scholarly journals Epidemiology and Potential Pathomechanisms of Cardiovascular Comorbidities in Psoriasis: A Report from the GRAPPA 2010 Annual Meeting

2012 ◽  
Vol 39 (2) ◽  
pp. 441-444 ◽  
Author(s):  
WOLF-HENNING BOEHNCKE

There is increasing awareness that psoriasis is more than “skin deep.” Several recent reviews focused on biomarkers have indicated the systemic dimension of psoriasis and the comorbidity that psoriasis shares with other chronic inflammatory diseases. Of emerging significance is the relationship to cardiovascular disease, which contributes substantially to patients’ increased mortality. This article examines currently available evidence favoring the concept of a causal link between psoriasis and cardiovascular disease, and summarizes a report represented at the 2010 Annual Meeting of GRAPPA (Group for Research and Assessment of Psoriasis and Psoriatic Arthritis).

2013 ◽  
Vol 40 (8) ◽  
pp. 1434-1437 ◽  
Author(s):  
April W. Armstrong ◽  
Joel M. Gelfand ◽  
Wolf-Henning Boehncke ◽  
Ehrin J. Armstrong

At the 2012 annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) in Stockholm, Sweden, several GRAPPA members led a panel discussion on cardiovascular (CV) comorbidities of psoriasis and psoriatic arthritis (PsA). The panelists discussed the role of insulin resistance in the pathophysiology of psoriasis, the possible effect of tumor necrosis factor inhibitors on CV comorbidities, and the effect of 12/23 monoclonal antibodies on CV outcomes. The panelists also addressed how lessons from CV comorbidity research could be applied to other areas of comorbidity research in psoriasis and PsA and identified future research directions in this area.


2018 ◽  
Vol 24 (3) ◽  
pp. 281-290 ◽  
Author(s):  
Peter Riis Hansen

Inflammation plays a significant role in atherosclerosis and cardiovascular disease (CVD). Patients with chronic inflammatory diseases are at increased risk of CVD, but it is debated whether this association is causal or dependent on shared risk factors, other exposures, genes, and/or inflammatory pathways. The current review summarizes epidemiological, clinical, and experimental data supporting the role of shared inflammatory mechanisms between atherosclerotic CVD and rheumatoid arthritis, psoriasis, inflammatory bowel disease, and periodontitis, respectively, and provides insights to future prospects in this area of research. Awareness of the role of inflammation in CVD in patients with chronic inflammatory diseases and the potential for anti-inflammatory therapy, e.g., with tumor necrosis factor-α inhibitors, to also reduce atherosclerotic CVD has evolved into guideline- based recommendations. These include regular CVD risk assessment, aggressive treatment of traditional CVD risk factors, and recognition of reduced CVD as an added benefit of strict inflammatory disease control. At present, chronic inflammatory diseases would appear to qualify as partners in crime and not merely innocent bystanders to CVD. However, definite incremental contributions of inflammation versus effects of the complex interplay with other CVD risk factors may never be fully elucidated and for the foreseeable future, inflammation is posed to maintain its current position as both a marker and a maker of CVD, with clinical utility both for identification of patient at risk of CVD and as target for therapy to reduce CVD.


2012 ◽  
Vol 39 (11) ◽  
pp. 2204-2210 ◽  
Author(s):  
APRIL W. ARMSTRONG ◽  
KRISTINA CALLIS DUFFIN ◽  
AMIT GARG ◽  
JOEL M. GELFAND ◽  
ALICE B. GOTTLIEB ◽  
...  

At the 2011 annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) in Naples, Italy, the GRAPPA dermatology members led discussions on priority research areas in psoriasis and psoriatic arthritis (PsA). These discussions centered on 3 primary areas: evaluation of PsA screening tools, updates on psoriasis comorbidities, and new developments in genetics and comparative effectiveness research. Introductory presentations were followed by engaging panel discussions and audience interaction. The members agreed that screening tools are highly valuable in early detection of PsA among dermatology patients and that efforts are necessary to develop tools suitable for adoption in clinical practice. Members also agreed that a collaborative investigation to evaluate the effect of psoriasis treatments on cardiovascular comorbidities would be highly informative. Finally, the members supported continued efforts to explore the genetic basis of psoriasis and more studies focused on comparative effectiveness of existing treatments.


2021 ◽  
Author(s):  
Rune Matthiesen ◽  
Chris Lauber ◽  
Julio L. Sampaio ◽  
Neuza Domingues ◽  
Liliana Alves ◽  
...  

