Cigarette smoking and colorectal cancer: long-term, subsite-specific risks in a cohort study of postmenopausal women.

BACKGROUND & AIMS: Cigarette smoking is a putative risk factor for colorectal cancer (CRC). However, long-term CRC risk estimates among female smokers remain limited and inconsistent. The goal of this prospective study was to assess cigarette smoking and CRC risk, overall and by anatomic subsite, among postmenopausal women. METHODS: Data were drawn from a large population-based cohort (n = 41836) of randomly selected women, age 55-69 years at baseline (Iowa Women's Health Study). Cigarette smoking and other CRC risk factors were characterized at baseline (1986). Incident (n = 869) and fatal (n = 249) CRC cases were identified through December 31, 1999. CRC risks were estimated using Cox proportional hazards regression models. RESULTS: Compared with never smokers, ever smokers had slightly increased risks for both incident (relative risk [RR], 1.17; 95% confidence interval [CI], 1.00-1.36) and fatal (RR, 1.31; 95% CI, 0.98-1.74) CRC in multivariate analyses. Incident CRC risks increased progressively by lengthening induction period (P trend=0.01), reaching a 30% increase (RR, 1.30; 95% CI, 1.04-1.63) after age 45 years. By anatomic subsite, ever smoked cigarettes and induction period were more strongly associated with incident proximal CRC (P = 0.03 and P trend = 0.03, respectively) than incident distal CRC (P=0.44 and P trend=0.10, respectively). CONCLUSIONS: In this long-term cohort study of postmenopausal women, cigarette smoking was positively associated with CRC risk. Onset of smoking in the distant past appeared to confer the greatest risk, especially for incident proximal CRC. These data support a potential subsite-specific role for cigarette smoking in colorectal carcinogenesis, at least among women. Based on emerging data, an epigenetic pathway for smoking-induced CRC is proposed.     

Impact of cigarette smoking on the incidence of Type 2 diabetes mellitus in middle-aged Japanese men: the Osaka Health Survey.

AIMS: To assess the impact of cigarette smoking on the incidence of Type 2 diabetes mellitus (DM) in middle-aged Japanese men. METHODS: The study enrolled 6250 men aged 35-60 years and free of diabetes, impaired fasting glucose and hypertension at entry. Type 2 DM was defined by a fasting plasma glucose level > or =7.0 mmol/l or physician-diagnosed Type 2DM. RESULTS: Four hundred and fifty cases of Type 2 DM were confirmed during the 60904 person-years follow-up. After adjustment for multiple covariates, including age, body mass index, alcohol consumption, physical activity, parental history of diabetes and the level of fasting plasma glucose, total cholesterol, triglycerides, high-density lipoprotein cholesterol and haematocrit, the relative risk of Type 2 DM among current smokers compared with non-smokers was 1.47 (95% confidence interval (CI) 1.14-1.92). Men who smoked >30 cigarettes/day had a multivariate-relative risk of 1.73 (95% CI 1.20-2.48) compared with non-smokers. The number of cigarettes smoked daily and the pack-year values were positively related to the development of Type 2 DM in a dose-dependent manner (P for trends = 0.0026 and 0.001, respectively). CONCLUSIONS: A cigarette smoking habit is an independent risk factor for Type 2 DM.     

Association of type 2 diabetes mellitus and the risk of colorectal cancer: A meta-analysis and systematic review

