Transfusion History and Risk of Non-Hodgkin Lymphoma (NHL): an Interlymph Pooled Analysis

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3039-3039
Author(s):  
James R Cerhan ◽  
Silvia de Sanjosé ◽  
Bracci M Paige ◽  
John J. Spinelli ◽  
Claire M Vajdic ◽  
...  

Abstract Background. A recent meta-analysis of 9 case-control and 5 cohort studies reported a positive association of transfusion history with risk of NHL (RR=1.20; 95% CI 1.07-1.35), which was only evident in cohort (RR=1.25) and not case-control (RR=1.05) studies (Castillo et al., Blood 2010;116:2897-2907). Risk was similar in men and women, and for transfusions before or after 1992. In subset analyses, elevated risk was only apparent for chronic lymphocytic leukemia (CLL) and not diffuse large B-Cell lymphoma (DLBCL) or follicular lymphoma, but power was low. To further investigate these findings, particularly from studies conducted after 1990, better assess confounding, and address heterogeneity by NHL subtypes, we conducted an individual-level, pooled analysis of 13 case-control studies in the InterLymph Consortium (including 11 studies conducted after 1990; 8 studies were not included in the published meta-analysis). Methods. There were a total of 10,805 cases and 14,026 controls with transfusion data from 13 studies conducted in Europe, North America, and Australia. Transfusion history and other risk factors were self-reported in interviewer-administered or self-administered questionnaires. All risk factor data were harmonized centrally, and cases were grouped into NHL subtypes according to the WHO classification using guidelines from the InterLymph Pathology Working Group. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression, adjusted for age, sex, and study center. Results. The median age at diagnosis was 60 years for cases (range, 18-97) and 59 years for controls (range, 16-97). The overall prevalence of a history of any transfusion in controls was 15.5%, was higher in women (18.6%) than men (13.0%), and increased with age, but was not associated with race/ethnicity (Asian, Black, Hispanic, White, other) or geographic region after adjusting for age and sex. Among whites, history of any transfusion was inversely associated with NHL risk among men (OR=0.74; 95% CI 0.65-0.83) but not women (OR=0.92; 95% CI 0.83-1.03); there were no significant results for other race/ethnicity groups, and ORs were highly variable and imprecise due to small sample sizes. Thus analyses were restricted to white men, where there was no trend with the number of transfusions, time since first transfusion, age at first transfusion, or decade of first transfusion. Further adjustment for socioeconomic status, body mass index, smoking, alcohol use or hepatitis C virus (HCV) seropositivity did not alter these results. The associations were stronger in hospital-based (OR=0.56; 95% CI 0.45-0.70) than population-based (OR=0.84; 95% CI 0.72-0.98) studies, and were stronger in studies from Southern Europe (OR=0.53; 95% CI 0.36-0.79) than northern Europe (OR=0.67; 95% CI 0.53-0.83) or North America (OR=0.82; 95% CI 0.70-0.98). For NHL subtypes, statistically significant inverse associations were observed for follicular lymphoma (OR=0.70; 95% CI 0.56-0.88), DLBCL (OR=0.72; 95% CI 0.59-0.87), and CLL/SLL (OR=0.67; 95% CI 0.52-0.87), whereas weaker and non-statistically significant associations were observed for mantle cell (OR=0.81; 95% CI 0.54-1.23), marginal zone (OR=0.78; 95% CI 0.54-1.15), lymphoplasmacytic (OR=0.82; 95% CI 0.47-1.42) and peripheral T-cell (OR=0.83; 95% CI 0.49-1.40) lymphomas. Conclusion. Contrary to earlier results, transfusion history was inversely associated with risk of NHL and the common subtypes of follicular lymphoma, DLBCL and CLL/SLL among white men, whereas associations were null among white women and other racial/ethnic groups. These results were not explained by confounding by lifestyle factors or HCV seropositivity, era of first transfusion, hospital versus population-based study design, or geographic location. Despite dramatic changes in transfusion practice over the past 40 years, results were similar for decade of first transfusion, suggesting secular trends are a less likely explanation. Our results are unexpected and bias cannot be ruled out. Further studies, particularly cohort studies, are needed to clarify the role of transfusion history in NHL risk. Disclosures No relevant conflicts of interest to declare.

