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Annunziata G, Verde L, Zink A, Muscogiuri G, Albanesi C, Paganelli A, Barrea L, Scala E. Plant-Based Foods for Chronic Skin Diseases: A Focus on the Mediterranean Diet. Curr Nutr Rep 2025; 14:42. [PMID: 40048018 PMCID: PMC11885338 DOI: 10.1007/s13668-025-00632-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 02/22/2025] [Indexed: 03/09/2025]
Abstract
PURPOSE OF REVIEW In this narrative review, we provide an overview of how adherence to a Mediterranean dietary pattern can complement traditional treatment strategies for psoriasis, acne, and hidradenitis suppurativa. We emphasize the importance of an integrated approach, with dietary interventions as a key component of holistic patient care. RECENT FINDINGS Psoriasis, acne, and hidradenitis suppurativa are immune-mediated chronic diseases marked by systemic inflammation, with genetic and environmental factors influencing their onset. The Mediterranean diet, rich in plant-based foods with antioxidant and anti-inflammatory properties-such as whole-grain cereals, extra-virgin olive oil, vegetables, legumes, fruits, and nuts-has been shown to reduce the clinical severity of these conditions. It also supports weight control and positively impacts metabolic and cardiovascular risk factors, which are closely linked to these diseases. Dietary education, particularly about the Mediterranean diet, plays a crucial role in the management of these skin diseases and serves as an important non-pharmacological treatment option that can influence patient prognosis. This review offers specific nutrition recommendations for prescribing the Mediterranean diet to patients with chronic inflammatory skin diseases.
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Affiliation(s)
- Giuseppe Annunziata
- Facoltà Di Scienze Umane, Della Formazione E Dello Sport, Università Telematica Pegaso, Via Porzio, Centro Direzionale, Isola F2, 80143, Naples, Italy
| | - Ludovica Verde
- Department of Public Health, University of Naples Federico II, Via Sergio Pansini 5, 80131, Naples, Italy
| | - Alexander Zink
- Department of Dermatology and Allergy, TUM School of Medicine and Health, Technical University of Munich, Munich, Germany
| | - Giovanna Muscogiuri
- Diabetologia E Andrologia, Dipartimento Di Medicina Clinica E Chirurgia, Unità Di Endocrinologia, Università Degli Studi Di Napoli Federico II, Via Sergio Pansini 5, 80131, Naples, Italy
- Dipartimento Di Medicina Clinica E Chirurgia, Centro Italiano Per La Cura E Il Benessere del Paziente Con Obesità (C.I.B.O), Università Degli Studi Di Napoli Federico II, Via Sergio Pansini 5, 80131, Naples, Italy
- Cattedra Unesco "Educazione Alla Salute E Allo Sviluppo Sostenibile", University Federico II, 80131, Naples, Italy
| | - Cristina Albanesi
- Laboratory of Experimental Immunology, IDI-IRCCS, Via Monti Di Creta, 104, 00167, Rome, Italy
| | | | - Luigi Barrea
- Dipartimento Di Psicologia E Scienze Della Salute, Università Telematica Pegaso, Centro Direzionale, Via Porzio, Isola F2, 80143, Naples, Italy
| | - Emanuele Scala
- Laboratory of Experimental Immunology, IDI-IRCCS, Via Monti Di Creta, 104, 00167, Rome, Italy.
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Cho H, Kim YJ, Moon IJ, Lee WJ, Won CH, Lee MW, Chang SE, Jung JM. Risk of major adverse cardiovascular events and all-cause mortality among patients with psoriatic disease treated with tumor necrosis factor-α and interleukin-12/23 inhibitors: a nationwide population-based cohort study in Korea. J DERMATOL TREAT 2024; 35:2321194. [PMID: 38403279 DOI: 10.1080/09546634.2024.2321194] [Citation(s) in RCA: 2] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/17/2023] [Accepted: 02/13/2024] [Indexed: 02/27/2024]
Abstract
PURPOSE Few studies have investigated the impact of biologics on the risk of major adverse cardiovascular events (MACEs) among Korean patients with psoriatic diseases. We compared the risk of MACEs and all-cause mortality among patients with psoriatic disease treated with tumor necrosis factor (TNF)-α and interleukin (IL)-12/23 inhibitors in Korea. METHODS Patients with psoriatic disease prescribed with TNF-α and IL-12/23 inhibitors since 2016 were selected from the Korean National Health Insurance Service (NHIS) Database. Follow-up data for MACEs and all-cause mortality between 2016 and 2020 were collected. A total of 2886 individuals were included, including 1987 IL-12/23 inhibitor users and 899 TNF-α inhibitor users. RESULTS Compared with IL-12/23 inhibitor users, TNF-α inhibitor users had a higher prevalence of dyslipidemia and a significantly higher risk of all-cause mortality but not MACE. After controlling for age, female TNF-α inhibitor users had a significantly increased risk of all-cause mortality. Meanwhile, after controlling for sex, TNF-α inhibitor users aged 60 years or older demonstrated a significantly elevated risk of all-cause mortality. In conclusion, No statistically significant difference in MACE risk was observed between patients who used TNF-α and IL-12/23 inhibitors. Nevertheless, the use of IL-12/23 inhibitors, especially among older and female patients, resulted in a lower overall mortality.
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Affiliation(s)
- Hyesoo Cho
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Ye-Jee Kim
- Department of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Ik Jun Moon
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Woo Jin Lee
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Chong Hyun Won
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Mi Woo Lee
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Sung Eun Chang
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
| | - Joon Min Jung
- Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
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3
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Huong NTK, Long B, Doanh LH, Thoai TM, Hang NT, Khoi L, Nu PT. Associations of different inflammatory factors with atherosclerosis among patients with psoriasis vulgaris. Front Med (Lausanne) 2024; 11:1396680. [PMID: 39104857 PMCID: PMC11298419 DOI: 10.3389/fmed.2024.1396680] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2024] [Accepted: 07/08/2024] [Indexed: 08/07/2024] Open
Abstract
Background This study aimed to measure the associations between different inflammatory factors, namely interleukin (IL)-17A, tumor necrosis factor (TNF)-α, and high-sensitivity C-reactive protein (hs-CRP), and atherosclerosis in patients with psoriasis vulgaris. Methods A cross-sectional study was conducted at two hospitals in Hanoi, Vietnam. A total of 125 patients with psoriasis vulgaris and 50 healthy controls were recruited. Clinical characteristics and atherosclerosis were assessed. IL-17A, TNF-α, and hs-CRP levels were measured. Results Psoriasis vulgaris patients with atherosclerosis had higher levels of hs-CRP (median = 1.22; interquartile range-IQR = 0.34-12.11) and IL-17A (median = 1.30; IQR = 0.43-4.28), but a lower level of TNF-α (median = 0.54; IQR = 0.13-3.41) compared to those without atherosclerosis (p < 0.05). Only LogIL-17A was positively related to atherosclerosis in psoriasis patients (Odds Ratio-OR = 2.16, 95% CI = 1.06-4.38, p < 0.05). After excluding systemically treated patients, LogIL-17A and Log TNF-α were associated with the likelihood of atherosclerosis (p < 0.05). Conclusion This study suggests a link between elevated levels of IL-17A and TNF-α and subclinical atherosclerosis. Further investigation on a larger scale is required to establish the causality of this relationship.
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Affiliation(s)
- Nguyen Thi Kim Huong
- Hanoi Medical University, Hanoi, Vietnam
- Department of Dermatology, Friendship Hospital, Hanoi, Vietnam
| | - Bui Long
- Department of Interventional Cardiology, Friendship Hospital, Hanoi, Vietnam
| | | | - Tran Minh Thoai
- Department of Interventional Cardiology, Friendship Hospital, Hanoi, Vietnam
| | - Nguyen Thi Hang
- Department of Interventional Cardiology, Friendship Hospital, Hanoi, Vietnam
| | - Le Khoi
- Department of Interventional Cardiology, Friendship Hospital, Hanoi, Vietnam
| | - Pham Thi Nu
- Department of Cardiology, Friendship Hospital, Hanoi, Vietnam
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4
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Potestio L, Tommasino N, Lauletta G, Martora F, Megna M. Psoriasis and Molecular Target Therapies: Evidence of Efficacy in Preventing Cardiovascular Comorbidities. Dermatol Ther (Heidelb) 2024; 14:841-852. [PMID: 38592640 PMCID: PMC11052943 DOI: 10.1007/s13555-024-01152-w] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/05/2024] [Accepted: 03/26/2024] [Indexed: 04/10/2024] Open
Abstract
Psoriasis is now considered a systemic disease, and several comorbidities have been described such as cardiovascular diseases, neurologic and psychiatric disorders, chronic inflammatory bowel disease, psoriatic arthritis, etc. Regarding cardiovascular comorbidities, major adverse cardiovascular events have been reported in psoriasis patients by multiple epidemiologic studies. Moreover, smoking, obesity, metabolic syndrome, hypertension, dyslipidemia, diabetes and reduced physical activity are associated with psoriasis, increasing cardiovascular risk. Consequently, several aspects should be considered when making the treatment decision. The aim of this review manuscript was to investigate the effectiveness and safety of biologic drugs acting on molecular mechanisms involved in the pathogenesis of psoriasis in preventing cardiovascular complications.
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Affiliation(s)
- Luca Potestio
- Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Via Pansini 5, 80131, Naples, Italy.
| | - Nello Tommasino
- Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Via Pansini 5, 80131, Naples, Italy
| | - Giuseppe Lauletta
- Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Via Pansini 5, 80131, Naples, Italy
| | - Fabrizio Martora
- Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Via Pansini 5, 80131, Naples, Italy
| | - Matteo Megna
- Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Via Pansini 5, 80131, Naples, Italy
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Palmer V, Cornier MA, Waring A, Valdebran M. Evaluation and treatment of metabolic syndrome and cardiovascular disease in adult patients with psoriasis. Int J Dermatol 2023; 62:1437-1446. [PMID: 37845786 DOI: 10.1111/ijd.16873] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/03/2023] [Revised: 09/21/2023] [Accepted: 09/27/2023] [Indexed: 10/18/2023]
Abstract
Psoriasis is strongly associated with cardiovascular disease (CVD) and metabolic syndrome, with patients having an approximately twofold increased risk of each compared to the general population. This increased risk is based on shared underlying genetic and cytokine profiles, as well as similar environmental risks. Many screening guidelines do not address the development of CVD and metabolic syndrome in these predisposed patients. These deficits are evidenced by the exclusion of psoriasis as a risk factor in validated 10-year CVD risk calculators for adult patients with chronic inflammatory diseases, as well as insufficient screening guidelines for insulin resistance in patients with psoriasis. This manuscript aims to discuss and propose allopathic and lifestyle recommendations for the screening and management of the aforementioned comorbidities in adult patients with psoriasis.
