Association of psoriasis with risk of COVID-19: A 2-sample Mendelian randomization study.
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ABSTRACT:
SUBMITTER: Gu X
PROVIDER: S-EPMC8815194 | biostudies-literature | 2022 Sep
REPOSITORIES: biostudies-literature
Publications
Association of psoriasis with risk of COVID-19: A 2-sample Mendelian randomization study.
Gu Xiaoyu X Chen Xiang X Shen Minxue M
Journal of the American Academy of Dermatology 20220204 3
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Project description:BackgroundAs a common chronic recurrent inflammatory skin disease, psoriasis is characterized by erythema and scaly skin lesions, with infection as an integral part of the pathogenesis of many diseases. Many previous cases reported the impact of psoriasis on infection. However, the existing research fails to completely clarify the infection factors associated with the potential of these diseases and causality.Materials and methodsThirteen kinds of pathogens and their immune responses and psoriasis in the phenotype of 46 species of SNPs data were respectively obtained from the GWAS catalog database and the UK biobank database. With the help of R software, three methods of inverse variance weighted (IVW), weighted median (WME), and MR-Egger regression were used to analyze the causality of the dataset.ResultsAccording to the results of IVW analysis, there is a causal relationship between anti-Epstein Barr virus antibody and psoriasis (OR: 1.003, 95% CI: 1.001∼1.006, P = 0.046) with a positive correlation.ConclusionBased on the results of MR analysis, there is a causal relationship between psoriasis and EBV infection, which indicates that EBV infection can increase the risk or severity of psoriasis. Therefore, in clinical scenarios, patients afflicted with psoriasis should be prevented from contracting the infection and recurrence of EBV as well as symptoms of psoriasis. The underlying immunological mechanism also provides a new perspective for experimental research.
| S-EPMC11337910 | biostudies-literature
Project description: Not available
| S-EPMC9561435 | biostudies-literature
Project description:Background and objectiveEpidemiological studies report associations between coronavirus disease 2019 (COVID-19) and periodontitis; however, causality has not been proven. The aim of this study is to assess the associations between COVID-19 susceptibility and periodontitis with two-sample Mendelian randomization (MR) analyses.MethodsA two-sample summary MR analysis was performed using data for outcome and exposure from the OpenGWAS database on people of European descent. Periodontal complex traits (PCTs) were chosen as a proxy for the periodontitis phenotype. The causal association between PCT3 (Aggregatibacter actinomycetemcomitans), PCT5 (Porphyromonas gingivalis), and gingival crevicular fluid (GCF) interleukin-1β (IL-1β) and COVID-19 were considered. Genome-wide association study (GWAS) data with the two largest sample sizes were selected as COVID-19 outcomes (datasets ebi-a-GCST010776 and ebi-a-GCST010777). Single-nucleotide polymorphisms (SNPs) associated with PCT3, PCT5, and GCF IL-1β at statistical significance at genome-wide level (P < 5 × 10-8) were identified as genetic instruments. We used two-sample summary MR methods and tested the existence of a pleiotropic effect with MR-Egger.ResultsInverse-variance weighted (IVW) estimates showed that there was a positive association between COVID-19 risk and periodontitis (ebi-a-GCST010776: odds ratio [OR] = 1.02 (95% confidence interval (CI), 1.00-1.05), P = 0.0171; ebi-a-GCST010777: OR = 1.03 (95% CI, 1.00-1.05), P = 0.0397). The weighted median also showed directionally similar estimates. Exploration of the causal associations between other PCTs and COVID-19 identified a slight effect of local inflammatory response (GCF IL-1β) on COVID-19 risk across the two datasets (ebi-a-GCST010776: IVW OR = 1.02 (95% CI, [1.01-1.03]), P < 0.001; ebi-a-GCST010777: IVW OR = 1.03 (95% CI, [1.02-1.04]), P < 0.001). The intercepts of MR-Egger yielded no proof for significant directional pleiotropy for either dataset (ebi-a-GCST010776: P = 0.7660; ebi-a-GCST010777: P = 0.6017).ConclusionsThe findings suggests that periodontitis and the higher GCF IL-1β levels is causally related to increase susceptibility of COVID-19. However, given the limitations of our study, the well-designed randomized controlled trials are needed to confirm its findings, which may represent a new non-pharmaceutical intervention for preventing COVID-19.
