Prevalence of hepatitis B and C viruses in patients with lymphoproliferative disorders.
The etiology of most lymphoproliferative disorders remains unclear, though several hypotheses have been proposed. One of the conjectured mechanisms is infection of a tumor clone by an oncologic virus. Recently, evidence has arisen implicating both hepatitis B and, even more so, hepatitis C viruses in the pathogenesis of lymphoproliferative disease. Based on this information, we surveyed the prevalence of hepatitis B and C virus in patients with lymphoproliferative disease. A total of 334 newly-diagnosed lymphoproliferative disease patients (200 males, 134 females) and 1,014 (133 females, 881 males) healthy controls were randomly recruited from the university blood bank. Serologic evaluation for hepatitis B and C viruses was conducted and confirmed using PCR analyses. Those with hepatitis B and/or C, controls, and subgroups of patients with lymphoproliferative disease were compared using Pearson Chi-square analysis. Among patients with lymphoid tumors, the seropositivity of HbsAg and/or anti-HCV was 8.7% (29/334), and among the controls 6.1% (49/802), however this difference did not achieve statistical significance (P = 0.23, OR: 1.36, 95% CI: 0.82-2.26). We found no significant gender- or age-related differences for either hepatitis B or C seropositivity. There were no significant differences between the seropositivity rates of hepatitis B, C, or both in either NHL or Hodgkin's lymphoma. However, in the diffuse large cell lymphoma and follicular lymphoma subgroups, the HbsAg seropositivity rate was significantly higher than that in the controls (P = 0.017, P = 0.048, respectively), as was the seropositivity rate for hepatitis C in those with diffuse B cell lymphoma versus controls (P = 0.008). We did not identify any significant difference in the combined prevalence of hepatitis B or C seropositivity between patients with lymphoproliferative disorders and controls. However, significant differences were revealed among certain patient subgroups versus the controls. These two viruses could play a role in the development of certain specific lymphoproliferative disorders. Nevertheless, larger epidemiological studies are necessary and should focus, particularly on specific patient subgroups.
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey. vahapokan@yahoo.com.
Vahap
V
Okan
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Mehmet
M
Yilmaz
Department of Microbiology and Clinical Microbiology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Aysen
A
Bayram
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Cem
C
Kis
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Sami
S
Cifci
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Hakan
H
Buyukhatipoglu
Department of Hematology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Mustafa
M
Pehlivan
D000367:Age Factors; D005260:Female; D016174:Hepacivirus; D006508:Hepatitis Antibodies / Q000097:blood; D006509:Hepatitis B / Q000097:blood / Q000453:epidemiology*; D006515:Hepatitis B virus; D006526:Hepatitis C / Q000097:blood / Q000453:epidemiology*; D006801:Humans; D008232:Lymphoproliferative Disorders / Q000097:blood / Q000453:epidemiology* / Q000821:virology; D008297:Male; D015995:Prevalence; D012367:RNA, Viral / Q000097:blood; D012737:Sex Factors
D006508:Hepatitis Antibodies; D012367:RNA, Viral