AIM: To provide a quantitative assessment of the association between type 2 diabetes mellitus(T2DM)and the risk of colorectal cancer(CRC).METHODS: Systematic review was conducted thorough MEDLINE, EMBASE, Cochrane Library, andISI Web of knowledge databases till 31 st January 2014.This meta-analysis included the cohort studies that illustrated relative risk(RR) or odds ratio estimates with 95%CI for the predictive risk of CRC by T2 DM.Summary relative risks with 95%CI were analyzed by using an effects summary ratio model. Heterogeneity among studies was assessed by the Cochran's Q and I 2statistics.RESULTS: The meta analysis of 8 finally selected studies showed a positive correlation of T2 DM with the risk of CRC as depicted by effects summary RR of 1.21(95%CI: 1.02-1.42). Diabetic women showed greater risk of developing CRC as their effect summary RR of 1.22(95%CI: 1.01-49) with significant overall Z test at 5% level of significance was higher than the effect summary RR of 1.17(95%CI: 1.00-1.37) of men showing insignificant Z test. The effect summary RR of 1.19 with 95%CI of 1.07-1.33 indicate a positive relationship between DM and increased risk of CRC with significant heterogeneity(I 2 = 92% and P-value 0.05).CONCLUSION: Results from this systematic review and meta-analysis report that diabetic people have an increased risk of CRC as compared to non-diabetics.     

A prospective study of cigarette smoking and the incidence of diabetes mellitus among US male physicians

PURPOSE: To determine the association between cigarette smoking and the incidence of type 2 diabetes mellitus. SUBJECTS AND METHODS: We studied 21,068 US male physicians aged 40 to 84 years in the Physicians' Health Study who were initially free of diagnosed diabetes mellitus, cardiovascular disease, and cancer. Information about cigarette smoking and other risk indicators was obtained at baseline. The primary outcome was reported diagnosis of type 2 diabetes mellitus. RESULTS: During 255,830 person-years of follow-up, 770 new cases of type 2 diabetes mellitus were identified. Smokers had a dose-dependent increased risk of developing type 2 diabetes mellitus: compared with never smokers, the age-adjusted relative risk was 2.1 (95% confidence interval [CI]: 1.7 to 2.6) for current smokers of > or = 20 cigarettes per day, 1.4 (95% CI: 1.0 to 2.0) for current smokers of <20 cigarettes per day, and 1.2 (95% CI: 1.0 to 1.4) for past smokers. After multivariate adjustment for body mass index, physical activity, and other risk factors, the relative risks were 1.7 (95% CI: 1.3 to 2.3) for current smokers of > or = 20 cigarettes per day, 1.5 (95% CI: 1.0 to 2.2) for current smokers of <20 cigarettes per day, and 1.1 (95% CI: 1.0 to 1.4) for past smokers. Total pack-years of cigarette smoking was also associated with the risk of type 2 diabetes mellitus (P for trend <0.001). CONCLUSIONS: These prospective data support the hypothesis that cigarette smoking is an independent and modifiable determinant of type 2 diabetes mellitus.     

Exocrine pancreatic cancer,cigarette smoking,and diabetes mellitus: a case-control study in northern Italy

The role of cigarette smoking and diabetes mellitus as risk factors for exocrine pancreatic cancer (PC) was investigated in a hospital based case-control study. Current smokers were at increased risk for PC (OR = 2.36, 95% CI 1.53-3.63): the magnitude of the risk was related to the lifetime amount of smoking (chi2(trend) = 17.00; P < 0.0001). Among former smokers, after 15 years from ceasing smoking, the risk for PC dropped to the level of a lifetime non-smoker, whichever the lifetime smoking amount. Diabetes was associated with a 2.89-fold increased risk for PC (95% CI 1.71-4.86): the risk was 4.76 (95% CI 1.99-11.53) for diabetes diagnosed up to 2 years before the diagnosis of PC and dropped to 2.07 (95% CI 1.02-4.20) for diabetes diagnosed more than 5 years before PC. The risk for PC was estimated according to the treatment used to control diabetes: it was 6.49 (95% CI 2.28-18.48) for insulin treated diabetes and 2.12 (95% CI 1.16-3.87) for diabetes treated with oral hypoglycemic drugs. The risk of PC for diabetes treated for more than 5 years before the diagnosis of PC was 6.21 (95% CI 1.61-23.96) for patients treated with insulin and 1.21 (95% CI 0.50-2.92) for those treated with oral hypoglycemic drugs: the type of treatment needed to control the disease may discriminate between the diabetes that represents a consequence of cancer from the diabetes that could represent an etiological co-factor. More studies are needed to clarify whether long-lasting insulin-treated diabetes is an etiological co-factor in PC.     

