for hepatitis B
surface antigen
(HBsAg) while 52.7% of cirrhosis cases were positive. There rates were statistically significant when compared with HBsAg positivity rates of 9.1% and 18.2% in the
liver fibrosis
and miscellaneous groups. The role of hepatitis C virus (HCV) may be secondary or additive in the causation of chronic liver disease and hepatocellular carcinoma in this environment in which hepatitis B virus (HBV) is highly endemic.
...
PMID:Prevalence of antibodies to hepatitis C virus in Saudi patients with chronic liver disease. 1759 Jul 80
We present the preoperative findings of 102 patients who underwent successful splenectomy for advanced schistosomiasis japonica. All patients were symptomatic for schistosomiasis and had splenomegaly greater than or equal to II according to the Hackett criteria. Before surgery, all patients underwent clinical examination including full blood count; fibrinogen and serum protein levels; liver function tests; and serology for hepatitis B, C, and D. Ultrasound examination of the liver and spleen and liver histology for evidence of pathology were also undertaken. Ninety patients had a treatment history for schistosomiasis. Fifty-six patients were seropositive for hepatitis B virus antibody, and 6 patients were seropositive for hepatitis C virus antibody. Immunohistochemical testing of the liver samples confirmed that 45 patients were positive for hepatitis B virus
surface antigen
, thereby indicating active infection. A total of 66.7% of patients had fibrosis stages II to III by ultrasound; and 76.5% of patients had portal vein inner diameter greater than 12 mm, indicating portal vein hypertension. A total of 83.2% of patients showed various stages of esophageal varicosis via x-ray, and 81.4% had fibrotic stages III to IV by liver biopsy. Coinfection with hepatitis B virus accelerated the development of
liver fibrosis
. There was moderate concordance between the fibrosis assessed by ultrasonography and histopathology, indicating that ultrasound underestimates the true pathology. Combined assessment is needed to improve the diagnosis of clinical hepatic fibrosis.
...
PMID:Severe hepatosplenic schistosomiasis: clinicopathologic study of 102 cases undergoing splenectomy. 2097 Jan 62
Chronic hepatitis B is a major cause of liver disease worldwide, ranking as the first cause of cirrhosis and hepatocellular carcinoma. Hepatitis B
surface antigen
(HBsAg) is usually used as a qualitative marker for the diagnosis of hepatitis B virus (HBV) infection. HBsAg clearance is the closest to cure outcome as one can expect to achieve in hepatitis B. Support for this comes from natural history studies demonstrating increased length of survival, lower rates of hepatic decompensation, reduction in the frequency of hepatocellular carcinoma, and regression of
liver fibrosis
in patients who clear HBsAg. HBsAg seroclearance may occur spontaneously at a yearly incidence of 1-2%, preceded usually by a long period of inactive disease. Interferon treatment enhanced HBsAg seroclearance by approximately three-fold in western studies and sixfold in Asian studies compared with non-treated patients. Pegylated interferon induced a 10-15% yearly rate of HBsAg seroclearance in patients who developed sustained virological response in clinical trials. By contrast, treatment with nucleos (t) ides analogues did not significantly affect the rate of HBsAg seroclearance, especially in patients with hepatitis B e antigen (HBeAg) - negative disease. Recently, serum HBsAg has been shown to be a surrogate marker of covalently closed circular DNA (cccDNA) concentration in the liver. Quantification of serum HBsAg has also been recently shown to be a promising tool for monitoring virologic response in HBeAg-negative patients treated with pegylated interferon.
...
PMID:[HBsAg seroclearance: prognostic value for the response to treatment and the long-term outcome]. 2109 15
Chronic hepatitis B virus (HBV) infection is a major health problem in the Asia-Pacific region. In the past decade, much progress has been made in the understanding and management of this disease. The introduction of universal vaccination has significantly reduced the incidence of perinatal infection in most Asia-Pacific countries. As the majority of the adult population have not been immunized at birth, we are still facing a large population of young HBV-infected patients in the coming two decades. The study of long-term longitudinal databases has provided deeper insight into the clinical significance of HBV DNA suppression, hepatitis B e antigen (HBeAg) seroconversion and hepatitis B
surface antigen
(HBsAg) seroclearance in chronic hepatitis B. With a better understanding on the natural history of HBV infection, one can now stratify the risk of chronic hepatitis B patients for adverse clinical outcomes and use this to individualize management. The introduction of non-invasive assessment of
liver fibrosis
can potentially reduce the necessity of liver biopsy. There have also been great advances in the development of antiviral therapy in the past decade. However, the high cost of HBV antiviral drugs poses major challenges to health authorities in many Asia-Pacific countries. Properly performed cost-effective analysis and understanding on the best timing of stopping antiviral drugs will be important to facilitate the most appropriate allocation of resources.