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Affiliation(s)
- Victoria Palmer
- Department of Medicine, Richmond University Medical Center, Staten Island, NY, USA
| | - Marc-André Cornier
- Division of Endocrinology, Diabetes and Metabolic Diseases, Department of Medicine, Medical University of South Caroline, Charleston, SC, USA
| | - Ashley Waring
- Heart and Vascular Center, Division of Cardiology, Medical University of South Carolina, Charleston, SC, USA
| | - Manuel Valdebran
- Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston, SC, USA
- Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA
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Looking beyond the Skin: Pathophysiology of Cardiovascular Comorbidity in Psoriasis and the Protective Role of Biologics. Pharmaceuticals (Basel) 2022; 15:ph15091101. [PMID: 36145322 PMCID: PMC9503011 DOI: 10.3390/ph15091101] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/01/2022] [Revised: 08/23/2022] [Accepted: 08/25/2022] [Indexed: 11/16/2022] Open
Abstract
Psoriasis is a chronic systemic inflammatory disease associated with a higher incidence of cardiovascular disease, especially in patients with moderate to severe psoriasis. It has been estimated that severe psoriasis confers a 25% increase in relative risk of cardiovascular disease, regardless of traditional risk factors. Although the underlying pathogenic mechanisms relating psoriasis to increased cardiovascular risk are not clear, atherosclerosis is emerging as a possible link between skin and vascular affection. The hypothesis that the inflammatory cascade activated in psoriasis contributes to the atherosclerotic process provides the underlying basis to suggest that an anti-inflammatory therapy that improved atherosclerosis would also reduce the risk of MACEs. In this sense, the introduction of biological drugs which specifically target cytokines implicated in the inflammatory cascade have increased the expectations of control over the cardiovascular comorbidity present in psoriasis patients, however, their role in vascular damage processes remains controversial. The aim of this paper is to review the mechanistic link between psoriasis and cardiovascular disease development, as well as analyzing which of the biological treatments could also reduce the cardiovascular risk in these patients, fueling a growing debate on the modification of the general algorithm of treatment.
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Merzel Šabović EK, Starbek Zorko M, Janić M. Killing Two Birds with One Stone: Potential Therapies Targeting Psoriasis and Atherosclerosis at the Same Time. Int J Mol Sci 2022; 23:ijms23126648. [PMID: 35743091 PMCID: PMC9224172 DOI: 10.3390/ijms23126648] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2022] [Revised: 06/10/2022] [Accepted: 06/12/2022] [Indexed: 01/27/2023] Open
Abstract
Psoriasis is a chronic systemic inflammatory disease. Due to systemic inflammation, it is associated with many comorbidities. Among them, cardiovascular diseases represent the most common causes of morbidity and mortality in this population. Therefore, physicians treating patients with psoriasis should keep in mind that, as important as the treatment of psoriasis, awareness of cardiovascular risk deserves additional attention. Thus, in parallel with psoriasis treatment, a cardiovascular risk assessment must also be performed and addressed accordingly. In addition to encouraging non-pharmacologic strategies for a healthy lifestyle, physicians should be familiar with different pharmacologic options that can target psoriasis and reduce cardiovascular risk. In the present article, we present the pathophysiological mechanisms of the psoriasis and cardiometabolic interplay, our view on the interaction of psoriasis and cardiovascular disease, review the atherosclerotic effect of therapeutic options used in psoriasis, and vice versa, i.e., what the effect of medications used in the prevention of atherosclerosis could be on psoriasis.
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Affiliation(s)
- Eva Klara Merzel Šabović
- Department of Dermatovenerology, University Medical Centre Ljubljana, Gradiškova Ulica 10, SI-1000 Ljubljana, Slovenia;
- Faculty of Medicine, University of Ljubljana, Vrazov Trg 2, SI-1000 Ljubljana, Slovenia;
- Correspondence:
| | - Mateja Starbek Zorko
- Department of Dermatovenerology, University Medical Centre Ljubljana, Gradiškova Ulica 10, SI-1000 Ljubljana, Slovenia;
- Faculty of Medicine, University of Ljubljana, Vrazov Trg 2, SI-1000 Ljubljana, Slovenia;
| | - Miodrag Janić
- Faculty of Medicine, University of Ljubljana, Vrazov Trg 2, SI-1000 Ljubljana, Slovenia;
- Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Centre Ljubljana, Zaloška Cesta 7, SI-1000 Ljubljana, Slovenia
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Dongliang Y, Yang R, Peng S, Deng J, Huo Y, Deng Z, Yau Y, Liu J, Liao D, Cheng C. Guanxin Xiaoban capsules could treat atherosclerosis by affecting the gut microbiome and inhibiting the AGE-RAGE signalling pathway. J Med Microbiol 2022; 71. [PMID: 35580023 DOI: 10.1099/jmm.0.001530] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/18/2022] Open
Abstract
Introduction. Atherosclerosis is a chronic disorder in which plaque builds up in the arteries and is associated with several cardiovascular and cerebrovascular diseases such as coronary artery disease, cerebral infarction and cerebral haemorrhage. Therefore, there is an urgent need to discover new medications to treat or prevent atherosclerosis.Hypothesis/Gap Statement. The active components of Guanxin Xiaoban capsules may have an effect on the gut microbiome of patients with atherosclerosis and have a role in their therapeutic targets.Aim. The aim of this study was to identify genes and pathways targeted by active ingredients in Guanxin Xiaoban capsules for the treatment of atherosclerosis based on network pharmacology and analysis of changes to the gut microbiome.Methods. Mice were treated with Guanxin Xiaoban capsules. The 16S rDNA genome sequence of all microorganisms from each group of faecal samples was used to evaluate potential structural changes in the gut microbiota after treatment with Guanxin Xiaoban capsules. Western blotting and real-time quantitative PCR were used to detect gene targets in aortic and liver tissues. Haematoxylin and eosin staining was used to observe improvements in mouse arterial plaques.Results. The gut microbiota of atherosclerotic mice is disturbed. After Guanxin Xiaoban treatment, the abundance of bacteria in the mice improved, with an increase in the proportion of Akkermansia and a significant decrease in the proportion of Faecalibaculum. The main ingredients of Guanxin Xiaoban capsules are calycosin, liquiritin, ferulic acid, ammonium glycyrrhizate, aloe emodin, rhein and emodin. The core genes of this network were determined to be glutathione S-transferase mu 1 (GSTM1), vascular endothelial growth factor A (VEGFA) and cyclin-dependent kinase inhibitor 1A (CDKN1A). The compound-target gene network revealed an interaction between multiple components and targets and contributed to a better understanding of the potential therapeutic effects of the capsules on atherosclerosis. In addition, expression of the AGE-receptor for the AGE (RAGE) pathway was significantly inhibited and the mice showed signs of arterial plaque reduction. Guanxin Xiaoban capsules may improve atherosclerosis and reduce the plaque area by inhibiting the AGE-RAGE signalling pathway to delay the development of atherosclerosis. This mechanism appears to involve changes in the gut microbiota. Therefore, Guanxin Xiaoban capsules have potential value as a treatment for atherosclerosis.
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Affiliation(s)
- Yin Dongliang
- College of Pharmacy, Hunan University of Chinese Medicine, Changsha, PR China.,Department of Rehabilitation Medicine, Third Xiangya Hospital, Central South University, Changsha, PR China
| | - Rong Yang
- College of Pharmacy, Hunan University of Chinese Medicine, Changsha, PR China
| | - Sha Peng
- College of Pharmacy, Hunan University of Chinese Medicine, Changsha, PR China
| | - Jing Deng
- Hunan Key Laboratory for Quality Evaluation of Bulk Herbs, Hunan University of Chinese Medicine, Changsha, PR China
| | - Yanjie Huo
- College of Pharmacy, Hunan University of Chinese Medicine, Changsha, PR China
| | - Zhe Deng
- Department of Internal Medicine, College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, PR China
| | - Yuenming Yau
- School of Medicine, Xiamen University, Xiamen, PR China
| | - Jianhe Liu
- Department of Cardiovascular Diseases, The First Hospital of Hunan University of Chinese Medicine, Changsha, PR China
| | - Duanfang Liao
- College of Pharmacy, Hunan University of Chinese Medicine, Changsha, PR China
| | - Choufu Cheng
- Department of Cardiovascular Diseases, The First Hospital of Hunan University of Chinese Medicine, Changsha, PR China
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Wang Y, Zang J, Liu C, Yan Z, Shi D. Interleukin-17 Links Inflammatory Cross-Talks Between Comorbid Psoriasis and Atherosclerosis. Front Immunol 2022; 13:835671. [PMID: 35514987 PMCID: PMC9063001 DOI: 10.3389/fimmu.2022.835671] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/14/2021] [Accepted: 03/23/2022] [Indexed: 11/13/2022] Open
Abstract
Psoriasis is a chronic, systemic, immune-mediated inflammatory disorder that is associated with a significantly increased risk of cardiovascular disease (CVD). Studies have shown that psoriasis often coexists with atherosclerosis, a chronic inflammatory disease of large and medium-sized arteries, which is a major cause of CVD. Although the molecular mechanisms underlying this comorbidity are not fully understood, clinical studies have shown that when interleukin (IL)-17A inhibitors effectively improve psoriatic lesions, atherosclerotic symptoms are also ameliorated in patients with both psoriasis and atherosclerosis. Also, IL-17A levels are highly expressed in the psoriatic lesions and atherosclerotic plaques. These clinical observations implicit that IL-17A could be a crucial link for psoriasis and atherosclerosis and IL-17A-induced inflammatory responses are the major contribution to the pathogenesis of comorbid psoriasis and atherosclerosis. In this review, the current literature related to epidemiology, genetic predisposition, and inflammatory mechanisms of comorbidity of psoriasis and atherosclerosis is summarized. We focus on the immunopathological effects of IL-17A in both diseases. The goal of this review is to provide the theoretical base for future preventing or treating psoriasis patients with atherosclerosis comorbidity. The current evidence support the notion that treatments targeting IL-17 seem to be hold some promise to reduce cardiovascular risk in patients with psoriasis.
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Affiliation(s)
- Yan Wang
- College of Clinical Medicine, Jining Medical University, Jining, China
| | - Jinxin Zang
- Department of Neurology, Jining No.1 People's Hospital, Jining, China
| | - Chen Liu
- Laboratory of Medical Mycology, Jining No.1 People's Hospital, Jining, China
| | - Zhongrui Yan
- Department of Neurology, Jining No.1 People's Hospital, Jining, China
| | - Dongmei Shi
- Laboratory of Medical Mycology, Jining No.1 People's Hospital, Jining, China.,Department of Dermatology, Jining No.1 People's Hospital, Jining, China
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10
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Wang X, Kaiser H, Kvist-Hansen A, McCauley BD, Skov L, Hansen PR, Becker C. IL-17 Pathway Members as Potential Biomarkers of Effective Systemic Treatment and Cardiovascular Disease in Patients with Moderate-to-Severe Psoriasis. Int J Mol Sci 2022; 23:ijms23010555. [PMID: 35008981 PMCID: PMC8745093 DOI: 10.3390/ijms23010555] [Citation(s) in RCA: 15] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2021] [Revised: 12/30/2021] [Accepted: 12/30/2021] [Indexed: 02/01/2023] Open
Abstract
Psoriasis is a chronic inflammatory condition associated with atherosclerotic cardiovascular disease (CVD). Systemic anti-psoriatic treatments mainly include methotrexate and biological therapies targeting TNF, IL-12/23 and IL-17A. We profiled plasma proteins from patients with moderate-to-severe psoriasis to explore potential biomarkers of effective systemic treatment and their relationship to CVD. We found that systemically well-treated patients (PASI < 3.0, n = 36) had lower circulating levels of IL-17 pathway proteins compared to untreated patients (PASI > 10, n = 23). Notably, IL-17C and PI3 were decreased with all four examined systemic treatment types. Furthermore, in patients without CVD, we observed strong correlations among IL-17C/PI3/PASI (r ≥ 0.82, p ≤ 1.5 × 10−12) pairs or between IL-17A/PASI (r = 0.72, p = 9.3 × 10−8). In patients with CVD, the IL-17A/PASI correlation was abolished (r = 0.2, p = 0.24) and the other correlations were decreased, e.g., IL-17C/PI3 (r = 0.61, p = 4.5 × 10−5). Patients with moderate-to-severe psoriasis and CVD had lower levels of IL-17A compared to those without CVD (normalized protein expression [NPX] 2.02 vs. 2.55, p = 0.013), and lower IL-17A levels (NPX < 2.3) were associated with higher incidence of CVD (OR = 24.5, p = 0.0028, 95% CI 2.1–1425.1). As a result, in patients with moderate-to-severe psoriasis, we propose circulating IL-17C and PI3 as potential biomarkers of effective systemic anti-psoriatic treatment, and IL-17A as potential marker of CVD.