Alcohol abuse and the risk of pancreatic cancer

BACKGROUND: Although most epidemiological studies do not support a role for alcohol in the aetiology of pancreatic cancer, an increased risk among heavy drinkers cannot be excluded. METHODS: In a retrospective cohort based on the Swedish Inpatient Register, we analysed the risk of pancreatic cancer among patients admitted to hospital for alcoholism (n=178 688), alcoholic chronic pancreatitis (n=3500), non-alcoholic chronic pancreatitis (n=4952), alcoholic liver cirrhosis (n=13 553), or non-alcoholic liver cirrhosis (n=7057) from 1965 to 1994. Follow up through to 1995 was accomplished by linkage to nationwide registers. Standardised incidence ratios (SIRs) express the relative risks by taking the general Swedish population as reference. To minimise the possible influence of selection bias, we excluded the first year observations. RESULTS: Alcoholics had only a modest 40% excess risk of pancreatic cancer (SIR 1.4, 95% confidence interval (CI) 1.2-1.5). Overrepresented smokers among alcoholics might confound a true SIR of unity among alcoholics to approximately 1.4. SIR among alcoholic chronic pancreatitis patients (2.2, 95% CI 0.9-4.5) was considerably lower than that among non-alcoholic chronic pancreatitis patients (8.7, 95% CI 6.8-10.9), and decreased with increasing duration of follow up in both groups, indicating that most of the excess might be explained by reversed causation from undiagnosed cancers. Among patients with alcoholic liver cirrhosis, the increased risk of pancreatic cancer was also moderate (SIR 1.9, 95% CI 1.3-2.8) while no significant excess risk was found among non-alcoholic liver cirrhosis patients (SIR 1.2, 95% CI 0.6-2.2). CONCLUSIONS: The excess risk for pancreatic cancer among alcoholics is small and could conceivably be attributed to confounding by smoking.     

Risk of intestinal cancer in inflammatory bowel disease: a population-based study from olmsted county, Minnesota

BACKGROUND & AIMS: The risk for colorectal cancer in Crohn's disease and ulcerative colitis patients from the United States currently is unknown. We estimated the risk for small-bowel and colorectal cancer in a population-based cohort of 692 inflammatory bowel disease patients from Olmsted County, Minnesota, from 1940 to 2001. METHODS: The Rochester Epidemiology Project was used to identify cohort patients with colorectal and small-bowel cancer. The cumulative probability of cancer and standardized incidence ratios (SIR) were estimated using expected rates from Surveillance, Epidemiology, and End Results, white patients from Iowa, from 1973 to 2000, and Olmsted County, from 1980 to 1999. RESULTS: Colorectal cancer was observed in 6 ulcerative colitis patients vs 5.38 expected (SIR, 1.1; 95% confidence interval [CI], 0.4-2.4), but 4 of these occurred among those with extensive colitis or pancolitis (SIR, 2.4; 95% CI, 0.6-6.0). Six Crohn's disease patients (vs 3.2 expected) developed colorectal cancer (SIR, 1.9; 95% CI, 0.7-4.1). Three Crohn's disease patients developed small-bowel cancer vs 0.07 expected (SIR, 40.6; 95% CI, 8.4-118). CONCLUSIONS: The risk for colorectal cancer was not increased among ulcerative colitis patients overall, but appeared to be increased among those with extensive colitis. The colorectal cancer risk was increased slightly among Crohn's disease patients, who also had a 40-fold excess risk for small-bowel cancer.     

