Thrombocytopenia In Chronic Hepatitis Research Articles

Assessment Prevalence of Thrombocytopenia in Chronic Hepatitis B and C

Assessment Prevalence of Thrombocytopenia in Chronic Hepatitis B and C

Pattern and burden of thrombocytopenia in chronic hepatitis C virus patients at a tertiary care hospital

Objective: To determine the frequency of thrombocytopenia in chronic Hepatitis C virus infection. Material and Methods: This Descriptive cross-sectional study was conducted at department of Hematology, King Edward Medical University, Lahore from February 2023 to October 2023. A total of 143 patients of either gender with chronic Hepatitis C virus infection were included in the study. For every patient, a fresh 3 ml blood sample was collected by syringe using aseptic technique in a vacutainer containing EDTA. A complete blood count was carried out using Automated Hematology Analyzer and peripheral blood smear was prepared using Wright Giemsa stain to establish whether thrombocytopenia was present or not. Thrombocytopenia was assessed by Neubauer chamber. Results: Age range in this study was from 18 to 65 years with mean age of 44.132±7.34 years, mean duration of HCV 12.685±4.53 months and mean platelet count was 238076.923 ± 100165.08/µL. Thrombocytopenia was seen in 37.1% patients. Conclusion: Our results show that chronic hepatitis C infection is related to high frequency of thrombocytopenia. The higher the duration of disease process, higher is the risk of thrombocytopenia in these patients. This study highlights that identification by screening, timely diagnosis and treatment of Hepatitis C infection can prevent thrombocytopenia and its complications. Serial hematological follow up can play a pivotal role in such patients. Keywords: Chronic hepatitis, Hepatitis C virus, Thrombocytopenia

A STUDY OF PREVALENCE OF THROMBOCYTOPENIA IN CHRONIC HEPATITIS B PATIENTS AND ITS ASSOCIATION WITH THE SEVERITY OF HEPATIC FIBROSIS IN A TERTIARY CARE HOSPITAL OF NORTH EAST INDIA.

Background: Thrombocytopenia which is dened as circulating platelet count below 150×109/L, is one of the uncommon extra-hepatic manifestation of Chronic hepatitis B infection.1 Thrombocytopenia in Chronic hepatitis B infection mainly attributes to hepatic cirrhosis of liver, autoimmune destruction of direct platelets and megakaryocytes, impaired production of platelets due to impaired thrombopoietin production.2–4 Objective: To assess the platelet count in chronic hepatitis B patients and its association with the severity of hepatic brosis. Materials and methodology: Ahospital based observational study was conducted among 70 chronic hepatitis B patients where chronic hepatitis B infection was conrmed by HbcIg-Total and HbcIgM ELISA kit test. Platelets were being counted with the help of microscope and neubauer slide. Severity of brosis is graded by liver point shear wave elastography machine. Results:Among the 70 Chronic hepatitis B patients 24 patients were found have thrombocytopenia. Value of mean platelet count (in ×109/L) were 327.14±62.07, 224.14±72.56, 191.88±18.89, 157.55±13.24 and 121.43±60.71 in normal hepatic status; mild, signicant, severe brosis and cirrhosis respectively. Conclusion: From the study thrombocytopenia can be considered as one of the extra-hepatic manifestations in CHB patients where the platelet count is found to be inversely proportional to the severity of hepatic brosis with signicant association (p value < 0.0001).

Introduction of direct-acting antiviral agents alters frequencies of anti-GPIIb/IIIa antibody-producing B cells in chronic hepatitis C patients with thrombocytopenia

The pathogenesis of thrombocytopenia in chronic hepatitis C (CHC) conceivably involves autoimmunity; however, the dynamics of autoantibodies and other autoimmune mechanisms remain unclear. In this study, we examined the changes in the frequency of anti-glycoprotein (GP) IIb/IIIa antibody-producing B cells and the levels of plasma B-cell-activating factor (BAFF), a proliferation-inducing ligand (APRIL), and interleukin (IL)-21 following treatment of CHC with direct-acting antiviral agents (DAA). We recruited 28 patients with CHC who underwent treatment with DAA for 8–12 weeks and subsequently tested negative for serum hepatitis C virus RNA. Thirty healthy controls were recruited for comparison. Platelet counts increased significantly (p = .016), and the frequency of anti-GPIIb/IIIa antibody-producing B cells decreased significantly (p = .002) in CHC patients with thrombocytopenia at the end of treatment (EOT) than before DAA treatment (baseline). However, these changes were not observed in CHC patients without thrombocytopenia. Plasma BAFF levels in CHC patients with thrombocytopenia significantly decreased from baseline to EOT (p = .002). Anti-GPIIb/IIIa antibody-producing B cells were positively correlated with plasma BAFF levels in these patients (r = 0.669, p = .039). These results suggest that DAA treatment suppresses the autoimmune response against platelets and improves thrombocytopenia.

