Association of inflammatory factors with occurrence and recurrence of atrial fibrillation: A meta-analysis

Wu, Na; Xu, Bin; Xiang, Ying; Wu, Long; Zhang, Yao; Ma, Xiangyu; Shi-fei, Tong; Shu, Maoqing; Zhang, Song; Li, Yafei; Zhong, Li

doi:10.1016/j.ijcard.2013.08.078

Cited by 190 publications

(136 citation statements)

References 136 publications

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“…It is noteworthy that one of these studies (negative for an association) had enrolled a cohort, 45% of which had diabetes, cardiac failure, and/or myocardial infarction as comorbidities, all known to be associated with inflammation (Kimmel et al, 2013), while the other two (one negative and one weakly positive for the association) included no information on comorbidities. Furthermore, and perhaps more crucially significant, there is a well-documented relationship between atrial fibrillation, the major indication for use of warfarin and other vitamin K antagonists in these studies, and raised inflammatory biomarkers, especially IL-6 (Henningsen et al, 2009;Marcus et al, 2010;Celebi et al, 2011;Smit et al, 2012;Wu et al, 2013). Inevitably, a question arises concerning the extent to which the CYP2C9 genotype of the cohorts of these three studies was predictive of their CYP2C9 phenotype.…”

Section: Discussionmentioning

confidence: 99%

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

Shah¹,

2014

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Phenoconversion transiently converts genotypic extensive metabolizers (EMs) into phenotypic poor metabolizers (PMs) of drugs, potentially with corresponding changes in clinical response. This phenomenon, typically resulting from coadministration of medications that inhibit certain drug metabolizing enzymes (DMEs), is especially well documented for enzymes of the cytochrome P450 family. Nonclinical evidence gathered over the last two decades also strongly implicates elevated levels of some proinflammatory cytokines, released during inflammation, in down-regulation of drug metabolism, especially by certain DMEs of the P450 family, thereby potentially causing transient phenoconversion. Clinically, phenoconversion of NAT2, CYP2C19, and CYP2D6 has been documented in inflammatory conditions associated with elevated cytokines, such as human immunodeficiency virus infection, cancer, and liver disease. The potential of other inflammatory conditions to cause phenoconversion has not been studied but experimental and anecdotal clinical evidence supports infectioninduced down-regulation of CYP1A2, CYP3A4, and CYP2C9 as well. Collectively, the evidence supports a hypothesis that certain inflammatory conditions associated with elevated proinflammatory cytokines may cause phenoconversion of certain DMEs. Since inflammatory conditions associated with elevated levels of proinflammatory cytokines are highly prevalent, phenoconversion of genotypic EM patients into transient phenotypic PMs may be more frequent than appreciated. Since drug pharmacokinetics, and therefore the clinical response, is influenced by DME phenotype rather than genotype per se, phenoconversion (whatever its cause) can have a significant impact on the analysis and interpretation of genotype-focused clinical outcome association studies. There is a risk that focusing on genotype alone may miss important associations between clinical outcomes and DME phenotypes, thus compromising future prospects of personalized medicine.

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Section: Discussionmentioning

confidence: 99%

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

Shah¹,

2014

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“…In the case of multiple publications reporting the same or overlapping data, only the most recent study or the study using the largest population were included, as recommended by Wu et al [51]. In cases where a study reported insufficient data, the authors were contacted, and if no response was received, the study was excluded.…”

Section: Selection Criteriamentioning

confidence: 99%

WITHDRAWN: Prognostic value of circulating tumor DNA in breast cancers

Gui¹,

Chen²,

Xu³

et al. 2018

Oncotarget

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Circulating tumor DNA (ctDNA) comprises single-or double-stranded DNA that likely originates from cancer cells. The prognostic value of ctDNA detection in breast cancer patients is currently under debate. Here, we conducted the first comprehensive meta-analysis of the published literature on the prognostic relevance of ctDNA, in patients with early-and advanced-stage disease.The PubMed and Embase databases were searched for studies on ctDNA in breast cancer patients.The main outcomes analyzed were overall survival (OS) and disease-free survival (DFS) in early-stage breast cancer patients as well as progression-free survival (PFS) and OS in metastatic breast cancer patients. Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using random and fixed-effects models. A total of 16 studies involving 2070 participants were identified as eligible for inclusion in our meta-analysis, and the results of the pooled analysis showed that the presence of ctDNA was significantly associated with poor OS (HR = 1.98; 95% CI: 1.38-2.83, P = 0.0002) and DFS/PFS (HR = 1.87; 95% CI: 1.35-2.60, P = 0.0002) in the total breast cancer population. Furthermore, subgroup analysis revealed that associations between the presence of ctDNA and the outcome endpoints (OS and PFS) were significant within the metastatic breast cancer patient group and in patients with TP53 or ESR1 mutations in ctDNA.The TP53 and ESR1 mutations in ctDNA are potential prognostic biomarkers and promising therapeutic targets for advanced breast cancer.www.impactjournals.com/oncotarget/

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“…Increased levels of IL-6, TNF-α and CRP have all been associated with POAF (Elahi, Flatman, & Matata, 2008;Ucar, et al, 2007;Wu, et al, 2013).…”

Section: Inflammatory Response and Factors That Alter Incidence Of Poafmentioning

confidence: 99%

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

Zakkar

Ascione

James

et al. 2015

Pharmacology & Therapeutics

169

115

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Postoperative atrial fibrillation (POAF) is a common complication of cardiac surgery that occurs in up to 60% of patients. POAF is associated with increased risk of cardiovascular mortality, stroke and other arrhythmias that can impact on early and long term clinical outcomes and health economics. Many factors such as disease-induced cardiac remodelling, operative trauma, changes in atrial pressure and chemical stimulation and reflex sympathetic/parasympathetic activation have been implicated in the development of POAF. There is mounting evidence to support a major role for inflammation and oxidative stress in the pathogenesis of POAF. Both are consequences of using cardiopulmonary bypass and reperfusion following ischaemic cardioplegic arrest. Subsequently, several anti-inflammatory and antioxidant drugs have been tested in an attempt to reduce the incidence of POAF. However, prevention remains suboptimal and thus far none of the tested drugs has provided sufficient efficacy to be widely introduced in clinical practice. A better understanding of the cellular and molecular mechanisms responsible for the onset and persistence of POAF is needed to develop more effective prediction and interventions.

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Association of inflammatory factors with occurrence and recurrence of atrial fibrillation: A meta-analysis

Cited by 190 publications

References 136 publications

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

Inflammation-Induced Phenoconversion of Polymorphic Drug Metabolizing Enzymes: Hypothesis with Implications for Personalized Medicine

WITHDRAWN: Prognostic value of circulating tumor DNA in breast cancers

Inflammation, oxidative stress and postoperative atrial fibrillation in cardiac surgery

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