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Cancer may impair sexual function in women. We provide an overview of studies that address Female Sexual Dysfunction (FSD) in women with cancer with a meta-analysis of observational studies that used a validated diagnostic tool. Searches included MEDLINE, Scopus, and Google Scholar for studies published from January 2000 to 31 December 2014. Every included study had to involve at least 30 cancer patients, to investigate FSD based on the Female Sexual Function Index (FSFI), and to have been published in peer-review journals. Duplicate independent data extraction and quality assessment were performed. Data were pooled using a random effects model if statistical heterogeneity was present. The main outcomes were FSFI total score and FSD prevalence. FSFI is a 19-item self-report instrument for assessing key dimensions of female sexual function. A value less than 26.55 is consistent with FSD. Thirty-five studies met the inclusion criteria. Among these, 27 reported FSFI scores, and 16 FSD prevalence. Most studies (56 %) had low to moderate quality. The mean value of FSFI was lower than 20 at all cancer sites: 16.25 (pooled random effect, 95 % CI 14.91-17.58, I (2) = 14.5 %) for colorectal cancer, 18.11 (95 % CI 14.45-21.77, I (2) = 97.8 %) for gynecological cancer, and 19.58 (95 % CI 17.64-21.53, I (2) = 90.9 %) for breast cancer. FSD prevalence was higher than 60 % at all cancer sites, with the highest value for gynecological cancer (78.44 %, 95 % CI 68.36-88.52 %, I (2) = 94.1 %). Women with cancer showed low FSFI scores with a high prevalence of FSD. Cancer may impair sexual function in women. We provide an overview of studies that address Female Sexual Dysfunction (FSD) in women with cancer with a meta-analysis of observational studies that used a validated diagnostic tool. Searches included MEDLINE, Scopus, and Google Scholar for studies published from January 2000 to 31 December 2014. Every included study had to involve at least 30 cancer patients, to investigate FSD based on the Female Sexual Function Index (FSFI), and to have been published in peer-review journals. Duplicate independent data extraction and quality assessment were performed. Data were pooled using a random effects model if statistical heterogeneity was present. The main outcomes were FSFI total score and FSD prevalence. FSFI is a 19-item self-report instrument for assessing key dimensions of female sexual function. A value less than 26.55 is consistent with FSD. Thirty-five studies met the inclusion criteria. Among these, 27 reported FSFI scores, and 16 FSD prevalence. Most studies (56 %) had low to moderate quality. The mean value of FSFI was lower than 20 at all cancer sites: 16.25 (pooled random effect, 95 % CI 14.91–17.58, I2 = 14.5 %) for colorectal cancer, 18.11 (95 % CI 14.45–21.77, I2 = 97.8 %) for gynecological cancer, and 19.58 (95 % CI 17.64–21.53, I2 = 90.9 %) for breast cancer. FSD prevalence was higher than 60 % at all cancer sites, with the highest value for gynecological cancer (78.44 %, 95 % CI 68.36–88.52 %, I2 = 94.1 %). Women with cancer showed low FSFI scores with a high prevalence of FSD.

The purpose of this study was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing the effect of intensified insulin regimens (basal-bolus versus premixed) on glycemic control in patients with type 2 diabetes. We conducted an electronic search until March 2015 on many electronic databases including online registries of ongoing trials. All RCTs comparing basal-bolus with premixed insulin regimens, with a duration of >12 weeks and with >30 patients per arm, were included. Investigators extracted data on study characteristics, outcome measures, and methodological quality. We found thirteen RCTs lasting 16-60 weeks and involving 5255 patients assessed for the primary endpoint (reduction of HbA1c from baseline). Meta-analysis of change in HbA1c level between basal-bolus and premixed insulin regimens resulted in a small and non-significant difference of 0.09% (95% CI -0.03 to 0.21), with substantial heterogeneity between studies (I(2) = 74.4%). There was no statistically significant difference in the event rate for overall hypoglycemia (0.16 episode/patient/year, 95%CI -2.07 to 2.3), weight change (-0.21 kg, -0.164 to 0.185), and daily insulin dose (-0.54 U/day, -2.7 to 1.6). The likelihood for reaching the HbA1c

