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Background Functional gastrointestinal symptoms such as abdominal pain, bloating, distension, constipation, diarrhea and flatulence have been noted in patients with irritable bowel syndrome (IBS) or inflammatory bowel disease (IBD). The diversity of symptoms has meant that finding an effective treatment has been challenging with most treatments alleviating only the primary symptom. A novel treatment option for IBS and IBD currently generating much excitement is the low fermentable, oligo-, di-, mono-saccharides and polyol (FODMAP) diet. The aim of this meta-analysis was to determine the evidence of the efficacy of such a diet in the treatment of functional gastrointestinal symptoms. Methods Electronic databases were searched through to March 2015 to identify relevant studies. Pooled odds ratios (ORs) and 95 % confidence intervals were calculated for the effect of a low FODMAP diet on the reduction in IBS [Symptoms Severity Score (SSS)] score and increase in IBS quality of life (QOL) score for both randomized clinical trials (RCTs) and non-randomized interventions using a random-effects model. Results Six RCTs and 16 non-randomized interventions were included in the analysis. There was a significant decrease in IBS SSS scores for those individuals on a low FODMAP diet in both the RCTs (OR 0.44, 95 % CI 0.25–0.76; I 2  = 35.52, p  = 0.00) and non-randomized interventions (OR 0.03, 95 % CI 0.01–0.2; I 2  = 69.1, p  = 0.02). In addition, there was a significant improvement in the IBS-QOL score for RCTs (OR 1.84, 95 % CI 1.12–3.03; I 2  = 0.00, p  = 0.39) and for non-randomized interventions (OR 3.18, 95 % CI 1.60–6.31; I 2  = 0.00, p  = 0.89). Further, following a low FODMAP diet was found to significantly reduce symptom severity for abdominal pain (OR 1.81, 95 % CI 1.13–2.88; I 2  = 0.00, p  = 0.56), bloating (OR 1.75, 95 % CI 1.07–2.87; I 2  = 0.00, p  = 0.45) and overall symptoms (OR 1.81, 95 % CI 1.11–2.95; I 2  = 0.00, p  = 0.4) in the RCTs. In the non-randomized interventions similar findings were observed. Conclusion The present meta-analysis supports the efficacy of a low FODMAP diet in the treatment of functional gastrointestinal symptoms. Further research should ensure studies include dietary adherence, and more studies looking at greater number of patients and long-term adherence to a low FODMAP diet need to be conducted.

Introduction and hypothesisFemale pelvic organ prolapse (POP) is a common condition, with a lifetime risk for surgery of 10–20%. Prolapse procedures are known to have a high reoperation rate. It is assumed that etiological factors for POP may also be risk factors for POP recurrence after surgery. There are few reviews available evaluating risk factors for prolapse and recurrence or recently updated meta-analysis on this topic. Our aim was to perform a systematic review and quantitative meta-analysis to determine risk factors for prolapse recurrence after reconstructive surgery.MethodsFour electronic databases (MEDLINE, PubMed, EMBASE, and Google Scholar) were searched between 1995 and 1 January 2017, with no language restrictions.ResultsTwenty-five studies met inclusion criteria for a total of 5082 patients with an average recurrence rate of 36%. Variables on which a meta-analysis could be performed were body mass index (BMI) (n = 12), age (n = 11), preoperative stage (n = 9), levator avulsion (n = 8), parity (n = 8), constipation/straining (n = 6), number of compartments involved (n = 4), prior hysterectomy (n = 4), familiy history (n = 3), and several other predictors evaluated in only three studies. The following meta- analyses identified significant predictors: levator avulsion [odds ratio (OR) 2.76, P < 0.01], preoperative stage 3–4 (OR 2.11, P < 0.001), family history (OR 1.84, P = 0.006), and hiatal area (OR 1.06/cm2, P = 0.003).ConclusionsLevator avulsion, prolapse stage, and family history are significant risk factors for prolapse recurrence.