Cancer risk among men with, or at risk of, HIV infection in southern Europe

OBJECTIVE: To evaluate the cancer risk in southern European men with, or at risk of, HIV infection. DESIGN: An analysis of longitudinal data to assess time-dependent rare events. METHODS: Data from a cohort of HIV seroconverters, and from two hospital-based HIV seroprevalent cohorts were combined and analysed. The number of cancer cases observed was compared with the expected number, obtained from cancer incidence rates among men in the general population. Age-standardized incidence ratios (SIR) and their 95% confidence intervals (CI) were computed. RESULTS: A total of 19,609 person-years of observation were accumulated among HIV-positive men, and 7957 person-years among HIV-negative men. Among HIV-positive men, statistically significant increased SIR were seen for Hodgkin's disease (HD) (SIR = 8.7), liver cancer (SIR = 11.0), and cancer of the salivary glands (SIR = 33.6). An excess of lung cancer was seen among intravenous drug users (IDU), but not among homosexual men. When the risk of all non-AIDS-defining cancers was considered, HIV-positive men had a nearly twofold excess (95% CI: 1.2-2.8). A risk of similar magnitude emerged among HIV-negative IDU (95% CI: 1.0-4.5), largely attributable to lung cancer and HD. CONCLUSION: These findings confirm that HIV infection increases the risk of HD, whereas they suggest that the risk of hepatocellular carcinoma may also be enhanced by HIV infection. The observation of an elevated risk of lung cancer in both HIV-positive and HIV-negative IDU points to personal behaviours unrelated to HIV infection.     

Increased risk of left sided colon cancer in patients with diverticular disease.

Certain similar epidemiological characteristics suggest a common aetiology for colon cancer and diverticulosis of the colon. The hypothesis that patients with diverticulosis are at increased risk of developing colon cancer was tested in a retrospective, population based, cohort study in Sweden. A total of 7159 patients (2478 men and 4681 women) who had been given a hospital discharge diagnosis of diverticulosis or diverticulitis of the colon between 1965 and 1983 were followed up during 1985 by means of record linkage procedures. After excluding the first 2 years of follow up, there was not a significant increase in risk (SIR) overall for colon cancer (SIR = 1.2; 95% confidence intervals (CI) 0.9, 1.6) or for rectal cancer (SIR = 1.1; 95% CI 0.7, 1.7). The observed number of right sided colon cancers was as expected (SIR = 0.9; 95% CI 0.5, 1.5). In contrast, an increased risk of left sided colon cancer was found both overall (SIR = 1.8; 95% CI 1.1, 2.7) and consistently in men and women as well as in different age groups. This risk increased the longer the follow up (p value for trend < 0.001). These results do not support the hypothesis of a common aetiology in diverticular disease and colonic cancer but suggest a causal relationship between diverticular disease and cancer of the left colon.     

Increased cancer incidence in a Swedish cohort of patients with systemic lupus erythematosus

OBJECTIVE: To assess the risk of cancer in patients with systemic lupus erythematosus (SLE). METHODS: A population-based cohort of 5 715 hospitalised SLE patients was followed 1964-1995 through linkage of the Hospital Discharge Register to the National Swedish Cancer Register. RESULTS: In all, 443 malignancies occurred during the observation-period. The overall risk was increased by 25% (SIR= 1.25, CI 95% 1.14-1.37) and lymphomas constituted the major excess risk. The risk of non-Hodgkin's lymphoma (NHL) was nearly 3-fold increased (SIR = 2.86, CI 95% 1.96-4.04). There was also an increased risk of lung cancer (SIR= 1.73, CI 95% 1.25-2.32) and squamous cell skin cancer (SIR= 1.53, CI 95% 0.98-2.28), which was most pronounced at more than 15 years of follow-up. CONCLUSION: The major finding was a bimodal incidence pattern with an increased risk of lymphoma, mainly NHL, early during follow-up, but lung cancer and squamous skin cancer later on.     

