Nancy D Berkman, Stacey L Sheridan, Katrina E Donahue, David J Halpern, Anthony Viera, Karen Crotty, Audrey Holland, Michelle Brasure, Kathleen N Lohr, Elizabeth Harden, Elizabeth Tant, Ina Wallace, Meera Viswanathan
{"title":"Health literacy interventions and outcomes: an updated systematic review.","authors":"Nancy D Berkman, Stacey L Sheridan, Katrina E Donahue, David J Halpern, Anthony Viera, Karen Crotty, Audrey Holland, Michelle Brasure, Kathleen N Lohr, Elizabeth Harden, Elizabeth Tant, Ina Wallace, Meera Viswanathan","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To update a 2004 systematic review of health care service use and health outcomes related to differences in health literacy level and interventions designed to improve these outcomes for individuals with low health literacy. Disparities in health outcomes and effectiveness of interventions among different sociodemographic groups were also examined.</p><p><strong>Data sources: </strong>We searched MEDLINE®, the Cumulative Index to Nursing and Allied Health Literature, the Cochrane Library, PsychINFO, and the Educational Resources Information Center. For health literacy, we searched using a variety of terms, limited to English and studies published from 2003 to May 25, 2010. For numeracy, we searched from 1966 to May 25, 2010.</p><p><strong>Review methods: </strong>We used standard Evidence-based Practice Center methods of dual review of abstracts, full-text articles, abstractions, quality ratings, and strength of evidence grading. We resolved disagreements by consensus. We evaluated whether newer literature was available for answering key questions, so we broadened our definition of health literacy to include numeracy and oral (spoken) health literacy. We excluded intervention studies that did not measure health literacy directly and updated our approach to evaluate individual study risk of bias and to grade strength of evidence.</p><p><strong>Results: </strong>We included good- and fair-quality studies: 81 studies addressing health outcomes (reported in 95 articles including 86 measuring health literacy and 16 measuring numeracy, of which 7 measure both) and 42 studies (reported in 45 articles) addressing interventions. Differences in health literacy level were consistently associated with increased hospitalizations, greater emergency care use, lower use of mammography, lower receipt of influenza vaccine, poorer ability to demonstrate taking medications appropriately, poorer ability to interpret labels and health messages, and, among seniors, poorer overall health status and higher mortality. Health literacy level potentially mediates disparities between blacks and whites. The strength of evidence of numeracy studies was insufficient to low, limiting conclusions about the influence of numeracy on health care service use or health outcomes. Two studies suggested numeracy may mediate the effect of disparities on health outcomes. We found no evidence concerning oral health literacy and outcomes. Among intervention studies (27 randomized controlled trials [RCTs], 2 cluster RCTs, and 13 quasi-experimental designs), the strength of evidence for specific design features was low or insufficient. However, several specific features seemed to improve comprehension in one or a few studies. The strength of evidence was moderate for the effect of mixed interventions on health care service use; the effect of intensive self-management inventions on behavior; and the effect of disease-management interventions on disease prevale","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 199","pages":"1-941"},"PeriodicalIF":0.0,"publicationDate":"2011-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31027709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ronald A Booth, Mohammed T Ansari, Andrea C Tricco, Evelin Loit, Laura Weeks, Steve Doucette, Becky Skidmore, Jeffrey S Hoch, Sophia Tsouros, Margaret Sears, Richmond Sy, Jacob Karsh, Suja Mani, James Galipeau, Alexander Yurkiewich, Raymond Daniel, Alexander Tsertsvadze, Fatemeh Yazdi
