Association between antipsychotic medication and venous thromboembolism

2010 ◽  
Vol 27 (1) ◽  
pp. 22-26
Author(s):  
Santhana Gunasekaran

AbstractObjective: This study aims to identify and review available evidence in the literature to determine the strength of association between antipsychotic medications and thromboembolism as an adverse effect.Method: Electronic databases were searched for evidence.Results: A total of 15 case reports, 14 case series, two observational studies and three case-control studies were found in the literature. Two case control studies found significantly increased risk of venous thromboembolism (OR 13.3 and 7.1 respectively). The risk was high for low potency antipsychotics. Studies were critically appraised to determine the strength of evidence.Conclusion: The studies reviewed indicate a significant association between antipsychotics and venous thromboembolism. Patients using the antipsychotics and those who prescribe them should be aware of this association.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2560-2560
Author(s):  
Samir Dalia ◽  
Jorge J. Castillo

Abstract Abstract 2560 Introduction: Few risk factors for the development of Hodgkin lymphoma (HL) have been described. A relationship between smoking and the subsequent development of HL has been suggested from previous reports; however, the available data are largely conflicting. The primary objective of this meta-analysis of observational studies is to evaluate the potential epidemiologic relationship, if any, between smoking and HL. Methods: We searched MEDLINE from January 1, 1960 to June 30, 2010 for observational studies on the association between smoking and HL in adults using the keywords “smoking” and “lymphoma”. Prospective cohort studies and case-control studies that reported relative risks (RR), hazard ratios, or odds ratios with 95% confidence intervals (CI) were included. Literature search, study selection and data gathering were performed independently by the two of authors. Cases were subdivided in ever smokers and current smokers and analyzed separately. Fixed-effect model (FEM) and random-effects models (REM) were used to assess the combined outcome of individual studies. The outcome measured in our study is reported as RR (95% CI). REM was used, if needed, to account for heterogeneity between studies. Heterogeneity was evaluated using the Cochrane Q and I2 statistics. Publication bias was assessed by direct observation of a funnel plot as well as trim-and-fill statistics. Quality of the studies was assessed using the Newcastle-Ottawa scale. Results: Our initial search rendered 577 articles. After reviewing the titles and abstracts, 36 papers were selected for full-text retrieval and reference list search, from which 4 prospective and 11 case-control studies were included in the final analysis. All studies were of high quality with both case-control and prospective studies averaging a score of 8 on the Newcastle-Ottawa scale. When pooling all studies, ever smokers had a RR of 1.20 (95% CI 1.07–1.34; p=0.001); there was no heterogeneity between studies or dissemination bias. Current smokers had a RR of 1.42 (95% CI 1.20–1.68; p<0.001, Figure); there was mild heterogeneity between studies (Q=28.5, I2=45.8%, p=0.046) but no dissemination bias was identified. Based on case-control studies, ever smoking was associated with a RR of 1.16 (95% CI 1.02–1.31; p=0.02) while current smoking was associated with a RR of 1.39 (95% CI 1.14–1.69; p<0.001). Based on prospective studies, ever smoking had a RR 1.40 (95% CI 1.10–1.77; p=0.005) while current smoking had a RR 1.49 (1.02-2.18; p=0.04). Conclusions: In both retrospective and prospective studies, there is a 20% increased risk of developing HL in those patients who have ever smoked. However, the risk increases to 42% in those who were current smokers at time of diagnosis of HL. Our findings confirm a previously reported association between smoking and the development of HL, giving additional support in favor of smoking cessation. The lymphomagenic mechanism of smoking is currently unclear but could be related to a direct carcinogenic effect of tobacco-related agents or the immunomodulatory effect of smoking. Disclosures: No relevant conflicts of interest to declare.


2010 ◽  
Vol 33 (6) ◽  
pp. 349 ◽  
Author(s):  
Gideon Koren ◽  
Sheri Nickel

Every year scores of new pharmaceuticals enter the market, almost never with human fetal safety data. Such data typically accumulate during the first years of clinical use, in the form of case reports, case series, prospective and retrospective cohorts and case control studies. All of these methods suffer from serious sources of bias, often leading to alarming signals of teratogenicity that are later found to be false. This review highlights major sources of bias, including the bias against the null hypothesis in its different forms, ascertainment and recall bias, in fetal exposure to pharmaceutical molecules.


