Glycemic load in relation to hepatocellular carcinoma among patients with chronic hepatitis infection

BackgroundChronic infections with hepatitis B virus (HBV) and hepatitis C virus (HCV) are of paramount etiologic importance for hepatocellular carcinoma (HCC), but other factors are likely to be important. The association of diabetes mellitus and obesity with HCC raises the possibility that dietary glycemic load (GL) may interact with chronic hepatitis infection in the causation of HCC.Patients and methodsWe conducted a case–control study of 333 HCC patients and 360 controls in Athens, Greece. Third-generation assays were used to determine chronic HBV and HCV infection and information from a semiquantitative food frequency questionnaire to estimate dietary GL.ResultsAfter adjustment for possible confounding factors through multiple logistic regression, we found a nonsignificant positive association between GL and HCC, which was exclusively accounted for by a positive association between GL and HCC cases with chronic infection with hepatitis B and/or C. For the latter group of patients, the odds ratio at the highest compared with the lowest GL quintile was 1.95 (95% confidence interval 1.09–3.48). The association was strengthened after exclusion of subjects with diabetes.ConclusionOur results indicate that, among patients with chronic infection with HBV and/or HCV, reduction of dietary GL could reduce risk or delay development of HCC.     

The impact of obesity and diabetes mellitus on the risk of hepatocellular carcinoma

Background: Obesity has been associated to increased hepatocellularcarcinoma (HCC) risk, but studies on the topic do not fullyaccount for hepatitis B virus (HBV) and hepatitis C virus (HCV)infections. Likewise, an increased risk has been reported fordiabetes mellitus (DM) but whether DM is an independent riskfactor has not been established yet. To evaluate the associationof obesity and DM with HCC risk, we conducted a hospital-based,case–control study in two Italian areas. Patients and methods: From 1999 to 2003, 185 HCC cases and 404hospital controls were enrolled. Blood samples were obtainedfor HBV and HCV screening. Results: After allowance for known risk factors, body mass index30 kg/m² [odds ratio (OR) = 1.9, 95% confidence interval (CI)0.9–3.9] and DM (OR = 3.7, 95% CI 1.7–8.4) wereassociated to HCC risk. These associations persisted (OR = 3.5,95% CI 1.6–7.7 for obesity; OR = 3.5, 95% CI 1.3–9.2for DM) among subjects without HBV and/or HCV infection. Overall,23% of HCC cases seemed attributable to these conditions, andthis figure rose to 37% among subjects without HBV and/or HCVinfections. Conclusions: The present study provides further evidence thatobesity and DM increase HCC risk and that these factors mayexplain a relevant proportion of cases among subjects withoutmarkers of HBV/HCV infection. Key words: attributable risk, diabetes mellitus, HBV, HCV, hepatocellular carcinoma, obesity Received for publication April 29, 2008. Accepted for publication July 18, 2008.     

Consumption of fish and meats and risk of hepatocellular carcinoma: the European Prospective Investigation into Cancer and Nutrition (EPIC)

BackgroundWhile higher intake of fish and lower consumption of red/processed meats have been suggested to play a protective role in the etiology of several cancers, prospective evidence for hepatocellular carcinoma (HCC) is limited, particularly in Western European populations.MethodsThe associations of fish and meats with HCC risk were analyzed in the EPIC cohort. Between 1992 and 2010, 191 incident HCC were identified among 477 206 participants. Baseline diet was assessed using validated dietary questionnaires. A single 24-h diet recall from a cohort subsample was used for calibration. Multivariable proportional hazard regression was utilized to estimate hazard ratios (HR) and 95% confidence intervals (CI). In a nested case–control subset (HCC = 122), HBV/HCV status and liver function biomarkers were measured.ResultsHCC risk was inversely associated with intake of total fish (per 20 g/day increase, HR = 0.83, 95% CI 0.74–0.95 and HR = 0.80, 95% CI 0.69–0.97 before and after calibration, respectively). This inverse association was also suggested after adjusting for HBV/HCV status and liver function score (per 20-g/day increase, RR = 0.86, 95% CI 0.66–1.11 and RR = 0.74, 95% CI 0.50–1.09, respectively) in a nested case–control subset. Intakes of total meats or subgroups of red/processed meats, and poultry were not associated with HCC risk.ConclusionsIn this large European cohort, total fish intake is associated with lower HCC risk.     

