In mild acute diverticulitis, outpatient therapy without antibiotics was noninferior to antibiotics.

SOURCE CITATION: Mora-López L, Ruiz-Edo N, Estrada-Ferrer O, et al. Efficacy and safety of nonantibiotic outpatient treatment in mild acute diverticulitis (DINAMO-study): a multicentre, randomised, open-label, noninferiority trial. Ann Surg. 2021;274:e435-42. 34183510.

Pancreatic panniculitis in active systemic lupus erythematosus.

This report documents the case of a 64-year-old African-American female with new end-stage renal disease (ESRD), diagnosed with systemic lupus erythematosus (SLE) on renal biopsy and serologies including a positive ANA (>1:2560), positive anti-Sm antibodies, low titer anti-RNP antibodies, high titer anti-Ro antibodies, anti-dsDNA antibodies, lupus anticoagulant, and hypocomplementemia. She was also noted to have tender nodules on the bilateral shins. Excisional biopsy of one of the nodules showed marked fat necrosis with "ghost cells" and patchy basophilic granular debris consistent with pancreatic panniculitis. Further examination for pancreatic pathology showed an elevated lipase of 585 U/L (reference range 8-78 U/L) and amylase of 214 U/L (reference range 25-125 U/L). However, computed tomography imaging showed no evidence of pancreatitis or pancreatic tumors. This is very similar to another case recently reported in the literature. Similarities of these two cases (African-American females with lupus nephritis on dialysis) may represent a particular subset of SLE patients at increased risk for pancreatic panniculitis.

Diabetes risk reduction in primary care: Evaluation of the Ontario Primary Care Diabetes Prevention Program.

OBJECTIVES: Lifestyle interventions can reduce type 2 diabetes risk. The Primary Care Diabetes Prevention Program (PCDPP) was implemented by the Government of Ontario to lower diabetes risk. This study first evaluated the program, and second used a validated tool to estimate a potential population impact if the program were implemented more broadly in the province. METHODS: PCDPP was implemented in six primary care settings serving communities with high mortality risk due to chronic diseases. In total, 1916 adults with prediabetes or metabolic syndrome were enrolled from January 2011 to December 2012. Body weight was the primary outcome variable, and was modeled using four time periods (i.e., baseline, 3rd, 6th and 9th month). The intervention effect was estimated using multilevel mixed-effects linear regression, and was stratified by gender and age. In the population impact analysis, a number needed to treat (NNT) for the intervention to prevent one case of diabetes and an absolute number of diabetes cases averted were estimated. RESULTS: Weight loss over 9 months was 7.5% (or 6.8 kg), with 7.4% (or 6.4 kg) in females and 8.6% (or 8.6 kg) in males. When modeled, changes in weight were all statistically significant. The models for male participants predicted, however, some gains in weight in the last 3 months of the program. Dropout rates were 26.8%, 46.8% and 63.0% at 3rd, 6th and 9th month respectively. Scaling up the program would produce an NNT of approximately 36 and would avert 6401 cases of diabetes in five years. CONCLUSION: PCDPP may represent a potentially effective tool for population-level diabetes risk reduction.

Dietary N-nitroso compounds and risk of colorectal cancer: a case-control study in Newfoundland and Labrador and Ontario, Canada.