2006 ◽  
Vol 4 (S2) ◽  
pp. 101-119 ◽  
Author(s):  
Gunther F. Craun ◽  
Rebecca L. Calderon

Observational studies have assessed endemic waterborne risks in a number of countries. Time-series analyses associated increased water turbidity with increased gastroenteritis risks in several public water systems. Several cohort studies reported an increased risk of gastroenteritis in populations using certain public or individual water systems. Although several case-control studies found increased waterborne risks, they also found increased risks associated with other exposures. An increased risk of campylobacteriosis was associated with drinking untreated water from non-urban areas and some tap waters; other significant risks included contaminated poultry and foreign travel. Increased risks of cryptosporidiosis and giardiasis were associated with drinking water in some populations; other risk factors included foreign travel, day care exposures, and swimming. These observational studies provide evidence that some populations may be at an increased risk of endemic or sporadic illness from waterborne exposures, but not all studies found an increased risk. Differences in waterborne risks may be due to differences in water quality. System vulnerabilities and contamination likely differed in the areas that were studied. The information from these studies may help inform estimates of waterborne illness for the US population but is inadequate to estimate a population attributable risk.


2017 ◽  
Vol 43 (06) ◽  
pp. 614-620 ◽  
Author(s):  
Vera Gessi ◽  
Rossella Marcucci ◽  
Monica Gianni ◽  
Anna Grandi ◽  
Massimo Franchini ◽  
...  

AbstractElevated plasma levels of lipoprotein(a) (Lp(a)) are associated with increased cardiovascular risk in several clinical studies. However, there is a lack of data supporting a positive association between elevated Lp(a) levels and venous thromboembolism (VTE). Thus, we conducted a systematic review of the literature to better clarify its role as a risk factor for VTE. Medline and the Embase (up to May 2015) electronic databases were used to identify potentially eligible studies. Studies measuring Lp(a) values in adult patients with deep vein thrombosis and/or pulmonary embolism and in a population of patients without a VTE were selected. Studies on patients with major venous thromboembolic events occurring at other unusual site, case reports, and case series were excluded. The odds ratios (ORs) of the association between high values of Lp(a) and VTE and the weighted mean difference (WMD) in Lp(a) levels in cases and in controls were calculated using a random-effect model. Results were presented with 95% confidence interval (CI). Fourteen studies for a total of more than 14,000 patients were finally included in our analysis. Lp(a) was slightly but significantly associated with an increased risk of VTE (OR: 1.56, 95% CI: 1.36, 1.79; 10 studies, 13,541 patients). VTE patients had significantly higher Lp(a) values compared with controls (WMD: 14.46 mg/L, 95% CI: 12.14, 16.78; 4 studies, 470 patients). Lp(a) appeared to be significantly associated with increased risk of VTE. However, Lp(a) levels were only slightly increased in VTE patients compared with controls.


Cephalalgia ◽  
2014 ◽  
Vol 35 (2) ◽  
pp. 118-131 ◽  
Author(s):  
G Roberto ◽  
E Raschi ◽  
C Piccinni ◽  
V Conti ◽  
L Vignatelli ◽  
...  

Background Apart from the underlying cardiovascular (CV) risk associated with migraine, both triptans and ergotamines can induce vasoconstriction and potentially increase the risk of serious ischemic events. Because of the low frequency of such events in eligible patients, randomized controlled trials are not exhaustive to assess the drug-related CV risk. Observational studies are, therefore, an essential source of information to clarify this matter of concern. Aim The aim of this study was to systematically review the available published observational studies investigating the risk of serious CV events in triptan or ergotamine users, as compared to unexposed migraineur controls. Methods We systematically searched MEDLINE and EMBASE electronic databases for cohort or case-control studies up to December 1, 2013. Studies retrieved from CDSR, DARE and HTA databases of the Cochrane Library were used for snowballing. Studies investigating the risk of any CV outcome in patients with a migraine diagnosis and exposed to triptans or ergotamines were considered for inclusion. Selection of studies, data extraction, and risk of bias assessment were conducted independently by two reviewers. Pooled odds ratios (ORs) with 95% confidence interval (95% CI) were computed using a random-effects model for studies and outcomes judged eligible for quantitative data synthesis. Results From a total of 3370 citations retrieved, after duplicate removal and screening, only four studies met the inclusion criteria (three nested case-control analyses and one retrospective cohort study). These studies investigated the risk of different CV outcomes associated with either the recency or the intensity of exposure to the studied drugs. As for the intensity of use, the pooled OR of serious ischemic events was 2.28 (95% CI 1.18–4.41; I2 = 0%) for ergotamine use (two studies), whereas for triptans (three studies) it was 0.86 (95% CI 0.52–1.43; I2 = 24.5%). Recent use of ergotamines was not significantly associated with any CV outcome (only one available study). Two studies investigated the risk of stroke related to recent triptan use: the first study reported an OR of 0.90 (0.64–1.26), and the second one suggested an increased risk of 2.51 (1.10–5.71). In this case, because of the high degree of heterogeneity, results were not pooled. Conclusions To date, few comparative observational studies have investigated the CV safety of migraine-specific drugs in clinical practice. Evidence gathered here suggests that intense consumption of ergotamines may be associated with an increased risk of serious ischemic complications. As for triptans, available studies do not suggest strong CV safety issues, although no firm conclusions can be drawn. In particular, evidence on stroke risk is conflicting. However, if an increase of the absolute stroke risk in recently exposed patients does actually exist, it must be small. Overall, residual uncontrolled confounding factors reduce the confidence in the risk estimates collected from the included studies. Further investigations are needed to better define the risk for rare but serious CV events related to triptan and ergotamine use for treatment of migraine.