Glycemic index,glycemic load,dietary carbohydrate,and dietary fiber intake and risk of liver and biliary tract cancers in Western Europeans

BackgroundThe type and quantity of dietary carbohydrate as quantified by glycemic index (GI) and glycemic load (GL), and dietary fiber may influence the risk of liver and biliary tract cancers, but convincing evidence is lacking.Patients and methodsThe association between dietary GI/GL and carbohydrate intake with hepatocellular carcinoma (HCC; N = 191), intrahepatic bile duct (IBD; N = 66), and biliary tract (N = 236) cancer risk was investigated in 477 206 participants of the European Prospective Investigation into Cancer and Nutrition cohort. Dietary intake was assessed by country-specific, validated dietary questionnaires. Hazard ratios and 95% confidence intervals were estimated from proportional hazard models. HBV/HCV status was measured in a nested case–control subset.ResultsHigher dietary GI, GL, or increased intake of total carbohydrate was not associated with liver or biliary tract cancer risk. For HCC, divergent risk estimates were observed for total sugar = 1.43 (1.17–1.74) per 50 g/day, total starch = 0.70 (0.55–0.90) per 50 g/day, and total dietary fiber = 0.70 (0.52–0.93) per 10 g/day. The findings for dietary fiber were confirmed among HBV/HCV-free participants [0.48 (0.23–1.01)]. Similar associations were observed for IBD [dietary fiber = 0.59 (0.37–0.99) per 10 g/day], but not biliary tract cancer.ConclusionsFindings suggest that higher consumption of dietary fiber and lower consumption of total sugars are associated with lower HCC risk. In addition, high dietary fiber intake could be associated with lower IBD cancer risk.     

Hepatitis B and C Viruses Infection, Lifestyle and Genetic Polymorphisms as Risk Factors for Hepatocellular Carcinoma in Haimen, China

A case‐control study was carried out to investigate the impact of factors including virus infection, aflatoxin B1, microcystins, smoking/drinking and dietary habits as well as genetic polymorphisms of aldehyde dehydrogenase 2 (ALDH2) and cytochrome P4502E1 (CYP2E1), on susceptibility to hepatocellular carcinoma (HCC) in Haimen, China. A total of 248 patients with HCC and 248 sex‐, age‐ and residence‐matched population‐based controls were recruited into the study. Virus infection, and ALDH2 and CYP2E1 gene polymorphisms were assessed in 134 paired cases and controls. By univariate analysis, hepatitis B virus (HBV) infection (odds ratio [OR]=9.75; 95% confidence interval [CI] =4.71–20.2), history of intravenous injection (OR=1.50; 95%CI=1.02–2.22), average income (OR=0.63; 95% CI=0.43–0.92), frequent intake of foods rich in protein, e.g., egg (OR=0.6; 95% CI=0.42–0.87), chicken (OR=0.53; 95% CI=0.35–0.79), pork (OR=0.67; 95% CI=0.46–0.98) and fresh fish (OR=0.58; 95% CI=0.39–0.87) significantly differed between cases and controls. However, peanut intake (OR=0.66; 95% CI=0.43–1.01), source of drinking water, including tap (OR=1.33; 95% CI=0.81–2.20), deep well (OR=0.94; 95% CI=0.56–1.55), shallow well (OR=0.85; 95% CI=0.55‐–1.30), river (OR=0.95; 95% CI=0.65–1.38), ditch (OR=1.09; 95% CI=0.76–1.55) and pond water (OR=1.0; 95% CI=0.14–7.10) were not significantly associated with risk. Univariate analysis also indicated that the 1–1 genotype of ALDH2 (OR=1.38; 95% CI=0.86–2.23) as well as the Pst1‐ and Rsa1‐digested c1/c1 genotype of CYP2E1 (OR=1.36; 95% CI=0.81–2.28), was slightly more frequent in the case group. On multivariate analysis, HBV infection (OR=13.9; 95% CI=5.78–33.6) and history of intravenous injection (OR=2.72; 95% CI=1.24–6.00) were still associated with significantly increased risk of HCC, while frequent intake of fresh fish (OR=0.32; 95% CI=0.12–0.86) decreased this risk. These findings suggest that whereas peanut intake, water sources as well as genetic polymorphisms in ALDH2 and CYP2E1 do not significantly correlate with the risk of HCC, HBV infection is a main risk factor, and dietary items rich in protein, especially fresh fish, might protect against the risk of HCC in Haimen, China.     

