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Published on: May 7, 2012
Hepatitis B and hepatitis C viral infections in patients with chronic lymphocytic leukemia
Insights
Chronic hepatitis B (HBV) and C (HCV) infections do not appear to influence the development or progression of chronic lymphocytic leukemia (CLL). This study found no significant difference in disease aggressiveness or survival between infected and uninfected CLL patients.
Area of Science:
- Hematology
- Virology
- Oncology
Background:
- The role of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections in the pathogenesis and progression of chronic lymphocytic leukemia (CLL) remains unclear.
- Investigating potential links between viral infections and hematological malignancies is crucial for understanding disease development.
Purpose of the Study:
- To determine the prevalence of HBV and HCV infections among patients diagnosed with chronic lymphocytic leukemia.
- To assess whether HBV or HCV infection is associated with more aggressive chronic lymphocytic leukemia disease or altered patient outcomes.
Main Methods:
- Sera from 222 chronic lymphocytic leukemia patients and 72 healthy controls were tested for HBV and HCV antibodies using ELISA.
- Real-time polymerase chain reaction was employed to detect HBV-DNA and HCV-RNA in patient sera and lymphocytes, irrespective of antibody status.
- Prognostic markers including Rai stage, IgVH mutational status, β2-microglobulin, Zap-70, and CD38 were analyzed.
Main Results:
- Prevalence of HBV infection was 6.3% in CLL patients versus 2.8% in controls (P=0.25); HCV markers were found in 1.8% of CLL patients and 1.4% of controls (P=0.81).
- No significant differences in aggressive disease indicators or survival times were observed between HBV/HCV-infected and uninfected CLL patients.
- Occult HBV and HCV infections were infrequent in the studied CLL cohort.
Conclusions:
- The findings do not support a significant role for HBV or HCV infections in the pathogenesis or clinical course of chronic lymphocytic leukemia.
- Further research may be warranted to explore other potential co-factors or pathogenetic mechanisms in CLL.
Background:
Whether chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infections contribute to the pathogenesis and⁄or course of chronic lymphocytic leukemia is unclear.
Objective:
To document the prevalences of HBV and HCV infections in chronic lymphocytic leukemia patients, and to determine whether infected patients experience more aggressive disease than those without infection.
Methods:
Patient sera were screened for antibodies to HBV core antigen and HCV (anti-HCV) using ELISA; both sera and peripheral blood lymphocytes were further tested (regardless of antibody results) for HBV-DNA and HCV-RNA using real-time polymerase chain reaction. Prognostic markers for chronic lymphocytic leukemia included Rai stage, IgVH mutational status, β2-microglobulin levels, Zap-70 and CD38 status.
Results:
Fourteen of 222 (6.3%) chronic lymphocytic leukemia patients and two of 72 (2.8%) healthy controls tested positive for previous or ongoing HBV infection (OR 2.4 [95% CI 0.5 to 7.7]; P=0.25) while four of 222 (1.8%) chronic lymphocytic leukemia patients and one of 72 (1.4%) controls tested positive for HCV markers (OR 1.3 [95% CI 0.2 to 6.4]; P=0.81). The levels and distribution of the various indicators of aggressive chronic lymphocytic leukemia disease were similar among HBV- and HCV-infected and uninfected patients. Survival times were also similar. Occult HBV and HCV infection (HBV-DNA or HCV-RNA positive in the absence of diagnostic serological markers) were uncommon in chronic lymphocytic leukemia patients (0.5% and 1.8%, respectively).
Conclusions:
The results of the present study do not support the hypothesis that HBV or HCV infections play an important role in the pathogenesis or course of chronic lymphocytic leukemia.
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