Objective Previous meta-analyses have examined the prognosis of women with pregnancy-associated breast cancer (PABC) as well as pregnancy that follows breast cancer diagnosis. Since then, many additional studies have been performed. We conducted an updated meta-analysis to examine the prognosis for women who become pregnant before, during and after a diagnosis of breast cancer. We also performed analyses on the various subgroups within PABC such as pregnancy and postpartum cases, as well as on time periods postpartum. Methods We identified studies that reported on overall (OS) and disease-free survival (DFS) in patients diagnosed with breast cancer during pregnancy or up to 5 years postpartum from four electronic databases. We also identified studies that reported on OS and DFS where pregnancy up to 5 years occurred after a breast cancer diagnosis. Results 41 studies met our inclusion criteria (cases = 4929; controls = 61,041) for pregnancy occurring during or before breast cancer diagnosis. There was an overall increased risk of death amongst patients compared to non-pregnant controls [HR 1.57; 95 % CI 1.35–1.82]. Subgroup analysis indicated poor survival outcomes for those diagnosed either during pregnancy or postpartum (PABC) [HR 1.46; 95 % CI 1.17–1.82] as well as those diagnosed during pregnancy alone [HR 1.47; 95 % CI 1.04–2.08]. Those diagnosed postpartum had the poorest overall survival [HR 1.79; 95 % CI 1.39–2.29]. Similarly, patients with PABC had decreased DFS compared to controls [HR 1.51; 95 % CI 1.22–1.88]. Those diagnosed postpartum were the most at risk of disease progression or relapse [HR 1.86; 95 % CI 1.17–2.93]. 19 studies met our inclusion criteria (cases = 1829; controls = 21,907) for pregnancy following breast cancer diagnosis. Such women had a significantly reduced risk of death compared to those who did not become pregnant [pHR 0.63; 95 % CI 0.51–0.79]. A subgroup analysis to account for the “healthy mother effect” generated similar results [pHR 0.65; 95 % CI 0.52–0.81]. Conclusion Pregnancy that occurs before or concurrently with a diagnosis of breast cancer is more likely to result in death and decreased disease-free survival. On the other hand, pregnancy occurring after a breast cancer diagnosis reduces the risk of death.

BACKGROUND:It has been posited that there is an association between perineal talc use and the incidence of ovarian cancer. To date, this has only been explored in observational studies. OBJECTIVES:To perform a meta-analysis to evaluate the association between perineal talc use and risk of ovarian cancer. METHODS:Studies were identified using six electronic databases. Observational studies involving at least 50 cases of ovarian cancer were eligible for inclusion. We analyzed the association between ovarian cancer, including specific types, and any perineal talc use, long-term (>10 years) use, total lifetime applications, and use on diaphragms or sanitary napkins. A subgroup analysis was performed, stratifying by study design and population. RESULTS:We identified 24 case–control (13,421 cases) and three cohort studies (890 cases, 181,860 person-years). Any perineal talc use was associated with increased risk of ovarian cancer (OR = 1.31; 95% CI = 1.24, 1.39). More than 3600 lifetime applications (OR = 1.42; 95% CI = 1.25, 1.61) were slightly more associated with ovarian cancer than <3600 (OR = 1.32; 95% CI = 1.15, 1.50). An association with ever use of talc was found in case–control studies (OR = 1.35; 95% CI = 1.27, 1.43), but not cohort studies (OR = 1.06; 95% CI = 0.90, 1.25). However, cohort studies found an association between talc use and invasive serous type ovarian cancer (OR = 1.25; 95% CI = 1.01, 1.55). We found an increased risk of serous and endometrioid, but not mucinous or clear cell subtypes. CONCLUSIONS:In general, there is a consistent association between perineal talc use and ovarian cancer. Some variation in the magnitude of the effect was found when considering study design and ovarian cancer subtype.

Background Benzodiazepine use is highly prevalent in elderly and late middle-aged populations and may be associated with an increased risk of dementia. Observational studies have suggested that benzodiazepine use may increase the risk of dementia, however there have been significant concerns regarding protopathic bias in these studies, precluding conclusive findings. Objective The aim of our study was to investigate the risk of dementia associated with the use of benzodiazepines in elderly patients, after controlling for protopathic bias. Methods We identified observational studies with more than 50 cases, adequate assessment of benzodiazepine exposure, and reliable dementia diagnosis ascertainment, from the MEDLINE, PubMed, EMBASE, CINAHL, LILACS and CENTRAL electronic databases through to 5 June 2018, with no language limits. The association of any current or former use of short- or long-acting benzodiazepines with incident dementia was analysed. A subgroup analysis was performed by the introduction of lag time to assess the effect of protopathic bias. We also performed analyses considering the effect of higher benzodiazepine cumulative doses and adjustment for psychiatric covariates. Study quality was investigated using the Newcastle–Ottawa Scale. Results We identified 15 studies reported in 14 articles, involving 159,090 cases. Ever use of benzodiazepines was associated with a significantly increased risk of dementia [odds ratio (OR) 1.39, 95% confidence interval (CI) 1.21–1.59]. Those studies that implemented the longest lag times of ≥ 5 years, and hence most likely to overcome protopathic bias, found a risk estimate that was marginally attenuated, but still significant (OR 1.30, 95% CI 1.14–1.48). Long-acting benzodiazepines were associated with a marginally higher magnitude risk (OR 1.21, 95% CI 0.99–1.49) than short-acting benzodiazepines (OR 1.13, 95% CI 1.02–1.26), although the former failed to reach statistical significance ( p  = 0.059). Conclusions Our findings indicate that the association between benzodiazepine use and dementia incidence is not purely an artefact due to protopathic bias. Reduction of inappropriate benzodiazepine prescription is likely to attenuate dementia risk.