Risk Profile of Hepatocellular Carcinoma Reveals Dichotomy among US Veterans

Background

Hepatocellular carcinoma (HCC) is traditionally associated with chronic liver injury resulting from hepatitis B virus (HBV) and hepatitis C virus (HCV) infection or excessive consumption of alcohol. In addition, recent evidence links HCC to diabetes.

Aims

Since these risk factors are prevalent among US veterans, we analyzedcontribution of various etiologies toHCC incidence in this population.

Methods

Clinicopathological correlates of 150 male US veterans diagnosed with HCC between 2001 and 2010 were analyzed and compared to frequency-matched (2:1) non-cancer controls in a single center.

Results

HCC was associated with cirrhosis (odds ratio [OR], 250.84; 95 % confidence interval [CI], 86.92–723.88; p?<?0.0001), chronic hepatitis B (OR, 34.30 95 % CI, 1.97–598.47; p?=?0.015), chronic hepatitis C (OR, 6.84; 95 % CI, 3.89–12.04; p?<?0.0001), alcohol use (OR, 6.76; 95 % CI, 4.35–10.52; p?<?0.0001), and smoking (OR, 1.83; 95 % CI, 1.23–2.89; p?=?0.009), but surprisingly not with diabetes. Only in a subgroup of HCC patients with no “traditional” risk factors did diabetes become a strong independent predictor of HCC when compared to HCC patients with at least one such risk factor (OR, 10.69; 95 % CI, 1.88–60.63, p?=?0.007). This subgroup was further distinguished by older age, increased prevalence of hypertension, nonsmoking, and a trend to develop noncirrhotic HCC.

Conclusions

While HCC in US veterans is overwhelmingly linked to cirrhosis due to “traditional” risk factors, it also occurs with a separate clinical profile characterized by diabetes and no evidence of cirrhosis, suggesting distinct mechanisms of hepatocarcinogenesis and needs for surveillance.     

Hepatitis C virus genotype 1b increases cumulative lifetime risk of hepatocellular carcinoma

The association between subtypes of hepatitis C virus (HCV) and risk of hepatocellular carcinoma (HCC) remained inconclusive and evaluated in both case–control and cohort studies. In the case–control study, 397 HCC cases from medical centers were compared with 410 community‐based non‐HCC controls. All of them were anti‐HCV‐seropositive, HBsAg‐seronegative with serum HCV RNA levels ≥1,000 IU/mL. Logistic regression models were used to estimate the odds ratio (OR) with 95% confidence interval (95% CI) of HCV subtype after controlling for other HCC risk factors. In the cohort study, 866 anti‐HCV‐seropositive individuals were followed from 1991 to 2008 to assess the long‐term HCC predictability of HCV subtypes. Newly developed HCC cases were ascertained by follow‐up health examinations and computerized linkage with national databases. The percentage of HCV 1b subtype was higher among HCC cases than controls (64 vs. 55%, p < 0.001). Participant infected with HCV 1b had a higher mean serum HCV RNA level (2.0 × 10⁶ IU/mL) than those infected with HCV non‐1b (1.2 × 10⁶ IU/mL, p < 0.001). The multivariate‐adjusted OR (95% CI) of developing HCC for HCV 1b comparing to non‐1b was 1.43 (1.02–2.02). After the long‐term follow‐up, the cumulative lifetime (30–80 years old) HCC risk was 19.2 and 29.7% for patients infected with HCV non‐1b and 1b, respectively (p < 0.001). The multivariate‐adjusted hazard ratio (95% CI) was 1.85 (1.06–3.22) for HCV 1b compared to non‐1b. HCV subtype 1b, the most prevalent subtype in Taiwan, was associated with an increased HCC risk and a proactive clinical management is suggested for patients with HCV 1b.     

Case-control study on hepatitis C virus (HCV) as a risk factor for hepatocellular carcinoma: the role of HCV genotypes and the synergism with hepatitis B virus and alcohol. Brescia HCC Study.