{"title":"Assessment of thiopurine methyltransferase activity in patients prescribed azathioprine or other thiopurine-based drugs.","authors":"Ronald A Booth, Mohammed T Ansari, Andrea C Tricco, Evelin Loit, Laura Weeks, Steve Doucette, Becky Skidmore, Jeffrey S Hoch, Sophia Tsouros, Margaret Sears, Richmond Sy, Jacob Karsh, Suja Mani, James Galipeau, Alexander Yurkiewich, Raymond Daniel, Alexander Tsertsvadze, Fatemeh Yazdi","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To examine whether pretreatment determination of thiopurine methyltransferase (TPMT) enzymatic activity (phenotyping) or TPMT genotype, to guide thiopurine therapy in chronic autoimmune disease patients, reduces treatment harms. Other objectives included assessing: preanalytic, analytic, and postanalytic requirements for TPMT testing; diagnostic accuracy of TPMT genotyping versus phenotyping; association of thiopurine toxicity with TPMT genotypic or phenotypic status; and costs of testing, care, and treating drug-associated complications.</p><p><strong>Data sources: </strong>MEDLINE®, EMBASE®, and Healthstar were searched from inception to May 2010; the Cochrane Library® to October 2009; and BIOSIS®, Genetics Abstracts, and EconLit™ to May 2009, for English language records.</p><p><strong>Review methods: </strong>A reviewer screened records, and a second reviewer verified exclusions and subsequent selection of relevant studies. Studies in patients with leukemia and organ transplant were excluded. Additionally, laboratories that provide TPMT analytical services were surveyed to assess means of TPMT testing in practice. Where possible, risk of bias was assessed using standard criteria. Meta-analyses estimated diagnostic sensitivity, and specificity; and odds ratios of associations.</p><p><strong>Results: </strong>1790 titles or abstracts, and 538 full text records were screened. 114 observational studies and one RCT were included. Majority of studies were rated fair quality, except for diagnostic studies with 37 percent of studies rated poor. In general, there were few patients who were homozygous (or compound heterozygous) for TPMT variant alleles in the included studies limiting applicability. There is insufficient evidence examining effectiveness of pretesting in terms of reduction in clinical adverse events. Sufficient preanalytical data were available regarding preferred specimen collection, stability and storage conditions for TPMT testing. There was no clinically significant effect of age, gender, various coadministered drugs, or most morbidities (with the exception of renal failure and dialysis). TPMT phenotyping methods had coefficients of variation generally below 10 percent. TPMT genotyping reproducibility is generally between 95-100 percent. The sensitivity of genotyping to identify patients with low or intermediate TPMT enzymatic activity is imprecise, ranging from 70.70 to 82.10 percent (95 percent CI, lower bound range 37.90 to 54.00 percent; upper bound range 84.60 to 96.90 percent). Sensitivity of homozygous TPMT genotype to correctly identify patients with low to absent enzymatic activity was 87.10 percent (95 percent CI 44.30 to 98.30 percent). Genotyping specificity approached 100 percent. Leukopenia was significantly associated with low and intermediate enzymatic activity (low activity OR 80.00, 95 percent CI 11.5 to 559; and intermediate activity OR 2.96, 95 percent CI 1.18 to 7.42), and hom","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 196","pages":"1-282"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31027437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paul G Shekelle, Glenn Takata, Sydne J Newberry, Tumaini Coker, Mary Ann Limbos, Linda S Chan, Martha M Timmer, Marika J Suttorp, Jason Carter, Aneesa Motala, Di Valentine, Breanne Johnsen, Roberta Shanman
{"title":"Management of Acute Otitis Media: update.","authors":"Paul G Shekelle, Glenn Takata, Sydne J Newberry, Tumaini Coker, Mary Ann Limbos, Linda S Chan, Martha M Timmer, Marika J Suttorp, Jason Carter, Aneesa Motala, Di Valentine, Breanne Johnsen, Roberta Shanman","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Context: </strong>Acute Otitis Media (AOM), a viral or bacterial infection of the ear, is the most common childhood infection for which antibiotics are prescribed in the United States. In 2001, the Southern California Evidence-based Practice Center conducted a systematic review of the evidence comparing treatments of AOM.</p><p><strong>Objectives: </strong>This review updates the 2001 review findings on diagnosis and treatment of uncomplicated AOM, assesses the evidence for treatment of recurrent AOM, and assesses the impact of the heptavalent pneumococcal conjugate (PCV7) vaccine on the microbiology of AOM.</p><p><strong>Data sources and study selection: </strong>Searches of PubMed® and the Cochrane databases were conducted from January 1998 to July 2010 using the same search strategies used for the 2001 report, with the addition of terms not considered in the 2001 review. The Web of Science was also searched for citations of the 2001 report and its peer-reviewed publications.