•There was no relationship between vaccination and autism (OR: 0.99; 95% CI: 0.92 to 1.06).•There was no relationship between vaccination and ASD (autism spectrum disorder) (OR: 0.91; 95% CI: 0.68 to 1.20).•There was no relationship between [autism/ASD] and MMR (OR: 0.84; 95% CI: 0.70 to 1.01).•There was no relationship between [autism/ASD] and thimerosal (OR: 1.00; 95% CI: 0.77 to 1.31).•There was no relationship between [autism/ASD] and mercury (Hg) (OR: 1.00; 95% CI: 0.93 to 1.07).•Findings of this meta-analysis suggest that vaccinations are not associated with the development of autism or autism spectrum disorder. There has been enormous debate regarding the possibility of a link between childhood vaccinations and the subsequent development of autism. This has in recent times become a major public health issue with vaccine preventable diseases increasing in the community due to the fear of a ‘link’ between vaccinations and autism. We performed a meta-analysis to summarise available evidence from case-control and cohort studies on this topic (MEDLINE, PubMed, EMBASE, Google Scholar up to April, 2014). Eligible studies assessed the relationship between vaccine administration and the subsequent development of autism or autism spectrum disorders (ASD). Two reviewers extracted data on study characteristics, methods, and outcomes. Disagreement was resolved by consensus with another author. Five cohort studies involving 1,256,407 children, and five case-control studies involving 9,920 children were included in this analysis. The cohort data revealed no relationship between vaccination and autism (OR: 0.99; 95% CI: 0.92 to 1.06) or ASD (OR: 0.91; 95% CI: 0.68 to 1.20), nor was there a relationship between autism and MMR (OR: 0.84; 95% CI: 0.70 to 1.01), or thimerosal (OR: 1.00; 95% CI: 0.77 to 1.31), or mercury (Hg) (OR: 1.00; 95% CI: 0.93 to 1.07). Similarly the case-control data found no evidence for increased risk of developing autism or ASD following MMR, Hg, or thimerosal exposure when grouped by condition (OR: 0.90, 95% CI: 0.83 to 0.98; p=0.02) or grouped by exposure type (OR: 0.85, 95% CI: 0.76 to 0.95; p=0.01). Findings of this meta-analysis suggest that vaccinations are not associated with the development of autism or autism spectrum disorder. Furthermore, the components of the vaccines (thimerosal or mercury) or multiple vaccines (MMR) are not associated with the development of autism or autism spectrum disorder.

Randomised and sham-controlled trials (RCTs) of repetitive transcranial magnetic stimulation (rTMS) in the treatment of obsessive-compulsive disorder (OCD) have yielded conflicting results, which may be due to the variability in rTMS parameters used. We performed an updated systematic review and meta-analysis on the effectiveness of rTMS for the treatment of OCD and aimed to determine whether certain rTMS parameters, such as cortical target, may be associated with higher treatment effectiveness. After conducting a systematic literature review for RCTs on rTMS for OCD through to 1 December 2016 using MEDLINE, PubMed, Web of Science, PsycINFO, Google, and Google Scholar, we performed a random-effects meta-analysis with the outcome measure as pre-post changes in Yale-Brown Obsessive Compulsive Scale (Y-BOCS) scores. To determine whether rTMS parameters may have influenced treatment effectiveness, studies were further analysed according to cortical target, stimulation frequency, and length of follow-up. Data were obtained from 18 RCTs on rTMS in the treatment of OCD. Overall, rTMS yielded a modest effect in reducing Y-BOCS scores with Hedge’s g of 0.79 (95% CI = 0.43–1.15, p < 0.001). Stimulation of the supplementary motor area yielded the greatest reductions in Y-BOCS scores relative to other cortical targets. Subgroup analyses suggested that low frequency rTMS was more effective than high frequency rTMS. The effectiveness of rTMS was also greater at 12 weeks follow-up than at four weeks follow-up. Our meta-analysis implies that low frequency rTMS applied over the supplementary motor area may offer the greatest effectiveness in the treatment of OCD. The therapeutic effects of rTMS also appear to persist post-treatment and may offer beneficial long-term effectiveness. With our findings, it is suggested that future large-scale studies focus on the supplementary motor area and include follow-up periods of 12 weeks or more.