We performed a case-control study to evaluate the risk of hepatocellular carcinoma (HCC) for hepatitis C virus (HCV) infection. A total of 305 newly diagnosed HCC cases (80% males) and 610 subjects (81% males) unaffected by clinically evident hepatic disease admitted to the 2 main hospitals in Brescia, North Italy, were recruited as cases and controls, respectively. Among the 122 HCC cases positive for HCV RNA, genotype 1b was found in 83 patients (68%), genotype 2 in 36 (29.5%) and genotype 1a in 3 (2.5%). Among the controls, 15 were infected with genotype 1b and 15 with type 2. Analysis of HCV envelope 1 nucleotide sequence among 25 cases and 8 controls infected with genotype 2 showed subtype 2c in 96% of cases and in all controls, and subtype 2a in 1 HCC case. The odds ratio (OR) for HCV RNA positivity adjusted for hepatitis B virus (HBV) markers and alcohol intake was 26.3 [95% confidence interval (CI): 15.8-44], and it was higher for genotype 1b (OR = 34.2) than type 2 (OR = 14.4). The OR for HCV RNA was 35.6 (95% CI: 14.5-87.1) when the HBV markers were all negative and 132 (15.3-890) when HBsAg positivity was present; the OR was 26.1 (95% CI: 12.6-54.0) among subjects with alcohol intake of 0-40 g/day and increased to 62.6 (23.3-168) and 126 (42.8-373) with an alcohol intake of 41-80 and >80 g/day, respectively. In conclusion, synergism was found between HCV infection and HBV infection and alcohol intake in causing HCC.     

A meta-analysis of epidemiological studies on the combined effect of hepatitis B and C virus infections in causing hepatocellular carcinoma

The aim of the study was to assess whether co-infection by hepatitis-B virus (HBV) and hepatitis-C virus (HCV) is associated with a higher risk of developing hepatocellular carcinoma (HCC) than each infection alone. A meta-analysis of data published up to June 1997 was performed. HBsAg and anti-HCV antibodies or HCV RNA (anti-HCV/HCV RNA) were considered as serological markers of current HBV and HCV infection respectively. A total of 32 case-control studies were suitable for a quantitative overview. The summary odds ratios (OR) were 13.7 for HBsAg positivity and 11.5 for anti-HCV/HCV RNA positivity. The OR for anti-HCV was lower among studies using second- or third-generation anti-HCV or HCV RNA (OR, 8.2) with respect to studies with first-generation anti-HCV test (OR, 19.1). When combining data from the studies with second- or third-generation anti-HCV or HCV RNA, the OR for HBsAg positivity and anti-HCV/HCV RNA negativity was 22.5 (95% confidence interval (CI), 19.5–26.0), the OR for anti-HCV/HCV RNA positivity and HBsAg negativity was 17.3 (95% CI, 13.9–21.6), and the OR for both markers positivity was 165 (95% CI: 81.2–374, based on 191 cases and 8 controls exposed). A synergism was found between HBV and HCV infections, the OR for co-infection being greater than the sum and lower than the product of those for each infection alone. The interaction was therefore negative according to the multiplicative model, providing epidemiological evidence both of an independent effect and of interference between the 2 viruses in the carcinogenic process. Int. J. Cancer 75:347–354, 1998. © 1998 Wiley-Liss, Inc.     