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Affiliation(s)
- Xing Wang
- Department of Medicine, Division of Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; (X.W.); (B.D.M.)
| | - Hannah Kaiser
- Department of Cardiology, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark; (H.K.); (A.K.-H.); (P.R.H.)
- Department of Dermatology and Allergy, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark;
- Department of Clinical Medicine, University of Copenhagen, 2200 Copenhagen, Denmark
| | - Amanda Kvist-Hansen
- Department of Cardiology, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark; (H.K.); (A.K.-H.); (P.R.H.)
- Department of Dermatology and Allergy, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark;
| | - Benjamin D. McCauley
- Department of Medicine, Division of Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; (X.W.); (B.D.M.)
| | - Lone Skov
- Department of Dermatology and Allergy, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark;
- Department of Clinical Medicine, University of Copenhagen, 2200 Copenhagen, Denmark
| | - Peter Riis Hansen
- Department of Cardiology, University Hospital—Herlev and Gentofte, 2900 Hellerup, Denmark; (H.K.); (A.K.-H.); (P.R.H.)
- Department of Clinical Medicine, University of Copenhagen, 2200 Copenhagen, Denmark
| | - Christine Becker
- Department of Medicine, Division of Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; (X.W.); (B.D.M.)
- Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
- Correspondence:
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11
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Cai J, Cui L, Wang Y, Li Y, Zhang X, Shi Y. Cardiometabolic Comorbidities in Patients With Psoriasis: Focusing on Risk, Biological Therapy, and Pathogenesis. Front Pharmacol 2021; 12:774808. [PMID: 34803716 PMCID: PMC8600112 DOI: 10.3389/fphar.2021.774808] [Citation(s) in RCA: 18] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/13/2021] [Accepted: 10/14/2021] [Indexed: 12/23/2022] Open
Abstract
Psoriasis is a chronic inflammatory disease characterized by erythematous scaly plaques, accompanied by systemic damage that leads to the development of multiple comorbidities. In particular, the association between psoriasis and cardiometabolic comorbidities, including cardiovascular diseases (CVDs), obesity, diabetes mellitus, and metabolic syndrome, has been verified in a considerable number of clinical trials. Moreover, the increased risk of cardiometabolic comorbidities positively correlates with psoriasis severity. Biologic therapy targeting inflammatory pathways or cytokines substantially improves the life quality of psoriasis patients and may affect cardiometabolic comorbidities by reducing their incidences. In this review, we focus on exploring the association between cardiometabolic comorbidities and psoriasis, and emphasize the benefits and precautions of biologic therapy in the management of psoriasis with cardiometabolic comorbidities. The pathogenic mechanisms of cardiometabolic comorbidities in psoriasis patients involve common genetic factors, lipid metabolism, insulin resistance, and shared inflammatory pathways such as tumor necrosis factor-α and interleukin-23/Th-17 pathways.
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Affiliation(s)
- Jiangluyi Cai
- Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.,Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China
| | - Lian Cui
- Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China.,Department of Dermatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China
| | - Yu Wang
- Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.,Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China
| | - Ying Li
- Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.,Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China
| | - Xilin Zhang
- Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.,Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China
| | - Yuling Shi
- Department of Dermatology, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.,Institute of Psoriasis, Tongji University School of Medicine, Shanghai, China
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12
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Psoriasis and Atherosclerosis-Skin, Joints, and Cardiovascular Story of Two Plaques in Relation to the Treatment with Biologics. Int J Mol Sci 2021; 22:ijms221910402. [PMID: 34638740 PMCID: PMC8508744 DOI: 10.3390/ijms221910402] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2021] [Revised: 09/21/2021] [Accepted: 09/24/2021] [Indexed: 02/06/2023] Open
Abstract
It is known that both psoriasis (PSO) limited to the skin and psoriatic arthritis (PSA) increase the risk of cardiovascular complications and atherosclerosis progression by inducing systemic inflammatory response. In recent decades, the introduction of biological medications directed initially against TNF-α and, later, different targets in the inflammatory cascade brought a significant breakthrough in the efficacy of PSO/PSA treatment. In this review, we present and discuss the most recent findings related to the interplay between the genetics and immunology mechanisms involved in PSO and PSA, atherosclerosis and the development of cardiac dysfunction, as well as the current PSO/PSA treatment in view of cardiovascular safety and prognosis.
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13
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Bazid H, Hammam M, Aboashour M, Ellaithy M, Mostafa M, Holah NS. Study of serum level and immunohistochemical expression of von Willebrand factor in psoriasis. J Immunoassay Immunochem 2021; 43:54-66. [PMID: 34225585 DOI: 10.1080/15321819.2021.1941097] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/11/2023]
Abstract
Von Willebrand factor (vWF) is angiogenic, hypercoagulable, and inflammatory marker that increases inflammation and vasculitis and reflects endothelial cells dysfunction. vWF could play a role in psoriasis pathogenesis and prognosis. To assess the serum and immunohistochemical expression of vWF in psoriasis to evaluate its possible role in disease pathogenesis and prognosis. This case-control study included 30 cases of psoriasis vulgaris with different degrees of severity and 30 age- and sex-matched healthy controls. Serum level of vWF was measured by ELISA. Immunohistochemical staining of skin biopsies for von Willebrand factor (vVF) antibody was done. Significantly higher vWF serum level in cases (24.3 ± 14.0) vs (15.7 ± 6.85) for controls (p = .002) and significantly higher epidermal expression intensity in patients than in controls (P value = .001). There was also significant difference between cases and control regarding the dermal expression of vWF in inflammatory cells, adenexa, and endothelial cell (P value = .001, 0.065, 0.004, respectively,). Von Willebrand factor could be used as an indicator of the hypercoaguable state which may develop in patients with psoriasis and may serve as a new therapeutic target in psoriasis treatment protocols. Patients with psoriasis especially those with high PASI score are more prone to develop vascular complication. Serum vWF could be used as a better marker for psoriasis severity than PASI which is considered the gold-standard noninvasive assessment but it only measures skin involvement, while psoriasis is considered a systemic disease.
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Affiliation(s)
- Heba Bazid
- Dermatology and Andrology Department, Menoufia University Faculty of Medicine, Shebin El-Kom, Egypt
| | - Mostafa Hammam
- Department of Dermatology and Andrology, Menoufia University Faculty of Medicine, Shebin El-Kom, Egypt
| | - Marwa Aboashour
- Department of Dermatology and Andrology, Menoufia Egypt, Sadat Hospital, Shebin El-Kom, Egypt
| | - Manal Ellaithy
- Medical Biochemistry department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt
| | - Mohammed Mostafa
- Clinical Pathology department, National Research Center, Cairo, Egypt
| | - Nanis Shawky Holah
- Pathology Department, Menoufia University Faculty of Medicine, Shebin El-Kom, Egypt
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14
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Sileno S, Beji S, D'Agostino M, Carassiti A, Melillo G, Magenta A. microRNAs involved in psoriasis and cardiovascular diseases. VASCULAR BIOLOGY 2021; 3:R49-R68. [PMID: 34291190 PMCID: PMC8284950 DOI: 10.1530/vb-21-0007] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 05/17/2021] [Accepted: 06/03/2021] [Indexed: 12/14/2022]
Abstract
Psoriasis is a chronic inflammatory disease involving the skin. Both genetic and environmental factors play a pathogenic role in psoriasis and contribute to the severity of the disease. Psoriasis, in fact, has been associated with different comorbidities such as diabetes, metabolic syndrome, gastrointestinal or kidney diseases, cardiovascular disease (CVD), and cerebrovascular diseases (CeVD). Indeed, life expectancy in severe psoriasis is reduced by up to 5 years due to CVD and CeVD. Moreover, patients with severe psoriasis have a higher prevalence of traditional cardiovascular (CV) risk factors, including dyslipidemia, diabetes, smoking, and hypertension. Further, systemic inflammation is associated with oxidative stress increase and induces endothelial damage and atherosclerosis progression. Different miRNA have been already described in psoriasis, both in the skin tissues and in the blood flow, to play a role in the progression of disease. In this review, we will summarize and discuss the most important miRNAs that play a role in psoriasis and are also linked to CVD.
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Affiliation(s)
- Sara Sileno
- Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy
| | - Sara Beji
- Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy
| | - Marco D'Agostino
- Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy
| | - Alessandra Carassiti
- Istituto Dermopatico dell'Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy
| | - Guido Melillo
- Unit of Cardiology, IDI-IRCCS, Via Monti di Creta, Rome, Italy
| | - Alessandra Magenta
- Institute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Fosso del Cavaliere, Rome, Italy
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15
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Porta S, Otero-Losada M, Kölliker Frers RA, Cosentino V, Kerzberg E, Capani F. Adipokines, Cardiovascular Risk, and Therapeutic Management in Obesity and Psoriatic Arthritis. Front Immunol 2021; 11:590749. [PMID: 33643281 PMCID: PMC7902722 DOI: 10.3389/fimmu.2020.590749] [Citation(s) in RCA: 12] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/02/2020] [Accepted: 12/21/2020] [Indexed: 12/13/2022] Open
Abstract
Psoriatic arthritis is a chronic inflammatory disease with skin and joint pathology as the dominant characteristics. Scientific evidence supports its systemic nature and relevant relationship with obesity, metabolic syndrome, and associated conditions. Metabolic syndrome and obesity share common signaling pathways with joint inflammation, reinforcing the idea that adipose tissue is a major contributor to disease development and severity. The adipose tissue is not a mere energy store but also an endocrine organ participating in the immune response. In the search for the best therapeutic strategy for a patient, we should appraise the adipose tissue as an endocrine and immune organ responsible for mild chronic inflammation. Today, our challenge is not only to achieve disease remission but to control the associated comorbidities as well. In light of the high prevalence of obesity in psoriatic arthritis patients and the importance of the adipose tissue in the development of chronic inflammation, we aimed to identify the most relevant articles in this regard published in English until June 2020 using the PubMed database. Search terms included psoriatic arthritis, in combination with metabolic syndrome, obesity, adipokines, cardiovascular disease, and treatment. This review summarizes the current evidence regarding the role of adipose tissue as an adipokine-secreting endocrine organ, discussing its influence on disease development and severity, and ultimately in meeting successful disease management.