...
PMID:Chronic hepatitis B in Asia-new insights from the past decade. 2119 24
Occult hepatitis B infection (OBI) is characterized by hepatitis B virus (HBV) DNA in serum in the absence of hepatitis B
surface antigen
(HBsAg) presenting HBsAg-negative and anti-HBc positive serological patterns. Occult HBV status is associated in some cases with mutant viruses undetectable by HBsAg assays; but more frequently it is due to a strong suppression of viral replication and gene expression. OBI is an entity with world-wide diffusion. The failure to detect HBsAg, despite the persistence of the viral DNA, is due in most cases to the strong suppression of viral replication and gene expression that characterizes this "occult" HBV infection; although the mechanisms responsible for suppression of HBV are not well understood. The majority of OBI cases are secondary to overt HBV infection and represent a residual low viremia level suppressed by a strong immune response together with histological derangements which occurred during acute or chronic HBV infection. Much evidence suggests that it can favour the progression of
liver fibrosis
and the development of hepatocellular carcinoma.
...
PMID:Pathogenesis of occult chronic hepatitis B virus infection. 2147 18
Occult hepatitis B virus (HBV) infection (OBI) is defined by the presence of HBV DNA in the liver tissue of individuals who test negative for hepatitis B
surface antigen
(HBsAg). Patients who have recovered from acute hepatitis B can carry HBV genomes for a long time and show histological patterns of mild necro-inflammation, even fibrosis, years after the resolution of acute hepatitis, without showing any clinical or biochemical evidence of liver disease. At least in conditions of immunocompetence, OBI is inoffensive itself, but when other relevant causes of liver damage are present it might make the course of the liver disease worse. The risk of HBV transmission through transfusion is related to blood donations negative for HBsAg that have been collected during the pre-seroconversion period or during chronic OBI. Use of HBV nucleic acid amplification testing and multivalent anti-HBs antibodies in the HBsAg assays is recommended for detection of true and false OBI, respectively. It is not known if prior hepatitis B immunization with an optimal anti-HBs response in cases of HBV transmission through organ transplantation can effectively modulate or abort the infection. Use of antiviral agents as prophylaxis in patients with serological evidence of past HBV infection prevents reactivation of OBI after transplantation in most cases. Reactivation of OBI has been observed in other conditions that cause immunosuppression, in which antiviral therapy could be delayed until the HBV DNA or HBsAg becomes detectable. OBI might contribute to the progression of
liver fibrosis
and hepatocellular carcinoma development in patients with chronic liver disease.
...
PMID:Management of occult hepatitis B virus infection: an update for the clinician. 2147 22
Both optimism and frustration exist regarding therapy for patients with chronic hepatitis B virus infection. Due to the recent advent of several drugs with potent antiviral capacities and comparatively low rates of adverse effects, considerable optimism has developed regarding the treatment of these patients. Chronic hepatitis B is now a treatable disease, and suppression of hepatitis B virus replication, normalization of alanine aminotransferase levels, seronegativity/seroconversion of hepatitis B e antigen and hepatitis B
surface antigen
, and decreased hepatic inflammation and
liver fibrosis
have been documented in chronic hepatitis B virus-infected patients treated with antiviral therapy. In contrast, many frustrations regarding antiviral therapy for chronic hepatitis B have arisen, because the disease, although treatable, is not curable. The present regimens of antiviral therapy modulate some intermediate parameters or so-called surrogate markers in chronic hepatitis B virus-infected patients, but usually fail to improve all intermediate parameters or ultimate clinical outcomes. In addition, major concerns remain about the applicability and use of antiviral drugs in developing and resource-constrained countries in which healthcare delivery systems do not support the proper use of antiviral therapy. New and more effective therapeutic regimens for chronic hepatitis B patients are needed that take into account potential surrogate markers of treatment outcomes and allow for effective collaboration between resource-constrained and advanced countries.
...
PMID:Future aspects of therapy for hepatitis B virus infection: value of surrogate markers, innovative therapy, and global collaboration. 2152 71
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