</p><p><strong>Data extraction: </strong>After review by two investigators against pre-determined inclusion/exclusion criteria, we included existing systematic reviews and randomized controlled clinical trials for assessment of treatment efficacy and safety. Pooled analysis was performed for comparisons with three or more trials.</p><p><strong>Results and conclusions: </strong>Few studies were found that examined the accuracy and precision of the diagnosis of AOM. Since PCV7's introduction, AOM microbiology has shifted significantly, with Streptococcus pneumoniae becoming less prevalent and Haemophilus influenzae (HF) increasing in importance. For uncomplicated AOM, pooled analysis indicates that nine children (95% CI: 6, 20) would need to be treated with ampicillin or amoxicillin rather than placebo to note a difference in the rate of clinical success. However, in four studies of delayed treatment approaches for uncomplicated AOM, two had higher rates of clinical success with immediate antibiotic therapy while two did not, and in three studies, a marked decrease in antibiotic utilization was noted. We are unable to draw definitive conclusions regarding the comparative effectiveness of different antibiotics for AOM in children with recurrent otitis media (ROM). For ROM, long-term antibiotic administration will decrease AOM episodes from 3 to 1.5 for every 12 months of treatment per otitis prone child during active treatment (95% CI: 1.2, 2.1); however, potential consequences of long-term treatment need to be considered. Data were insufficient to draw conclusions about comparative effectiveness of different treatment strategies in subgroups of children with uncomplicated AOM. Adverse events were generally more frequent for amoxicillin-clavulanate than for cefdinir, ceftriaxone, or azithromycin. Higher quality studies and improved reporting of study characteristics related to quality are needed to provide definitive conclusions for AOM and ROM treatment options.</p","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 198","pages":"1-426"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31028347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olu Oyesanmi, David Snyder, Nancy Sullivan, James Reston, Jonathan Treadwell, Karen M Schoelles
{"title":"Alcohol consumption and cancer risk: understanding possible causal mechanisms for breast and colorectal cancers.","authors":"Olu Oyesanmi, David Snyder, Nancy Sullivan, James Reston, Jonathan Treadwell, Karen M Schoelles","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the risk of developing breast and colorectal cancers.</p><p><strong>Data sources: </strong>We searched 11 external databases, including PubMed® and Embase, for studies on possible mechanisms. These searches used Medical Subject Headings and free text words to identify relevant evidence.</p><p><strong>Review methods: </strong>Two reviewers independently screened search results, selected studies to be included, and reviewed each trial for inclusion. We manually examined the bibliographies of included studies, scanned the content of new issues of selected journals, and reviewed relevant gray literature for potential additional articles.</p><p><strong>Results: </strong>Breast Cancer. Five human and 15 animal studies identified in our searches point to a connection between alcohol intake and changes in important metabolic pathways that when altered may increase the risk of developing breast cancer. Alterations in blood hormone levels, especially elevated estrogen-related hormones, have been reported in humans. Several cell line studies suggest that the estrogen receptor pathways may be altered by ethanol. Increased estrogen levels may increase the risk of breast cancer through increases in cell proliferation and alterations in estrogen receptors. Human studies have also suggested a connection with prolactin and with biomarkers of oxidative stress. Of 15 animal studies, six reported increased mammary tumorigenesis (four administered a co-carcinogen and two did not). Other animal studies reported conversion of ethanol to acetaldehyde in mammary tissue as having a significant effect on the progression of tumor development. Fifteen cell line studies suggested the following mechanisms: Increased hormonal receptor levels. Increased cell proliferation. A direct stimulatory effect. DNA adduct formation. Increase cyclic adenosine monophosphate (camp). Change in potassium channels. Modulation of gene expression. Colorectal Cancer. One human tissue study, 