Risk of pancreatic cancer after cholecystectomy: a cohort study in Sweden

BACKGROUND: Although some experimental studies have indicated that cholecystectomy may increase the risk of pancreatic cancer, data from epidemiological studies are conflicting. AIMS: We conducted a register based retrospective cohort study to explore the relationship between cholecystectomy and pancreatic cancer. SUBJECTS: The cohort included 87 263 men and 181 049 women with a documented cholecystectomy for cholelithiasis between 1965 and 1997. METHODS: By record linkage to the nationwide and virtually complete registers of Cancer, Emigration, and Causes of Death, the cohort was followed up until the occurrence of any cancer, emigration, death, or the end of follow up, 31 December 1997, whichever came first. Relative risk was estimated by standardised incidence ratio (SIR) using the Swedish nationwide sex, age, and calendar year specific cancer incidence rates as reference. RESULTS: During the period of observation, 1053 cases of pancreatic cancer were found, among which 231 (22%) occurred within 12 months after operation. After excluding cases and person years accrued during the first two years of follow up, we observed a non-significant 6% excess risk for pancreatic cancer (95% confidence interval (CI) -2 to 14%). The relative risk did not increase with increasing follow up duration, with a SIR equal to 0.98 (95% CI 0.79-1.20) 20 years or more after operation. Patients with a comorbidity of diabetes or chronic pancreatitis had higher relative risks (SIR=1.79, 95% CI 1.39-2.28; SIR=3.17, 95% CI 1.37-6.24, respectively). After excluding patients with recorded diabetes or chronic pancreatitis, the relative risk was close to unity (SIR=1.01, 95% CI 0.94-1.09). CONCLUSIONS: Our findings do not support the hypothesis that cholecystectomy increases the subsequent risk of pancreatic cancer.     

Risk of adenocarcinomas of the esophagus and gastric cardia in patients with gastroesophageal reflux diseases and after antireflux surgery.

BACKGROUND & AIMS: Gastroesophageal reflux has been proposed as an important risk factor for esophageal and gastric cardia adenocarcinoma, but prospective data are lacking. Furthermore, the effect of antireflux surgery has not yet been studied. We conducted a population-based retrospective cohort study to fill these gaps. METHODS: A cohort of 35,274 male and 31,691 female patients with a discharge diagnosis of gastroesophageal reflux diseases, and another cohort of 6406 male and 4671 female patients who underwent antireflux surgery, were identified in the Swedish Inpatient Register. Follow-up was attained through record linkage with several nationwide registers. Standardized incidence ratio (SIR) was used to estimate relative risk of upper gastrointestinal cancers, using the general Swedish population as reference. RESULTS: After exclusion of the first year follow-up, 37 esophageal and 36 gastric cardia adenocarcinomas were observed among male patients who did not have surgery (SIR, 6.3, 95% confidence interval [CI], 4.5-8.7; SIR, 2.4, 95% CI, 1.7-3.3, respectively). SIR for esophageal adenocarcinoma increased with follow-up time (P = 0.03 for trend). Among male patients who had undergone antireflux surgeries, risks were also elevated (16 esophageal adenocarcinoma, SIR, 14.1, 95% CI, 8.0-22.8; 15 gastric cardia adenocarcinomas, SIR, 5.3, 95% CI, 3.0-8.7) and remained elevated with time after surgery. The cancer risk pattern in women was similar to that for men, but the number of cases were much smaller. CONCLUSIONS: Gastroesophageal reflux is strongly associated with the risk of esophageal adenocarcinoma, and to a lesser extent, with gastric cardia adenocarcinoma. The risk of developing adenocarcinomas of the esophagus and gastric cardia remains increased after antireflux surgery.     

