Project description:ContextStudies from different geographical regions have assessed the relations between indoor dampness and mold problems and the risk of asthma, but the evidence has been inconclusive.ObjectiveTo assess the relations between indicators of indoor dampness and mold problems and the risk of developing new asthma, and to investigate whether such relations differ according to the type of exposure.Data sourcesA systematic literature search of PubMed database from 1990 through March 2012 and the reference lists of recent reviews and of relevant articles identified in our search.Study selectionCohort/longitudinal and incident case-control studies assessing the relation between mold/dampness and new asthma were included.Data extractionThree authors independently evaluated eligible articles and extracted relevant information using a structured form.SynthesisSIXTEEN STUDIES WERE INCLUDED: 11 cohort and 5 incident case-control studies. The summary effect estimates (EE) based on the highest and lowest estimates for the relation between any exposure and onset of asthma were for the highest estimates 1.48 (95% confidence interval [CI] 1.23-1.78, random-effects model, Q-statistic 38.75 (16), P = 0.001) ; and for the lowest estimates: 1.27 (95% CI 1.06-1.53, random-effects model, Q-statistic 38.12 (16), P = 0.000) [corrected].The summary effect estimates were significantly elevated for dampness (fixed-effects model: EE 1.33, 95% CI 1.12-1.56, Q-statistic 8.22 (9), P?=?0.413), visible mold (random-effects model; EE 1.29, 95% CI 1.04-1.60, 30.30 (12), P?=?0.001), and mold odor (random-effects model; EE 1.73, 95% CI 1.19-2.50, Q-statistics 14.85 (8), P?=?0.038), but not for water damage (fixed-effects model; EE 1.12, 95% CI 0.98-1.27). Heterogeneity was observed in the study-specific effect estimates.ConclusionThe evidence indicates that dampness and molds in the home are determinants of developing asthma. The association of the presence of visible mold and especially mold odor to the risk of asthma points towards mold-related causal agents.

Project description:BackgroundIbuprofen is one of the most commonly used analgesic and antipyretic drugs in children. However, its potential causal role in childhood asthma pathogenesis remains uncertain. In this systematic review, we assessed the association between ibuprofen administration in children and the risk of developing or exacerbating asthma.MethodsWe searched MEDLINE, Embase, Cochrane Library, CINAHL, Web of Science, and Scopus from inception to May 2022, with no language limits; searched relevant reviews; and performed citation searching. We included studies of any design that were primary empirical peer-reviewed publications, where ibuprofen use in children 0-18 years was reported. Screening was performed in duplicate by blinded review. In total, 24 studies met our criteria. Data were extracted according to PRISMA guidelines, and the risk of bias was assessed using RoB2 and NOS tools. Quantitative data were pooled using fixed effect models, and qualitative data were pooled using narrative synthesis. Primary outcomes were asthma or asthma-like symptoms. The results were grouped according to population (general, asthmatic, and ibuprofen-hypersensitive), comparator type (active and non-active) and follow-up duration (short- and long-term).ResultsComparing ibuprofen with active comparators, there was no evidence of a higher risk associated with ibuprofen over both the short and long term in either the general or asthmatic population. Comparing ibuprofen use with no active alternative over a short-term follow-up, ibuprofen may provide protection against asthma-like symptoms in the general population when used to ease symptoms of fever or bronchiolitis. In contrast, it may cause asthma exacerbation for those with pre-existing asthma. However, in both populations, there were no clear long-term follow-up effects.ConclusionsIbuprofen use in children had no elevated risk relative to active comparators. However, use in children with asthma may lead to asthma exacerbation. The results are driven by a very small number of influential studies, and research in several key clinical contexts is limited to single studies. Both clinical trials and observational studies are needed to understand the potential role of ibuprofen in childhood asthma pathogenesis.

Project description:BackgroundDampness and mold have been shown in qualitative reviews to be associated with a variety of adverse respiratory health effects, including respiratory tract infections. Several published meta-analyses have provided quantitative summaries for some of these associations, but not for respiratory infections. Demonstrating a causal relationship between dampness-related agents, which are preventable exposures, and respiratory tract infections would suggest important new public health strategies. We report the results of quantitative meta-analyses of published studies that examined the association of dampness or mold in homes with respiratory infections and bronchitis.MethodsFor primary studies meeting eligibility criteria, we transformed reported odds ratios (ORs) and confidence intervals (CIs) to the log scale. Both fixed and random effects models were applied to the log ORs and their variances. Most studies contained multiple estimated ORs. Models accounted for the correlation between multiple results within the studies analyzed. One set of analyses was performed with all eligible studies, and another set restricted to studies that controlled for age, gender, smoking, and socioeconomic status. Subgroups of studies were assessed to explore heterogeneity. Funnel plots were used to assess publication bias.ResultsThe resulting summary estimates of ORs from random effects models based on all studies ranged from 1.38 to 1.50, with 95% CIs excluding the null in all cases. Use of different analysis models and restricting analyses based on control of multiple confounding variables changed findings only slightly. ORs (95% CIs) from random effects models using studies adjusting for major confounding variables were, for bronchitis, 1.45 (1.32-1.59); for respiratory infections, 1.44 (1.31-1.59); for respiratory infections excluding nonspecific upper respiratory infections, 1.50 (1.32-1.70), and for respiratory infections in children or infants, 1.48 (1.33-1.65). Little effect of publication bias was evident. Estimated attributable risk proportions ranged from 8% to 20%.ConclusionsResidential dampness and mold are associated with substantial and statistically significant increases in both respiratory infections and bronchitis. If these associations were confirmed as causal, effective control of dampness and mold in buildings would prevent a substantial proportion of respiratory infections.