| S-EPMC9884046 | biostudies-literature
Project description:BackgroundObservational studies reported an association between psoriasis and risk of lung cancer. However, whether psoriasis is causally associated with lung cancer is unclear.MethodsGenetic summary data of psoriasis were retrieved from two independent genome-wide association studies (GWAS). Genetic information of lung cancer was retrieved from GWAS of International Lung Cancer Consortium. A set of quality control steps were conducted to select instrumental tools. We performed two independent two-sample Mendelian randomization (MR) analyses and a meta-analysis based on the two independent MR estimates to assess the causal relationship between psoriasis and lung cancer (LUCA) as well as its subtypes, squamous cell carcinoma (LUSC) and adenocarcinoma (LUAD).ResultsBetween-SNP heterogeneity was present for most MR analyses, whereas horizontal pleiotropy was not detected for all MR analyses. Multiplicative random-effect inverse variance weighted (IVW-MRE) method was therefore selected as the primary MR approach. Both IVW-MRE estimates from the two independent MR analyses suggested that there was no significant causal relationship between psoriasis and LUCA as well as its histological subtypes. Sensitivity analyses using other four MR methods gave similar results. Meta-analysis of the two IVW-MRE derived MR estimates yielded an odds ratio (OR) of 1.00 (95% CI 0.95-1.06) for LUCA, 1.01 (95% CI 0.93-1.08) for LUSC, and 0.97 (95% CI 0.90-1.06) for LUAD.ConclusionOur results do not support a genetic association between psoriasis and lung cancer and its subtypes. More population-based and experimental studies are warranted to further dissect the complex correlation between psoriasis and lung cancer.
| S-EPMC9814449 | biostudies-literature
Project description:BackgroundSepsis and COVID-19 have a well-established observable relationship. Whether COVID-19 increases the likelihood of developing sepsis and whether patients with sepsis are at increased risk for COVID-19 infection is unknown. Using a bidirectional 2-sample Mendelian randomization (TSMR) analysis techniques in sizable cohorts, we sought to answer this question.MethodsThe current study performed Mendelian randomization (MR) on publicly accessible genome-wide association study (GWAS) summary data in order to investigate the causal linkages between COVID-19 and sepsis. A Two-Sample MR(TSMR) analyses was performed. As instrumental variables, a COVID-19 dataset of single nucleotide polymorphisms (SNPs) with significance value smaller than 5*10-8 was employed and Sepsis dataset of SNPs with significance value smaller than 5*10-7was employed.ResultsThe results suggested that Very severe respiratory confirmed COVID-19(VSRC), hospitalized COVID-19(HC) and Infected COVID-19(IC) had no causal influence on sepsis risk using the inverse variance weighted (IVW) technique (VSRC OR = 1.000, 95% CI, 0.956-1.046, P = 0.996, HC OR = 0.976, 95% CI, 0.920-1.036, P = 0.430, IC OR = 0.923, 95% CI, 0.796-1.071, P = 0.291) and there was no causal effect of sepsis on the risk of VSRC, HC and IC (VSRC OR = 0.955, 95% CI, 0.844-1.173, P = 0.953, HC OR = 0.993, 95% CI, 0.859-1.147, P = 0.921, IC OR = 1.001, 95% CI, 0.959-1.045, P = 0.961).ConclusionsOur findings do not support a causal relationship between COVID-19 and sepsis risk, nor do they suggest a causal link between sepsis and COVID-19. The bidirectional relationship between COVID-19 and sepsis warrants further investigation in large cohorts.
| S-EPMC10591217 | biostudies-literature
Project description:Primary Sjögren's Syndrome (PSS) and psoriasis are frequently observed to co-occur in clinical settings. However, the causal associations and underlying mechanisms between PSS and psoriasis remain poorly defined. In this study, we conducted bidirectional MR analysis to explore the causal relationship between PSS and psoriasis using four MR methods: inversevariance weighted, MR-Egger regression, weighted median, and weighted mode. Sensitivity analyses were carried out, employing different models and testing methods for comparison to assess the influence of heterogeneity and pleiotropy on our findings and to confirm the robustness of these results. We primarily employed the Inverse Variance Weighting (IVW) method for our analysis. A p-value of less than 0.05 indicates a significant causal relationship, while a p-value greater than 0.05 suggests the absence of such a relationship. The IVW analysis confirmed a causal relationship between psoriasis and primary Sjögren's syndrome (PSS) (OR: 3.149E-10, 95% CI 1.114E-18-0.089, P = 0.028), with the weighted median yielding similar results. Conversely, there was no causal association found between PSS and the risk of developing psoriasis (OR: 1.000, 95% CI 0.999-1.000, P = 0.328). This study reveals a causal relationship between primary Sjögren's syndrome (PSS) and psoriasis, demonstrating that psoriasis increases the risk of developing PSS, while the reverse is not true. This potential causal link offers new insights into the etiology of both PSS and psoriasis.