The influence of maternal body mass index,maternal diabetes mellitus,and maternal smoking during pregnancy on the risk of childhood‐onset type 1 diabetes mellitus in the offspring: Systematic review and meta‐analysis of observational studies

There is emerging evidence that events occurring before and shortly after birth may be important in determining the risk of childhood‐onset type 1 diabetes mellitus (T1DM). We aimed to summarize and synthesize the associations between maternal body mass index (BMI), maternal diabetes mellitus (DM), and maternal smoking during pregnancy and the risk of childhood‐onset T1DM in the offspring by performing a systematic review and meta‐analysis of observational studies. A random effects model was used to generate the summary risk estimates. The PubMed and Web of Science databases were searched to identify relevant observational studies. Twenty one observational studies were included in the present meta‐analysis. Compared with offspring of mothers with normal weight, offspring of women with overweight or obesity were at an increased risk of developing childhood‐onset T1DM (overweight: relative risk [RR] 1.09, 95% confidence interval [CI], 1.03‐1.15; obesity: RR 1.25, 95% CI, 1.16‐1.34; per 5 kg m^?2 increase in BMI: RR 1.10, 95% CI, 1.06‐1.13). No association was found for maternal underweight (RR 0.92, 95% CI, 0.75‐1.13). Maternal DM was associated with an increased risk of childhood‐onset T1DM (RR 3.26, 95% CI, 2.84‐3.74). Regarding the type of maternal DM, the greatest risk of T1DM in the offspring appeared to be conferred by maternal T1DM (RR 4.46, 95% CI, 2.89‐6.89), followed by maternal gestational diabetes mellitus (RR 1.66, 95% CI, 1.16‐2.36), and lastly by maternal type 2 diabetes mellitus (RR 1.11, 95% CI, 0.69‐1.80). Additional analysis of studies comparing maternal versus paternal T1DM within the same population revealed that offspring of fathers with T1DM had a 1.5 times higher risk of developing childhood‐onset T1DM than offspring of mothers with T1DM (RR 9.58, 95% CI, 6.33‐14.48 vs. RR 6.24, 95% CI, 5.52‐7.07). Furthermore, a reduced risk of childhood‐onset T1DM was observed in infants born to mothers who smoked during pregnancy compared with infants born to mothers who did not smoke during pregnancy (RR 0.79, 95% CI, 0.71‐0.87). In summary, our findings add further evidence that early‐life events or environmental factors may play a role in modulating infants' risk of developing T1DM later in life.     

CHRNA5/CHRNA3 Locus Associates with Increased Mortality among Smokers

Polymorphisms in the nicotinic acetylcholine receptor gene (CHRNA5/CHRNA3 locus) have been associated with several smoking related traits such as nicotine dependence, cigarette consumption, smoking cessation, lung cancer, and COPD. The aim of this candidate gene study was to study the locus among the Finnish COPD patients and long-term smokers with regard to COPD risk, smoking behavior, cancer, and all-cause mortality. Genotyping of rs1051730, the locus tagging SNP was done in two longitudinal cohorts: Finnish COPD patients (N = 575, 74% men) and long-term smokers, all men (N = 1911). Finnish population sample (N = 1730) was used as controls. The analyses were done using logistic and Cox regression. The main findings were that the minor allele increased the risk of COPD when compared to the Finnish population at large (OR = 1.4, 95% CI 1.2-1.7, p = 3.2 × 10-5). Homozygosity for the risk allele was associated in both cohorts with all-cause mortality (crude HR 2.2, 95% CI 1.2–3.8 and 1.3, 95% CI 1.1–1.5, respectively), with any type of cancer (crude OR 2.3, 95% CI 1.0–5.1) among the COPD patients and with the number of pack-years (crude OR 1.4, 95% CI 1.1–1.9) among the male smokers. CHRNA5/CHRNA3 locus tagged by rs1051730, which has been previously associated with several smoking related diseases was now shown to be associated also with increased all-cause mortality among long-term smokers with or without clinical COPD further emphasizing the clinical importance of the finding.     