2020 ◽  
Vol 34 (5) ◽  
pp. 703-714
Author(s):  
Xiaoping Gao ◽  
Mei Yin ◽  
Pei Yang ◽  
Xia Li ◽  
Lingling Di ◽  
...  

Background Controversies persist regarding whether exposure to cat or dog increases the risk of asthma and allergic rhinitis. Objective This meta-analysis aimed to assess the associations between exposure to cats or dogs and the development of asthma and allergic rhinitis. Methods A systematic review was performed to identify case-control and cohort studies before May 2019, evaluating the association between exposure to cats and dogs and the risk of asthma and rhinitis. The risk of bias was assessed using the Newcastle–Ottawa Scale. The odds ratios (ORs) and risk ratios (RRs) were pooled for case-control and cohort studies, respectively. Subgroup analyses were performed on prespecified study-level characteristics. Results The meta-analysis of 34 cohort studies showed a protective role of exposure to cats [RR: 0.88, 95% confidence interval (CI): 0.77–0.99] or dogs (RR: 0.85, 95% CI: 0.73–0.97) in the development of asthma. The subgroup analysis of birth cohort (RR: 0.74, 95% CI: 0.56–0.93) and children population (RR: 0.83, 95% CI: 0.70–0.96) also suggested a favorable role of exposure to dogs in the development of asthma. Pooled evidence from 13 case-control studies indicated no significant impact of cats (OR: 1.66, 95% CI: 0.39–2.94) and dogs (OR: 1.22, 95% CI: 0.92–1.52) on the development of asthma. A pooled analysis of five cohort studies showed a favorable effect of exposure to cats (RR: 0.60, 95% CI: 0.33–0.86) or dogs (RR: 0.68, 95% CI 0.44–0.90) on the development of allergic rhinitis. Conclusion The findings indicated a protective effect of exposure to cats and dogs, especially ownership, on the development of asthma and allergic rhinitis.


2021 ◽  
Vol 7 ◽  
Author(s):  
Long Wang ◽  
Zi-Ru Deng ◽  
Mei-Dan Zu ◽  
Juan Zhang ◽  
Yu Wang

Objective: Recent studies have indicated a pathophysiologic link between migraine and asthma. This meta-analysis aimed to comprehensively estimate the risk ratio for migraine in asthma as well as that of asthma in migraine based on available evidence.Method: We systematically searched the electronic databases including PubMed, Web of Science, and SCOPUS for population-based studies that measured either the odds or the risk of asthma in subjects with migraine as well as that of migraine in subjects with asthma. The titles and abstracts were screened by two independent reviewers to identify eligible studies, and this was followed by full-text review of the included studies. Newcastle–Ottawa Scale (NOS) was used to assess the risk of bias of included literature. A meta-analysis was conducted with Review Manager 5.3 Software to calculate the odds ratio (OR) for case-control and cross-sectional studies and either relative ratio (RR) or hazard ratio (HR) for cohort studies, and the source of heterogeneity was assessed. Subgroup and sensitivity analyses were conducted, and the I2 test were used to assess the source of heterogeneity. The funnel plot, Galbraith plot, and Egger's test were used to evaluate publication bias.Results: Fifteen published studies covering a total of 1,188,780 individuals were identified. Pooled analysis indicated that migraine was associated with increased odds (OR = 1.54; 95% CI: 1.34~1.77) and risk for asthma (HR = 1.42; 95% CI: 1.26~1.60), and asthma associated with increased odds (OR = 1.45; 95% CI: 1.22~1.72) and risk for migraine (HR = 1.47; 95% CI: 1.41~1.52).Conclusion: Migraine is a potential risk indicator for asthma, and vice versa, asthma is a potential risk indicator for migraine. However, future prospective cohort studies are warranted to provide more evidence concerning the detailed association between migraine and asthma.


2019 ◽  
Vol 25 (4) ◽  
pp. 486-503 ◽  
Author(s):  
Nina Shigesi ◽  
Marina Kvaskoff ◽  
Shona Kirtley ◽  
Qian Feng ◽  
Hai Fang ◽  
...  