19 animal studies (of which 12 administered a co-carcinogen and seven did not), and 10 cell line studies indicate that ethanol and acetaldehyde may alter metabolic pathways and cell structures that increase the risk of developing colon cancer. Exposure of human colonic biopsies to acetaldehyde suggests that acetaldehyde disrupts epithelial tight junctions. Among 19 animal studies the mechanisms considered included: Mucosal damage after ethanol consumption. Increased degradation of folate. Stimulation of rectal carcinogenesis. Increased cell proliferation. Increased effect of carcinogens. Ten cell line studies suggested: Folate uptake modulation. Tumor necrosis factor modulation. Inflammation and cell death. DNA adduct formation. Cell differentiation. Modulation of gene expression. One study used a combination of a","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 197","pages":"1-151"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31025175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marilee C Allen, Pamela Donohue, Maureen Gilmore, Elizabeth Cristofalo, Renee F Wilson, Jonathan Z Weiner, Karen Robinson
{"title":"Inhaled nitric oxide in preterm infants.","authors":"Marilee C Allen, Pamela Donohue, Maureen Gilmore, Elizabeth Cristofalo, Renee F Wilson, Jonathan Z Weiner, Karen Robinson","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To systematically review the evidence on the use of inhaled nitric oxide (iNO) in preterm infants born at or before 34 weeks gestation age who receive respiratory support.</p><p><strong>Data sources: </strong>We searched MEDLINE, EMBASE, the Cochrane Central Register of Controlled Studies (CENTRAL) and PsycInfo in June 2010. We also searched the proceedings of the 2009 and 2010 Pediatric Academic Societies Meeting and ClinicalTrials.gov. We identified additional studies from reference lists of eligible articles and relevant reviews, as well as from technical experts.</p><p><strong>Review methods: </strong>Questions were developed in collaboration with technical experts, including the chair of the upcoming National Institutes of Health Office of Medical Applications of Research Consensus Development Conference. We limited our review to randomized controlled trials (RCTs) for the question of survival or occurrence of bronchopulmonary dysplasia (BPD) and for the question on short-term risks. All study designs were considered for long-term pulmonary or neurodevelopmental outcomes, and for questions about whether outcomes varied by subpopulation or by intervention characteristics. Two investigators independently screened search results, and abstracted data from eligible articles.</p><p><strong>Results: </strong>We identified a total of 14 RCTs, reported in 23 articles, and eight observational studies. Mortality rates in the NICU did not differ for infants treated with iNO versus those not treated with iNO (RR 0.97 (95% CI 0.82, 1.15)). BPD at 36 weeks for iNO and control groups also did not differ (RR 0.93 (0.86, 1.003) for survivors). A small difference was found between iNO and control infants in the composite outcome of death or BPD (RR 0.93 (0.87, 0.99)). There was inconsistent evidence about the risk of brain injury from individual RCTs, but meta-analyses showed no difference between iNO and control groups. We found no evidence of differences in other short term risks. There was no evidence to suggest a difference in the incidence of cerebral palsy (RR 1.36 (0.88, 2.10)), neurodevelopmental impairment (RR 0.91 (0.77, 1.12)), or cognitive impairment (RR 0.72 (0.35, 1.45)). Evidence was limited on whether the effect of iNO varies by subpopulation or by characteristics of the therapy (timing, dose and duration, mode of delivery, or concurrent therapies).</p><p><strong>Conclusions: </strong>There was a seven percent reduction in the risk of the composite outcome of death or BPD at 36 weeks PMA for infants treated with iNO compared to controls, but no reduction in death or BPD alone. Further studies are needed to explore particular subgroups of infants and to assess long term outcomes including function in childhood. There is currently no evidence to support the use of iNO in preterm infants with respiratory failure outside the context of rigorously conducted randomized clinical trials.</p>","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 195","pages":"1-315"},"PeriodicalIF":0.0,"publicationDate":"2010-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31028135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andrea D Furlan, Fatemeh Yazdi, Alexander Tsertsvadze, Anita Gross, Maurits Van Tulder, Lina Santaguida, Dan Cherkin, Joel Gagnier, Carlo Ammendolia, Mohammed T Ansari, Thomas Ostermann, Trish Dryden, Steve Doucette, Becky Skidmore, Raymond Daniel, Sophia Tsouros, Laura Weeks, James Galipeau