A systematic review and meta-analysis of familial colorectal cancer risk

OBJECTIVE: The aim of this study was to identify published studies quantifying familial colorectal cancer (CRC) risks in first-degree relatives of CRC and colorectal adenoma (CRA) cases and, through a meta-analysis, obtain more precise estimates of familial risk according to the nature of the family history and type of neoplasm. METHODS: Twenty-seven case-control and cohort studies were identified, which reported risks of CRC in relatives of CRC cases and nine, which reported the risk of CRC in relatives of CRA cases. Pooled estimates of risk for various categories of family history were obtained by calculating the weighted average of the log relative risk estimates from studies. RESULTS: The pooled estimates of relative risk were as follows: a first-degree relative with CRC 2.25 (95% CI = 2.00-2.53), colon 2.42 (95% CI = 2.20-2.65), and rectal 1.89 (95% CI = 1.62-2.21) cancer; parent with CRC 2.26 (95% CI = 1.87-2.72); sibling with CRC 2.57 (95% CI = 2.19-3.02); more than one relative with CRC 4.25 (95% CI = 3.01-6.08); relative diagnosed with CRC before age 45, 3.87 (95% CI = 2.40-6.22); and a relative with CRA 1.99 (95% CI = 1.55-2.55). CONCLUSIONS: Individuals with a family history of CRC and CRA have a significantly elevated risk of developing CRC compared with those without such a history. Risks are greatest for relatives of patients diagnosed young, those with two or more affected relatives, and relatives of patients with colonic cancers.     

Childhood risk factors predict cardiovascular disease, impaired fasting glucose plus type 2 diabetes mellitus, and high blood pressure 26 years later at a mean age of 38 years: the Princeton-lipid research clinics follow-up study

The objective was to assess whether pediatric risk factors predict cardiovascular disease (CVD), impaired fasting glucose (IFG) + type 2 diabetes mellitus (T2DM), and high blood pressure (HBP) in young adulthood. We performed a prospective follow-up of 909 public-parochial suburban schoolchildren first studied at ages 6 to 18 years and 26 years later at a mean age of 38 years. Pediatric triglycerides (TGs), blood pressure, low-density lipoprotein cholesterol, body mass index, and glucose above and high-density lipoprotein cholesterol below established pediatric cutoffs, along with race, cigarette smoking, family history of CVD, T2DM, and HBP, were assessed as determinants of young adult CVD, a composite variable including IFG + T2DM and HBP. By stepwise logistic regression, adult CVD (19 yes, 862 no) was associated with pediatric high TG (odds ratio [OR], 5.85; 95% confidence interval [CI], 2.3-14.7). High TG in pediatric probands with young adult CVD was familial and was associated with early CVD in their high-TG parents. Adult IFG + T2DM (114 yes, 535 no) was associated with parental T2DM (OR, 2.2; 95% CI, 1.38-3.6), high childhood glucose (OR, 4.43; 95% CI, 2-9.7), and childhood cigarette smoking (OR, 1.64; 95% CI, 1.03-2.61). Adult HBP (133 yes, 475 no) was associated with pediatric high body mass index (OR, 2.7; 95% CI, 1.7-4.3) and HBP (OR, 2.5; 95% CI, 1.5-4.3). Pediatric risk factors are significantly, independently related to young adult CVD, IFG + T2DM, and HBP. Identification of pediatric risk factors for CVD, IFG + T2DM, and HBP facilitates initiation of primary prevention programs to reduce development of adult CVD, IFG + T2DM, and HBP.     