Abstract BACKGROUND Endometriosis is a chronic gynaecological disorder that affects 2–10% of women of reproductive age. The aetiology of endometriosis is largely under-explored, yet abnormalities in the immune system have been suggested to explain the origin of ectopic endometrial tissues, and an association between endometriosis and autoimmune diseases has been proposed. Evaluation of current evidence investigating the association between endometriosis and autoimmune diseases from population-based studies will facilitate our understanding of the causes and consequences of endometriosis and provide a reference for better healthcare practices population-wide. OBJECTIVE AND RATIONALE The aim of this study was to systematically review the literature on population-based studies investigating an association between endometriosis and autoimmune diseases and to conduct a meta-analysis of combinable results to investigate the extent and robustness of evidence. SEARCH METHODS Four electronic databases were searched (MEDLINE, Embase, Web of Science, and CINAHL) from each database inception date until 7 April 2018. Search terms included a combination of database-specific controlled vocabulary terms and free-text terms relating to ‘endometriosis’ and ‘autoimmune diseases’. Study inclusion criteria focused on peer-reviewed published articles that reported an association between endometriosis and autoimmune diseases, excluding case reports/series, review papers, meta-analyses, organizational guidelines, editorial letters, expert opinions, and conference abstracts. Quality assessment of included studies was performed based on GRADE criteria. Key information of eligible studies was abstracted into a standard form. Meta-analysis was performed for autoimmune diseases with combinable study results from at least three studies investigating an association with endometriosis. For cross-sectional studies and case–control studies, raw data from each study were documented to calculate a Mantel–Haenszel odds ratio with 95% CIs. For cohort studies, an inverse variance probability weighted model was used to pool study results to calculate a rate ratio (a hazard ratio or a standardized incidence rate) with 95% CIs. OUTCOMES A total of 26 published population-based cross-sectional, case–control, and cohort studies that investigated the association between endometriosis and autoimmune diseases met all eligible criteria and were included in the review. The studies quantified an association between endometriosis and several autoimmune diseases, including systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS), rheumatoid arthritis (RA), autoimmune thyroid disorder, coeliac disease (CLD), multiple sclerosis (MS), inflammatory bowel disease (IBD), and Addison’s disease. However, the quality of the evidence was generally poor due to the high risk of bias in the majority of the chosen study designs and statistical analyses. Only 5 of the 26 studies could provide high-quality evidence, and among these, 4 supported a statistically significant association between endometriosis and at least 1 autoimmune disease: SLE, SS, RA, CLD, MS, or IBD. WIDER IMPLICATIONS The observed associations between endometriosis and autoimmune diseases suggest that clinicians need to be aware of the potential coexistence of endometriosis and autoimmune diseases when either is diagnosed. Scientists interested in research studies on endometriosis or autoimmune diseases should consider the likelihood of comorbidity when studying these two types of health conditions. Well-designed large prospective cohort studies with confounding control and mediation quantification, as well as genetic and biological studies, are needed to generate further insights into whether endometriosis is a risk factor for, or a consequence of, autoimmune diseases, and whether these two types of disorders share pathophysiological mechanisms even if they arise independently. Such insights may offer opportunities for the development of novel non-hormonal medications such as immuno-modulators or repurposing of existing immunomodulatory therapies for endometriosis.


2021 ◽  
Vol 9 ◽  
Author(s):  
Hailuo Che ◽  
Dunmei Long ◽  
Qian Sun ◽  
Lina Wang ◽  
Yunbin Li