Several N-nitroso compounds (NOC) have been shown to be carcinogenic in a variety of laboratory animals, but evidence of their carcinogenicity in humans is lacking. We aimed to examine the association between NOC intake and colorectal cancer (CRC) risk and possible effect modification by vitamins C and E and protein in a large case-control study carried out in Newfoundland and Labrador and Ontario, Canada. A total of 1760 case patients with pathologically confirmed adenocarcinoma and 2481 population controls were asked to complete a self-administered FFQ to evaluate their dietary intakes 1 year before diagnosis (for cases) or interview (for controls). Adjusted OR and 95 % CI were calculated across the quintiles of NOC (measured by N-nitrosodimethylamine (NDMA)) intake and relevant food items using unconditional logistic regression. NDMA intake was found to be associated with a higher risk of CRC (highest v. lowest quintiles: OR 1·42, 95 % CI 1·03, 1·96; P for trend = 0·005), specifically for rectal carcinoma (OR 1·61, 95 % CI 1·11, 2·35; P for trend = 0·01). CRC risk also increased with the consumption of NDMA-containing meats when the highest tertile was compared with the lowest tertile (OR 1·47, 95 % CI 1·03, 2·10; P for trend = 0·20). There was evidence of effect modification between dietary vitamin E and NDMA. Individuals with high NDMA and low vitamin E intakes had a significantly increased risk than those with both low NDMA and low vitamin E intakes (OR 3·01, 95 % CI 1·43, 6·51; P for interaction = 0·017). The present results support the hypothesis that NOC intake may be positively associated with CRC risk in humans. Vitamin E, which inhibits nitrosation, could modify the effect of NDMA on CRC risk.

Intake of coffee and tea and risk of ovarian cancer: a prospective cohort study.

There is some evidence from case-control studies that coffee consumption might be positively associated with ovarian cancer risk, whereas the epidemiologic evidence regarding tea consumption and ovarian cancer is inconsistent. To date, there have been few prospective studies of these associations. Therefore, we examined ovarian cancer risk in association with both coffee and tea intake in a prospective cohort study of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the food frequency questionnaire were used to estimate daily intake of coffee and tea. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between categories of coffee and tea intake and ovarian cancer risk. During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. Tea intake was not associated with ovarian cancer risk in our study population. In contrast, a borderline positive association was observed among women who drank > 4 cups coffee/day compared to women who did not drink coffee (HR = 1.62, 95% CI = 0.95-2.75, P(trend) = 0.06). Given the pervasive use of these beverages, the associations between coffee and tea consumption and ovarian cancer risk warrant investigation in further prospective studies.

Dietary iron and heme iron intake and risk of breast cancer: a prospective cohort study.

Recent studies suggest that elevated body iron levels may contribute to breast carcinogenesis; however, epidemiologic evidence is lacking. We used data from a large cohort study of Canadian women to assess breast cancer in association with total iron and heme iron intake. Among 49,654 women ages 40 to 59 followed for an average of 16.4 years, we identified 2,545 incident breast cancer cases. Data from a food frequency questionnaire administered at baseline were used to calculate total dietary iron and heme iron intake. Using Cox proportional hazards models, we found no association of iron or heme iron intake with risk of breast cancer overall, in women consuming 30+ g of alcohol per day, or in women who had ever used hormone replacement therapy. The present study offers no support for an association of iron or heme iron intake with breast cancer risk or for a modification by iron of the effect of alcohol or estrogen. However, further cohort studies with repeated measurement of iron intake are warranted.

Glycaemic index, glycaemic load and ovarian cancer risk: a prospective cohort study.

BACKGROUND: There is some evidence that plasma insulin levels might influence ovarian cancer risk. Glycaemic index (GI) and glycaemic load (GL) are measures that allow the carbohydrate content of individual foods to be classified according to their postprandial glycaemic effects and hence their effects on circulating insulin levels. Therefore, we examined ovarian cancer risk in association with GI and GL, and intake of dietary carbohydrate and sugar. METHODS: The study was conducted in a prospective cohort of 49 613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food-frequency questionnaire (FFQ) between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the FFQ were used to estimate overall GI and GL, and Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between energy-adjusted quartile levels of GL, overall GI, total carbohydrates, total sugar and ovarian cancer risk. RESULTS: During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. GI and total carbohydrate and sugar intakes were not associated with ovarian cancer risk in the total cohort. GL was positively associated with a 72% increase in risk of ovarian cancer (HR=1.72, 95% CI=1.13-2.62, Ptrend=0.01) and the magnitude of the association was slightly greater among postmenopausal (HR=1.89, 95% CI=0.98-3.65, Ptrend=0.03) than among premenopausal women (HR=1.64, 95% CI=0.95-2.88, Ptrend=0.07). CONCLUSIONS: Our data suggest that consumption of diets with high GL values may be associated with increased risk of ovarian cancer.