2019 ◽  
Vol 62 (4) ◽  
pp. 137-146 ◽  
Author(s):  
Jamal Jafari-Nedooshan ◽  
Seyed Alireza Dastgheib ◽  
Saeed Kargar ◽  
Mohammad Zare ◽  
Ali Raee-Ezzabadi ◽  
...  

Background: The −174G>C (rs1800795) polymorphism at interleukin 6 (IL-6) gene has been reported to be related with the occurrence of colorectal (CRC) and gastric (GC) cancers. However, the results had been conflicting and controversial. In order to give a comprehensive and precise result, we summarized available data to analyze the association of this polymorphism with CRC and GC risk. Methods: A comprehensive literature search on PubMed, Elsevier Science Direct, and CNKI database was performed to identify all eligible studies up to May 15, 2019. The strength of association was assessed by odds ratios (ORs) with 95% confidence intervals (CI). Results: A total of 29 case-control studies including 16 studies with 7,560 cases and 9,574 controls on CRC and 13 studies with 1,445 cases and 2,918 controls on GC were selected. Overall, pooled data showed that the IL-6 −174G>C polymorphism was not significantly associated with increased risk of CRC and GC in overall. When stratified by ethnicity, we found a statistically significant association between the IL-6 −174 G>C polymorphism and CRC risk in Asians (CC vs. GG: OR = 1.860, 95% CI 1.061–3.258, p = 0.030; and CC vs. CG+GG: OR = 1.941, 95% CI 1.131–3.331, p = 0.016). Conclusion: The meta-analysis suggests that IL-6 −174G>C polymorphism was not significantly associated with the increased risk of CRC and GC in overall population. However, the results showed that IL-6 −174G>C polymorphism may be associated with risk of GC in Asians. Further studies including a larger sample size will be necessary to clarify these results.


2018 ◽  
Vol 5 (1) ◽  
pp. e000249 ◽  
Author(s):  
Cristina Ardura-Garcia ◽  
Paul Garner ◽  
Philip J Cooper

IntroductionHigh asthma prevalence in Latin-American cities is thought to be caused by poor hygiene and infections. This contradicts the widely accepted ‘hygiene hypothesis’ for asthma aetiology.MethodsSystematic review of observational studies evaluating the association between poor hygiene exposures or infections and asthma/wheeze among Latin-American children aged 4–16 years. MEDLINE, EMBASE, LILACS and CINAHL electronic databases were searched following a predefined strategy to 18 December 2017. We quantified outcomes measured and reported, assessed risk of bias and tabulated the results.ResultsForty-five studies included: 6 cohort, 30 cross-sectional and 9 case–control studies. 26 cross-sectional studies were school-based surveys (14 of over 3000 children), whereas 5 case–control studies were hospital/health centre-based. Exposures measured and reported varied substantially between studies, and current wheeze was the most common outcome reported. Data showed selective reporting based on statistical significance (P value <0.05): 17/45 studies did not clearly describe the number of exposures measured and 15/45 studies reported on less than 50% of the exposures measured. Most exposures studied did not show an association with wheeze or asthma, except for a generally increased risk associated with acute respiratory infections in early life. Contradictory associations were observed frequently between different studies.ConclusionSelective reporting is common in observational studies exploring the association between environmental exposures and risk of wheeze/asthma. This, together with the use of different study outcomes (wheeze/asthma) associated with possibly distinct causal mechanisms, complicates inferences about the role of poor hygiene exposures and childhood infections in explaining asthma prevalence in Latin-American children.