Objective: Birth weight, an important indicator of fetal nutrition and degree of development, may affect the risk of subsequent leukemia. At present, little is known about the effect of birth weight on acute myeloid leukemia (AML) and whether there is a dose-dependent relationship of birth weight with acute lymphoid leukemia (ALL) and AML. To address these questions, the present work aimed to systematically investigate the relationship between birth weight and the risk of subsequent leukemia based on the current epidemiological studiesMethods: Relevant studies were systematically retrieved from electronic databases PubMed, Embase, and Cochrane Library, from inception to May 15th, 2021. Finally, 28 studies (including 21 case-control studies and 7 cohort studies) were included for the final meta-analysis. Results in cohort studies were performed by risk ratios (RRs), while those in case-control studies by odds ratios (ORs), and all results were assessed by adopting the random-effect model. Besides, a dose-dependent analysis was conducted based on the cohort studies.Results: Compared with the population with normal birth weight (NBW), the population with high birth weight (HBW) might have an increased risk of leukemia (OR 1.33, 95%CI 1.20–1.49; I2 0%). Meanwhile, low birth weight (LBW) was associated with a decreased risk of ALL, as evidenced from the pooled analysis of case-control studies (OR 0.83, 95% CI 0.75–0.92; I2 23.3%). However, relative to NBW population, the HBW population might have an increased risk of ALL (OR 1.28, 95% CI 1.20–1.35; I2 7%). There was no obvious evidence supporting the relationship between LBW and the risk of AML from the pooled analysis of case-control studies (OR, 1.11 95% CI 0.87–1.42; I2 31.7%).Conclusions: Overall, in children and young adults, HBW population may be associated with the risks of subsequent leukemia and AML relative to NBW population, but the supporting dose-dependent evidence is lacking. In addition, compared with NBW population, there is stronger evidence supporting a significantly increased risk of subsequent ALL in HBW population, and a decreased risk in LBW population in a dose-dependent manner. More prospective studies with large samples are warranted in the future to validate and complement these findings.


2017 ◽  
Vol 89 (4) ◽  
pp. 259 ◽  
Author(s):  
Gianpaolo Perletti ◽  
Elena Monti ◽  
Vittorio Magri ◽  
Tommaso Cai ◽  
Anne Cleves ◽  
...  

Objective: The main outcome of this review was the association between a history of clinical chronic prostatitis (NIH category II or III) and a histologically confirmed diagnosis of prostate cancer. Materials and methods: Crude odds ratios and 95% confidence intervals (CI) were calculated to analyze dichotomous data. For analysis of pooled data we adopted a random-effects model and the inverse variance weighing method. Heterogeneity was assessed by calculating the I2 value. Results: Out of 2794 screened records, we retrieved 16 full-text articles written in English, reporting the data of 15 case-control studies, involving 422.943 patients. Pooled analysis resulted in a significant crude odds ratio of 1.83 (95% CI: 1.43 to 2.35; P < 0.00001). The total set of data showed considerable heterogeneity (I2 = 91%). Both the Egger’s test and the Begg's test for funnel plot asymmetry did not reach statistical significance. The ‘trim and fill’ method applied to the funnel plot imputed 3 missing studies and the resulting adjusted estimate of the odds ratio was 2.12 (95% CI: 1.38 to 3.22). According to GRADE criteria, the overall quality of the meta-analysis data is low, mainly due to the presence of bias, confounders and extreme effect size outliers. Five among the included studies reported data assessed in 8015 African-American subjects. Pooled analysis resulted in a non-significant crude odds ratio of 1.59 (95% CI: 0.71 to 3.57; P = 0.26), and considerable heterogeneity (I2 = 90%). Conclusions: Meta-analysis of 15 case-control studies shows that a history of clinical chronic prostatitis can significantly increase the odds for prostate cancer in the general population, whereas such association in African-American individuals remains uncertain.


BMJ Open ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. e040137
Author(s):  
Lihai Wang ◽  
Lei Zhong ◽  
Bin Xu ◽  
Min Chen ◽  
Hongxiao Huang

ObjectiveEmerging evidence from observational studies (cohort and case–control studies) suggests that a history of diabetes mellitus (DM) has been linked to increased risk of ovarian cancer (OC), but the association between them remains inconclusive. The aim of this systematic review and meta-analysis of observational studies was to clarify this association.DesignSystematic review and meta-analysis.MethodsWe searched PubMed, Embase and the Cochrane library databases published from the inception through 9 April 2020 without language restriction. Observational studies that evaluated the correlation between DM and the incidence of OC were included in our study. Relative risk (RR) with 95% CI was pooled by use of a random-effects model.ResultsA total of 36 epidemiological articles, including 9 case–control and 27 cohort studies, were finally enrolled, consisting of 14 496 incident cases of OC. Synthesised RRs of developing OC by history of DM were 1.20 (95% CI=1.10 to 1.31) for all eligible studies, 1.08 (95% CI=0.77 to 1.53) for case–control studies and 1.22 (95% CI=1.11 to 1.33) for cohort studies. The above-mentioned positive association persisted across most of subgroup analyses, whereas it was not significant among studies from North American and European countries, level of unadjusted, and patients with low-quality and gestational DM group. The cumulative meta-analysis and sensitivity analysis showed pooled effect was stable and reliable, and no apparent publication bias was identified in this study.ConclusionsOur study found weaker but still association between DM and OC risk. However, further well-designed prospective studies that control for potential confounders are warranted.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eric Lontchi-Yimagou ◽  
Charly Feutseu ◽  
Sebastien Kenmoe ◽  
Alexandra Lindsey Djomkam Zune ◽  
Solange Fai Kinyuy Ekali ◽  
...  

