370 research outputs found
Hepatitis C Virus–Associated Non-Hodgkin Lymphomas: Biology, Epidemiology, and Treatment
No full textEradication of hepatitis C virus (HCV) in indolent non-Hodgkin lymphomas (NHLs), especially in marginal zone lymphomas, determines the regression of the hematologic disorder in a significant fraction of cases. Because direct antiviral agents show an excellent profile in terms of efficacy, safety, and rapid onset of action, these drugs can be used in any clinical situation and in the presence of any comorbidities. To avoid the progression of the NHL, despite HCV eradication, antiviral therapy should be provided as soon as the viral infection is discovered; before that, the chronic antigenic stimulation determines the irreversible proliferation of neoplastic B cells
Hepatitis C virus and non-Hodgkin's lymphoma ten years later
No full textHepatitis C virus is associated with chronic liver disease as well as with lymphoproliferative disorders such as mixed cryoglobulinemia and, likely, non-Hodgkin's lymphomas. The association between hepatitis C virus infection and B-cell lymphoma is controversial since it shows a strong regional variation. In fact, the prevalence of hepatitis C virus infection in non-Hodgkin's lymphoma shows a prevalence ranging between 7.4 and 37.0%. However, the intimate pathogenetic mechanism involved in hepatitis C virus-associated lymphomas remains considerably unknown. Hepatitis C virus may exert its oncogenic potential via an indirect mechanism or utilise other pathways directly. It is reasonable to assume that several different pathogenetic mechanisms operate in the wide spectrum of hepatitis C virus-related lymphoproliferative disorders, which include the intermediate to high-grade lymphoma, and the more common indolent, low-grade lymphoma, preceded by long standing symptomatic mixed cryoglobulinemia Type II. In this review, the etiopathogenetic role of hepatitis C virus in non-Hodgkin's lymphoma is discussed on the basis of molecular, clinical and epidemiological considerations. The management of hepatitis C virus-associated non-Hodgkin's lymphoma is similar to that of conventional lymphoma, although viral reactivation or the underlying chronic liver disease can complicate chemotherapy. Whether to treat low-grade hepatitis C virus-related lymphomas with anti-viral therapy is still debatable, but encouraging data emerge from some recent studie
HCV and lymphoproliferative disorders
No full textThe etiology of non-Hodgkin's lymphomas (NHL) remains a controversial matter, but, in the last few years, considerable evidence suggests that aberrations of the immune system and viruses may act as etiologic agents, in at least some cases of NHL. In fact, patients with primary immuno-deficiencies, or those suffering from diseases characterized by autoimmune dysfunction, show an increased risk for the development of NHL. Several viruses have been identified as possible etiologic agents for NHL; one of the best studied is the Epstein-Barr virus, which was detected in cultures of tumor cells from patients with Burkitt's lymphoma. The pathogenetic potential of this virus is illustrated by its association with an increasing number of malignant diseases. In addition, the human T-cell lymphotropic virus family (HTLV), was also recognized as possible etiologic agents for several lymphomas, such as cutaneous T-cell lymphoma and T-cell leukemia-lymphoma syndrome (HTLV-I), and T-cell hairy cell leukemia (HTLV-II). Recently, the presence of hepatitis C virus infection has also been recognized in several hematological malignancies such as mixed cryoglobulinemia, low-grade malignant lymphomas and Waldenström's disease. The possible etiopathogenetic role of this virus in non-Hodgkin's lymphomas is discussed on the basis of molecular, clinical, and epidemiological considerations
Hepatitis C virus, mixed cryoglobulinemia and non-Hodgkin’s lymphoma
No full textThere is increasing evidence from recent studies that a
large number of diseases are related to infections. In the
field of haematology, many malignant disorders are now
related to some infectious agents, such as Epstein-Barr
virus (EBV) in Burkitt's lymphoma, human T lymphocyte
virus I (HTLV-I) in T-cell leukaemia-lymphoma,
Helicobacter pylori in gastric B-cell lymphoma, human
herpes virus (HHV-6, -7, -8) in Kaposi's sarcoma and
Castelman's disease and, perhaps, parvovirus B19 in pure
red cell aplasia. However, all these infectious agents are
widespread in the general population, but only a very small
fraction of infected patients develop the neoplastic disease,
indicating the crucial role of some, at present unknown,
underlying genetic factors.
An association between HCV infection and B-cell
lymphoma has been demonstrated in several geographical
areas. Although controversy remains, a pathogenetic
linkage between HCV and NHL is strongly suggested by
molecular and epidemiological evidence. However, despite
this evidence, the pathogenetic mechanisms underlying
HCV-associated lymphomas are still unknown. HCV-related
lymphomas could, therefore, represent an important model
for analysing virus–induced lymphomas in humans.
It has not been elucidated whether HCV exerts its
oncogenic effect through an indirect mechanism or whether
it uses other pathways directly. It can be said that in most
cases the viral infection does not have a significant impact
on either response to chemotherapy or survival of
lymphoma patients. Chemotherapy is relatively safe and
treatment regimes do not usually need to be interrupted.
Since the treatment of HCV infection can lead to
regression not only of chromosomal and molecular
abnormalities, but even of clinically evident low-grade
NHL118.119, new therapeutic strategies (pegylated interferons
plus ribavirin), currently recognised as the gold standard
for HCV antiviral therapy and able to eradicate HCV in a
high percentage of treated subjects (from 60 to 90% of
complete responders on the basis of HCV genotype: 1 vs.
non-1) are likely to drastically reduce the number of HCV
infected patients and, consequently, the number of HCVrelated
NHL
Hepatitis C virus-associated indolent B-cell lymphomas: A review on the role of the new direct antiviral agents therapy
No full textSeveral studies have suggested that hepatitis C virus (HCV) may be the causative agent of some B-cell non-Hodgkin lymphomas (B-NHL). Several authors have demonstrated that pegylated interferon (Peg-IFN) plus ribavirin (RBV) can revert indolent low-grade B-NHL by inducing HCV eradication. Presently, the combination therapy (IFN plus RBV) has been abandoned since the direct antiviral agents (DAAs) have shown very high efficacy in achieving sustained virologic response (SVR) (range: 95%-100%). This review analyzed DAAs efficacy in HCV-associated indolent low-grade NHL, providing a detailed literature review. Overall, 122 B-cell NHL patients were treated with DAAs: complete/partial hematological response, particularly in those with marginal zone lymphoma, was obtained in most cases. Hematological response, obtained either with DAAs or IFN-based therapy, was similar. Nonetheless, DAAs therapy showed better tolerability and higher SVR. A fraction of the patients, despite SVR, underwent hematologic relapse or progression. In these cases, a recovery treatment with immunotherapy, or chemoimmunotherapy, had to be planned. In conclusion, data obtained from published studies mostly agree that HCV eradication with DAAs should be considered as the first-line treatment in HCV-related NHL. In fact, the chronic viral stimulation of the immune system might be the primary pathogenic mechanism in disease development and progression
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