| S-EPMC11787228 | biostudies-literature
Project description:[Figure: see text].
| S-EPMC8545250 | biostudies-literature
Project description:BackgroundPrevious observational studies have found an association between inflammatory bowel disease (IBD) and psoriasis. Using the mendelian randomization (MR) approach, we aim to determine whether there was a causal association between IBD and psoriasis.MethodsWe performed a two-sample MR with the genetic instruments identified for IBD and its main subtypes, Crohn's disease (CD) and ulcerative colitis (UC), from a genome-wide association study (GWAS) involving 25,042 cases with an IBD diagnosis and 34,915 controls. Summarized data for psoriasis were obtained from different GWAS studies which included 4510 cases and 212,242 controls without psoriasis. Causal estimates are presented as odds ratios (ORs) with 95% confidence intervals (CIs).ResultsThe overall outcome of MR analysis was to demonstrate that genetic predisposition to IBD was associated with an increased risk of psoriasis (OR: 1.1271; 95% CI: 1.0708 to 1.1864). Psoriatic arthritis (PsA) had a significant association with total IBD (OR: 1.1202; 95% CI: 1.0491 to 1.1961). Casual relationship was also identified for CD-psoriasis (OR: 1.1552; 95% CI: 1.0955 to 1.2182) and CD-PsA (OR: 1.1407; 95% CI: 1.0535 to 1.2350). The bidirectional analysis did not demonstrate that a genetic predisposition to psoriasis was associated with total IBD, although psoriasis showed association with CD (OR: 1.2224; 95% CI: 1.1710 to 1.2760) but not with UC. A genetic predisposition to PsA had a borderline association with IBD (OR: 1.0716; 95% CI: 1.0292 to 1.1157) and a suggestive association with CD (OR: 1.0667; 95% CI: 1.0194 to 1.1162).ConclusionThere appears to be a causal relationship between IBD and psoriasis, especially for PsA, but for psoriasis and IBD, only total psoriasis and PsA were associated with CD. Understanding that specific types of psoriasis and IBD constitute mutual risk factors facilitates the clinical management of two diseases.
| S-EPMC9226443 | biostudies-literature
Project description:BackgroundThe association between psoriasis vulgaris and bullous pemphigoid (BP) remains largely unknown.ObjectivesTo investigate whether there is a causal effect between psoriasis vulgaris and BP.MethodsTwo-sample bidirectional Mendelian randomization (MR) analyses were conducted using publicly released genome-wide association studies (GWAS) summary statistics. The GWAS summary statistics for BP were downloaded online from FinnGen Biobank Documentation of the R12 release, which includes 219 BP cases and 218,066 controls. The GWAS data for psoriasis vulgaris were extracted from Sakaue et al., which comprises 5072 cases and 478,102 controls. Single-nucleotide polymorphisms (SNPs) associated with exposure were selected as instrumental variables by performing additional quality control steps. The inverse-variance-weighted (IVW) method was used for the primary MR analyses, and the MR-Egger regression, weighted mode method, weighted median method, and simple mode were employed for sensitivity analyses. The MR-Egger intercept test and "leave-one-out" sensitivity analysis were performed to evaluate the horizontal pleiotropy and the potentially influential SNPs, respectively.ResultsGenetically determined log odds of psoriasis vulgaris were associated with an increased risk of BP (IVW: odds ratio (OR) = 1.263, 95% confidence interval (CI): 1.013-1.575, P=0.038). Sensitivity analyses by the weighted mode (OR=1.255, 95%CI: 0.973-1.618, P=0.106), MR Egger (OR=1.315, 95%CI: 0.951-1.817, P=0.126), simple mode (OR=1.414, 95%CI: 0.823-2.429, P=0.234) and weighted median method (OR=1.177, 95%CI: 0.889-1.559, P=0.254) derived directionally consistent relationship between the genetically predicted log odds of psoriasis vulgaris and risks of developing BP. On the contrary, we found that genetically predicted BP had no significant effect on psoriasis vulgaris (IVW: OR=0.996, P= 0.707), indicating the unidirectionality of the relationship. MR-Egger intercept tests showed no evidence of horizontal pleiotropy. No influential SNP driving the results was detected by the leave-one-out sensitivity analysis.ConclusionsOur results suggested that psoriasis vulgaris causally increases the risk of BP, highlighting the need for potential strategies for the prevention and early diagnosis of comorbid BP in patients with psoriasis vulgaris. Further researches into this association and underlying mechanisms are warranted.
| S-EPMC10965669 | biostudies-literature
Project description: Not available
| S-EPMC10656872 | biostudies-literature