Etiology of hepatocellular carcinoma in West Africa,a case–control study

Hepatocellular carcinoma (HCC) is a leading cause of cancer in West Africa where HBV infection is endemic. However, limited information is available on other risk factors such as alcohol use, HCV and HIV infection. A case–control study was conducted in referral hospitals of Abidjan (Cote d'Ivoire), Bamako (Mali) and Lome (Togo). Cases were matched with controls on age, gender and participating site. The diagnosis of HCC relied on the combination of one or more space‐occupying lesions suggestive of an HCC on a standardized abdominal ultrasound and an α‐fetoprotein level ≥400 ng/ml. HIV, HBV and HCV serology were performed. Hazardous alcohol use was assessed using the AUDIT questionnaire. A conditional logistic regression model was used to measure odds ratio (OR) with their 95% confidence intervals (CI). A total of 160 cases and 320 controls were included. Cases were predominantly men (80.0%) with a median age of 47 years (IQR 38–57). Hazardous alcohol use (OR = 4.5 [CI 1.1–18.5]), HBV infection (OR = 62.5 [CI 20.5–190.7]) and HCV infection OR = 35.9 [CI 10.0–130.3]) were independently associated with HCC. Combining the effect of HBV infection and alcohol, HBV‐infected hazardous drinkers had an OR = 149.8 (CI 13.5–1 667.0), HBV mono‐infected had an OR = 57.4 (CI 18.8–175.3) (ref: HBV‐negative). Aside the independent association of alcohol use and HBV and HCV infection with HCC, a synergic effect between alcohol use and HBV infection was identified. Timely screening and care of HBV infection and hazardous drinking might prevent a significant number of HCC in West Africa.     

Carbohydrate intake,glycemic load,glycemic index,and risk of ovarian cancer

BackgroundOur objective was to determine the relationship between dietary glycemic load (GL), glycemic index (GI), carbohydrate intake, and ovarian cancer risk in a population-based case–control study.Patients and methodsA self-administered questionnaire was used to collect data on demographic and lifestyle factors, and a food frequency questionnaire was used to collect dietary information from 1366 women with ovarian cancer and 1414 population controls.ResultsGL was positively associated with ovarian cancer. The adjusted odds ratio (OR) for the highest versus the lowest quartile of intake was 1.24 [95% confidence interval (CI) 1.00–1.55, P for trend = 0.03]. Fiber intake was inversely associated with risk. The OR comparing women in the highest fiber-intake group with those in the lowest was 0.78 (95% CI 0.62–0.98, P for trend = 0.11). We found no association between GI, carbohydrate intake, and ovarian cancer. In analyses stratified by body mass index, the risk estimates for GL, carbohydrate, and sugar were higher among overweight/obese women; however, the interaction term was only significant for sugar (P for interaction = 0.004).ConclusionsOur results suggest that diets with a high GL may increase the risk of ovarian cancer, particularly among overweight/obese women, and a high intake of fiber may provide modest protection.     

Population attributable risk of aflatoxin-related liver cancer: Systematic review and meta-analysis

BackgroundOver 4 billion people worldwide are exposed to dietary aflatoxins, which cause liver cancer (hepatocellular carcinoma, HCC) in humans. However, the population attributable risk (PAR) of aflatoxin-related HCC remains unclear.MethodsIn our systematic review and meta-analysis of epidemiological studies, summary odds ratios (ORs) of aflatoxin-related HCC with 95% confidence intervals were calculated in HBV+ and HBV− individuals, as well as the general population. We calculated the PAR of aflatoxin-related HCC for each study as well as the combined studies, accounting for HBV status.ResultsSeventeen studies with 1680 HCC cases and 3052 controls were identified from 479 articles. All eligible studies were conducted in China, Taiwan, or sub-Saharan Africa. The PAR of aflatoxin-related HCC was estimated at 17% (14–19%) overall, and higher in HBV+ (21%) than HBV− (8.8%) populations. If the one study that contributed most to heterogeneity in the analysis is excluded, the summarised OR of HCC with 95% CI is 73.0 (36.0–148.3) from the combined effects of aflatoxin and HBV, 11.3 (6.75–18.9) from HBV only and 6.37 (3.74–10.86) from aflatoxin only. The PAR of aflatoxin-related HCC increases to 23% (21–24%). The PAR has decreased over time in certain Taiwanese and Chinese populations.ConclusionsIn high exposure areas, aflatoxin multiplicatively interacts with HBV to induce HCC; reducing aflatoxin exposure to non-detectable levels could reduce HCC cases in high-risk areas by about 23%. The decreasing PAR of aflatoxin-related HCC reflects the benefits of public health interventions to reduce aflatoxin and HBV.     

miR-146a G > C polymorphisms and risk of hepatocellular carcinoma in a Chinese population

