Ford J.A.,University of East Anglia |
Pereira A.,Public Health Direct.
Journal of Evaluation in Clinical Practice | Year: 2015
Rationale, aims and objectives Referrals to dermatology for skin lesions is increasing. Teledermatology allows patients to obtain specialist advice remotely. The aim of this study is to assess if teledermatology reduces secondary care dermatology referrals and evaluate its acceptability to patients and clinicians. Methods A 24-month before and after comparative evaluation of a teledermatology service was undertaken involving four non-randomly allocated intervention practices and 18 control practices. Referral data for 12 months before and after the introduction of teledermatology was compared in intervention and control practices. Patient questionnaires explored their satisfaction and structured user dialogues explored the usefulness and benefits to clinicians. Time series analysis, adjusted for age and sex, was undertaken to assess the impact on secondary care referrals. Results There were 195 Telederm referrals during the 12-month pilot period. Seborrhoeic keratosis was the commonest diagnosis. No action was required in 86 patients. Urgent referral to secondary care was recommended in 64 patients and routine referral in 19. The difference in referral rate before and after was +2.11 referrals per 1000 practice population in the teledermatology group and +1.39 in the control group. This was statistically significant in the adjusted, but not unadjusted, analysis. There was a 14% response rate for the questionnaire. The service was very popular with patients and clinicians. Clinicians highlighted the significant educational benefit. Conclusion We did not find any evidence that teledermatology reduced secondary care referral rates but in this small pilot, we found that it increased referrals in the short term. It was very popular among patients and clinicians, especially for its educational value. © 2015 John Wiley & Sons, Ltd. Source
Duell E.J.,Catalan Institute of Oncology ICO IDIBELL |
Bonet C.,Catalan Institute of Oncology ICO IDIBELL |
Munoz X.,Catalan Institute of Oncology ICO IDIBELL |
Lujan-Barroso L.,Catalan Institute of Oncology ICO IDIBELL |
And 53 more authors.
International Journal of Cancer | Year: 2015
ABO blood serotype A is known to be associated with risk of gastric cancer (GC), but little is known how ABO alleles and the fucosyltransferase (FUT) enzymes and genes which are involved in Lewis antigen formation [and in Helicobacter pylori (H. pylori) binding and pathogenicity] may be related to GC risk in a European population. The authors conducted an investigation of 32 variants at ABO and FUT1-7 loci and GC risk in a case-control study of 365 cases and 1,284 controls nested within the EPIC cohort (the EPIC-Eurgast study). Four variants (including rs505922) in ABO, and allelic blood group A (AO1AA, odds ratio51.84, 95%CI51.20-2.80) were associated with diffuse-type GC; however, conditional models with other ABO variants indicated that the associations were largely due to allelic blood group A. One variant in FUT5 was also associated with diffuse-type GC, and four variants (and haplotypes) in FUT2 (Se), FUT3 (Le) and FUT6 with intestinal-type GC. Further, one variant in ABO, two in FUT3 and two in FUT6 were associated with H. pylori infection status in controls, and two of these (in FUT3 and FUT6) were weakly associated with intestinal-type GC risk. None of the individual variants surpassed a Bonferroni corrected p-value cutoff of 0.0016; however, after a gene-based permutation test, two loci [FUT3(Le)/FUT5/FUT6 and FUT2(Se)] were significantly associated with diffuse- and intestinal-type GC, respectively. Replication and functional studies are therefore recommended to clarify the role of ABO and FUT alleles in H. pylori infection and subtype-specific gastric carcinogenesis. © 2014 UICC. Source
De Batlle J.D.,International Agency for Research on Cancer IARC |
Ferrari P.,International Agency for Research on Cancer IARC |
Chajes V.,International Agency for Research on Cancer IARC |
Park J.Y.,International Agency for Research on Cancer IARC |
And 55 more authors.