Risk for gastric cancer after cholecystectomy

BACKGROUND: It is becoming increasingly evident that chronic inflammation may predispose cancer development. In the stomach, inflammation caused by Helicobacter pylori infection is linked to gastric cancer. Cholecystectomy is regularly followed by duodenogastric bile reflux and reactive gastritis. To test whether a noninfectious long-standing inflammation impels gastric carcinogenesis as well, we assessed the risk of gastric cancer in a large, population-based cohort of cholecystectomized patients. METHODS: We identified 251,672 individuals, in the Swedish National Inpatient Register, who had undergone cholecystectomy between 1970 and 1997. All incident cases of gastric cancer were identified through linkage to the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for comparisons with cancer rates of the general population in Sweden. RESULTS: We found an 11% greater overall risk of distal gastric cancer (SIR=1.11, 95% CI 1.04-1.19). The risk increase was only observed among men (SIR=1.21, 95% CI 1.10-1.32), whereas no excess risk was evident for women. For men, the risk was elevated for up to 10 yr after surgery, but this elevation disappeared with longer follow-up time. There was no clear association between cholecystectomy and cardia cancer (SIR=0.95, 95% CI 0.76-1.16). CONCLUSIONS: Inconsistency over gender strata, implausibly short induction and latency time, and disappearance of the effect over time makes a causal relationship between cholecystectomy and distal gastric cancer less likely. The findings set aside concerns of harmful long-term consequences of cholecystectomy.     

Is there a risk of cancer development after Campylobacter infection?

Abstract

Objective. All Campylobacter jejuni species produce a genotoxin, which induce DNA double strand breaks, could lead to an increased risk of cancer especially in the gastro-intestinal tract. Material and methods. All individuals in Stockholm County who tested positive with C. jejuni between 1989 and 2006 were included. The cohort was followed-up until December 31, 2007 for the occurrence of cancer, overall and site specific. Standard incidence ratios (SIR) with 95% confidence intervals (CI) were calculated by comparisons with the background population. Results. There were 16,276 individuals who tested positive for C. jejuni generating 124,387 person years. Excluding the first year of follow-up the overall risk for cancer did neither differ from that expected SIR = 0.95 (95% CI 0.82–1.09) nor after10 years or more of follow-up; SIR = 0.91 (95% CI 0.71–1.16). There was no increased risk for cancer in the gastro-intestinal tract, but there were significantly increased risks for melanomas SIR = 1.84 (95% CI 1.27–2.57) and squamous cell skin cancer SIR = 1.52 (95% CI 1.01–2.19) while a significantly decreased risk of respiratory cancers among males SIR = 0.32 (95% CI 0.12–0.70) was observed. Conclusions. Our results indicate no excess risks of malignancies following an infection by C. jejuni at least during the first decade. Furthermore, the finding of a decreased risk of respiratory cancers could be of interest, if the results are reproduced in future studies in other populations.     

Long-term predictors of survival for the Seven Countries Study cohort from Crete: from 1960 to 2000

BACKGROUND: In 1960, all male inhabitants of a series of villages in rural Crete, born between 1900 and 1919, were invited to participate in the Seven Countries Study. Analysis of 25-year mortality data from the 16 cohorts of participants indicated that the cohort from Crete had the lowest age-standardised all-cause and coronary heart disease death rates. METHODS: At baseline, 686 Cretan men (98% of those invited) participated in health examinations. Mortality data were collected over 40 years. Time-fixed and updated covariate survival analysis techniques were applied to assess eight cardiovascular disease risk factors as long-term predictors of all-cause and cardiovascular disease mortality. RESULTS: The median survival time was 32 years. All-cause and cardiovascular mortality rates were 26 and 11 per 1000 person-years, respectively. Age (relative risk 1.11, 95% CI 1.09-1.13), diastolic blood pressure (relative risk 1.02, 95% CI 1.01-1.03), and smoking (relative risk 1.37, 95% CI 1.14-1.64) were positively associated and forced expiratory volume (relative risk 0.50, 95% CI 0.36-0.68) was negatively associated with all-cause mortality. Age (relative risk 1.13, 95% CI 1.09-1.16), diastolic blood pressure (relative risk 1.01, 95% CI 1.001-1.03), and forced expiratory volume (relative risk 0.53, 95% CI 0.32-0.89) were independent predictors of cardiovascular mortality. Serum cholesterol concentration and body mass index were not independently associated with death risk. CONCLUSIONS: The Cretan cohort displays favourable 40-year survival. Even so, long-term predictors of the hazard of both all-cause and cardiovascular disease mortality are present.