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Affiliation(s)
- Sabrina Porta
- Rheumatology Department, J. M. Ramos Mejía Hospital, Buenos Aires, Argentina
| | - Matilde Otero-Losada
- Biomedical Research Center, Interamerican Open University, National Research Council (CAECIHS-UAI. CONICET), Buenos Aires, Argentina
| | - Rodolfo A Kölliker Frers
- Rheumatology Department, J. M. Ramos Mejía Hospital, Buenos Aires, Argentina.,Biomedical Research Center, Interamerican Open University, National Research Council (CAECIHS-UAI. CONICET), Buenos Aires, Argentina
| | - Vanesa Cosentino
- Rheumatology Department, J. M. Ramos Mejía Hospital, Buenos Aires, Argentina
| | - Eduardo Kerzberg
- Rheumatology Department, J. M. Ramos Mejía Hospital, Buenos Aires, Argentina
| | - Francisco Capani
- Biomedical Research Center, Interamerican Open University, National Research Council (CAECIHS-UAI. CONICET), Buenos Aires, Argentina.,Department of Biology, University John F. Kennedy, Buenos Aires, Argentina.,Universidad Autónoma de Chile, Santiago, Chile
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16
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Nair KM, Kannayiram SS, Guraya A, Idolor ON, Aihie OP, Sanwo EJ, Muojieje CC. Reasons for Hospitalization of Psoriasis Patients: A Report From the National Inpatient Sample. Cureus 2020; 12:e12271. [PMID: 33520487 PMCID: PMC7834545 DOI: 10.7759/cureus.12271] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Background We used a large United States population-based database to analyze the reasons for hospitalization of psoriasis patients. Methods International Classification of Diseases, 10th revision (ICD-10) code was used to identify hospitalizations in National Inpatient Sample (NIS) 2017 with a principal or secondary diagnosis of psoriasis. The reasons for hospitalization were divided into 19 categories based on their principal discharge ICD-10 diagnosis code. We also ranked the five most common specific reasons for hospitalization of psoriasis patients. Results There were over 35 million discharges included in the 2017 NIS database. A total of 165215 hospitalizations had either a principal or secondary ICD 10 code for psoriasis. Based on ICD-10 code categories, the top five reasons for hospitalization in patients with history of psoriasis were: Cardiovascular (CV) (26605, 16.10%), rheumatologic (19555, 11.84%), digestive (18465, 11.18%), infection (16395, 9.92%), and respiratory (14865, 9.00%). Sepsis was the most common principal diagnosis of psoriasis hospitalizations. Conclusion CV diseases were the most common ICD category, and sepsis was the most common principal diagnosis for psoriasis hospitalization. Management of medical co-morbidities is important in reducing rates of hospitalization of psoriasis patients.
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Affiliation(s)
- Karun M Nair
- Internal Medicine, John H. Stroger, Jr. Hospital of Cook County, Chicago, USA
| | | | - Armaan Guraya
- Medicine, Midwestern University Chicago College of Osteopathic Medicine, Downers Grove, USA
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17
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Chernomordik F, Cercek B, Lio WM, Mihailovic PM, Yano J, Herscovici R, Zhao X, Zhou J, Chyu KY, Shah PK, Dimayuga PC. The Role of T Cells Reactive to the Cathelicidin Antimicrobial Peptide LL-37 in Acute Coronary Syndrome and Plaque Calcification. Front Immunol 2020; 11:575577. [PMID: 33123157 PMCID: PMC7573569 DOI: 10.3389/fimmu.2020.575577] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/23/2020] [Accepted: 09/11/2020] [Indexed: 11/13/2022] Open
Abstract
The human cationic anti-microbial peptide LL-37 is a T cell self-antigen in patients with psoriasis, who have increased risk of cardiovascular events. However, the role of LL-37 as a T cell self-antigen in the context of atherosclerosis remains unclear. The objective of this study was to test for the presence of T cells reactive to LL-37 in patients with acute coronary syndrome (ACS). Furthermore, the role of T cells reactive to LL-37 in atherosclerosis was assessed using apoE-/- mice immunized with the LL-37 mouse ortholog, mCRAMP. Peripheral blood mononuclear cells (PBMCs) from patients with ACS were stimulated with LL-37. PBMCs from stable coronary artery disease (CAD) patients or self-reported subjects served as controls. T cell memory responses were analyzed with flow cytometry. Stimulation of PBMCs with LL-37 reduced CD8+ effector T cell responses in controls and patients with stable CAD but not in ACS and was associated with reduced programmed cell death protein 1 (PDCD1) mRNA expression. For the mouse studies, donor apoE-/- mice were immunized with mCRAMP or adjuvant as controls, then T cells were isolated and adoptively transferred into recipient apoE-/- mice fed a Western diet. Recipient mice were euthanized after 5 weeks. Whole aortas and hearts were collected for analysis of atherosclerotic plaques. Spleens were collected for flow cytometric and mRNA expression analysis. Adoptive transfer experiments in apoE-/- mice showed a 28% reduction in aortic plaque area in mCRAMP T cell recipient mice (P < 0.05). Fifty six percent of adjuvant T cell recipient mice showed calcification in atherosclerotic plaques, compared to none in the mCRAMP T cell recipient mice (Fisher's exact test P = 0.003). Recipients of T cells from mice immunized with mCRAMP had increased IL-10 and IFN-γ expression in CD8+ T cells compared to controls. In conclusion, the persistence of CD8+ effector T cell response in PBMCs from patients with ACS stimulated with LL-37 suggests that LL-37-reactive T cells may be involved in the acute event. Furthermore, studies in apoE-/- mice suggest that T cells reactive to mCRAMP are functionally active in atherosclerosis and may be involved in modulating plaque calcification.
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Affiliation(s)
- Fernando Chernomordik
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Bojan Cercek
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Wai Man Lio
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Peter M Mihailovic
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Juliana Yano
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Romana Herscovici
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Xiaoning Zhao
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Jianchang Zhou
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Kuang-Yuh Chyu
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Prediman K Shah
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Paul C Dimayuga
- Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States
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18
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Abstract
Psoriasis is caused by a complex interplay among the immune system, genetic background, autoantigens, and environmental factors. Recent studies have demonstrated that patients with psoriasis have a significantly higher serum homocysteine (Hcy) level and a higher prevalence of hyperhomocysteinaemia (HHcy). Insufficiency of folic acid and vitamin B12 can be a cause of HHcy in psoriasis. Hcy may promote the immuno-inflammatory process in the pathogenesis of psoriasis by activating Th1 and Th17 cells and neutrophils, while suppressing regulatory T cells. Moreover, Hcy can drive the immuno-inflammatory process by enhancing the production of the pro-inflammatory cytokines in related to psoriasis. Hcy can induce nuclear factor kappa B activation, which is critical in the immunopathogenesis of psoriasis. There may be a link between the oxidative stress state in psoriasis and the effect of HHcy. Hydrogen sulfide (H2S) may play a protective role in the pathogenesis of psoriasis and the deficiency of H2S in psoriasis may be caused by HHcy. As the role of Hcy in the pathogenesis of psoriasis is most likely established, Hcy can be a potential therapeutic target for the treatment of psoriasis. Systemic folinate calcium, a folic acid derivative, and topical vitamin B12 have found to be effective in treating psoriasis.
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19
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Kapniari E, Papadimitriou P, Dalamaga M, Makavos G, Piaserico S, Egeberg A, Ikonomidis I, Papadavid E. Investigating the Link between Psoriasis and Cardiovascular Disease: Current Evidence, Therapeutic Implications and Perspectives. Curr Vasc Pharmacol 2020; 18:592-609. [DOI: 10.2174/1570161118666200523154318] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/25/2020] [Revised: 04/24/2020] [Accepted: 04/27/2020] [Indexed: 02/07/2023]
Abstract
Psoriasis; a chronic inflammatory disease is characterized by symmetric hyperkeratotic
plaques affecting any part of the body. Psoriasis is nowadays considered as a systemic inflammation
linked with several comorbidities as metabolic syndrome, depression, anxiety and increased prevalence
of cardiovascular (CV) disease. The hypothesis that psoriasis is an independent CV risk factor leading to
atherosclerosis via inflammation is now widely accepted. Deciphering the underlying mechanisms interconnecting
psoriasis and CV disease may have significant implications in treatment decisions. Accumulating
evidence suggests that systematic therapies and recently introduced biologic agents, that control
psoriasis by suppressing the chronic and systemic inflammation, may alter the progression of CV disease.
We herein attempt a review of current evidence analysing the relationship between psoriasis and
CV comorbidities, comment on the mechanisms underlying this association and investigate the consequences
for the management of psoriasis.
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Affiliation(s)
- Eirini Kapniari
- 2nd Department of Dermatology and Venereology, National and Kapodistrian University of Athens Medical School, Attikon Hospital, Athens, Greece
| | | | - Marianna Dalamaga
- Department of Biological Chemistry, Medical School, National & Kapodistrian University of Athens, Athens, Greece
| | - George Makavos
- 2nd Department of Cardiology, National and Kapodistrian University of Athens Medical School, Attikon Hospital, Athens, Greece
| | | | - Alexander Egeberg
- Departments of Dermatology and Allergy, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
| | - Ignatios Ikonomidis
- 2nd Department of Cardiology, National and Kapodistrian University of Athens Medical School, Attikon Hospital, Athens, Greece
| | - Evangelia Papadavid
- 2nd Department of Dermatology and Venereology, National and Kapodistrian University of Athens Medical School, Attikon Hospital, Athens, Greece
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20
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Cardiovascular risk in patients with plaque psoriasis and psoriatic arthritis without a clinically overt cardiovascular disease: the role of endothelial progenitor cells. Postepy Dermatol Alergol 2020; 37:299-305. [PMID: 32774211 PMCID: PMC7394160 DOI: 10.5114/ada.2020.96085] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2018] [Accepted: 02/20/2019] [Indexed: 11/26/2022] Open
Abstract
Psoriasis is an autoimmune, chronic disease determined by environmental and genetic factors. The occurrence of psoriasis is accompanied by metabolic diseases, cardiovascular diseases (CVD) and depression, disturbances on interpersonal interactions and a tendency towards social isolation. Regardless of the form of psoriasis and the severity of the disease, early arterial lesions are recorded in arterial vessels of patients. Nevertheless, the chance of CVD is higher in the population of patients with severe psoriasis than in patients with mild to moderate psoriasis. The correlation between the presence of atherosclerotic plaque and psoriatic plaque is partially explained by: (1) a similar inflammatory pathway – via the T helper cells, (2) impaired angiogenesis, and (3) endothelial dysfunction. In the considered tests, the diagnostic tools used showed a reduced level of endothelial progenitor cells in the circulation of patients with psoriasis. Endogenous angiopoietin stimulation in patients with psoriasis leads to deterioration of endothelial regeneration, atherosclerosis which secondarily contributes to the progression of heart failure. Clinical and experimental data confirm the potential of immunomodulatory methods to combat both autoimmune and cardiovascular diseases through the use of immunosuppressive drugs. Full understanding of the way in which CVD develops in patients with autoimmune diseases would enable the implementation of targeted cell therapy allowing the quality and life expectancy of patients to be improved. Modern cellular diagnostic tools allow the use of highly specific biomarkers, which in the near future will enable a reduction in morbidity and mortality due to CVD.
