A hepatitis C vírus-infekció és B-sejtes non-Hodgkin-lymphoma.

Translated title of the contribution: Hepatitis C virus infection and B-cell non-Hodgkin's lymphoma

B. Gasztonyi, A. Pár, A. Szomor, A. Nagy, L. Kereskai, H. Losonczy, L. Pajor, M. Horányi, G. Mózsik

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Oncogenesis is a multifactorial process in which environmental, genetical and infectious factors may be of importance. Specific viruses are supposed to have etiological role in about 15% of human tumors. Recently the B-cell proliferation inducing effect of the hepatotropic and lymphotropic hepatitis-C virus (HCV) came into the limelight based on the high prevalence of HCV positivity in B-cell non-Hodgkin's lymphoma (NHL) patients. The aim of the authors was to establish the prevalence of HCV infection in NHL patients. Paralelly the HBV, CMV and EBV markers, and the alterations of the humoral immune response (immunoglobulins, cryoglobulins, rheumatoid factor) were determined. 42 patients (24 male, 18 female; the mean age: 54.1 years, range 22-80 years) classified as 16 indolent (low risk), and 25 aggressive (intermediate risk) NHL and one with very aggressive Burkitt's lymphoma, according to the modified REAL classification were examined. Enzyme-linked immunosorbent assay (ELISA) for HBsAg and anti-HCV, HBsAg, anti EBV, anti CMV, furthermore polymerase chain reaction (PCR) for HCV-RNA were used. Anti-HCV was found in 6/42 NHL patients (14.3%), while anti-HCV and/or HCV-RNA PCR positivity revealed on overall HCV infection in 10/42 (23.8%) patients. None of them were HBsAg positive. Our findings support the hypothesis, that HCV might have an aetiological role in the lymphoproliferation leading to B-cell NHL.

Original languageHungarian
Pages (from-to)2649-2651
Number of pages3
JournalOrvosi Hetilap
Volume141
Issue number49
Publication statusPublished - Dec 3 2000

Fingerprint

B-Cell Lymphoma
Virus Diseases
Hepacivirus
Non-Hodgkin's Lymphoma
Hepatitis B Surface Antigens
Human Herpesvirus 4
Cryoglobulins
Polymerase Chain Reaction
Burkitt Lymphoma
Rheumatoid Factor
DNA-Directed RNA Polymerases
Humoral Immunity
Immunoglobulins
Carcinogenesis
B-Lymphocytes
Enzyme-Linked Immunosorbent Assay
Cell Proliferation
RNA
Viruses

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A hepatitis C vírus-infekció és B-sejtes non-Hodgkin-lymphoma. / Gasztonyi, B.; Pár, A.; Szomor, A.; Nagy, A.; Kereskai, L.; Losonczy, H.; Pajor, L.; Horányi, M.; Mózsik, G.

In: Orvosi Hetilap, Vol. 141, No. 49, 03.12.2000, p. 2649-2651.

Research output: Contribution to journalArticle

Gasztonyi, B. ; Pár, A. ; Szomor, A. ; Nagy, A. ; Kereskai, L. ; Losonczy, H. ; Pajor, L. ; Horányi, M. ; Mózsik, G. / A hepatitis C vírus-infekció és B-sejtes non-Hodgkin-lymphoma. In: Orvosi Hetilap. 2000 ; Vol. 141, No. 49. pp. 2649-2651.
@article{77ffbd1e83344b33a578c28833b41198,
title = "A hepatitis C v{\'i}rus-infekci{\'o} {\'e}s B-sejtes non-Hodgkin-lymphoma.",
abstract = "Oncogenesis is a multifactorial process in which environmental, genetical and infectious factors may be of importance. Specific viruses are supposed to have etiological role in about 15{\%} of human tumors. Recently the B-cell proliferation inducing effect of the hepatotropic and lymphotropic hepatitis-C virus (HCV) came into the limelight based on the high prevalence of HCV positivity in B-cell non-Hodgkin's lymphoma (NHL) patients. The aim of the authors was to establish the prevalence of HCV infection in NHL patients. Paralelly the HBV, CMV and EBV markers, and the alterations of the humoral immune response (immunoglobulins, cryoglobulins, rheumatoid factor) were determined. 42 patients (24 male, 18 female; the mean age: 54.1 years, range 22-80 years) classified as 16 indolent (low risk), and 25 aggressive (intermediate risk) NHL and one with very aggressive Burkitt's lymphoma, according to the modified REAL classification were examined. Enzyme-linked immunosorbent assay (ELISA) for HBsAg and anti-HCV, HBsAg, anti EBV, anti CMV, furthermore polymerase chain reaction (PCR) for HCV-RNA were used. Anti-HCV was found in 6/42 NHL patients (14.3{\%}), while anti-HCV and/or HCV-RNA PCR positivity revealed on overall HCV infection in 10/42 (23.8{\%}) patients. None of them were HBsAg positive. Our findings support the hypothesis, that HCV might have an aetiological role in the lymphoproliferation leading to B-cell NHL.",
author = "B. Gasztonyi and A. P{\'a}r and A. Szomor and A. Nagy and L. Kereskai and H. Losonczy and L. Pajor and M. Hor{\'a}nyi and G. M{\'o}zsik",
year = "2000",
month = "12",
day = "3",
language = "Hungarian",
volume = "141",
pages = "2649--2651",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "49",