Unfortunately, although the authors mentioned collecting data on month, season, and atmospheric temperature, however, there was very little real data presented in the paper. [...]it might have been useful to graph the minimum and maximum temperatures over the course of the study period and was the temperature data collected for Naples, as it is not stated in the paper. Conversely, abdominal pain was not linked to inadequate bowel preparation (OR: 0.39, 95% CI: 0.05–3.01), nor was having a fecal occult blood test (FOBT) (OR: 0.38, 95% CI: 0.54–2.68), or iron deficiency (OR: 0.53, 95% CI: 0.07–4.12).

BackgroundOver the last three decades, laparoscopic appendicectomy (LA) has become the routine treatment for uncomplicated acute appendicitis. The role of laparoscopic surgery for complicated appendicitis (gangrenous and/or perforated) remains controversial due to concerns of an increased incidence of post-operative intra-abdominal abscesses (IAA) in LA compared to open appendicectomy (OA). The aim of this study was to compare the outcomes of LA versus OA for complicated appendicitis.MethodsA systematic literature search following PRISMA guidelines was conducted using MEDLINE, EMBASE, PubMed and Cochrane Database for randomised controlled trials (RCT) and case–control studies (CCS) that compared LA with OA for complicated appendicitis.ResultsData from three RCT and 30 CCS on 6428 patients (OA 3,254, LA 3,174) were analysed. There was no significant difference in the rate of IAA (LA = 6.1% vs. OA = 4.6%; OR = 1.02, 95% CI = 0.71–1.47, p = 0.91). LA for complicated appendicitis has decreased overall post-operative morbidity (LA = 15.5% vs. OA = 22.7%; OR = 0.43, 95% CI: 0.31–0.59, p < 0.0001), wound infection, (LA = 4.7% vs. OA = 12.8%; OR = 0.26, 95% CI: 0.19–0.36, p < 0.001), respiratory complications (LA = 1.8% vs. OA = 6.4%; OR = 0.25, 95% CI: 0.13–0.49, p < 0.001), post-operative ileus/small bowel obstruction (LA = 3.1% vs. OA = 3.6%; OR = 0.65, 95% CI: 0.42–1.0, p = 0.048) and mortality rate (LA = 0% vs. OA = 0.4%; OR = 0.15, 95% CI: 0.04–0.61, p = 0.008). LA has a significantly shorter hospital stay (6.4 days vs. 8.9 days, p = 0.02) and earlier resumption of solid food (2.7 days vs. 3.7 days, p = 0.03).ConclusionThese results clearly demonstrate that LA for complicated appendicitis has the same incidence of IAA but a significantly reduced morbidity, mortality and length of hospital stay compared with OA. The finding of complicated appendicitis at laparoscopy is not an indication for conversion to open surgery. LA should be the preferred treatment for patients with complicated appendicitis.

We performed a systematic review and meta-analysis to explore whether type 2 diabetes mellitus (T2DM) increases the risk of Alzheimer's disease (AD). We also reviewed interactions with smoking, hypertension, and apolipoprotein E ɛ4. Using a series of databases (MEDLINE, EMBASE, PubMed, Current Contents Connect, and Google Scholar), we identified a total of 15 epidemiologic studies. Fourteen studies reported positive associations, of which 9 were statistically significant. Risk estimates ranged from 0.83 to 2.45. The pooled adjusted risk ratio was 1.57 (95% confidence interval: 1.41, 1.75), with a population-attributable risk of 8%. Smoking and hypertension, when comorbid with T2DM, had odds of 14 and 3, respectively. Of the 5 studies that investigated the interaction between T2DM and apolipoprotein E ɛ4, 4 showed positive associations, of which 3 were significant, with odds ranging from 2.4 to 4.99. The pooled adjusted risk ratio was 2.91 (95% confidence interval: 1.51, 5.61). Risk estimates were presented in the context of a key confounder—cerebral infarcts—which are more common in those with T2DM and might contribute to the manifestation of clinical AD. We provide evidence from clinico-neuropathologic studies that demonstrates the following: First, cerebral infarcts are more common than AD-type pathology in those with T2DM and dementia. Second, those with dementia at postmortem are more likely to have both AD-type and cerebrovascular pathologies. Finally, cerebral infarcts reduce the number of AD lesions required for the manifestation of clinical dementia, but they do not appear to interact synergistically with AD-type pathology. Therefore, the increased risk of clinically diagnosed AD seems to be mediated through cerebrovascular pathology.