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21
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Abstract
Psoriasis is a systemic inflammatory disorder that involves complex pathogenic interactions between the innate and adaptive immune systems. Individuals with psoriasis have an increased risk of developing other chronic health diseases such cardiovascular disorders. The high incidence of cardiovascular events in the population with psoriasis could be explained by several mechanisms. The high prevalence of traditional cardiovascular risk factors and metabolic abnormalities contributes to the high cardiovascular burden in patients with psoriasis. Likewise, the presence of systemic inflammation in combination with metabolic abnormalities may act in a synergistic manner to increase cardiovascular risk in these patients. This review focused on epidemiologic and clinical evidence linking psoriasis to cardiovascular risk factors and cardiovascular disease. We described the possible pathophysiological mechanisms that justify this association and analyzed the best way to stratify the cardiovascular risk in patients with psoriasis. We also described the usefulness of the therapies frequently used in cardiovascular prevention and analyzed the impact of the specific psoriasis medication on cardiovascular risk factors or major atherosclerotic events. Knowledge of the application of different cardiovascular prevention strategies could mean an advantage in performing the difficult task of estimating cardiovascular risk and treating cardiovascular risk factors in this particular group of patients.
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Affiliation(s)
- Walter Masson
- Hospital Italiano de Buenos Aires, Perón 4190, C1199ABB, Buenos Aires, Argentina.
- Council of Epidemiology and Cardiovascular Prevention, Argentine Society of Cardiology, Azcuénaga 980, C1115AAD, Buenos Aires, Argentina.
| | - Martín Lobo
- Council of Epidemiology and Cardiovascular Prevention, Argentine Society of Cardiology, Azcuénaga 980, C1115AAD, Buenos Aires, Argentina
| | - Graciela Molinero
- Council of Epidemiology and Cardiovascular Prevention, Argentine Society of Cardiology, Azcuénaga 980, C1115AAD, Buenos Aires, Argentina
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22
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Duman H, Dilek N, Demirelli S, Inci S, Duman H, Çetin M, Durakoğlugil ME. The relationship between total atrial conduction time and left atrial global strain in patients with psoriasis vulgaris. Arch Med Sci 2019; 15:865-871. [PMID: 31360181 PMCID: PMC6657257 DOI: 10.5114/aoms.2019.82678] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/27/2016] [Accepted: 03/30/2017] [Indexed: 11/18/2022] Open
Abstract
INTRODUCTION Psoriasis vulgaris is a chronic, multisystem disease that results in the development of atrial fibrillation (AF) over time. In this study, our goal was to assess predictors of AF in patients with psoriasis, including total atrial conduction time (TACT) and left atrial global longitudinal strain (LAGLS). MATERIAL AND METHODS A total of 80 individuals, including 40 psoriasis patients and 40 healthy controls, were enrolled in the study. A physical examination was performed, biochemical parameters were studied, and Holter electrocardiography was carried out. Conventional echocardiography, atrial tissue Doppler, and speckle tracking echocardiography were recorded. RESULTS No significant difference was observed between psoriasis patients and healthy controls with regard to age, and the average duration of psoriasis was 5.7 years. High-sensitivity C reactive protein levels were higher in the patient group compared to the control group (respectively, group 1: 1 ±0.8; group 2: 0.6 ±0.3, p < 0.05). Atrial arrhythmia was not detected in the Holter ECG monitoring. A significant moderate negative correlation between TACT and LAGLS (r = -0.57, p < 0.05) was observed, and there was a significant moderate positive correlation between the duration of disease and TACT (r = 0.52, p < 0.05). CONCLUSIONS In the current study, we determined that LAGLS decreased, TACT was prolonged, and P-wave dispersion increased in patients with psoriasis. The current results may improve predictions of AF risk in psoriasis patients in clinical practice.
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Affiliation(s)
- Hakan Duman
- Department of Cardiology, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Nursel Dilek
- Department of Dermatology, Rize University Medical Faculty, Rize, Turkey
| | - Selami Demirelli
- Department of Cardiology, Erzurum Education and Research Hospital, Erzurum, Turkey
| | - Sinan Inci
- Department of Cardiology, Aksaray State Hospital, Aksaray, Turkey
| | - Handan Duman
- Department of Family Medicine, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Mustafa Çetin
- Department of Cardiology, Recep Tayyip Erdoğan University, Rize, Turkey
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23
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Duman H, Dilek N, Değirmenci H, Duman H, Tüfekçi D, Uslu A, Şatiroğlu Ö, Çiçek Y. Decreased left atrial strain parameters are associated with prolonged total atrial conduction time in lichen planus. Interv Med Appl Sci 2019; 10:150-156. [PMID: 30713754 PMCID: PMC6343578 DOI: 10.1556/1646.10.2018.11] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022] Open
Abstract
Background Lichen planus (LP) carries the increased risk of cardiovascular events as it is a chronic inflammatory disease. This study aimed at determining the relationship between total atrial conduction time (TACT), P-wave dispersion, and the left atrium (LA) global strain in the patients with LP. Methods Forty people as a control group and 40 patients with LP were included in this study. Patient assessed global longitudinal LA strain by two-dimensional speckle-tracking strain echocardiography. Results The global peak systolic LA myocardium strain during the left ventricular systole (LAGLSRs) and the global peak negative LA myocardial strain rate during the early ventricular diastole (LAGLSRe) values were significantly lower in the patients with LP in proportion to the control group according to the strain measurements (1.7 ± 0.07 vs. 1.9 ± 0.1%, p = 0.001; 1.23 ± 0.04 vs. 1.2 ± 0.08 s−1, p = 0.001), respectively. TACT value was found to be significantly longer (102.6 ± 6.3 ms) in the patients with LP than the control group (96.3 ± 5.3 ms, p = 0.001), considering the terms of the artial conduction features. Conclusion This study demonstrated that the subclinical cardiac involvement in LP can determine the prolonged TACT and the impaired left atrial myocardial deformation values.
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Affiliation(s)
- Hakan Duman
- Faculty of Medicine, Department of Cardiology, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Nursel Dilek
- Faculty of Medicine, Department of Dermatology, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Hüsnü Değirmenci
- Faculty of Medicine, Department of Cardiology, Erzincan University, Erzincan, Turkey
| | - Handan Duman
- Family Care Center Rize, Ministry of Health, Rize, Turkey
| | - Damla Tüfekçi
- Faculty of Medicine, Department of Internal Medicine, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Abdulkadir Uslu
- Cardiology Clinic, Kartal Kosuyolu Training and Research Hospital, Istanbul, Turkey
| | - Ömer Şatiroğlu
- Faculty of Medicine, Department of Cardiology, Recep Tayyip Erdoğan University, Rize, Turkey
| | - Yüksel Çiçek
- Faculty of Medicine, Department of Cardiology, Recep Tayyip Erdoğan University, Rize, Turkey
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24
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Asha K, Singal A, Sharma SB, Arora VK, Aggarwal A. Dyslipidaemia & oxidative stress in patients of psoriasis: Emerging cardiovascular risk factors. Indian J Med Res 2018; 146:708-713. [PMID: 29664028 PMCID: PMC5926341 DOI: 10.4103/ijmr.ijmr_717_16] [Citation(s) in RCA: 25] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Background & objectives: Psoriasis is a recurrent hyper-proliferative skin disease which is often associated with free radical generation, abnormal lipid metabolism and increased inflammatory secretion that induce cardiovascular risk in these patients. The present study was intended to evaluate serum lipids, lipoprotein and oxidants-antioxidants status and to establish their relationship with atherogenic risk markers [oxidized low-density lipoprotein (oxLDL) and high-sensitivity C-reactive protein (hsCRP)] in patients with psoriasis. Methods: The study was conducted on 150 psoriasis patients and 150 age- and sex-matched healthy controls. Overnight fasting blood samples were obtained for lipids, lipoproteins, lipid oxidation and peroxidation products [oxLDL, malondialdehyde (MDA)], antioxidant enzymes [reduced glutathione (GSH) and total antioxidant status] levels and hsCRP estimations. Results: The mean levels of atherogenic lipids [total cholesterol (P<0.001), triacylglycerol (P<0.01)], lipid peroxidation products (P<0.001) and oxLDL and hsCRP (P<0.001) levels in patients with psoriasis were found to be significantly higher than those of healthy controls. On the other hand, ferric-reducing ability of plasma (FRAP, P<0.001) and antioxidant enzyme activities (reduced GSH, P<0.01) were significantly lower when compared to healthy controls. The plasma oxLDL was positively correlated to LDL cholesterol (P<0.001) and MDA (P<0.001) and negatively associated with antioxidant status in these patients. Serum MDA, FRAP and oxLDL were correlated with risk of atherosclerosis in the patients with psoriasis; however, no significant association was found between reduced GSH and hsCRP. Interpretation & conclusions: The study results suggest that LDL oxidation and reactive oxygen species in addition to inflammatory markers may play a pivotal role in inducing atherosclerosis in patients of psoriasis.
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Affiliation(s)
- Kumari Asha
- Department of Biochemistry, University College of Medical Sciences (University of Delhi), Delhi, India
| | - Archana Singal
- Department of Dermatology, University College of Medical Sciences (University of Delhi), Delhi, India
| | - Suman Bala Sharma
- Department of Biochemistry, University College of Medical Sciences (University of Delhi), Delhi, India
| | - Vinod Kumar Arora
- Department of Pathology, University College of Medical Sciences (University of Delhi), Delhi, India
| | - Amitesh Aggarwal
- Department of Medicine, University College of Medical Sciences (University of Delhi), Delhi, India
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Caiazzo G, Fabbrocini G, Di Caprio R, Raimondo A, Scala E, Balato N, Balato A. Psoriasis, Cardiovascular Events, and Biologics: Lights and Shadows. Front Immunol 2018; 9:1668. [PMID: 30150978 PMCID: PMC6099159 DOI: 10.3389/fimmu.2018.01668] [Citation(s) in RCA: 79] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/28/2018] [Accepted: 07/04/2018] [Indexed: 12/19/2022] Open
Abstract
Nowadays, it is well established a link between psoriasis and cardiovascular (CV) diseases. A series of different overlapping mechanisms including inflammation, homeostasis dysregulation, and genetic susceptibility are thought to underlie this association. Advances in understanding the molecular patterns involved in the complex scenario of psoriasis have highlighted a tight correlation with atherosclerosis. Indeed, common profiles are shared in term of inflammatory cytokines and cell types. In the last decade, the management of psoriasis patients has been revolutionized with the introduction of biological therapies, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-12/23, and IL-17 inhibitors. In clinical setting, the effectiveness of these therapies as well as the incidence of CV events is related to the type of biologics. In particular, anti-TNF-α agents seem to reduce these events in psoriasis patients whereas anti-IL-12/23 agents related CV events reduction still remain to clarify. It has to be taken into account that IL-12/23 inhibitors have a shorter post-marketing surveillance period. An even more restricted observational time is available for anti-IL-17 agents. IL-17 is associated with psoriasis, vascular disease, and inflammation. However, IL-17 role in atherosclerosis is still debated, exerting both pro-atherogenic and anti-atherogenic effects depending on the specific context. In this review, we will discuss the differences between the onset of CV events in psoriasis patients, referred to specific biological therapy and the underlying immunological mechanism. Given the development of new therapeutic strategies, the investigation of these inhibitors impact on heart failure outcome is extremely important.
