Posted on the OSN SuperSite October 25, 2010
Arch Ophthalmol. 2010;128(10):1295-1299.
The prevalence of hepatitis C infection may be relevant to ocular adnexal non-Hodgkin lymphoma, and hepatitis C may influence the initial appearance of the disease, a study said.
In the retrospective comparative study, medical records of 129 patients with ocular adnexal non-Hodgkin lymphoma were reviewed.
The prevalence of hepatitis C virus (HCV) infection among the patients was 17.8%, and seropositivity for infection was significantly associated with extraorbital lymphoma at the onset, the study said.
A high prevalence of mucosa-associated lymphoid tissue disease (79.8%) was also noted.
Ninety-nine patients who underwent radiotherapy and chemotherapy achieved complete remission, while 23.6% of patients with HCV-seronegative status and 21.7% of patients with HCV-seropositive status relapsed.
"However, the overall and disease-free survival of the infected patients are not statistically different than that of patients who are not infected," the authors said.
Source
Showing posts with label Lymphoma. Show all posts
Showing posts with label Lymphoma. Show all posts
September 1, 2010
Hepatitis B virus infection and risk of non-Hodgkin lymphoma in South Korea: a cohort study
The Lancet Oncology, Volume 11, Issue 9, Pages 827 - 834, September 2010
doi:10.1016/S1470-2045(10)70167-4 Cite or Link Using DOI
Published Online: 04 August 2010
Original Text
Eric A Engels MD a, Eo Rin Cho PhD b, Prof Sun Ha Jee PhD c
Summary
Background
Hepatitis B virus (HBV) infection is common throughout Asia and Africa. Whether chronic HBV infection increases risk of non-Hodgkin lymphoma (NHL) is unclear. We aimed to assess the association between chronic HBV infection and subsequent development of NHL in a South Korean cohort.
Methods
The Korean Cancer Prevention Study is a cohort study of South Korean workers and their dependants enrolled during 1992—95. From this cohort, we excluded individuals who died before Jan 1, 1993, who had cancer at or before the initial visit, who had missing information about weight, height, alanine aminotransferase or aspartate aminotransferase concentrations, or alcohol use, or who had evidence of HIV or HCV infection. Of 1 284 586 eligible participants, 603 585 had baseline data for serum hepatitis B surface antigen (HBsAg) status and were included in our study. We regarded HBsAg positivity at baseline as evidence of chronic HBV infection. Participants were followed up from baseline until Dec 31, 2006. We used national databases of inpatient and outpatient diagnoses and mortality records to ascertain occurrence of haematological malignancies. We assessed incidence of NHL overall and of NHL subtypes, malignant immunoproliferation, Hodgkin's lymphoma, multiple myeloma, and various leukaemias. We used Cox regression to evaluate associations with HBsAg status, adjusting for sex, age, and enrolment year.
Findings
53 045 (9%) of 603 585 participants tested positive for HBsAg at baseline. Subsequently, 133 HBsAg-positive and 905 HBsAg-negative individuals developed NHL. HBsAg-positive participants had an increased risk of NHL overall compared with those who were HBsAg-negative (incidence 19·4 vs 12·3 per 100 000 person-years; hazard ratio [HR] 1·74, 95% CI 1·45—2·09, adjusted for sex, age at baseline, and enrolment year). Among NHL subtypes, HBsAg positivity was associated with increased risk of diffuse large B-cell lymphoma (n=325, incidence 6·86 vs 3·79 per 100 000 person-years; adjusted HR 2·01, 1·48—2·75) and other or unknown subtypes (n=591, incidence 10·5 vs 7·07 per 100 000 person-years; adjusted HR 1·65, 1·29—2·11), compared with HBsAg negativity. Increased risk was also recorded for malignant immunoproliferation (n=14, incidence 0·44 vs 0·15 per 100 000 person-years; adjusted HR 3·79, 1·05—13·7). Risk of these malignancies was consistently raised in HBsAg-positive participants throughout 14 years of follow-up. HBsAg positivity was not associated with follicular or T-cell NHL, Hodgkin's lymphoma, multiple myeloma, or various leukaemias.
Interpretation
During extended follow-up, HBsAg-positive individuals had an increased risk of NHL, suggesting that chronic HBV infection promotes lymphomagenesis.
Funding
Korean Seoul City Research and the National Research and Development Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea; US National Cancer Institute.
a Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
b Institute of Human Genomic Study, College of Medicine, Korea University, Seoul, South Korea
c Department of Epidemiology, Institute for Health Promotion, Graduate School of Public Health, Seoul, South Korea
Correspondence to: Prof Sun Ha Jee, Department of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, South Korea
Source
doi:10.1016/S1470-2045(10)70167-4 Cite or Link Using DOI
Published Online: 04 August 2010
Original Text
Eric A Engels MD a, Eo Rin Cho PhD b, Prof Sun Ha Jee PhD c
Summary
Background
Hepatitis B virus (HBV) infection is common throughout Asia and Africa. Whether chronic HBV infection increases risk of non-Hodgkin lymphoma (NHL) is unclear. We aimed to assess the association between chronic HBV infection and subsequent development of NHL in a South Korean cohort.
