Platelet‐associated IgM elevated in patients with chronic hepatitis C contains no anti‐platelet autoantibodies

Kosugi, Satoru; Imai, Yumiko; Kurata, Yoshiyuki; Tomiyama, Yoshiaki; Shiraga, Masamichi; Honda, Susumu; Nishikawa, Masahiro; Yonezawa, Takeshi; Kanakura, Yuzuru; Matsuzawa, Yūji

doi:10.1111/j.1600-0676.1997.tb01023.x

Cited by 21 publications

(6 citation statements)

References 24 publications

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“…Various authors confirmed these findings, calling attention to the nonspecific character in relation to the cause of the event [21,22,23]. Other studies found an alteration in platelet adhesion function, which is evidenced earlier than aggregation defects, that in general are delayed, as demonstrated in the test of platelet function in patients with chronic hepatic insufficiency [24,25].…”

Section: Clinico-epidemiological Manifestationssupporting

confidence: 53%

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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Section: Clinico-epidemiological Manifestationssupporting

confidence: 53%

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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“…Antibody‐mediated thrombocytopenia has been assumed to be due to increased levels of platelet‐associated IgG or IgM (15, 33, 34). In contrast to AITP patients, eluates from platelets of HCV‐infected patients do not react with donor platelets (35), suggesting that immune complexes, rather than antibodies, were responsible for platelet‐associated immunoglobulins IgM (36). The MAIPA technique, however, is not influenced by the presence of immune complexes (37, 38), and it is therefore unlikely that our results are adulterated by the detection of immune complexes.…”

Section: Discussionmentioning

confidence: 99%

Platelet autoantibodies are common in hepatitis C infection, irrespective of the presence of thrombocytopenia

Panzer¹,

Seel²,

Brunner³

et al. 2006

European J of Haematology

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“…All serum samples were negative for HIV antibodies and HBsAg using a standard enzyme immunoassay technique. Platelet-associated antibodies were determined by immunot1uorescent flow cytometric analysis, as previously described by Li et al' 6 Abdominal ultrasound and portal power Doppler was performed in all patients at presentation to rule out hypersplenism and/or portal hypertension. Percutaneous liver biopsy was performed in all patients and evaluated according to the Ishak score.…”

Section: Methodsmentioning

confidence: 99%

“…The pathogenic mechanism of the thrombocytopenia in these patients has not been fully explained, but in at least some cases thrombocytopenia could be caused by an immune mechanism as a result of hepatitis C virus infection 1,4,5 . Some studies on patients with chronic HCV infection have pointed out the possible association between thrombocytopenia and elevated titres of platelet‐associated immunoglobulin G and/or antiphospholipid antibodies 4–8 …”

mentioning

confidence: 99%

THROMBOCYTOPENIA IN PATIENTS WITH HCV‐POSITIVE CHRONIC HEPATITIS: EFFICACY OF LEUCOCYTE INTERFERON‐α TREATMENT

Benci

Caremani

Tacconi

2003

Int J Clinical Practice

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SUMMARYTreating patients with HCV‐associated thrombocytopenia is a problem, because the pathogenesis of thrombocytopenia is still unclear. We evaluated the clinical and haematological response to leucocyte interferon‐α in 20 naive patients with chronic hepatitis C and thrombocytopenia (platelet count <140 × 109/l for at least six months) without portal hypertension and/or hypersplenism. They were treated with leucocyte interferon‐α (3 MU three times per week) for 12 months and followed up for 12 months. Biochemical (ALT) and virological (HCV‐RNA) responses were determined. Two patients discontinued treatment because of hyperthyroidism. Of the 18 patients who completed treatment, 12 (66%) showed a biochemical response, 10 of whom (55.5%) also showed a virological response. At the end of follow‐up, four patients (22%) showed a complete (biochemical and virological) response. During treatment, platelet counts decreased to less than 10–20% of pretreatment values in most patients. Three of the four patients with a complete response showed a platelet increase during treatment and throughout the follow‐up period. In HCV‐associated thrombocytopenia leucocyte interferon‐α is well tolerated and in cases of sustained virological inhibition is able to ameliorate the disease by increasing the platelet count.

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Platelet‐associated IgM elevated in patients with chronic hepatitis C contains no anti‐platelet autoantibodies

Cited by 21 publications

References 24 publications

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

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

Platelet autoantibodies are common in hepatitis C infection, irrespective of the presence of thrombocytopenia

THROMBOCYTOPENIA IN PATIENTS WITH HCV‐POSITIVE CHRONIC HEPATITIS: EFFICACY OF LEUCOCYTE INTERFERON‐α TREATMENT

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