{"title":"Complementary and alternative therapies for back pain II.","authors":"Andrea D Furlan, Fatemeh Yazdi, Alexander Tsertsvadze, Anita Gross, Maurits Van Tulder, Lina Santaguida, Dan Cherkin, Joel Gagnier, Carlo Ammendolia, Mohammed T Ansari, Thomas Ostermann, Trish Dryden, Steve Doucette, Becky Skidmore, Raymond Daniel, Sophia Tsouros, Laura Weeks, James Galipeau","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Back and neck pain are important health problems with serious societal and economic implications. Conventional treatments have been shown to have limited benefit in improving patient outcomes. Complementary and Alternative Medicine (CAM) therapies offer additional options in the management of low back and neck pain. Many trials evaluating CAM therapies have poor quality and inconsistent results.</p><p><strong>Objectives: </strong>To systematically review the efficacy, effectiveness, cost-effectiveness, and harms of acupuncture, spinal manipulation, mobilization, and massage techniques in management of back, neck, and/or thoracic pain.</p><p><strong>Data sources: </strong>MEDLINE, Cochrane Central, Cochrane Database of Systematic Reviews, CINAHL, and EMBASE were searched up to 2010; unpublished literature and reference lists of relevant articles were also searched. study selection: All records were screened by two independent reviewers. Primary reports of comparative efficacy, effectiveness, harms, and/or economic evaluations from randomized controlled trials (RCTs) of the CAM therapies in adults (age ≥ 18 years) with back, neck, or thoracic pain were eligible. Non-randomized controlled trials and observational studies (case-control, cohort, cross-sectional) comparing harms were also included. Reviews, case reports, editorials, commentaries or letters were excluded.</p><p><strong>Data extraction: </strong>Two independent reviewers using a predefined form extracted data on study, participants, treatments, and outcome characteristics.</p><p><strong>Results: </strong>265 RCTs and 5 non-RCTs were included. Acupuncture for chronic nonspecific low back pain was associated with significantly lower pain intensity than placebo but only immediately post-treatment (VAS: -0.59, 95 percent CI: -0.93, -0.25). However, acupuncture was not different from placebo in post-treatment disability, pain medication intake, or global improvement in chronic nonspecific low back pain. Acupuncture did not differ from sham-acupuncture in reducing chronic non-specific neck pain immediately after treatment (VAS: 0.24, 95 percent CI: -1.20, 0.73). Acupuncture was superior to no treatment in improving pain intensity (VAS: -1.19, 95 percent CI: 95 percent CI: -2.17, -0.21), disability (PDI), functioning (HFAQ), well-being (SF-36), and range of mobility (extension, flexion), immediately after the treatment. In general, trials that applied sham-acupuncture tended to produce negative results (i.e., statistically non-significant) compared to trials that applied other types of placebo (e.g., TENS, medication, laser). Results regarding comparisons with other active treatments (pain medication, mobilization, laser therapy) were less consistent Acupuncture was more cost-effective compared to usual care or no treatment for patients with chronic back pain. For both low back and neck pain, manipulation was significantly better than placebo or no treatment in r","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 194","pages":"1-764"},"PeriodicalIF":0.0,"publicationDate":"2010-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31027703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
John W Williams, B L Plassman, J Burke, S Benjamin