No specific diet is recommended to prevent type 2 diabetes. We did a meta-analysis of prospective cohort studies to assess the association between different diets and prevention of type 2 diabetes. We did a comprehensive search of multiple electronic databases (Medline, Scopus, EMBASE, and ISI web of knowledge) until August 2013 using predefined criteria. We included prospective cohort studies that evaluated the role of different diets in type 2 diabetes prevention. Studies were selected by 2 independent reviewers. We did random-effects meta-analyses to determine the relative risk (RR) of incident diabetes associated with healthful dietary patterns. A total of 21,372 cases of incident diabetes, from 18 prospective studies, with 20 cohorts, in 4 world regions were identified. In the random-effect meta-analysis of the 20 cohorts, RR was 0.80 (95 % confidence interval (CI) = 0.74-0.86, P < 0.001), with high heterogeneity (I 2 = 57 %, P = 0.001) and no evidence of publication bias (Egger's test, P = 0.653). Exclusion of two cohorts produced identical RR (0.80, 95 % CI 0.76-0.84), with nonsignificant heterogeneity (I 2 = 9 %). The risk of incident diabetes did not appreciably change considering the geography (USA, Europe, and Asia), the duration of follow-up (10 years), and type of diets (Mediterranean and DASH, Dietary Approaches to Stop Hypertension, diets). There was a difference between at risk and general population (P = 0.0487), but the evidence was limited to two studies only. The results of our study demonstrate that several healthy diets are equally and consistently associated with a 20 % reduced risk of future type 2 diabetes.

We performed a systematic review and meta-analysis of the empirical evidence on the association of metabolic syndrome and its components with colorectal cancer incidence and mortality. A systematic literature search of multiple electronic databases was conducted and complemented by cross-referencing to identify studies published before 31 October 2012. Every included study was to report risk estimates with 95 % confidence intervals for the association between metabolic syndrome and colorectal cancer (incidence or mortality). Core items of identified studies were independently extracted by two reviewers, and results were summarized by standard methods of meta-analysis. We identified 17 studies, which reported on 49 data sets with 11,462 cancer cases. Metabolic syndrome was associated with an increased risk of colorectal cancer incidence and mortality in both men (RR: 1.33, 95 % CI 1.18-1.50, and 1.36, 1.25-1.48, respectively) and women (RR: 1.41, 1.18-1.70, and 1.16, 1.03-1.30, respectively). The risk estimates changed little depending on type of study (cohort vs non cohort), populations (US, Europe, Asia), cancer site (colon and rectum), or definition of the syndrome. The risk estimates for any single factor of the syndrome were significant for higher values of BMI/waist (RR: 1.19, 95 % CI 1.10-1.28), dysglycemia (RR: 1.29, 1.11-1.49), and higher blood pressure (RR: 1.09, 1.01-1.18). Dysglycemia and/or higher BMI/waist explained most of the risk associated with metabolic syndrome. Metabolic syndrome is associated with an increased risk of colorectal cancer incidence and mortality in both sexes. The risk conveyed by the full syndrome is not superior to the sum of its parts.

Ability to predict which patients might benefit more of therapy might facilitate personalization of treatment. The aim of this study was to obtain information about clinical characteristics which might predict the HbA1c response to DPP-4 inhibitors. We conducted an electronic search without restriction for randomized controlled trials (RCTs) involving DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, linagliptin, and alogliptin). RCTs were included if they lasted at least 12 weeks, reported the effect of DPP-4 inhibitors on HbA1c level, and the number of patients in any arm was >30. We did a meta-regression analysis. Seventy-eight articles were eligible, with 79 arms and 20,503 patients. For all arms, the decrease of HbA1c was −0.74 % (95 % CI −0.80 to −0.67 %), with considerable heterogeneity (I 2 = 97 %, P