Journal of the National Cancer Institute | Year: 2015
Background: There is limited evidence on the association between dietary folate intake and the risk of breast cancer (BC) by hormone receptor expression in the tumors. We investigated the relationship between dietary folate and BC risk using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: A total of 367 993 women age 35 to 70 years were recruited in 10 European countries. During a median followup of 11.5 years, 11 575 women with BC were identified. Dietary folate intake was estimated from country-specific dietary questionnaires. Cox proportional hazards regression models were used to quantify the association between dietary variables and BC risk. BC tumors were classified by receptor status. Subgroup analyses were performed by menopausal status and alcohol intake. Intake of other B vitamins was considered. All statistical tests were two-sided. Results: A borderline inverse association was observed between dietary folate and BC risk (hazard ratio comparing top vs bottom quintile [HRQ5-Q1] = 0.92, 95% CI = 0.83 to 1.01, Ptrend =.037). In premenopausal women, we observed a statistically significant trend towards lower risk in estrogen receptor-negative BC (HRQ5-Q1 = 0.66, 95% CI = 0.45 to 0.96, Ptrend =.042) and progesterone receptor-negative BC (HRQ5-Q1 = 0.70, 95% CI = 0.51 to 0.97, Ptrend =.021). No associations were found in postmenopausal women. A 14% reduction in BC risk was observed when comparing the highest with the lowest dietary folate tertiles in women having a high (>12 alcoholic drinks/week) alcohol intake (HRT3-T1 = 0.86, 95% CI = 0.75 to 0.98, Pinteraction =.035). Conclusions: Higher dietary folate intake may be associated with a lower risk of sex hormone receptor-negative BC in premenopausal women. © The Author 2014. Published by Oxford University Press. Source
Aleksandrova K.,German Institute of Human Nutrition |
Bamia C.,National and Kapodistrian University of Athens |
Drogan D.,German Institute of Human Nutrition |
Lagiou P.,National and Kapodistrian University of Athens |
And 62 more authors.
American Journal of Clinical Nutrition | Year: 2015
Background: Higher coffee intake has been purportedly related to a lower risk of liver cancer. However, it remains unclear whether this association may be accounted for by specific biological mechanisms. Objective: We aimed to evaluate the potential mediating roles of inflammatory, metabolic, liver injury, and iron metabolism biomarkers on the association between coffee intake and the primary form of liver cancer hepatocellular carcinoma (HCC). Design: We conducted a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition among 125 incident HCC cases matched to 250 controls using an incidence-density sampling procedure. The association of coffee intake with HCC risk was evaluated by using multivariableadjusted conditional logistic regression that accounted for smoking, alcohol consumption, hepatitis infection, and other established liver cancer risk factors. The mediating effects of 21 biomarkers were evaluated on the basis of percentage changes and associated 95% CIs in the estimated regression coefficients of models with and without adjustment for biomarkers individually and in combination. Results: The multivariable-adjusted RR of having $4 cups (600mL) coffee/d compared with ,2 cups (300 mL)/d was 0.25 (95% CI: 0.11, 0.62; P-trend = 0.006). A statistically significant attenuation of the association between coffee intake and HCC risk and thereby suspected mediation was confirmed for the inflammatory biomarker IL-6 and for the biomarkers of hepatocellular injury glutamate dehydrogenase, alanine aminotransferase, aspartate aminotransferase (AST), g-glutamyltransferase (GGT), and total bilirubin, which in combination attenuated the regression coefficients by 72% (95% CI: 7%, 239%). Of the investigated biomarkers, IL-6, AST, and GGT produced the highest change in the regression coefficients: 40%, 56%, and 60%, respectively. Conclusion: These data suggest that the inverse association of coffee intake with HCC risk was partly accounted for by biomarkers of inflammation and hepatocellular injury. © 2015 American Society for Nutrition. Source
Cirera L.,11 Health |
Cirera L.,CIBER ISCIII |
Cirera L.,University of Murcia |
Huerta J.M.,11 Health |
And 27 more authors.
European Journal of Public Health | Year: 2016
Background: The literature has consistently shown that extreme social-economic groups predicted type 2 diabetes mellitus (T2D), rather than summarising the social gradient throughout all society stratification. Body mass index (BMI) was established as the principal mediator, with little support for other anthropometries. Our aim was to investigate an individual life-course social position (LiSoP) gradient and its mediators with T2D risk in the EPIC-Spain cohort. Methods: 36 296 participants (62% women), mostly aged 30-65 years, and free of T2D at baseline (1992-1996) were followed up for a mean of 12.1 years. A combined score of paternal occupation in childhood and own adult education assessed individual life-course social risk accumulation. Hazard ratios of T2D were estimated using Cox regression, stratifying by centre and age, and adjusting for different explanatory models, including anthropometric indices; dietary history; smoking and physical activity lifestyles; and clinical information. Results: Final models evidenced significant risks in excess of 63% for middle and 90% for lower classes of LiSoP in men; and of 104 and 126%, respectively, in women. Concurrently, LiSoP presented significant social gradients for T2D risk (P < 0.01) in both sexes. Waist circumference (WC) accounted for most of the risk excess in women, and BMI and WC in men. Conclusions: LiSoP gradient was related to T2D risk in Spanish men and women. WC mostly explained the relationship in both genders, together with BMI in men, yet LiSoP retained an independent effect in final models. © 2015 The Author. Published by Oxford University Press on behalf of the European Public Health Association. All rights reserved. Source