{"title":"Preventing Alzheimer's disease and cognitive decline.","authors":"John W Williams, B L Plassman, J Burke, S Benjamin","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To assess whether previous research on purported risk or protective factors for Alzheimer's disease (AD) and cognitive decline is of sufficient strength to warrant specific recommendations for behavioral, lifestyle, or pharmaceutical interventions/modifications targeted to these endpoints.</p><p><strong>Data sources: </strong>MEDLINE and the Cochrane Database of Systematic Reviews. Additional studies were identified from reference lists and technical experts.</p><p><strong>Review methods: </strong>A group of experts in the field developed the list of factors to be evaluated in preparation for an upcoming National Institutes of Health (NIH) Office of Medical Applications of Research (OMAR) State-of-the-Science Conference addressing the prevention of AD and cognitive decline. We grouped the factors into the following categories: nutritional factors, medical conditions and prescription and non-prescription medications, social/economic/behavioral factors, toxic environmental factors, and genetics. Outcomes of interest were the development of AD or cognitive decline. Both observational and intervention studies were evaluated. Studies were evaluated for eligibility and quality, and data were abstracted on study design, demographics, intervention or predictor factor, and cognitive outcomes.</p><p><strong>Results: </strong>A total of 25 systematic reviews and 250 primary research studies were included. Only a few factors showed a consistent association with AD or cognitive decline across multiple studies, including both observational studies and randomized controlled trials (when available). Such factors associated with increased risk of AD and cognitive decline were: diabetes, epsilon 4 allele of the apolipoprotein E gene (APOE e4), smoking, and depression. Factors showing a fairly consistent association with decreased risk of AD and cognitive decline were: cognitive engagement and physical activities. A consistent association does not imply that findings were robust, as the data were often limited, and the quality of evidence was typically low. In addition, the modification of risk for reported associations was typically small to moderate for AD, and small for cognitive decline. Some of the factors that did not show an association with AD or cognitive decline in this review may still play an influential role in late-life cognition, but there was not sufficient evidence to draw this conclusion. Many of the factors evaluated are not amenable to randomization, so rigorous observational studies are required to assess their effect on AD and cognitive decline.</p><p><strong>Conclusions: </strong>The current research on the list of putative risk or protective factors is largely inadequate to confidently assess their association with AD or cognitive decline. Further research that addresses the limitations of existing studies is needed prior to be able to make recommendations on interventions.</p>","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 193","pages":"1-727"},"PeriodicalIF":0.0,"publicationDate":"2010-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29822956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jeanne-Marie Guise, Karen Eden, Cathy Emeis, Mary Anna Denman, Nicole Marshall, Rongwei Rochelle Fu, Rosalind Janik, Peggy Nygren, Miranda Walker, Marian McDonagh
{"title":"Vaginal birth after cesarean: new insights.","authors":"Jeanne-Marie Guise, Karen Eden, Cathy Emeis, Mary Anna Denman, Nicole Marshall, Rongwei Rochelle Fu, Rosalind Janik, Peggy Nygren, Miranda Walker, Marian McDonagh","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To synthesize the published literature on vaginal birth after cesarean (VBAC). Specifically, to review the trends and incidence of VBAC, maternal benefits and harms, infant benefits and harms, relevant factors influencing each, and the directions for future research.</p><p><strong>Data sources: </strong>Relevant studies were identified from multiple searches of MEDLINE; DARE; the Cochrane databases (1966 to September 2009); and from recent systematic reviews, reference lists, reviews, editorials, Web sites, and experts.</p><p><strong>Review methods: </strong>Specific inclusion and exclusion criteria were developed to determine study eligibility. The target population includes healthy women of reproductive age, with a singleton gestation, in the U.S. with a prior cesarean who are eligible for a trial of labor (TOL) or elective repeat cesarean delivery (ERCD). All eligible studies were quality rated and data were extracted from good or fair quality studies, entered into tables, summarized descriptively and, when appropriate, pooled for analysis. The primary focus of the report was term pregnancies. However, due to a small number of studies on term pregnancies, general population studies including all gestational ages (GA) were included in appropriate areas.