MicroRNAs (miRNAs) are thought to have a role in cancer development. We investigated the association among miR-146a G?>?C genetic variations, hepatitis B (HBV), and C (HCV) infection, and risk of hepatocellular carcinoma (HCC). Unconditional logistical regression analysis suggested that the miR-146a GG genotype and G allele carried a 2.10- (95 % confidence interval (CI)?=?1.03–4.37) and 1.42-fold (95 % CI?=?1.07–1.92) increased HCC risk, respectively. HBV-positive subjects carrying the miR-146a GG genotype (odds ratio (OR)?=?2.95, 95 % CI?=?1.31–6.81) and G allele (OR?=?1.65, 95 % CI?=?1.15–2.58) had an increased risk of HCC. However, the miR-146a GG genotype and G allele did not carry a significantly enhanced risk of HCC in either hepatitis-negative or HCV-infected subjects. miR-146a G?>?C polymorphisms appear to influence susceptibility to HCC, especially in HBV-infected patients.     

Relationship of hepatocellular carcinoma to soya food consumption: a cohort-based, case-control study in Japan

To determine if the risk of hepatocellular carcinoma (HCC) is reduced by consumption of soya foods, we conducted a case-control study within a cohort of Japanese A-bomb survivors. We compared the prediagnosis consumption of isoflavone-rich miso soup and tofu to HCC risk, adjusting for hepatitis B (HBV) and C (HCV) viral infections, the major HCC risk factors in this population. The study included 176 pathologist-confirmed cases of HCC diagnosed in 1964-1988 and 560 controls who died of diseases other than liver cancer. We examined dietary information collected at least 2 years before diagnosis or death and tissue-based measures of viral hepatitis. Using logistic regression, crude ORs were 0.5 (95% CI 0.29-0.95) and 0.5 (95% CI 0.20-0.99) for high vs. low miso soup and tofu intake, respectively. Adjusting for year of birth, sex, HBV, HCV and other factors, the OR for miso soup was unchanged at 0.5 (95% CI 0.14-1.55), and miso results were similar when ORs were recalculated separately for earlier and later birth cohorts to assess consistency of results. The adjusted OR for tofu was 0.9 (95% CI 0.20-3.51). We also found a statistically significant (p < 0.0001) interaction between sex and HCV, with risk of HCC being substantially higher for women. We conclude that consumption of miso soup and other soya foods may reduce HCC risk.     

A meta-analysis of case-control studies on the combined effect of hepatitis B and C virus infections in causing hepatocellular carcinoma in China

We investigated whether concurrent infection by hepatitis B virus (HBV) and hepatitis C virus (HCV) in China, a hyperepidemic area for these infections, was associated with a higher risk of causing hepatocellular carcinoma (HCC) than each infection alone in a meta-analysis in China, 32 case-control studies involving 3201 cases and 4005 controls, identified from a computer-based literature search from 1966 to 2004. The pooled odds ratio and 95% confidence interval (CI) for HBsAg positivity was 14.1 (95% CI: 10.6-18.8); for anti-HCV/HCV RNA positivity was 4.6 (95% CI: 3.6-5.9); for HBsAg positivity and anti-HCV/HCV RNA negativity were 15.6 (95% CI: 11.5-21.3); for HBsAg negativity and anti-HCV/HCV RNA positivity were 8.1 (95% CI: 5.0-13.0); and positivity for both HBsAg and anti-HCV/HCV RNA was 35.7 (95% CI: 26.2-48.5). We conclude that HBV and HCV infections are important independent risk factors for HCC in China, and that dual infection by HBV and HCV is associated with a higher risk of causing HCC than each infection alone, suggesting a synergism between HBV and HCV.     

Synergism of alcohol, diabetes, and viral hepatitis on the risk of hepatocellular carcinoma in blacks and whites in the U.S