Project description:Rationale & objectiveOsmotic demyelination syndrome (ODS) is a rare but severe condition often attributed to the rate of sodium collection. We evaluated the association between the overly rapid sodium correction in adult hospitalized patients with ODS.Study designSystematic review and meta-analysis.Setting & study populationsAdults hospitalized hyponatremia patients.Selection criteria for studiesThe studies comparing the incidence of ODS with and without rapid sodium correction inception to January 2024.Data extractionTwo reviewers independently extracted data and assessed the risk of bias and the certainty of evidence.Analytic approachThe incidence of ODS following a rapid and nonrapid sodium correction was pooled using the random effects model. Subgroup and meta-regression analyses were performed for the robustness and the source of heterogeneity.ResultsEleven cohort studies were included with 26,710 hospitalized hyponatremia patients. The definition of hyponatremia varied from <116 to <130 mmol/L, and overly rapid sodium correction was defined as >8 to 12 mmol/L within 24 hours. The overall incidence of ODS was 0.23%. The incidence of ODS in rapid and nonrapid sodium correction was 0.73% and 0.10%, respectively. Meta-analysis demonstrated that a rapid rate of sodium correction was associated with a higher incidence of ODS (odds ratio 3.16, 95% CI, 1.54-6.49, I2 = 27%), whereas some patients with hyponatremia developed ODS without rapid sodium level correction. The sensitivity analysis based on the quality of the studies was consistent with the main result.LimitationVarious definition criteria for ODS diagnosis across studies, lack of potential electrolyte and treatment data that may affect the incidence of ODS.ConclusionsThe rapid rate of sodium correction had a statistical correlation with a higher incidence of ODS. Among ODS without rapid correction, further studies are recommended to evaluate and comprehend the relationship for better and proper management of hospitalized patients with hyponatremia.

Project description:BackgroundAsthma is a common complex chronic, inflammatory polygenic disease with heterogeneous manifestations, affecting individuals of all age groups and posing an immense burden on healthcare resources. A number of studies have identified the association between a disintegrin and metalloprotease 33 (ADAM33) polymorphisms and asthma risk, however, the results still remain inconclusive. The objective of the present study was to identify the effect of ADAM33 variants in asthma susceptibility.MethodsEligible case-control studies published between January 2000 and June 2018 was searched and retrieved from online electronic databases. The odds ratio (OR) with its 95% confidence interval (CI) was employed to calculate the effect.ResultsA total of 63 case-control studies were finally screened out, including 13,280 asthma patients and 13,340 controls. Eleven SNPs of ADAM33 gene were identified. Our results detected a significant association between ADAM33 T2, Q1, F + 1 and AA genotype of T + 1 polymorphisms and asthma risk in total population. Subgroup analysis by ethnicities showed that the alleles and genotypes of T2, Q1 and F + 1 polymorphisms were associated with asthma susceptibility among Asian populations, while V4 polymorphism was associated with asthma among Caucasian populations. Subgroup analysis by ages showed that T2, F + 1 and ST + 4 polymorphisms were associated with childhood asthma, while Q1 and V4 polymorphisms were associated with asthma risk in adults. Subgroup analysis by asthma severity showed that only the G allele of ADAM33 T1 polymorphism was associated with the severity of asthma when compared with the controls. In addition, T2, Q1 and F + 1 polymorphisms of ADAM33 were significantly associated with increased the asthma risk in Chinese asthma patients.ConclusionsOur results found that T2, Q1 and F + 1 polymorphisms of ADAM33 gene might contribute to asthma risk. Future well-designed case-control studies with large population and more ethnicities are still needed to estimate the association.

Project description:Chronic postsurgical pain (CPSP) is a significant detriment to postsurgical recovery and a risk factor for prolonged opioid use. Emerging evidence suggests the estimated heritability for chronic pain is 45% and that genetic factors partially explain individual susceptibility to CPSP. The aim of this study was to systematically review, assess quality, and summarize the studies in humans that have investigated genetic factors associated with CPSP. We also conducted a meta-analysis to derive a single effect size for evaluable genetic associations with CPSP. Our comprehensive literature search included review of 21 full-text articles evaluating variants of 69 genes for association with CPSP. We found significant gene variant associations reported for variants/haplotypes of 26 genes involved in neurotransmission, pain signaling, immune responses and neuroactive ligand-receptor interaction, with CPSP. Six variants of 5 genes (COMT: rs4680 and rs6269, OPRM1: rs1799971, GCH1: rs3783641, KCNS1: rs734784 and TNFA: rs1800629), were evaluated by more than one study and were included in the meta-analysis. At rs734784 (A>G) of KCNS1, presence of G allele marginally increased risk of CPSP (Additive genetic model; Odds ratio: 1.511; 95% CI 1-2.284; P value: .050), while the other variants did not withstand meta-analyses criteria. Our findings demonstrate the role of genetic factors with different functions in CPSP, and also emphasize that single genetic factors have small effect sizes in explaining complex conditions like CPSP. Heterogeneity in surgical cohorts, population structure, and outcome definitions, as well as small number of available studies evaluating same variants, limit the meta-analysis. There is a need for large-scale, homogenous, replication studies to validate candidate genes, and understand the underlying biological networks underpinning CPSP. PERSPECTIVE: Our systematic review comprehensively describes 21 studies evaluating genetic association with CPSP, and limitations thereof. A meta-analysis of 6 variants (5 genes) found marginally increased risk for CPSP associated with rs734784 A>G of the potassium voltage-gated channel gene (KCNS1). Understanding genetic predisposition for CPSP will enable prediction and personalized management.

Dataset Information

Correction: Residential Dampness and Molds and the Risk of Developing Asthma: A Systematic Review and Meta-analysis

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