2017 ◽  
Vol 2 (1) ◽  
Author(s):  
Annette O'Connor

The evidence pyramid for assessing the efficacy of interventions under real world conditions has been used in various forms for many years, and to a lesser extent the pyramid has been used for assessing evidence for disease risk factors. While acknowledging minor differences, many pyramids list the following information sources for interventions in decreasing order of “validity”: systematic review and meta-analysis of randomised control trials, randomised controlled trials, cohort studies, case control studies, case series and case reports. The evidence pyramid is often used as a teaching aid to help clinicians and students visualise the concept that all studies might not have equal evidentiary value when evaluating real world efficacy.The rationale for the hierarchy of the pyramid is partially based on the potential for bias in some designs and partially based on the external validity of the information source. Designs with greater potential for bias “on average” are placed lower on the pyramid. The greater risk of bias means a greater risk that effect size estimates from studies lower on the pyramid may be systematically incorrect (overestimated or underestimated). As such, the evidence pyramid makes very broad statements about the design “on average”. Of course, for any particular study or topic, the pyramid may not be correct. Regardless, the generalisations described in the evidence pyramid have over the years been considered useful and use of the tool continues likely because of its simplicity. However, the validity of most pyramids that we have seen (and used ourselves, and published ourselves) is predicated on two potentially false concepts. The first potentially false concept conveyed by most evidence pyramids, is that there is only one case-control design and it is of lesser evidentiary value than cohort studies. The second potentially false concept conveyed by evidence pyramids is that the terms cohort, case control, and case series can be used to “filter” out studies of lower evidentiary value.In this presentation Annette discusses the validity of the evidence pyramid on the interpretation of evidence from primary research. She proposes a new way to think about evidence from primary studies using the framework for classifying epidemiologic studies proposed by Pearce (2012) based on incident and prevalent cases. This would also result in a rethinking of the current evidence pyramid.


Author(s):  
Mark Harrison

This chapter describes types of trials as applied to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details and advantages and disadvantages of case reports, case series, cohort studies, case–control studies, randomized controlled trials, crossover trials, systematic reviews, and meta-analysis. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4829-4829
Author(s):  
Sheila Pascual ◽  
Cannon Milani ◽  
Joanna Mitri ◽  
Jorge Castillo

Abstract INTRODUCTION: The etiology of Hodgkin lymphoma (HL) is largely unknown. However, certain associations have been noted, such as familial factors and infection with viruses. Smoking has been associated with the development of multiple malignancies and some studies have reported an association between HL and smoking but the relationship of tobacco use with lymphomas in largely unclear. OBJECTIVE: To investigate the potential relationship between tobacco use and the development of HL using a meta-analysis methodology of retrospective, case-control studies. METHODS: An extensive search was conducted using Pubmed/MEDLINE through July 2008. Case-control studies that reported odds ratio (OR) and 95% confidence intervals (CI) or allow for those values to be calculated were included in our analysis. Case reports, editorials, letters to the editor, review articles and prospective studies were excluded. The smoking status was then subdivided in three groups: never smokers, former smokers and current smokers. Meta-analyses were performed comparing the risks of former and current smokers against the risk of never smokers of developing HL. Fixed and random effects models were used to assess for heterogeneity. RESULTS: Seven case-controls studies, accounting for 3201 cases and 15268 controls were included in the analysis. Most of the articles reported OR adjusted for age, sex and educational level. In former smokers, the OR was 0.73 (95% CI, 0.65 – 0.82) when compared to never smokers; no heterogeneity was detected. The current smoker group had an OR of 1.70 (95% CI, 1.36 – 2.13) when compared to the never smoker group; some heterogeneity was detected in this group (p &lt; 0.003, I2 = 69.6%). CONCLUSIONS: Despite the heterogeneity observed in the analysis, the current smoker group seems to have a 70% increased risk of developing HL. Although a cause-effect linkage between tobacco use and HL is difficult to prove, further basic and translational research is necessary to clarify the potential etiological role of smoking in HL.


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