BACKGROUND: Heavy alcohol consumption, viral hepatitis, and diabetes are risk factors for hepatocellular carcinoma (HCC). However, to the authors' knowledge, the information concerning their interaction effect in patients with risk of HCC is sparse. METHODS: A population-based, case-control study of HCC was conducted during 1984-2002. The study involved 295 HCC cases and 435 age-, gender-, and race-matched control subjects among Hispanic and non-Hispanic whites and blacks in Los Angeles County, California. Lifestyle risk factors were ascertained through in-person interviews. Infections with the hepatitis B and C (HCV) viruses were determined using their serologic markers. RESULTS: Fourteen HCC cases but no control subjects tested positive for the hepatitis B surface antigen. Seropositivity for antibodies to HCV was associated with an odds ratio (OR) of 125 (95% confidence interval [95% CI], 17-909) for HCC, whereas seropositivity for antibodies to the hepatitis B core antigen was related to an OR of 2.9 (95% CI, 1.7-5.0). Heavy alcohol consumption and cigarette smoking were found to be independently associated with a statistically significant two to threefold increase in risk of HCC after adjustment for hepatitis B and C serology. Subjects with a history of diabetes had an OR of 2.7 (95% CI, 1.6-4.3) for HCC compared with nondiabetic subjects. A synergistic interaction on HCC risk was observed between heavy alcohol consumption and diabetes (OR = 4.2; 95% CI, 2.6-5.8), heavy alcohol consumption and viral hepatitis (OR = 5.5; 95% CI, 3.9-7.0), or between diabetes and viral hepatitis (OR = 4.8; 95% CI, 2.7-6.9). CONCLUSIONS: Heavy alcohol consumption, diabetes, and viral hepatitis were found to exert independent and synergistic effects on risk of HCC in U.S. blacks and whites.     

Diabetes mellitus and postoperative blood glucose value help predict posthepatectomy liver failure in patients with hepatocellular carcinoma

BackgroundMany complications after hepatectomy can lead to perioperative death, among which posthepatectomy liver failure (PHLF) is the leading one. Existing studies suggest that one of the most important risk factors for PHLF is cirrhosis. Hepatitis B virus (HBV) infection is an important factor in the occurrence of cirrhosis, and the exact relationship between HBV infection and PHLF is not obvious. Diabetes mellitus and postoperative blood glucose are closely associated with liver regeneration, but its exact relationship with PHLF remains unclear.MethodsWe collected clinical indicators from 920 adult patients treated at the Liver Surgery and Transplantation Center of West China Hospital of Sichuan University from April 2009 and April 2019. We conducted a univariate analysis find out the risk factors of PHLF, follow by a multivariate analysis to ascertain the independent risk factors. Receiver operating characteristic (ROC) curves were plotted to evaluate the predictive efficiency of each risk factor.ResultsFollowing hepatectomy, 205 (22.2%) of patients were diagnosed with PHLF. Several variables were confirmed to related with PHLF significantly: diabetes [P<0.01, odds ratio (OR) =10.845, 95% confidence interval (CI): 5.450–21.579], HBV (P<0.01, OR =0.345, 95% CI: 0.187–0.635), blood glucose on the first postoperative day (post-BG1) (P=0.027, OR =1.059, 95% CI: 1.006–1.115), blood glucose on the third postoperative day (post-BG3) (P=0.021, OR =1.085, 95% CI: 1.012–1.162), blood glucose on the fifth postoperative day (post-BG5) (P=0.014, OR =1.119, 95% CI: 1.023–1.225), postoperative total bilirubin (post-TB) (P<0.01, OR =1.160, 95% CI: 1.133–1.187), and liver cirrhosis (P<0.01, OR =0.982, 95% CI: 0.561–1.717) identified to be independent risk factors of PHLF.ConclusionsDiabetes, HBV, post-BG1, post-BG3, and post-BG5 are related to the development of PHLF, and diabetes and post-BG can be used as predictors of the development of PHLF in patients with hepatocellular carcinoma (HCC).     

Hepatitis C Virus (HCV) genotypes distribution among hepatocellular carcinoma patients in Southern Italy: a three year retrospective study

Background

Hepatocellular carcinoma (HCC) is one of the major cause for cancer in the world. Aim of this case-control study was to investigate the distribution pattern of HCV genotypes among HCC patients and suggest whether infection with specific subtypes may be associated with an increased risk of progression to cancer.

Methods

152 HCC anti-HCV positive patients, fulfilling the criteria from the Barcelona 2000 EASL conference, and 568 patients HCV chronically infected but without HCC as control group were included in the study. Serum of each patient was evaluated for viral load estimation and genotyping.