Danazol one Month Treatment of Thrombocytopenia in Chronic Hepatitis C

Thrombocytopenia is frequently observed in patients with chronic hepatitis C virus. Moderate and severe thrombocytopenia (

Helicobacter pylori infection influences the severity of thrombocytopenia and its treatment response in chronic hepatitis B patients with compensatory cirrhosis: A multicenter, observational study

The role of Helicobacter pylori (H. pylori) infection on thrombocytopenia in chronic hepatitis B (CHB) related compensatory cirrhotic patients is unknown. We conducted an observational study to determine whether H. pylori plays a role in these patients. A total of 255 patients from three centers in China were enrolled in the study. All patients received nucleoside analogs (NA) therapy and were screened for H. pylori infection. Patients were divided into three groups based on their H. pylori infection status and the therapy administered: patients without H. pylori infection who received NA therapy alone (N = 146); patients with H. pylori infection who received NA therapy alone (n = 48); and patients with H. pylori infection who received H. pylori eradication combined with NA therapy (N = 61). We observed that in CHB compensatory cirrhotic patients with H. pylori infection, the platelets count was significantly lower relative to uninfected patients (31 versus 60 × 109/L, p < 0.01). During a 2-year follow-up, the elevation in platelet count was significantly higher in HBV/H. pylori co-infected patients who received the NA and H. pylori eradication treatment compared to the other two groups (p < 0.01). It suggested that H. pylori infection and eradication treatment combined with NA were independent risk factors associated with platelets response during treatment of thrombocytopenia in CHB compensatory cirrhosis (p < 0.01). In conclusion, H. pylori infection may associate with thrombocytopenia in CHB compensatory cirrhosis. H. pylori eradication combined with NA treatment may prove to be beneficial to CHB compensatory cirrhotic patients with thrombocytopenia who are infected with H. pylori.

Mechanism of thrombocytopenia in chronic hepatitis C as evaluated by the immature platelet fraction

Thrombocytopenia occurs frequently in chronic hepatitis C. The mechanism of this association was investigated utilizing the immature platelet fraction (IPF%) as an index of platelet production together with assay of thrombopoietin (TPO). In a cross-sectional study, 47 patients with chronic hepatitis C were studied, 29 with thrombocytopenia and 18 without thrombocytopenia (six patients in each group were on interferon therapy). IPF% was elevated in the thrombocytopenic compared with the nonthrombocytopenic group (9.0 ± 4.8% vs. 4.7 ± 2.4%, P < 0.001), and an increase in IPF% was significantly associated with thrombocytopenia on multivariable analysis (P < 0.05). Splenomegaly was more common in thrombocytopenic than in nonthrombocytopenic subjects (66% vs. 6%, P < 0.001), and on multivariable analysis, splenomegaly was the factor associated with the highest relative risk of thrombocytopenia (RR = 1.9, P < 0.05). IPF% values were elevated in a similar proportion of thrombocytopenic patients with and without splenomegaly (58% and 60%, respectively). There was no difference in TPO levels between thrombocytopenic and nonthrombocytopenic patients, and TPO levels were not related to the risk of thrombocytopenia on multivariable analysis. Significantly more thrombocytopenic than nonthrombocytopenic subjects had abnormal liver function tests, cirrhosis, and portal hypertension, and a decrease in serum albumin was significantly associated with thrombocytopenia (P < 0.005) on multivariable analysis. Factors associated with liver disease in general are associated with thrombocytopenia in chronic hepatitis C. Peripheral platelet destruction or sequestration is the major mechanism for thrombocytopenia, with hypersplenism being an important cause. Low TPO levels were not related to the occurrence of thrombocytopenia in this study.

Causes of Thrombocytopenia in Chronic Hepatitis C Viral Infection

We retrospectively studied 89 patients with chronic hepatitis C virus (HCV) infection, including 50 chronic hepatitis (CH) cases, 18 liver cirrhosis (LC) cases, and 21 LC with hepatocellular carcinoma (LC + HCC) cases, with regard to various factors related with thrombocytopenia. The platelet count decreased with the stage advancement of liver diseases. Multiple regression analysis revealed that splenomegaly and von Willebrand factor (vWF) were explanatory variables that correlated with thrombocytopenia. Splenomegaly appears to be the most responsible factor, although there are a considerable number of thrombocytopenic cases without splenomegaly, suggesting other factors may also be responsible. The vWF level is inversely correlated with the platelet count. Soluble thrombomodulin, a marker of endothelial dysfunction, increases with the advancement of liver fibrosis. It is positively correlated with vWF and inversely with the platelet count. Our present results imply that vascular endothelial dysfunction is also involved in thrombocytopenia during chronic HCV infection.