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Affiliation(s)
- Giuseppina Caiazzo
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Gabriella Fabbrocini
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Roberta Di Caprio
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Annunziata Raimondo
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Emanuele Scala
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Nicola Balato
- Department of Clinical Medicine and Surgery, University of Naples Federico II, Napoli, Italy
| | - Anna Balato
- Department of Advanced Biomedical Sciences, University of Naples Federico II, Napoli, Italy
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Tissue hemostasis is shifted toward thrombogenesis in the psoriatic plaques. Pathol Res Pract 2017; 213:1125-1129. [PMID: 28756988 DOI: 10.1016/j.prp.2017.07.011] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/08/2017] [Revised: 06/10/2017] [Accepted: 07/12/2017] [Indexed: 01/16/2023]
Abstract
BACKGROUND Psoriasis is a common autoimmune disease of unknown etiology. Recently, much attention has been paid to evidence that a local hypercoagulable state is an important contributing factor to the development of inflammatory skin diseases. Thus, the aim of this study was to characterize the local hemostasis in the affected skin of patients with psoriasis. METHODS Skin biopsies of psoriatic plaques were obtained from 73 consecutive patients (48M, 25F, average age 45 years) with at least a one year history of the disease. The studied patients had not received any specific systemic treatment for at least 4 weeks before the biopsy was done. As a control, normal skin biopsies were obtained from 16 healthy subjects. For immunohistological study, the En-Vision method (DAKO EnVision Kit ®/Alkaline Phosphatase detection system), and monoclonal antibodies anti-tissue factor (TF), anti-thrombomodulin (TM) and anti-von Willebrand Factor (vWF) were used. All these molecules were assessed semi-quantitatively in the frozen sections. RESULTS Clinically, the Body Surface Area index ranged between 1-90% and the Psoriasis Area Severity Index score ranged from 1.6 to 47. Immunohistochemistry revealed redistribution of TF antigens from the upper to lower layers of the epidermis as compared to the control. It was collaborated with the number of TF-positive cells in the psoriatic skin sections (78.3%) as compared with the healthy subjects (34.4%; P<0.001). In addition, TF was uniformly and moderately expressed on capillary endothelial cells of the plaque sections in 43 out of 73 patients (58.9%). As far as the thrombomodulin is concerned, TM was clearly down-regulated and localized mainly in the upper layers of the psoriatic epidermis. It was collaborated with the number of TM positive cells in the psoriatic skin sections (38.9%) as compared with the healthy subjects (66.7%; P<0.001). All capillary vessels found in the biopsy sections were positive for TM and vWF staining, with similar expression (≥2+) in both groups. In the current study, no relationship was found between the TF, TM and vWF expression and the PASI and BAS (NS). CONCLUSIONS A local procoagulable state found in psoriatic plaques suggests a significant role of local tissue hemostasis in pathogenesis of the disease. These findings indicate another potential target for a therapeutic approach in patients with psoriasis, although further research would help elucidate the exact mechanisms.
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Sundarrajan S, Arumugam M. A systems pharmacology perspective to decipher the mechanism of action of Parangichakkai chooranam , a Siddha formulation for the treatment of psoriasis. Biomed Pharmacother 2017; 88:74-86. [DOI: 10.1016/j.biopha.2016.12.135] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/27/2016] [Revised: 12/29/2016] [Accepted: 12/29/2016] [Indexed: 10/20/2022] Open
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Kim HJ, Bae IH, Son ED, Park J, Cha N, Na HW, Jung C, Go YS, Kim DY, Lee TR, Shin DW. Transcriptome analysis of airborne PM 2.5-induced detrimental effects on human keratinocytes. Toxicol Lett 2017; 273:26-35. [PMID: 28341207 DOI: 10.1016/j.toxlet.2017.03.010] [Citation(s) in RCA: 42] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/20/2016] [Revised: 03/09/2017] [Accepted: 03/10/2017] [Indexed: 11/24/2022]
Abstract
Ambient air pollution is becoming more severe worldwide, posing a serious threat to human health. Fine airborne particles of particulate matter (PM2.5) show higher cytotoxicity than other coarse fractions. Indeed, PM2.5 induces cardiovascular or respiratory damage; however, few studies have evaluated the detrimental effect of PM2.5 to normal human skin. We used a next-generation sequencing-based (RNA-Seq) method with transcriptome and Gene Ontology (GO) enrichment analysis to determine the harmful influences of PM2.5 on human normal epidermal keratinocytes. DAVID analysis showed that the most significantly enriched GO terms were associated with epidermis-related biological processes such as "epidermis development (GO: 0008544)" and "keratinocyte differentiation (GO: 0030216)", suggesting that PM2.5 has some deleterious effects to the human epidermis. In addition, Ingenuity Pathway Analysis predicted inflammation-related signaling as one of the major PM2.5-induced signaling pathways, and pro-inflammatory cytokines as upstream regulators with symptoms similar to psoriasis as downstream effects. PM2.5 caused considerable changes in the expression of pro-inflammatory cytokines and psoriatic skin disease-related genes, might lead to epidermal dysfunctions. Our results might help to understand the mechanism of air pollution-induced skin barrier perturbation and contribute to the development of a new strategy for the prevention or recovery of the consequent damage.
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Affiliation(s)
- Hyoung-June Kim
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - Il-Hong Bae
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea; College of Veterinary Medicine, Seoul National University, Seoul, 151-742 Republic of Korea
| | - Eui Dong Son
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - Juyearl Park
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - Nari Cha
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - Hye-Won Na
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - Changjo Jung
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea
| | - You-Seak Go
- Macrogen Inc., Seoul, 08511, Republic of Korea
| | - Dae-Yong Kim
- College of Veterinary Medicine, Seoul National University, Seoul, 151-742 Republic of Korea
| | - Tae Ryong Lee
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea.
| | - Dong Wook Shin
- Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea.
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Ertem AG, Erdogan M, Koseoglu C, Akoglu G, Ozdemir E, Koseoglu G, Sivri S, Keles T, Durmaz T, Aktas A, Bozkurt E. Epicardial fat tissue thickness is increased in patients with lichen planus and is linked to inflammation and dyslipidemia. Rev Port Cardiol 2016; 35:525-30. [DOI: 10.1016/j.repc.2016.04.010] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2016] [Revised: 03/24/2016] [Accepted: 04/05/2016] [Indexed: 12/12/2022] Open
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30
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Epicardial fat tissue thickness is increased in patients with lichen planus and is linked to inflammation and dyslipidemia. REVISTA PORTUGUESA DE CARDIOLOGIA (ENGLISH EDITION) 2016. [DOI: 10.1016/j.repce.2016.04.007] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
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Ozlu E, Karadag AS, Toprak AE, Uzuncakmak TK, Gerin F, Aksu F, Ozakpınar O, Akdeniz N. Evaluation of Cardiovascular Risk Factors, Haematological and Biochemical Parameters, and Serum Endocan Levels in Patients with Lichen Planus. Dermatology 2016; 232:438-443. [PMID: 27508489 DOI: 10.1159/000447587] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/28/2016] [Accepted: 06/01/2016] [Indexed: 02/05/2023] Open
Abstract
BACKGROUND AND OBJECTIVE The current study aimed to evaluate cardiovascular risk factors, haematological and biochemical parameters, and serum endocan concentrations in lichen planus (LP) patients. METHODS This study was conducted with 86 cases, including 43 LP patients and 43 healthy controls. Cardiovascular risk factors, haematological and biochemical parameters, and endocan levels were evaluated. RESULTS The serum endocan concentrations of LP patients were not significantly different from those of the healthy controls (p > 0.05). There were no significant differences in the serum endocan levels according to classification by cardiovascular risk factors and smoking history (p > 0.05). In the LP group, white blood cell count, platelet distribution width and monocyte count/high-density lipoprotein cholesterol ratios were significantly higher when compared to the healthy controls (p < 0.05). The LP group had a lower mean platelet volume than the healthy controls (p < 0.05). CONCLUSIONS Serum endocan levels did not change significantly in patients with LP, and there were significant differences in haematological and biochemical parameters.
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Affiliation(s)
- Emin Ozlu
- Department of Dermatology, Kayseri Training and Research Hospital, Kayseri, Turkey
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Yaman M, Arslan U, Beton O, Asarcıklı LD, Aksakal A, Dogdu O. Atrial Electromechanical Coupling in Patients with Lichen Planus. Korean Circ J 2016; 46:530-5. [PMID: 27482262 PMCID: PMC4965432 DOI: 10.4070/kcj.2016.46.4.530] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/23/2015] [Revised: 11/15/2015] [Accepted: 12/01/2015] [Indexed: 11/17/2022] Open
Abstract
Background and objectives A chronic inflammatory disease, lichen planus may cause disturbance of atrial electromechanical coupling and increase the risk of atrial fibrillation. The aim of this study was to evaluate atrial electromechanical delay with both electrocardiography (ECG) and echocardiography in patients with lichen planus (LP). Subjects and Methods Seventy-two LP patients (43 males [59.7%], mean age: 44.0±16.7 years) were enrolled in this cross-sectional case-control study. The control group was selected in a 1:1 ratio from 70 patients in an age and sex matched manner. P wave dispersion was measured by ECG to show atrial electromechanical delay. All of the patients underwent transthoracic echocardiography for measuring inter- and intra-atrial electromechanical delays. Results The baseline characteristics of the patients and the control group were similar except for the presence of LP. P-wave dispersion measured by ECG was significantly higher in patients with LP (p<0.001). Patients with LP had significantly prolonged intra- and interatrial electromechanical delays when compared to the control group (p<0.001). In addition, all of these variables were significantly correlated with high sensitive C-reactive protein (hsCRP) levels. Conclusion Atrial electromechanical coupling, which is significantly correlated with increased hsCRP levels, is impaired in patients with LP.