Results

Males with HCC significantly showed to have quite 2 times higher risk of exposure to HCV infection (OR?=?1.72; 95% CI?=?1.15–2.58). Moreover, HCC was significantly associated with older age. In fact, > 50 years older patients showed to have a higher risk of developing HCC (OR?=?17.4; 95% CI?=?4.24 to 71.36) compared to younger patients.HCV RNA rate was significantly higher (83.7%) among HCC patients than in the control group (61.4%, p?<?0.001) and the most prevalent genotype was 1b (68.0% in HCC vs 54.4% in the control group, p?<?0.005). HCC patients significantly have a risk of exposure to HCV 1b infection almost 2 times greater than the control group (OR?=?1.8; 95% CI?=?1.11–2.82). The multivariate-adjusted OR (95% CI) of developing HCC for HCV 1b comparing to non-1b was 1.65 (1.16–2.33).

Conclusions

Our study detected a significantly higher rate of HCV RNA positivity and a higher rate of HCV 1b infection in HCC patients, suggesting the strict association between subtype 1b infection and HCC. A prospective study with larger number of samples would be needed to confirm our results.

     

Association of diabetes duration and diabetes treatment with the risk of hepatocellular carcinoma

BACKGROUND:

Despite the observed association between diabetes mellitus and hepatocellular carcinoma (HCC), little is known about the effect of diabetes duration before HCC diagnosis and whether some diabetes medications reduced the risk of HCC development. This objective of the current study was to determine the association between HCC risk and diabetes duration and type of diabetes treatment.

METHODS:

A total of 420 patients with HCC and 1104 healthy controls were enrolled in an ongoing hospital‐based case‐control study. Multivariate logistic regression models were used to adjust for HCC risk factors.

RESULTS:

The prevalence of diabetes mellitus was 33.3% in patients with HCC and 10.4% in the control group, yielding an adjusted odds ratio (AOR) of 4.2 (95% confidence interval [95% CI], 3.0‐5.9). In 87% of cases, diabetes was present before the diagnosis of HCC, yielding an AOR of 4.4 (95% CI, 3.0‐6.3). Compared with patients with a diabetes duration of 2 to 5 years, the estimated AORs for those with a diabetes duration of 6 to 10 years and those with a diabetes duration >10 years were 1.8 (95% CI, 0.8‐4.1) and 2.2 (95% CI, 1.2‐4.8), respectively. With respect to diabetes treatment, the AORs were 0.3 (95% CI, 0.2‐0.6), 0.3 (95% CI, 0.1‐0.7), 7.1 (95% CI, 2.9‐16.9), 1.9 (95% CI, 0.8‐4.6), and 7.8 (95% CI, 1.5‐40.0) for those treated with biguanides, thiazolidinediones, sulfonylureas, insulin, and dietary control, respectively.

CONCLUSIONS:

Diabetes appears to increase the risk of HCC, and such risk is correlated with a long duration of diabetes. Relying on dietary control and treatment with sulfonylureas or insulin were found to confer the highest magnitude of HCC risk, whereas treatment with biguanides or thiazolidinediones was associated with a 70% HCC risk reduction among diabetics. Cancer 2010. © 2010 American Cancer Society.     

Hepatitis C virus and non-Hodgkin's lymphoma: Findings from the Swiss HIV Cohort Study

Infections with hepatitis C virus (HCV) and, possibly, hepatitis B virus (HBV) are associated with an increased risk of non-Hodgkin's lymphoma (NHL) in the general population, but little information is available on the relationship between hepatitis viruses and NHL among people with HIV (PHIV). We conducted a matched case-control study nested in the Swiss HIV Cohort Study (SHCS). Two hundred and ninety-eight NHL cases and 889 control subjects were matched by SHCS centre, gender, age group, CD4+ count at enrollment, and length of follow-up. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were computed using logistic regression to evaluate the association between NHL and seropositivity for antibodies against HCV (anti-HCV) and hepatitis B core antigen (anti-HBc), and for hepatitis B surface antigen (HBsAg). Anti-HCV was not associated with increased NHL risk overall (OR = 1.05; 95% CI: 0.63-1.75), or in different strata of CD4+ count, age or gender. Only among men having sex with men was an association with anti-HCV found (OR = 2.37; 95% CI: 1.03-5.43). No relationships between NHL risk and anti-HBc or HBsAg emerged. Coinfection with HIV and HCV or HBV did not increase NHL risk compared to HIV alone in the SHCS.