Non‐Hodgkin's lymphoma and hepatitis C virus: A case‐control study from northern and southern Italy

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105

Nutritional status is known to alter immune function, a suspected risk factor for non-Hodgkin lymphoma (NHL). To investigate whether long-term over, or under, nutrition is associated with NHL, self-reported anthropometric data on weight and height from over 10,000 cases of NHL and 16,000 controls were pooled across 18 case-control studies identified through the International Lymphoma Epidemiology Consortium. Study-specific odds ratios (OR) were estimated using logistic regression and combined using a random-effects model. Severe obesity, defined as BMI of 40 kg m 22 or more, was not associated with NHL overall (pooled OR 5 1.00, 95% confidence interval (CI) 0.70-1.41) or the majority of NHL subtypes. An excess was however observed for diffuse large B-cell lymphoma (pooled OR 5 1.80, 95% CI 1.24-2.62), although not all study-specific ORs were raised.Among the overweight (BMI 25-29.9 kg m 22 ) and obese (BMI 30-39.9 kg m 22 ), associations were elevated in some studies and decreased in others, while no association was observed among the underweight (BMI < 18.5 kg m 22 ). There was little suggestion of increasing ORs for NHL or its subtypes with every 5 kg m 22 rise in BMI above 18.5 kg m 22 . BMI components height and weight were also examined, and the tallest men, but not women, were at marginally increased risk (pooled OR 5 1.19, 95% CI 1.06-1.34). In summary, whilst we conclude that there is no evidence to support the hypothesis that obesity is a determinant of all types of NHL combined, the association between severe obesity and diffuse large B-cell lymphoma may warrant further investigation.

Section: Methodsmentioning

confidence: 99%

Non‐Hodgkin lymphoma and obesity: A pooled analysis from the InterLymph Consortium

Willett

Morton

Hartge

et al. 2008

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105

Section: Methodsmentioning

confidence: 99%

“…Controls were more often females and were younger than HCC cases as matching was conducted according to the distribution by age and gender of cancer cases in the entire study, which also included lymphomas. 23,24 All study participants signed an informed consent form, in agreement with the requirements of the Ethical Committee of the Aviano National Cancer Institute, approving the study.…”

Section: Methodsmentioning

confidence: 99%

Coffee and tea consumption and risk of hepatocellular carcinoma in Italy

Montella

Polesel

Vecchia

et al. 2007

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The role of coffee in the aetiology of hepatocellular carcinoma has raised great interest. In Italy, coffee consumption is high, thus allowing the investigation of the topic over a broad range of consumption. A hospital-based case-control study was conducted in Italy in [1999][2000][2001][2002], including 185 incidents, histologically confirmed cases of hepatocellular carcinoma aged 43-84 years. Controls were 412 subjects admitted to the same hospitals' networks for acute, non-neoplastic diseases unrelated to diet. Coffee and tea consumption were assessed using a validated food-frequency questionnaire. Odds ratios (ORs) and corresponding the 95% confidence intervals (CI) were computed using unconditional multiple logistic regression, adjusting for hepatitis viruses seropositivity, alcohol intake, smoking habits and other potential confounding factors. Compared to people who drunk <14 cups/week of coffee, the risk of hepatocellular carcinoma decreased for increasing levels of consumption (OR 5 0.4, 95% CI: 0.2-1.1 for 28 cups/week, p for trend 5 0.02). In the present study, inverse relations were observed across strata of hepatitis C and B virus infections and alcohol drinking. No significant association emerged with consumption of decaffeinated coffee (OR 5 0.7, 95% CI 5 0.2-2.5) or tea (OR 5 1.4, 95% CI 5 0.8-2.7). The present study supports the hypothesis of a favourable effect of coffee, though not decaffeinated coffee and tea, on the risk on hepatocellular carcinoma. ' 2006 Wiley-Liss, Inc.Key words: coffee; tea; hepatocellular carcinoma; case-control study Hepatocellular carcinoma (HCC) is a highly fatal cancer that, in Italy, accounts for 3.4% of all newly diagnosed cancers among men and for 1.9% among women. 1 Likewise, the burden of HCC on total cancer mortality was 4.4% among men and 2.7% among women. 2 Incidence and mortality have shown upward trends in most of the developed countries, 3-5 including Italy. 3 The major known risk factors are persistent infections with hepatitis C virus (HCV) and hepatitis B virus (HBV), 6 but other prevalent medical conditions (i.e., liver cirrhosis) or socio-demographic factors, such as alcohol drinking and tobacco smoking, may play an important role in HCC onset. 6,7 Several studies from Europe, Japan, and United States reported an inverse relation between coffee consumption, g-glutamyltransferase (GGT) 8-10 and alanine aminotransferase (ALT) 10,11 levels, which are markers of liver injuries. Recently, increasing evidence has emerged on the relation between coffee drinking and risk of cirrhosis 12-14 and HCC. [15][16][17][18] A consistent inverse association with coffee consumption against HCC was found in cohort 15,[17][18][19] and case-control studies. 16,20,21 A few studies have investigated tea consumption in relation to HCC incidence and mortality, 14,15,19,22 and their results were inconclusive.Italy ranked among the top European countries according to annual pro-capite consumption of coffee (about 6 kg) (www.ico.org). The present paper, based on a case-control ...

“…[23][24][25][26][27] However, the interaction between tobacco smoking and HCVinfection remains an open issue.…”

mentioning

confidence: 99%

Smoking and non‐Hodgkin lymphoma: Case‐control study in Italy

Talamini

Polesel

Montella

et al. 2005

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Tobacco smoking is a well-documented risk factor for several cancers, but the role of cigarette smoking in the etiology of non-Hodgkin lymphoma (NHL) is inadequately understood. Hepatitis C virus (HCV) has been associated with NHL, but the interaction between HCV and smoking habits has not yet been studied. Between 1999 and 2002, we conducted a case-control study on the association of HCV, smoking habits and NHL in 2 areas of northern and southern Italy. Cases were 225 consecutive patients (median age, 59 years) with a new diagnosis of NHL that were admitted to reference and general hospitals. Controls were 504 patients (median age, 63 years) admitted to the same hospitals as cases, for a wide spectrum of acute, nonneoplastic, nonimmune-, nor tobacco-related conditions. Current, heavy smokers (!20 cigarettes/day) had an odds ratio (OR) of NHL of 2.10 (95% confidence interval, CI: 1.07-4.12) compared to never smokers. The association between smoking and NHL was consistent across strata of sex and age. Compared to never smokers, current smokers of !20 cigarettes/day had ORs of 1.14 (95% CI: 0.37-3.56) for B-cell-low-grade, 2.10 (95% CI: 0.94-4.67) for B-cell-intermediate and high-grade, and 25.84 (95% CI: 1.95-342.17) for T-cell NHL. The effect of tobacco smoking and HCV were independent on the relative risk, leading a 4-fold elevated risk in current smokers HCV positive subjects. Tobacco smoking and hepatitis C virus (HCV) have been associated to non-Hodgkin lymphoma (NHL), but the interaction between HCV and smoking habits has not yet been studied. Our study confirms that tobacco is related to NHL, and reports on the combined effect of tobacco smoking and HCV. Infection acted together according to a multiplicative model, leading to a 4-fold elevated risk in current smokers HCV positive subjects. ' 2005 Wiley-Liss, Inc.