</p><p><strong>Results: </strong>We identified 3,134 citations and reviewed 963 papers for inclusion, of which 203 papers met inclusion and were quality rated. Studies of maternal and infant outcomes reported data based upon actual rather than intended router of delivery. The range for TOL and VBAC rates was large (28-82 percent and 49-87 percent, respectively) with the highest rates being reported in studies outside of the U.S. Predictors of women having a TOL were having a prior vaginal delivery and settings of higher-level care (e.g., tertiary care centers). TOL rates in U.S. studies declined in studies initiated after 1996 from 63 to 47 percent, but the VBAC rate remained unimproved. Hispanic and African American women were less likely than their white counterparts to have a vaginal delivery. Overall rates of maternal harms were low for both TOL and ERCD. While rare for both TOL and ERCD, maternal mortality was significantly increased for ERCD at 13.4 per 100,000 versus 3.8 per 100,000 for TOL. The rates of maternal hysterectomy, hemorrhage, and transfusions did not differ significantly between TOL and ERCD. The rate of uterine rupture for all women with prior cesarean is 3 per 1,000 and the risk was significantly increased with TOL (4.7/1,000 versus 0.3/1,000 ERCD). Six percent of uterine ruptures were associated with perinatal death. No models have been able to accurately predict women who are more likely to deliver by VBAC or to rupture. Women with one prior cesarean delivery and previa had a statistically significant increased risk of adverse events compared with previa patients without a prior cesarean delivery; blood transfusion (15 versus 32.2 percent), ","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 191","pages":"1-397"},"PeriodicalIF":0.0,"publicationDate":"2010-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29122274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Timothy J Wilt, Aasma Shaukat, Tatyana Shamliyan, Brent C Taylor, Roderick MacDonald, James Tacklind, Indulis Rutks, Sarah Jane Schwarzenberg, Robert L Kane, Michael Levitt
{"title":"Lactose intolerance and health.","authors":"Timothy J Wilt, Aasma Shaukat, Tatyana Shamliyan, Brent C Taylor, Roderick MacDonald, James Tacklind, Indulis Rutks, Sarah Jane Schwarzenberg, Robert L Kane, Michael Levitt","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>We systematically reviewed evidence to determine lactose intolerance (LI) prevalence, bone health after dairy-exclusion diets, tolerable dose of lactose in subjects with diagnosed LI, and management.</p><p><strong>Data sources: </strong>We searched multiple electronic databases for original studies published in English from 1967-November 2009.</p><p><strong>Review methods: </strong>We extracted patient and study characteristics using author's definitions of LI and lactose malabsorption. We compared outcomes in relation to diagnostic tests, including lactose challenge, intestinal biopsies of lactase enzyme levels, genetic tests, and symptoms. Fractures, bone mineral content (BMC) and bone mineral density (BMD) were compared in categories of lactose intake. Reported symptoms, lactose dose and formulation, timing of lactose ingestion, and co-ingested food were analyzed in association with tolerability of lactose. Symptoms were compared after administration of probiotics, enzyme replacements, lactose-reduced milk and increasing lactose load.</p><p><strong>Results: </strong>Prevalence was reported in 54 primarily nonpopulation based studies (15 from the United States). Studies did not directly assess LI and subjects were highly selected. LI magnitude was very low in children and remained low into adulthood among individuals of Northern European descent. For African American, Hispanic, Asian, and American Indian populations LI rates may be 50 percent higher in late childhood and adulthood. Small doses of lactose were well tolerated in most populations. Low level evidence from 55 observational studies of 223,336 subjects indicated that low milk consumers may have increased fracture risk. Strength and significance varied depended on exposure definitions. Low level evidence from randomized controlled trials (RCTs) of children (seven RCTs) and adult women (two RCTs) with low lactose intake indicated that dairy interventions may improve BMC in select populations. Most individuals with LI can tolerate up to 12 grams of lactose, though symptoms became more prominent at doses above 12 grams and appreciable after 24 grams of lactose; 50 grams induced symptoms in the vast majority. A daily divided dose of 24 grams was generally tolerated. We found insufficient evidence that use of lactose reduced solution/milk, with lactose content of 0-2 grams, compared to a lactose dose of greater than 12 grams, reduced symptoms of lactose intolerance. Evidence was insufficient for probiotics (eight RCTs), colonic adaptation (two RCTs) or varying lactose doses (three RCTs) or other agents (one RCT). Inclusion criteria, interventions, and outcomes were variable. Yogurt and probiotic types studied were variable and results either showed no difference in symptom scores or small differences in symptoms that may be of low clinical relevance.