Epidemiology of thrombocytopenia in patients with chronic hepatitis C: more than meets the eye

Thrombocytopenia is likely the most common haematological abnormality that can be diagnosed inpatients affected by chronic liver disease. In these patients,the presence of thrombocytopenia may have significant clinical implications. In fact, it can be a limiting factor when considering invasive procedures and may hamper the out come of antiviral therapy with interferon. The prevalence of decreased platelet count in patients with chronic hepatitis Chas been assessed in various studies that evaluated heterogenous patient populations and used various platelet count threshold to identify thrombocytopenia. This review shows that the prevalence of thrombocytopenia in these patients is variable and mainly depends upon the severity of the underlying liver disease and the criterion used to identify this haematological abnormality. Furthermore, the results of this epidemiological review provide an indirect evidence that confirms the multiplicity of aetiological factors underlying the pathophysiology of thrombocytopenia in chronic hepatitis C patients. Lastly, this study shows that up to 25% of patients treated with interferon may develop some degree of thrombocytopenia, and this may be associated with decreased sustained virological response rates.

PP-132 Thrombocytopenia in chronic hepatitis C patients treated with conventional interferon and ribavirin in a tertiary care hospital of Rawalpindi, Pakistan

PP-132 Thrombocytopenia in chronic hepatitis C patients treated with conventional interferon and ribavirin in a tertiary care hospital of Rawalpindi, Pakistan

Association of genetic polymorphisms with interferon‐induced haematologic adverse effects in chronic hepatitis C patients

Interferon (IFN)-based combination therapy with ribavirin has become the gold standard for the treatment of chronic hepatitis C virus infection. Haematologic toxicities, such as neutropenia, thrombocytopenia, and anaemia, however, frequently cause poor treatment tolerance, resulting in poor therapeutic efficacy. The aim of this study was to identify host genetic polymorphisms associated with the efficacy or haematologic toxicity of IFN-based combination therapy in chronic hepatitis C patients. We performed comprehensive single nucleotide polymorphism detection in all exonic regions of the 12 genes involved in the IFN signalling pathway in 32 healthy Japanese volunteers. Of 167 identified polymorphisms, 35 were genotyped and tested for an association with the efficacy or toxicity of IFN plus ribavirin therapy in 240 chronic hepatitis C patients. Multiple logistic regression analysis revealed that low viral load, viral genotypes 2 and 3, and a lower degree of liver fibrosis, but none of the genetic polymorphisms, were significantly associated with a sustained virologic response. In contrast to efficacy, multiple linear regression analyses demonstrated that two polymorphisms (IFNAR1 10848-A/G and STAT2 4757-G/T) were significantly associated with IFN-induced neutropenia (P = 0.013 and P = 0.011, respectively). Thrombocytopenia was associated with the IRF7 789-G/A (P = 0.031). In conclusion, genetic polymorphisms in IFN signalling pathway-related genes were associated with IFN-induced neutropenia and thrombocytopenia in chronic hepatitis C patients. In contrast to toxicity, the efficacy of IFN-based therapy was largely dependent on viral factors and degree of liver fibrosis.

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

The pathogenesis of thrombocytopenia in chronic hepatitis is not well known. This study evaluated the relationship between liver injury, serum thrombopoietin, splenomegaly and thrombocytopenia in chronic viral hepatitis. Two hundred and nine patients were enrolled, 85 with splenomegaly and 124 without. Thrombocytopenia was present in 71% and 23% of patients with or without splenomegaly respectively. In subjects with low platelet count, those with splenomegaly showed significantly lower platelet numbers than those without splenomegaly. The spleen size correlated with portal hypertension. An inverse correlation between spleen size and platelet count was observed (r = -0.54; P < 0.0001). In patients without splenomegaly, thrombocytopenia was associated with the grade of fibrosis; platelet counts were the highest in patients with fibrosis 0-2, lower in those with grade 3 (P < 0.008) and lowest in those with grade 4 (P < 0.05). These findings were independent of demographic and biochemical characteristics, hepatic necroinflammatory activity, portal hypertension and splenomegaly. Patients with normal platelet counts showed higher thrombopoietin levels than those with low platelet counts (P < 0.0001). An inverse correlation between thrombopoietin levels and fibrosis grade was observed (r = - 0.50; P < 0.0001). Median thrombopoietin levels were 58 and 27 pg/ml for fibrosis grade 0-1 and grade 4 respectively (P < 0.001). These data indicate that advanced hepatic fibrosis, causing an altered production of thrombopoietin and portal hypertension, plays the central role in the pathogenesis of thrombocytopenia in chronic viral hepatitis.

Pathogenesis of thrombocytopenia in chronic hepatitis (CH): hepatic fibrosis plays a central role

Pathogenesis of thrombocytopenia in chronic hepatitis (CH): hepatic fibrosis plays a central role

Pathogenesis of thrombocytopenia in chronic hepatitis (CH): hepatic fibrosis plays a central role

Pathogenesis of thrombocytopenia in chronic hepatitis (CH): hepatic fibrosis plays a central role