Hepatic fibrosis plays a central role in the pathogenesis of thrombocytopenia in patients with chronic viral hepatitis

Adinolfi, Luigi Elio; Giordano, Maria; Andreana, A; Tripodi, Marie‐Francoise; Utili, Riccardo; Cesaro, G.; Ragone, Enrico; Durante‐Mangoni, Emanuele; Ruggiero, Giuseppe

doi:10.1046/j.1365-2141.2001.02824.x

Cited by 171 publications

(148 citation statements)

References 22 publications

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“…Splenomegalia was the most frequent finding (40%) in the patients with hepatitis, suggesting complications of chronic infection with HBV, confirming the findings of other authors [20].…”

Section: Clinico-epidemiological Manifestationssupporting

confidence: 81%

Characterization of HBeAg-negative chronic hepatitis B in western Brazilian Amazonia

Victoria¹,

Oliveira²,

Victoria³

et al. 2008

Braz J Infect Dis

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The present study was conducted with 55 patients native from western Brazilian Amazonia, who were HBV-DNA positive after seroconversion of HBeAg. It is a descriptive case study, with the patients separated into two groups: with hepatitis and without hepatitis on histological examination. The aim of the present study was to describe the clinical and molecular characteristics of patients who are chronic carriers of HBsAg. The prevalence of hepatitis was 63.64%, with a predominance of males (41.82%) and a mean age of 42.5 years, occurring mostly in natives of the southeast sub-region (32.73%). Time was a variable proportional to the course of the disease and the most frequent symptoms were: dyspepsia, asthenia and loss of libido with the majority of the patients having history of prior contact with HBV or positive family history. Splenomegalia was the most frequent sign (40%). Among the tests, platelet count, serum albumin and prothrombin activity were significant in the diagnosis of hepatitis. Alphafetoprotein was greater in patients with hepatitis, and hepatocellular carcinoma was detected in 3.63% of the patients with hepatic cirrhosis. Three types of HBV genotypes were diagnosed: A, D and F in the samples amplified for gene S. Genotype A (AA) was observed in 54.54% of the cases with hepatitis, in contrast to other studies showing the predominance of genotype F in this region. We observed mutations in 36.36%, with a predominance of the mutations in the core promoter region (31.81%), due to the greater prevalence of genotype A in this study. Key-Words: HBeAg-negative chronic hepatitis B, western Brazilian Amazonia, mutations.Western Brazilian Amazonia is considered a region of high endemicity for hepatitis B virus (HBV), where a large part of the population is infected in perinatal period and during infancy. The prevalence of chronic carriers of HBV surface antigen (HBsAg) in these areas varies between 5% and 15% and approximately 50% to 95% of the population show serologic evidence of past infection with HBV [1,2,3]. Various factors are implicated in the development and outcome of HBV infection, but the progression to chronic hepatitis is proportionally greater in individuals infected by the vertical route or during the perinatal period [4]. Chronic hepatopathies related to HBV are seen in two forms: HBeAg positive and HBeAg negative. The HBeAg-negative chronic forms are represented by two groups of patients: chronic inactive HBsAg carriers and chronic hepatitis B (CHB) patients. The distinction between these two forms is difficult, particularly in patients with biochemical and intermittent virologic activity. It is estimated that in the world there are approximately 350 million inactive HBsAg carriers, and of these, 7% to 30% are infected with mutant forms of HBV, which despite the presence of anti-HBe antibody continue to be HBV-DNA positive [5]. Chronic HBsAg carriers who show HBeAg-negative/antiHBe-positive serologic status and have serum HBV-DNA detectable by PCR and active hepatic disease characterized by ...

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“…Splenomegalia was the most frequent finding (40%) in the patients with hepatitis, suggesting complications of chronic infection with HBV, confirming the findings of other authors [20].…”

Section: Clinico-epidemiological Manifestationssupporting

confidence: 81%

Characterization of HBeAg-negative chronic hepatitis B in western Brazilian Amazonia

Victoria¹,

Oliveira²,

Victoria³

et al. 2008

Braz J Infect Dis

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“…These factors have been consistently found to be associated with advanced fibrosis. 23,26,[39][40][41][42][43][44][45] The Virahep-C model was significantly more accurate in predicting severe hepatic fibrosis than were several other published models including the APRI (Fig. 3).…”

Section: Discussionmentioning

confidence: 95%

Modeling hepatic fibrosis in African American and Caucasian American patients with chronic hepatitis C virus infection

et al. 2006

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“…43 Nonimmune mechanisms might also contribute to chronic thrombocytopenia in patients with HCV infection and associated liver disease, including sequestration of platelets in the enlarged spleen secondary to portal hypertension (hyper-splenism) 45 and inadequate production of thrombopoietin. 45,46 Dysregulation of the host immune system triggering the production of autoantibodies against platelet glycoproteins has also been postulated. 41,42 There have been conflicting data reported with respect to the presence of specific antibodies in platelet eluates from patients with HCVrelated ITP.…”

Section: Hcv Infectionmentioning

confidence: 99%

Viral-Associated Immune Thrombocytopenic Purpura

Liebman

2008

Hematology

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Chronic immune thrombocytopenic purpura (CITP) is a diagnosis of exclusion that occurs either de novo or secondary to other underlying disorders. Chronic infection with human immunodeficiency virus (HIV)andChronic immune thrombocytopenic purpura (CITP) is characterized by accelerated platelet destruction and variably impaired platelet production resulting in thrombocytopenia. CITP has been classified either as a primary autoimmune disorder (idiopathic thrombocytopenic purpura) or as secondary to a number of underlying disorders. Common conditions associated with secondary CITP include lymphoproliferative disorders and other autoimmune collagen vascular diseases. CITP is also associated with certain chronic infections. While the association between human immunodeficiency virus (HIV) infection and immune thrombocytopenia has been well known for over 20 years, recent studies have suggested that infection with Helicobacter pylori or hepatitis C virus (HCV) may be an even more frequent cause of chronic thrombocytopenia.The relationship between these chronic infections and the development of immune-mediated thrombocytopenia represents a largely unexplored paradigm in which the host response to an infectious agent results in a loss of immune self-regulation. The pathophysiology of infection-related ITP involves diverse immunologic pathways as well as nonimmune mechanisms that accelerate platelet destruction and/or decrease platelet production. A diagnosis of CITP associated with these chronic infections must include consideration of other potential causes of thrombocytopenia. For example, thrombocytopenia with HCV infection can also result from the hepatic cirrhosis leading to portal hypertension with splenic platelet sequestration and/or decreased hepatic production of thrombopoietin. However, the relationship between the infectious agent itself and the development of thrombocytopenia is clearly demonstrated by the improvements in platelet counts that follows successful treatment of the underlying infection. Therefore, the diagnostic and therapeutic algorithm for managing infection-related ITP can differ significantly from that of primary, i.e., idiopathic, thrombocytopenic purpura.

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Hepatic fibrosis plays a central role in the pathogenesis of thrombocytopenia in patients with chronic viral hepatitis

Cited by 171 publications

References 22 publications

Characterization of HBeAg-negative chronic hepatitis B in western Brazilian Amazonia

Characterization of HBeAg-negative chronic hepatitis B in western Brazilian Amazonia

Modeling hepatic fibrosis in African American and Caucasian American patients with chronic hepatitis C virus infection

Viral-Associated Immune Thrombocytopenic Purpura

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