AbstractA significant number of studies invoked diabetes as a risk factor for virus infections, but the issue remains controversial. We aimed to examine whether non-autoimmune diabetes mellitus enhances the risk of virus infections compared with the risk in healthy individuals without non-autoimmune diabetes mellitus. In this systematic review and meta-analysis, we assessed case-control and cohort studies on the association between non-autoimmune diabetes and viruses. We searched PubMed, Embase, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, and Web of Science with no language restriction, to identify articles published until February 15, 2021. The main outcome assessment was the risk of virus infection in individuals with non-autoimmune diabetes. We used a random-effects model to pool individual studies and assessed heterogeneity (I2) using the χ2 test on Cochrane’s Q statistic. This study is registered with PROSPERO, number CRD42019134142. Out of 3136 articles identified, we included 68 articles (90 studies, as the number of virus and or diabetes phenotype varied between included articles). The summary OR between non-autoimmune diabetes and virus infections risk were, 10.8(95% CI: 10.3–11.4; 1-study) for SARS-CoV-2; 3.6(95%CI: 2.7–4.9, I2 = 91.7%; 43-studies) for HCV; 2.7(95% CI: 1.3–5.4, I2 = 89.9%, 8-studies;) for HHV8; 2.1(95% CI: 1.7–2.5; 1-study) for H1N1 virus; 1.6(95% CI: 1.2–2.13, I2 = 98.3%, 27-studies) for HBV; 1.5(95% CI: 1.1–2.0; 1-study) for HSV1; 3.5(95% CI: 0.6–18.3 , I2 = 83.9%, 5-studies) for CMV; 2.9(95% CI: 1–8.7, 1-study) for TTV; 2.6(95% CI: 0.7–9.1, 1-study) for Parvovirus B19; 0.7(95% CI: 0.3–1.5 , 1-study) for coxsackie B virus; and 0.2(95% CI: 0–6.2; 1-study) for HGV. Our findings suggest that, non-autoimmune diabetes is associated with increased susceptibility to viruses especially SARS-CoV-2, HCV, HHV8, H1N1 virus, HBV and HSV1. Thus, these viruses deserve more attention from diabetes health-care providers, researchers, policy makers, and stakeholders for improved detection, overall proper management, and efficient control of viruses in people with non-autoimmune diabetes.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ali Baradaran ◽  
Hojat Dehghanbanadaki ◽  
Sara Naderpour ◽  
Leila Mohammadi Pirkashani ◽  
Abdolhalim Rajabi ◽  
...  

Abstract Introduction The relationship between H. pylori infection and obesity development has remained controversial among various studies. The aim of this study was to clarify the pooled effect of H. pylori infection on the development of obesity and vice versa. Methods We searched international databases including Medline (PubMed), Web of sciences, Scopus, EMBASE, Cochrane, Ovid, and CINHAL to retrieve all case–control studies reporting the effect of H. pylori on obesity and vice versa, which had been published in English between January 1990 and June 2019. The quality of included studies was assessed by the Modified Newcastle–Ottawa Scale for Case–Control studies. The logarithm of the odds ratio (OR) and its standard error was used for the meta-analysis. Results Eight case–control studies with 25,519 participants were included for qualitative and quantitative analyses. The pooled analysis showed that obese participants had a higher risk of H. pylori infection than lean participants with an odds ratio of 1.46 (95%CI: 1.26, 1.68). Also, the pooled analysis revealed that participants infected by H. pylori had a higher risk of obesity than non-infected participants with an odds ratio of 1.01 (95%CI: 1.01, 1.02). Conclusion The results of this meta-analysis showed that there was a positive correlation between the risk of H. pylori infection and the prevalence of obesity development. Thus, H. pylori positive patients were more likely to be obese, and obese individuals had higher risks of H. pylori infection.


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