}

TY - JOUR

T1 - A hepatitis C vírus-infekció és B-sejtes non-Hodgkin-lymphoma.

AU - Gasztonyi, B.

AU - Pár, A.

AU - Szomor, A.

AU - Nagy, A.

AU - Kereskai, L.

AU - Losonczy, H.

AU - Pajor, L.

AU - Horányi, M.

AU - Mózsik, G.

PY - 2000/12/3

Y1 - 2000/12/3

N2 - Oncogenesis is a multifactorial process in which environmental, genetical and infectious factors may be of importance. Specific viruses are supposed to have etiological role in about 15% of human tumors. Recently the B-cell proliferation inducing effect of the hepatotropic and lymphotropic hepatitis-C virus (HCV) came into the limelight based on the high prevalence of HCV positivity in B-cell non-Hodgkin's lymphoma (NHL) patients. The aim of the authors was to establish the prevalence of HCV infection in NHL patients. Paralelly the HBV, CMV and EBV markers, and the alterations of the humoral immune response (immunoglobulins, cryoglobulins, rheumatoid factor) were determined. 42 patients (24 male, 18 female; the mean age: 54.1 years, range 22-80 years) classified as 16 indolent (low risk), and 25 aggressive (intermediate risk) NHL and one with very aggressive Burkitt's lymphoma, according to the modified REAL classification were examined. Enzyme-linked immunosorbent assay (ELISA) for HBsAg and anti-HCV, HBsAg, anti EBV, anti CMV, furthermore polymerase chain reaction (PCR) for HCV-RNA were used. Anti-HCV was found in 6/42 NHL patients (14.3%), while anti-HCV and/or HCV-RNA PCR positivity revealed on overall HCV infection in 10/42 (23.8%) patients. None of them were HBsAg positive. Our findings support the hypothesis, that HCV might have an aetiological role in the lymphoproliferation leading to B-cell NHL.

AB - Oncogenesis is a multifactorial process in which environmental, genetical and infectious factors may be of importance. Specific viruses are supposed to have etiological role in about 15% of human tumors. Recently the B-cell proliferation inducing effect of the hepatotropic and lymphotropic hepatitis-C virus (HCV) came into the limelight based on the high prevalence of HCV positivity in B-cell non-Hodgkin's lymphoma (NHL) patients. The aim of the authors was to establish the prevalence of HCV infection in NHL patients. Paralelly the HBV, CMV and EBV markers, and the alterations of the humoral immune response (immunoglobulins, cryoglobulins, rheumatoid factor) were determined. 42 patients (24 male, 18 female; the mean age: 54.1 years, range 22-80 years) classified as 16 indolent (low risk), and 25 aggressive (intermediate risk) NHL and one with very aggressive Burkitt's lymphoma, according to the modified REAL classification were examined. Enzyme-linked immunosorbent assay (ELISA) for HBsAg and anti-HCV, HBsAg, anti EBV, anti CMV, furthermore polymerase chain reaction (PCR) for HCV-RNA were used. Anti-HCV was found in 6/42 NHL patients (14.3%), while anti-HCV and/or HCV-RNA PCR positivity revealed on overall HCV infection in 10/42 (23.8%) patients. None of them were HBsAg positive. Our findings support the hypothesis, that HCV might have an aetiological role in the lymphoproliferation leading to B-cell NHL.

UR - http://www.scopus.com/inward/record.url?scp=0034602607&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034602607&partnerID=8YFLogxK

M3 - Article

VL - 141

SP - 2649

EP - 2651

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 49

ER -