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Affiliation(s)
- Mehmet Yaman
- Department of Cardiology, Samsun Education and Research Hospital, Samsun, Turkey
| | - Uğur Arslan
- Department of Cardiology, Samsun Education and Research Hospital, Samsun, Turkey
| | - Osman Beton
- Department of Cardiology, Diskapi Education and Research Hospital, Ankara, Turkey
| | - Lale Dinç Asarcıklı
- Department of Cardiology, Diskapi Education and Research Hospital, Ankara, Turkey
| | - Aytekin Aksakal
- Department of Cardiology, Samsun Education and Research Hospital, Samsun, Turkey
| | - Orhan Dogdu
- Department of Cardiology, Firat University, Faculty of Medicine, Elazig, Turkey
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Ganzetti G, Campanati A, Molinelli E, Offidani A. Psoriasis, non-alcoholic fatty liver disease, and cardiovascular disease: Three different diseases on a unique background. World J Cardiol 2016; 8:120-131. [PMID: 26981209 PMCID: PMC4766264 DOI: 10.4330/wjc.v8.i2.120] [Citation(s) in RCA: 29] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2015] [Revised: 09/04/2015] [Accepted: 12/18/2015] [Indexed: 02/06/2023] Open
Abstract
Psoriasis is a chronic inflammatory immune-mediated skin disease, frequently associated with systemic comorbidities. According to recent data, patients with psoriasis show a greater prevalence of metabolic syndrome, which confers a higher cardiovascular risk. The link between these pathological conditions appears to be a chronic low-grade inflammatory status. The aim of this review is to focus on the multiple epidemiological and physio-pathogenetic aspects linking non-alcoholic fatty liver disease, psoriasis, and cardiovascular disease.
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Rajappa M, Shanmugam R, Munisamy M, Chandrashekar L, Rajendiran KS, Thappa DM. Effect of antipsoriatic therapy on oxidative stress index and sialic acid levels in patients with psoriasis. Int J Dermatol 2015; 55:e422-30. [PMID: 26711230 DOI: 10.1111/ijd.13196] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/18/2014] [Revised: 07/09/2015] [Accepted: 08/24/2015] [Indexed: 11/28/2022]
Abstract
BACKGROUND AND OBJECTIVES Recent studies have implicated the association between oxidative stress and inflammation in pathogenesis of psoriasis and its associated comorbidities. Hence, we undertook to study inflammatory markers such as sialic acids and the oxidative stress index (OSI) in patients with psoriasis vulgaris. METHODS Sixty cases and 60 healthy controls were included in this cohort study. Disease severity was assessed by psoriasis area severity index scoring. Serum levels of oxidative stress (total oxidant status, total antioxidant status) and inflammation (highly sensitive C-reactive protein [hs-CRP], total sialic acid, protein bound sialic acid) markers were estimated in controls and cases at baseline and on follow-up. OSI was calculated as the ratio of total oxidant status to total antioxidant status. RESULTS Baseline serum levels of OSI, hs-CRP, and sialic acids were significantly higher in cases compared to controls. Baseline OSI and sialic acids demonstrated a significant correlation with disease severity. After 12 weeks of therapy, there was a significant decline in OSI and serum levels of hs-CRP and sialic acids. CONCLUSIONS Our results demonstrate that oxidative stress and inflammation are significantly associated with psoriasis, and treatment with methotrexate results in a significant decline of both the inflammatory and oxidative stress parameters.
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Affiliation(s)
- Medha Rajappa
- Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
| | - Rathika Shanmugam
- Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
| | - Malathi Munisamy
- Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
| | - Laxmisha Chandrashekar
- Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
| | - Kalai Selvi Rajendiran
- Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
| | - Devinder Mohan Thappa
- Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
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Abstract
Psoriasis is a systemic inflammatory disease that confers significant risk of metabolic derangements and adverse cardiovascular outcomes. Early detection and treatment of modifiable risk factors and modulation of the systemic inflammatory response are important treatment goals. Studies have shown that there is a significant lack of awareness of the relationship between psoriasis and cardiovascular disease, so future considerations should focus on education of and collaboration with health care providers, especially those in primary care, and development of updated, rigorous screening guidelines. In addition, targeted biologic therapies such as TNF-a inhibitors have shown immense promise in targeting the systemic inflammation associated with psoriatic disease, but whether they will impact long-term cardiovascular outcomes remains to be seen.
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Affiliation(s)
- Kathryn T Shahwan
- Clinical Unit for Research Trials and Outcomes in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, 50 Staniford Street, Suite 240, Boston, MA 02114, USA
| | - Alexa B Kimball
- Clinical Unit for Research Trials and Outcomes in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, 50 Staniford Street, Suite 240, Boston, MA 02114, USA.
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36
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Lüscher TF. Neglected cardiovascular risk factors. Eur Heart J 2015; 36:2621-3. [PMID: 26468255 DOI: 10.1093/eurheartj/ehv540] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/12/2022] Open
Affiliation(s)
- Thomas F Lüscher
- Editor-in-Chief, Zurich Heart House, Careum Campus, Moussonstrasse 4, 8091 Zurich, Switzerland
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37
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Affiliation(s)
- Thomas F Lüscher
- Editor-in-Chief, Zurich Heart House, Careum Campus, Moussonstrasse 4, 8091 Zurich, Switzerland
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Karbach S, Croxford AL, Oelze M, Schüler R, Minwegen D, Wegner J, Koukes L, Yogev N, Nikolaev A, Reißig S, Ullmann A, Knorr M, Waldner M, Neurath MF, Li H, Wu Z, Brochhausen C, Scheller J, Rose-John S, Piotrowski C, Bechmann I, Radsak M, Wild P, Daiber A, von Stebut E, Wenzel P, Waisman A, Münzel T. Interleukin 17 drives vascular inflammation, endothelial dysfunction, and arterial hypertension in psoriasis-like skin disease. Arterioscler Thromb Vasc Biol 2014; 34:2658-68. [PMID: 25341795 DOI: 10.1161/atvbaha.114.304108] [Citation(s) in RCA: 195] [Impact Index Per Article: 17.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
OBJECTIVE Interleukin (IL)-17A is regarded as an important cytokine to drive psoriasis, an inflammatory skin disease marked by increased cardiovascular mortality. We aimed to test the hypothesis that overproduction of IL-17A in the skin leading to dermal inflammation may systemically cause vascular dysfunction in psoriasis-like skin disease. APPROACH AND RESULTS Conditional overexpression of IL-17A in keratinocytes caused severe psoriasis-like skin inflammation in mice (K14-IL-17A(ind/+) mice), associated with increased reactive oxygen species formation and circulating CD11b(+) inflammatory leukocytes in blood, with endothelial dysfunction, increased systolic blood pressure, left ventricular hypertrophy, and reduced survival compared with controls. In K14-IL-17A(ind/+) mice, immunohistochemistry and flow cytometry revealed increased vascular production of the nitric oxide/superoxide reaction product peroxynitrite and infiltration of the vasculature with myeloperoxidase(+)CD11b(+)GR1(+)F4/80(-) cells accompanied by increased expression of the inducible nitric oxide synthase and the nicotinamide dinucleotide phosphate (NADPH) oxidase, nox2. Neutrophil depletion by anti-GR-1 antibody injections reduced oxidative stress in blood and vessels. Neutralization of tumor necrosis factor-α and IL-6 (both downstream of IL-17A) reduced skin lesions, attenuated oxidative stress in heart and blood, and partially improved endothelial dysfunction in K14-IL-17A(ind/+) mice. CONCLUSIONS Dermal overexpression of IL-17A induces systemic endothelial dysfunction, vascular oxidative stress, arterial hypertension, and increases mortality mainly driven by myeloperoxidase(+)CD11b(+)GR1(+)F4/80(-) inflammatory cells. Depletion of the GR-1(+) immune cells or neutralization of IL-17A downstream cytokines by biologicals attenuates the vascular phenotype in K14-IL-17A(ind/+) mice.
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Affiliation(s)
- Susanne Karbach
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.).
| | - Andrew L Croxford
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Matthias Oelze
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Rebecca Schüler
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Daniel Minwegen
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Joanna Wegner
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Lija Koukes
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Nir Yogev
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Alexei Nikolaev
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Sonja Reißig
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Alexander Ullmann
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Maike Knorr
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Maximilian Waldner
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Markus F Neurath
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Huige Li
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Zhixiong Wu
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Christoph Brochhausen
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Jürgen Scheller
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Stefan Rose-John
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Carolin Piotrowski
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Ingo Bechmann
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Markus Radsak
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Philipp Wild
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Andreas Daiber
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Esther von Stebut
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Philip Wenzel
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
| | - Ari Waisman
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.).
| | - Thomas Münzel
- From the Institute for Molecular Medicine (S.K., A.L.C., R.S., N.Y., A.N., S.R., A.W.), Department of Medicine 2 (S.K., M.O., D.M., M.K., P. Wild, A.D., P. Wenzel, T.M.), Department of Dermatology (J.W., L.K., E.v.S.), Department of Pharmacology (H.L., Z.W.), Institute for Pathology (C.B.), Center for Thrombosis and Hemostasis (P. Wild, P. Wenzel, T.M.), German Center for Cardiovascular Research (DZHK), partner site RhineMain (A.U., P.W.), and Department of Medicine 3 (M.R.), University Medical Center of the Johannes-Gutenberg University of Mainz, Germany; Department of Internal Medicine I, University Hospital Erlangen, Germany (M.W., M.F.N.); Institute of Anatomy, University of Leipzig, Germany (C.P., I.B.); Institute for Biochemistry, Christian-Albrechts-University of Kiel, Germany (S.R.-J.); Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany (J.S.)
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Balci A, Celik M, Balci DD, Karazincir S, Yonden Z, Korkmaz I, Celik E, Egilmez E. Patients with psoriasis have an increased amount of epicardial fat tissue. Clin Exp Dermatol 2013; 39:123-8. [PMID: 24164295 DOI: 10.1111/ced.12216] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/27/2013] [Indexed: 01/06/2023]
Abstract
BACKGROUND Psoriasis is associated with coronary artery disease, and ischemic heart disease is associated with increased amounts of epicardial fat tissue (EFT). There has as yet been no study published on the accumulation of EFT in patients with psoriasis. AIM To compare epicardial fat accumulation and coronary artery calcium score (CACS) in patients with psoriasis and controls. METHODS We enrolled 38 patients with psoriasis and 38 controls matched for age and gender. Epicardial fat area (EFA) and CACS were evaluated by multidetector computed tomography. RESULTS Mean EFA in patients with psoriasis was significantly higher than in controls (13.8 ± 8.4 vs. 9.7 ± 6.4 cm(2) , respectively, P = 0.02), but mean CACS did not differ significantly between the two groups (55.2 ± 65.4 vs. 27.8 ± 29.3; P > 0.05). Multiple linear regression analyses indicated that EFA was significantly associated with waist circumference and presence of coronary artery calcification in both patients and controls, whereas EFA was significantly associated waist circumference and age in patients only (P < 0.05). CONCLUSIONS Patients with psoriasis had a higher level of EFA compared with controls, and EFA was independently associated with the presence of CAC in all study subjects.