Dietary fiber intake and ovarian cancer risk: a prospective cohort study.

There is some evidence from case-control studies that dietary fiber intake might be inversely associated with ovarian cancer risk, but there are limited prospective data. Therefore, we examined ovarian cancer risk in association with intake of dietary fiber in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS), who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the food frequency questionnaire were used to estimate intake of total dietary fiber, of fiber fractions, and of fiber from various sources. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between energy-adjusted quartile levels of fiber intake and ovarian cancer risk. During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. Total dietary fiber and fiber fractions were not associated with ovarian cancer risk in this study population.

Dietary folate consumption and risk of ovarian cancer: a prospective cohort study.

Deficient dietary folate intake may be associated with increased cancer risk in humans owing to DNA damage resulting from impaired nucleotide excision repair. It is conceivable that an association with folate may be modified by alcohol and/or methionine intake given that alcohol consumption and low methionine intakes both increase dietary folate requirements. In the cohort study reported here, we examined the association between dietary folate intake and ovarian cancer risk, overall and within strata defined by alcohol and methionine intakes. The investigation was conducted in 49 613 Canadian women who were participants in the National Breast Screening Study and who completed self-administered lifestyle and food frequency questionnaires between 1980 and 1985. Linkages to cancer and national mortality databases yielded data on cancer incidence and deaths among cohort members, with follow-up ending between 1998 and 2000. During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases among 48 766 women for whom data were available. Dietary folate intake was associated with a 25% decrease in risk of ovarian cancer for the highest versus the lowest quartile level of intake (hazard ratio=0.75, 95% confidence interval=0.42-1.34, Ptrend=0.25). On stratification by alcohol intake, dietary folate was not associated with ovarian cancer risk among women consuming <4 g/day of alcohol, but there was some suggestion of reduced risk at relatively high levels of folate intake among women consuming > or =4 g/day of alcohol/day (Ptrend=0.09; Pinteraction=0.22). The association between folate and ovarian cancer risk did not vary by strata of methionine intake (Pinteraction=0.98). Our findings, while not statistically significant, suggest that relatively high dietary folate intake may be associated with a reduction in ovarian cancer risk among women with relatively high alcohol consumption and among those with relatively high methionine intake.

Energy balance and breast cancer risk: a prospective cohort study.

While there is evidence that breast cancer risk is positively associated with body mass index (in postmenopausal women) and energy intake and inversely associated with physical activity, few studies have examined breast cancer risk in association with energy balance, the balance between energy intake and expenditure. Therefore, in the cohort study reported here, we studied the independent and combined associations of vigorous physical activity, energy consumption, and body mass index (BMI), with breast cancer risk. The investigation was conducted in 49,613 Canadian women who were participants in the National Breast Screening Study (NBSS) and who completed self-administered lifestyle and food frequency questionnaires between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. During a mean 16.4 years of follow-up, we observed 2545 incident breast cancer cases. Due to exclusions for various reasons, the analyses were based on 40,318 subjects amongst whom there were 1673 incident cases of breast cancer. Participation in vigorous physical activity and body mass index were not independently associated with breast cancer risk in the total cohort. A statistically significant positive trend was observed, however, between energy intake and breast cancer risk (P (trend )= 0.01). Although there was some variation in risk associated with vigorous physical activity, and BMI when the analyses were stratified by menopausal status, these interactions were not statistically significant. The interaction between menopausal status and energy intake, however, was of borderline statistical significance (P (interaction )= 0.06), with a statistically significant increased risk of breast cancer associated with highest versus lowest quartile of energy intake among premenopausal women (Hazard Ratio [HR] = 1.45, 95% confidence interval [CI] = 1.13- 1.85, P (trend) = 0.001). There was evidence of an increased risk of breast cancer associated with a relatively high body mass index among postmenopausal women in the highest quartile level of energy intake (Hazard Ratio [HR] = 1.72, 95% confidence interval [CI] = 1.01- 2.93, P (trend) = 0.05). In addition, there was evidence of an increased risk of breast cancer among premenopausal, physically inactive, overweight/obese women who consumed > or =1972 kcal/day compared to physically active normal weight women who consumed <1972 kcal/day (HR = 1.60, 95% CI = 1.08-2.37). Our data suggest that obese premenopausal women with relatively high energy intake may be at increased risk of breast cancer. In addition, energy imbalance, represented by a relatively high energy intake, lack of participation in vigorous physical activity, and a relatively high body mass index, may be associated with increased breast cancer risk, particularly among premenopausal women.