</p><p><strong>Conclusions: </strong>There are race and age differences in LI prevalence. Evidence is insuffici","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 192","pages":"1-410"},"PeriodicalIF":0.0,"publicationDate":"2010-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29122272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Debra J Holden, Russell Harris, Deborah S Porterfield, Daniel E Jonas, Laura C Morgan, Daniel Reuland, Michael Gilchrist, Meera Viswanathan, Kathleen N Lohr, Brieanne Lyda-McDonald
{"title":"Enhancing the use and quality of colorectal cancer screening.","authors":"Debra J Holden, Russell Harris, Deborah S Porterfield, Daniel E Jonas, Laura C Morgan, Daniel Reuland, Michael Gilchrist, Meera Viswanathan, Kathleen N Lohr, Brieanne Lyda-McDonald","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Objectives: </strong>To conduct a systematic review of the use and quality (including underuse, overuse, and misuse) of appropriate colorectal cancer (CRC) screening, including factors associated with screening, effective interventions to improve screening rates, current capacity, and monitoring and tracking the use and quality. Trends in the use and quality of CRC screening tests is also presented.</p><p><strong>Data sources: </strong>We searched MEDLINE, the Cochrane Library, and the Cochrane Central Trials Registry, supplemented by handsearches, for studies published in English from January 1998 through September 2009.</p><p><strong>Review methods: </strong>We used standard Evidence-based Practice Center methods of dual review of abstracts, full text articles, abstractions, quality rating, and quality grading. We resolved disagreements by consensus.</p><p><strong>Results: </strong>We found multiple problems of underuse, overuse, and misuse of CRC screening. We identified a total of 116 articles for inclusion into the systematic review, including a total of 72 studies qualified for inclusion for key question (KQ) 2, 21 for KQ 3, 12 for KQ 4, and 8 for KQ 5. A number of patient-level factors are associated with lower screening rates, including having low income or less education, being uninsured or of Hispanic or Asian descent, not being acculturated into the United States, and having less or reduced access to care. Being insured, of higher income or education, and non-Hispanic white, participating in other cancer screenings, having a family history of CRC or personal history of another cancer, as well as receiving a physician recommendation to be screened, are associated with higher screening rates. Interventions that effectively increased CRC screening with high strength of evidence include patient reminders, one-on-one interactions, eliminating structural barriers, and system-level changes. The largest magnitude of improvement came from one-on-one interactions and eliminating barriers. Purely educational small-media interventions do not improve screening rates. Evidence is mixed for decision aids, although certain designs may be effective. No studies tested interventions to reduce overuse or misuse of CRC screening. We found no studies that assessed monitoring systems for underuse, overuse, and misuse of CRC screening. Modeling studies, using various assumptions, show that if the United States were to adopt a colonoscopy-only approach to CRC screening and everyone were to agree to be screened in this way, it is likely that colonoscopy capacity would need to be substantially increased.</p><p><strong>Conclusions: </strong>Both CRC screening and patient-physician discussions of CRC screening are underused, and important problems of overuse and misuse also exist. Some interventions hold promise for improvement. The research priority is to design and test interventions to increase screening and CRC screening discussions, building on the","PeriodicalId":72991,"journal":{"name":"Evidence report/technology assessment","volume":" 190","pages":"1-195, v"},"PeriodicalIF":0.0,"publicationDate":"2010-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29199822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}