Methods
The Korean Cancer Prevention Study is a cohort study of South Korean workers and their dependants enrolled during 1992—95. From this cohort, we excluded individuals who died before Jan 1, 1993, who had cancer at or before the initial visit, who had missing information about weight, height, alanine aminotransferase or aspartate aminotransferase concentrations, or alcohol use, or who had evidence of HIV or HCV infection. Of 1 284 586 eligible participants, 603 585 had baseline data for serum hepatitis B surface antigen (HBsAg) status and were included in our study. We regarded HBsAg positivity at baseline as evidence of chronic HBV infection. Participants were followed up from baseline until Dec 31, 2006. We used national databases of inpatient and outpatient diagnoses and mortality records to ascertain occurrence of haematological malignancies. We assessed incidence of NHL overall and of NHL subtypes, malignant immunoproliferation, Hodgkin's lymphoma, multiple myeloma, and various leukaemias. We used Cox regression to evaluate associations with HBsAg status, adjusting for sex, age, and enrolment year.
Findings
53 045 (9%) of 603 585 participants tested positive for HBsAg at baseline. Subsequently, 133 HBsAg-positive and 905 HBsAg-negative individuals developed NHL. HBsAg-positive participants had an increased risk of NHL overall compared with those who were HBsAg-negative (incidence 19·4 vs 12·3 per 100 000 person-years; hazard ratio [HR] 1·74, 95% CI 1·45—2·09, adjusted for sex, age at baseline, and enrolment year). Among NHL subtypes, HBsAg positivity was associated with increased risk of diffuse large B-cell lymphoma (n=325, incidence 6·86 vs 3·79 per 100 000 person-years; adjusted HR 2·01, 1·48—2·75) and other or unknown subtypes (n=591, incidence 10·5 vs 7·07 per 100 000 person-years; adjusted HR 1·65, 1·29—2·11), compared with HBsAg negativity. Increased risk was also recorded for malignant immunoproliferation (n=14, incidence 0·44 vs 0·15 per 100 000 person-years; adjusted HR 3·79, 1·05—13·7). Risk of these malignancies was consistently raised in HBsAg-positive participants throughout 14 years of follow-up. HBsAg positivity was not associated with follicular or T-cell NHL, Hodgkin's lymphoma, multiple myeloma, or various leukaemias.
Interpretation
During extended follow-up, HBsAg-positive individuals had an increased risk of NHL, suggesting that chronic HBV infection promotes lymphomagenesis.
Funding
Korean Seoul City Research and the National Research and Development Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea; US National Cancer Institute.
a Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
b Institute of Human Genomic Study, College of Medicine, Korea University, Seoul, South Korea
c Department of Epidemiology, Institute for Health Promotion, Graduate School of Public Health, Seoul, South Korea
Correspondence to: Prof Sun Ha Jee, Department of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, South Korea
Source
August 3, 2010
Hepatitis B linked to lymphoma in study
WASHINGTON
Tue Aug 3, 2010 6:37pm EDT
WASHINGTON (Reuters) - People infected with hepatitis B virus are around twice as likely to develop non-Hodgkin lymphoma, researchers reported on Tuesday.
Hepatitis B was already known to cause liver cancer and some scientists had suspected it might cause lymphoma, too. The study, published in Lancet Oncology, confirms this. Hepatitis C is also linked to lymphoma.
The blood cancer is not common and widespread vaccination against the viruses is unlikely to affect non-Hodgkin lymphoma rates much, the researchers noted. But it may be possible to treat the virus and help non-Hodgkin lymphoma patients, they said.
Dr. Eric Engels of the U.S. National Cancer Institute and Sun Ha Jee of Yonsei University in Seoul studied the records of more than 600,000 people in South Korea, where hepatitis B was extremely common before a vaccination campaign began in 1995.
Of these, 53,000 or about 9 percent had evidence of hepatitis B infection. After 14 years, rates of non-Hodgkin lymphoma were more common among the infected people -- 19.4 cases per 100,000 people compared to 12.3 per 100,000 who did not have hepatitis B.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation, according to the U.S. Centers for Disease Control and Prevention. The various hepatitis viruses are not closely related -- the word hepatitis means inflammation of the liver.
An estimated 350 million people worldwide are infected with hepatitis B virus, which causes 340,000 cases of liver cancer a year and kills between 500,000 and 1.2 million people a year.
Researchers think both hepatitis B and C may cause lymphoma by overstimulating the immune system as it tries to fight off the liver infection.
(Reporting by Maggie Fox, editing by Alan Elsner)
Source
Tue Aug 3, 2010 6:37pm EDT
WASHINGTON (Reuters) - People infected with hepatitis B virus are around twice as likely to develop non-Hodgkin lymphoma, researchers reported on Tuesday.
Hepatitis B was already known to cause liver cancer and some scientists had suspected it might cause lymphoma, too. The study, published in Lancet Oncology, confirms this. Hepatitis C is also linked to lymphoma.
The blood cancer is not common and widespread vaccination against the viruses is unlikely to affect non-Hodgkin lymphoma rates much, the researchers noted. But it may be possible to treat the virus and help non-Hodgkin lymphoma patients, they said.
Dr. Eric Engels of the U.S. National Cancer Institute and Sun Ha Jee of Yonsei University in Seoul studied the records of more than 600,000 people in South Korea, where hepatitis B was extremely common before a vaccination campaign began in 1995.
Of these, 53,000 or about 9 percent had evidence of hepatitis B infection. After 14 years, rates of non-Hodgkin lymphoma were more common among the infected people -- 19.4 cases per 100,000 people compared to 12.3 per 100,000 who did not have hepatitis B.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation, according to the U.S. Centers for Disease Control and Prevention. The various hepatitis viruses are not closely related -- the word hepatitis means inflammation of the liver.
An estimated 350 million people worldwide are infected with hepatitis B virus, which causes 340,000 cases of liver cancer a year and kills between 500,000 and 1.2 million people a year.
Researchers think both hepatitis B and C may cause lymphoma by overstimulating the immune system as it tries to fight off the liver infection.
(Reporting by Maggie Fox, editing by Alan Elsner)
Source
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