AbstractBackgroundInflammation impacts several acute and chronic diseases causing localized stress and cell death, releasing tissue-specific lipids into the circulation from inflamed cells and tissues. The plasma lipidome may be expected to reflect the type of inflammation and the specific cells and tissues involved. However, deep lipid profiles of major chronic inflammatory diseases have not been compared.MethodsWe compare the plasma lipidomes of patients suffering from two etiologically distinct chronic inflammatory diseases, atherosclerosis-related cardiovascular disease (CVD) including ischemic stroke (IS), and systemic lupus erythematosus (SLE), to each other and to age-matched controls. The controls had never suffered from any of these diseases. Blood plasma lipidomes were screened by a top-down shotgun MS-based analysis without liquid chromatographic separation. Lipid profiling based on MS was performed on a cohort of 427 individuals. The cohort constitutes 85 controls (control), 217 with cardiovascular disease (further classified into CVD 1-5), 21 ischemic stroke patients (IS), and 104 patients suffering from systemic lupus erythematosis (SLE). 596 lipids were profiled which were quality filtered for further evaluation and determination of potential biomarkers. Lipidomes were compared by linear regression and evaluated by machine learning classifiers.ResultsMachine learning classifiers based on the plasma lipidomes of patients suffering from CVD and SLE allowed clear distinction of these two chronic inflammatory diseases from each other and from healthy age-matched controls and body mass index (BMI). We demonstrate convincing evidence for the capability of lipidomics to separate the studied chronic and inflammatory diseases from controls based on independent validation test set classification performance (CVD vs control - Sensitivity: 0.90, Specificity: 0.98; IS vs control - Sensitivity: 1.0, Specificity: 1.0; SLE vs control – Sensitivity: 1, Specificity: 0.88) and from each other (SLE vs CVD □ Sensitivity: 0.91, Specificity: 1). Preliminary linear discriminant analysis plots using all data clearly separated the clinical groups from each other and from the controls. In addition, CVD severities, as classified into five clinical groups, were partially separable by linear discriminant analysis. Notably, significantly dysregulated lipids between pathological groups versus control displayed a reverse lipid regulation pattern compared to statin treated controls versus non treated controls.ConclusionDysregulation of the plasma lipidome is characteristic of chronic inflammatory diseases. Lipid profiling accurately identifies the diseases and in the case of CVD also identifies sub-classes. Dysregulated lipids are partially but not fully counterbalanced by statin treatment.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Simran Chadha ◽  
Adovich Rivera ◽  
Anna Pawlowski ◽  
Donald M Lloyd-jones ◽  
Matthew J Feinstein

Introduction: Several chronic inflammatory diseases (CID) are associated with elevated risks for cardiovascular diseases (CVDs). However, the relative magnitude of elevated CVD risk may differ considerably between chronic inflammatory diseases. Hypothesis: We hypothesized that not all CIDs are associated with elevated risk for diabetes mellitus (DM) and atherosclerotic cardiovascular disease (ASCVD), and that magnitudes of increased CVD risk differ considerably across CIDs. Methods: We estimated the incidence of DM and ASCVD in 18,373 patients with any of six CIDs [human immunodeficiency virus infection (HIV), Irritable bowel disease (IBD), psoriasis, rheumatoid arthritis (RA), scleroderma, and systemic lupus erythematosus (SLE)] in regular outpatient care, as well as controls without CIDs in regular primary care, in a large metropolitan health system since January 1 st , 2000. We assessed incidence of outcomes in patients with each CID compared to controls using quasi-Poisson regression adjusting for age, sex, insurance status, and common CVD risk factors. A 90-day blanking period was applied for identifying incident cases. Results: Psoriasis, HIV, male sex, black race, Hispanic ethnicity, and being on public insurance were all associated with significantly elevated risks for DM (Figure). HIV, RA, scleroderma, SLE, male sex, and public insurance were all associated with significantly elevated risks for ASCVD. The magnitude of increased risk for ASCVD was similarly high for HIV (incidence rate ratio 1.79, 95% confidence interval 1.57-2.05), scleroderma (1.79, 1.42-2.27), and SLE (1.95, 1.59-2.39). Conclusion: Several, but not all, CIDs are associated with elevated risks for DM and ASCVD, but the magnitude of risk elevation differs depending on the CID. These data demonstrate the importance of nuanced approaches to understanding CID- and inflammation-associated CVD risks.


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