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Affiliation(s)
- A Balci
- Department of Radiology, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey
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Bacaksiz A, Erdogan E, Sonmez O, Sevgili E, Tasal A, Onsun N, Topukcu B, Kulaç B, Uysal O, Goktekin O. Ambulatory blood pressure monitoring can unmask hypertension in patients with psoriasis vulgaris. Med Sci Monit 2013; 19:501-9. [PMID: 23800996 PMCID: PMC3699538 DOI: 10.12659/msm.889197] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Psoriasis vulgaris is one of the most prevalent chronic, inflammatory skin disorders. Patients with psoriasis have excess risk of essential hypertension. Masked hypertension (MH), defined as normal office blood pressure (BP) with elevated ambulatory BP (ABPM), has been drawing attention recently due to its association with increased risk of developing sustained hypertension, cardiovascular morbidity, and mortality. The aim of this study was to investigate the prevalence of MH in psoriatic patients. MATERIAL AND METHODS On hundred and ten middle-aged, normotensive, non-obese patients with psoriasis vulgaris and 110 age- and sex-matched normotensive controls were included in the study. ABPM was performed in all participants over a 24-h period. The clinical severity of the disease was determined according to current indexes. RESULTS The prevalence of MH among subjects with psoriasis vulgaris was 31.8% and increased compared to control subjects (p<0.01). Predictors of MH in patients with psoriasis vulgaris were detected as male sex, smoking, obesity-related anthropometric measures, and disease activity. Male sex, waist circumference, and diffuse psoriatic involvement were detected as independent predictors of MH. CONCLUSIONS MH is prevalent in patients with psoriasis vulgaris. Assessment with ABPM and close follow-up for development of hypertension is reasonable.
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Affiliation(s)
- Ahmet Bacaksiz
- Department of Cardiology, Bezmiâlem Foundation University, Istanbul, Turkey.
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Flammer J, Konieczka K, Flammer AJ. The primary vascular dysregulation syndrome: implications for eye diseases. EPMA J 2013; 4:14. [PMID: 23742177 PMCID: PMC3693953 DOI: 10.1186/1878-5085-4-14] [Citation(s) in RCA: 210] [Impact Index Per Article: 17.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/23/2013] [Accepted: 04/26/2013] [Indexed: 01/08/2023]
Abstract
Vascular dysregulation refers to the regulation of blood flow that is not adapted to the needs of the respective tissue. We distinguish primary vascular dysregulation (PVD, formerly called vasospastic syndrome) and secondary vascular dysregulation (SVD). Subjects with PVD tend to have cold extremities, low blood pressure, reduced feeling of thirst, altered drug sensitivity, increased pain sensitivity, prolonged sleep onset time, altered gene expression in the lymphocytes, signs of oxidative stress, slightly increased endothelin-1 plasma level, low body mass index and often diffuse and fluctuating visual field defects. Coldness, emotional or mechanical stress and starving can provoke symptoms. Virtually all organs, particularly the eye, can be involved. In subjects with PVD, retinal vessels are stiffer and more irregular, and both neurovascular coupling and autoregulation capacity are reduced while retinal venous pressure is often increased. Subjects with PVD have increased risk for normal-tension glaucoma, optic nerve compartment syndrome, central serous choroidopathy, Susac syndrome, retinal artery and vein occlusions and anterior ischaemic neuropathy without atherosclerosis. Further characteristics are their weaker blood–brain and blood-retinal barriers and the higher prevalence of optic disc haemorrhages and activated astrocytes. Subjects with PVD tend to suffer more often from tinnitus, muscle cramps, migraine with aura and silent myocardial ischaemic and are at greater risk for altitude sickness. While the main cause of vascular dysregulation is vascular endotheliopathy, dysfunction of the autonomic nervous system is also involved. In contrast, SVD occurs in the context of other diseases such as multiple sclerosis, retrobulbar neuritis, rheumatoid arthritis, fibromyalgia and giant cell arteritis. Taking into consideration the high prevalence of PVD in the population and potentially linked pathologies, in the current article, the authors provide recommendations on how to effectively promote the field in order to create innovative diagnostic tools to predict the pathology and develop more efficient treatment approaches tailored to the person.
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Affiliation(s)
- Josef Flammer
- Department of Ophthalmology, University of Basel, Mittlere Strasse 91, Basel CH-4031, Switzerland.
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Sahin M, Bilgili SG, Simsek H, Akdag S, Akyol A, Gumrukcuoglu HA, Yaman M, Bayram Y, Karadag AS. Increased P-wave dispersion in patients with newly diagnosed lichen planus. Clinics (Sao Paulo) 2013; 68:846-50. [PMID: 23778479 PMCID: PMC3674259 DOI: 10.6061/clinics/2013(06)20] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/04/2013] [Accepted: 03/27/2013] [Indexed: 02/04/2023] Open
Abstract
OBJECTIVE Lichen planus is a chronic inflammatory autoimmune mucocutaneous disease. Recent research has emphasized the strong association between inflammation and both P-wave dispersion and dyslipidemia. The difference between the maximum and minimum P-wave durations on an electrocardiogram is defined as P-wave dispersion. The prolongation of P-wave dispersion has been demonstrated to be an independent risk factor for developing atrial fibrillation. The aim of this study was to investigate P-wave dispersion in patients with lichen planus. METHODS Fifty-eight patients with lichen planus and 37 age- and gender-matched healthy controls were included in this study. We obtained electrocardiographic recordings from all participants and used them to calculate the P-wave variables. We also assessed the levels of highly sensitive C-reactive protein, which is an inflammatory marker, and the lipid levels for each group. The results were reported as the means ± standard deviations and percentages. RESULTS The P-wave dispersion was significantly higher in lichen planus patients than in the control group. Additionally, highly sensitive C-reactive protein, LDL cholesterol, and triglyceride levels were significantly higher in lichen planus patients compared to the controls. There was a significant positive correlation between highly sensitive C-reactive protein and P-wave dispersion (r=0.549, p<0.001) in lichen planus patients. CONCLUSIONS P-wave dispersion increased on the surface electrocardiographic measurements of lichen planus patients. This result may be important in the early detection of subclinical cardiac involvement. Increased P-wave dispersion, in terms of the tendency for atrial fibrillation, should be considered in these patients.
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Affiliation(s)
- Musa Sahin
- Yuzunci Yil University, Faculty of Medicine, Cardiology Department, Van, Turkey.
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Bacaksiz A, Erdogan E, Tasal A, Vatankulu MA, Kul S, Sevgili E, Ertas G, Dizman D, Onsun N, Uysal O. Electrocardiographic P-wave characteristics in patients with psoriasis vulgaris. Ups J Med Sci 2013; 118:35-41. [PMID: 23153368 PMCID: PMC3572669 DOI: 10.3109/03009734.2012.744372] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
Abstract
PURPOSE Psoriasis vulgaris is one of the most common skin disorders. Patients with psoriasis carry an excessive risk of atrial fibrillation (AF). The differences between the maximum (Pmax) and the minimum (Pmin) P-wave duration on ECG are defined as P-wave dispersion (PWD). Prolongation of PWD is an independent risk factor for the development of AF. The aim of this the study was to investigate P-wave duration and PWD in patients with psoriasis. METHODS Sixty-one adult patients with psoriasis vulgaris (group 1) and 58 age and sex-matched healthy individuals (group 2) were included in this study. ECG recordings were obtained, and the P-wave variables were calculated. Results were reported as mean ± standard deviation and percentages. Continuous variables were analysed using Student's t test. A value of P < 0.05 was considered statistically significant. RESULTS Pmax and PWD were significantly higher in group 1 than in group 2 (108.8 ± 21.3 ms versus 93.3 ± 13.0 ms, P < 0.001; 67.4 ± 22.9 ms versus 45.0 ± 19.6 ms, P < 0.001, respectively). Also, Pmin was significantly lower in group 1 (41.3 ± 12.3 ms versus 48.3 ± 14.3 ms, P = 0.04). The psoriasis disease activity score and hsCRP correlated with PWD (P < 0.01). CONCLUSIONS Atrial conduction of sinus impulses was impaired in patients with psoriasis vulgaris. It was more prominent in patients with severe disease. Physicians caring for patients with psoriasis vulgaris should screen them for AF development.
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Affiliation(s)
- Ahmet Bacaksiz
- Department of Cardiology, Faculty of Medicine, BezmiÂlem Foundation University, Istanbul, Turkey.
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Abstract
BACKGROUND Psoriasis vulgaris is one of the most prevalent chronic, inflammatory skin disorders. Patients with psoriasis carry an excess risk of hypertension and adverse cardiovascular (CV) events. Blood pressure (BP) has a circadian rhythm characterised with lower values at night. A blunted nocturnal BP decline defined as non-dipping accelerates the development of hypertension and CV diseases. The aim of this study is to evaluate circadian variation of blood pressure in normotensive middle-aged patients with psoriasis vulgaris. METHODS Seventy adult patients with psoriasis vulgaris (group 1) and 70 age and sex-matched healthy individuals (group 2) were included in the study. Ambulatory BP monitoring was performed in all participants over a 24-h period. Non-dippers are defined as those who show a reduction in BP of less than 10 % between the average day and night systolic BP. RESULTS Although mean 24-h BPs were similar in both groups, night-time BPs were significantly higher in psoriatic patients (115.1 ± 7.7 vs. 109.9 ± 6.0 mmHg and 72.1 ± 7.0 vs. 67.6 ± 5.5 mmHg, respectively; p < 0.05). The non-dipping pattern of BP changes was significantly more common in patients with psoriasis vulgaris compared with the control group (65.9 vs. 34.1 %, p < 0.01). Psoriasis severity and BMI are independent predictors of impaired nocturnal BP regulation. CONCLUSIONS Patients with psoriasis vulgaris had increased nocturnal BP and heart rate. This is the first study to demonstrate a blunted nocturnal BP decrease in normotensive patients with psoriasis.
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Holzer M, Wolf P, Curcic S, Birner-Gruenberger R, Weger W, Inzinger M, El-Gamal D, Wadsack C, Heinemann A, Marsche G. Psoriasis alters HDL composition and cholesterol efflux capacity. J Lipid Res 2012; 53:1618-24. [PMID: 22649206 DOI: 10.1194/jlr.m027367] [Citation(s) in RCA: 128] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open
Abstract
Psoriasis, a chronic inflammatory skin disease, has been linked to increased myocardial infarction and stroke. Functional impairment of HDL may contribute to the excess cardiovascular mortality of psoriatic patients. However, data available regarding the impact of psoriasis on HDL composition and function are limited. HDL from psoriasis patients and healthy controls was isolated by ultracentrifugation and shotgun proteomics, and biochemical methods were used to monitor changed HDL composition. We observed a significant reduction in apoA-I levels of HDL from psoriatic patients, whereas levels of apoA-II and proteins involved in acute-phase response, immune response, and endopeptidase/protease inhibition were increased. Psoriatic HDL contained reduced phospholipid and cholesterol. With regard to function, these compositional alterations impaired the ability of psoriatic HDL to promote cholesterol efflux from macrophages. Importantly, HDL-cholesterol efflux capability negatively correlated with psoriasis area and severity index. We observed that control HDL, as well as psoriatic HDL, inhibited dihydrorhodamine (DHR) oxidation to a similar extent, suggesting that the anti-oxidative activity of psoriatic HDL is not significantly altered. Our observations suggest that the compositional alterations observed in psoriatic HDL reflect a shift to a pro-inflammatory profile that impairs cholesterol efflux capacity of HDL and may provide a link between psoriasis and cardiovascular disease.
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Affiliation(s)
- Michael Holzer
- Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria
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