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      Relationship between psoriasis and non-alcoholic fatty liver disease

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          Abstract

          Introduction

          Various components of metabolic syndrome have an important role in the pathogenesis of both non-alcoholic fatty liver disease (NAFLD) and psoriasis, suggesting an association between these diseases. However, at present very few studies have reported on the systematic evaluations of the prevalence of NAFLD in patients with psoriasis disorder.

          Aim

          To investigate the prevalence of NAFLD in patients with psoriasis vulgaris. The study also evaluated the parallel relationship between both of the diseases.

          Material and methods

          Patients over18 years old and with a diagnosis of psoriasis vulgaris at the outpatient unit of Department of Dermatology were considered for enrolment and were followed up by the Department of Hepatology, Madras Medical College. Each and every patient completed a questionnaire, underwent a thorough skin evaluation, and had a right upper quadrant ultrasound and fasting blood workup.

          Results

          Two hundred and fifty patients were enrolled in the study. The participants were predominantly middle aged (mean: 44.74 ±11.989 years), overweight (average body mass index (BMI): 24.772 ±3.611 kg/m 2), and male (68%, n = 170). The overall prevalence of NAFLD among psoriasis was 45.2%.

          Conclusions

          Non-alcoholic fatty liver disease is highly prevalent among our cohort of patients with psoriasis, occurring in 45.2% of patients. Comorbidity of NAFLD is highly associated with psoriasis, which emphasises that both diseases may develop simultaneously. Health care providers should be mindful of this association since early evaluation and diagnosis of NAFLD in patients with psoriasis may play a vital role in alleviating the progression of liver disease.

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          Most cited references19

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          The natural history of nonalcoholic fatty liver disease: a population-based cohort study.

          The natural history of nonalcoholic fatty liver disease (NAFLD) in the community remains unknown. We sought to determine survival and liver-related morbidity among community-based NAFLD patients. Four hundred twenty patients diagnosed with NAFLD in Olmsted County, Minnesota, between 1980 and 2000 were identified using the resources of the Rochester Epidemiology Project. Medical records were reviewed to confirm diagnosis and determine outcomes up to 2003. Overall survival was compared with the general Minnesota population of the same age and sex. Mean (SD) age at diagnosis was 49 (15) years; 231 (49%) were male. Mean follow-up was 7.6 (4.0) years (range, 0.1-23.5) culminating in 3192 person-years follow-up. Overall, 53 of 420 (12.6%) patients died. Survival was lower than the expected survival for the general population (standardized mortality ratio, 1.34; 95% CI, 1.003-1.76; P = .03). Higher mortality was associated with age (hazard ratio per decade, 2.2; 95% CI, 1.7-2.7), impaired fasting glucose (hazard ratio, 2.6; 95% CI, 1.3-5.2), and cirrhosis (hazard ratio, 3.1, 95% CI, 1.2-7.8). Liver disease was the third leading cause of death (as compared with the thirteenth leading cause of death in the general Minnesota population), occurring in 7 (1.7%) subjects. Twenty-one (5%) patients were diagnosed with cirrhosis, and 13 (3.1%) developed liver-related complications, including 1 requiring transplantation and 2 developing hepatocellular carcinoma. Mortality among community-diagnosed NAFLD patients is higher than the general population and is associated with older age, impaired fasting glucose, and cirrhosis. Liver-related death is a leading cause of mortality, although the absolute risk is low.
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            Non alcoholic fatty liver disease and metabolic syndrome.

            Non-alcoholic fatty liver disease (NAFLD) is a clinicopathologic entity increasingly recognized as a major health burden in developed countries. It includes a spectrum of liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis, and rarely, progression to cirrhosis. Recent studies emphasize the role of insulin resistance, oxidative stress and subsequent lipid peroxidation, proinflammatory cytokines, adipokines and mitochondrial dysfunction in the development and progression of NAFLD. Furthermore, accumulating evidence supports an association between NAFLD and metabolic syndrome. Although the data are mainly epidemiological, the pathogenesis of NAFLD and metabolic syndrome seems to have common pathophysiological mechanisms, with focus on insulin resistance as a key factor. This review summarizes the current knowledge on the epidemiology, pathophysiology and diagnosis of both NAFLD and metabolic syndrome and the findings that strongly support the association of nonalcoholic fatty liver disease as a possible component in the cluster of metabolic syndrome.
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              Psoriasis and systemic inflammatory diseases: potential mechanistic links between skin disease and co-morbid conditions.

              Psoriasis is now classified as an immune-mediated inflammatory disease (IMID) of the skin. It is being recognized that patients with various IMIDs, including psoriasis, are at higher risk of developing "systemic" co-morbidities, e.g., cardiovascular disease (CVD), metabolic syndrome, and overt diabetes. In non-psoriatic individuals, the pathophysiology of obesity, aberrant adipocyte metabolism, diabetes, and CVDs involves immune-mediated or inflammatory pathways. IMIDs may impact these co-morbid conditions through shared genetic risks, common environmental factors, or common inflammatory pathways that are co-expressed in IMIDs and target organs. Given that pathogenic immune pathways in psoriasis are now well worked out and a large number of inflammatory mediators have been identified in skin lesions, in this review we will consider possible mechanistic links between skin inflammation and increased risks of (1) obesity or metabolic alterations and (2) CVD. In particular, we will discuss how well-established risk factors for CVD can originate from inflammation in other tissues.
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                Author and article information

                Journal
                Prz Gastroenterol
                Prz Gastroenterol
                PG
                Przegla̜d Gastroenterologiczny
                Termedia Publishing House
                1895-5770
                1897-4317
                26 February 2016
                2016
                : 11
                : 4
                : 263-269
                Affiliations
                [1 ]Department of Hepatology, Madras Medical College, Rajiv Gandhi Government General Hospital, Chennai, India
                [2 ]Institute of Internal Medicine, Madras Medical College, Rajiv Gandhi Government General Hospital, Chennai, India
                [3 ]Multi-disciplinary Research Unit (MRU), Madras Medical College, Rajiv Gandhi Government General Hospital, Chennai, India
                Author notes
                Address for correspondence: Prof. Krishnasamy Narayanasamy, Department of Hepatology, Madras Medical College, Rajiv Gandhi Government General Hospital, 600003 Chennai, India. phone: 91-9841170145. e-mail: drkns_1963@ 123456yahoo.com
                Article
                25606
                10.5114/pg.2015.53376
                5209456
                28053681
                f2b8b133-34ad-4ce5-8f91-3d08e7a19810
                Copyright: © 2016 Termedia Sp. z o. o.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                : 17 April 2015
                : 10 July 2015
                Categories
                Original Paper

                non-alcoholic fatty liver disease (nafld),psoriasis,metabolic syndrome

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