Glycaemic index, glycaemic load and risk of endometrial cancer: a prospective cohort study.

OBJECTIVE: High-glycaemic-load diets may increase endometrial cancer risk by increasing circulating insulin levels and, as a consequence, circulating oestrogen levels. Given the paucity of epidemiological data regarding the relationship between dietary glycaemic index and glycaemic load and endometrial cancer risk, we sought to examine these associations using data from a prospective cohort study. DESIGN, SETTING AND SUBJECTS: We examined the association between dietary glycaemic load and endometrial cancer risk in a cohort of 49,613 Canadian women aged between 40 and 59 years at baseline who completed self-administered food-frequency questionnaires between 1982 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. RESULTS: During a mean of 16.4 years of follow-up, we observed 426 incident cases of endometrial cancer. Hazard ratios for the highest versus the lowest quartile level of overall glycaemic index and glycaemic load were 1.47 (95% confidence interval (CI) = 0.90-2.41; P for trend = 0.14) and 1.36 (95% CI = 1.01-1.84; P for trend = 0.21), respectively. No association was observed between total carbohydrate or total sugar consumption and endometrial cancer risk. Among obese women (body mass index >30 kg m(-2)) the hazard ratio for the highest versus the lowest quartile level of glycaemic load was 1.88 (95% CI = 1.08-3.29; P for trend = 0.54) and there was a 55% increased risk for the highest versus the lowest quartile level of glycaemic load among premenopausal women. There was also evidence to support a positive association between glycaemic load and endometrial cancer risk among postmenopausal women who had used hormone replacement therapy. CONCLUSIONS: Our data suggest that diets with high glycaemic index or high glycaemic load may be associated with endometrial cancer risk overall, and particularly among obese women, premenopausal women and postmenopausal women who use hormone replacement therapy.

Glycemic index, glycemic load, and pancreatic cancer risk (Canada).

There is some evidence that plasma insulin and postload plasma glucose may be associated with risk of pancreatic cancer. Glycemic index and glycemic load are measures, which allow the carbohydrate content of individual foods to be classified according to their postprandial glycemic effects and hence their effects on circulating insulin levels. Therefore, we examined pancreatic cancer risk in association with glycemic index (GI), glycemic load (GL), and intake of dietary carbohydrate and sugar in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths, with follow-up ending between 1998 and 2000. During a mean 16.5 years of follow-up, we observed 112 incident pancreatic cancer cases. There was no association between overall glycemic index, glycemic load, total carbohydrate and total sugar intake and pancreatic cancer risk. In multivariate adjusted models, the hazard ratio (HR) for the highest versus lowest quartile levels of overall GI and GL were 1.43 (95% confidence interval [CI]=0.56-3.65, P(trend)=0.58) and 0.80 (95% CI=0.45-1.41, P(trend)=0.41), respectively. Our data suggest that overall glycemic index and glycemic load, as well as total sugar and total carbohydrate intake, are not associated with pancreatic cancer risk. However, given the limited literature regarding the role of diet in the etiology of pancreatic cancer, particularly with respect to glycemic index/load, further investigation is warranted.