Increased Amount of Visceral Fat in Patients with Psoriasis ...

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Original Paper

Dermatology 2010;220:32–37 DOI: 10.1159/000254482

Increased Amount of Visceral Fat in Patients with Psoriasis Contributes to Metabolic Syndrome

Ali Balci a Didem Didar Balci b Zafer Yonden c Inan Korkmaz a Julide Zehra Yenin b Ebru Celik b Nese Okumus c Ertugrul Egilmez a

Departments of a Radiology, b Dermatology and c Biochemistry, Faculty of Medicine, Mustafa Kemal University, Antakya , Turkey

Introduction

Psoriasis is a systemic, chronic, inflammatory skin disease that affects approximately 2% of the population [1] . Recently, associations have been recognized between psoriasis and an increased incidence of atherosclerotic diseases and metabolic syndrome (central obesity, diabe-tes or insulin resistance, hypertension, and dyslipidae-mia) [2–5] .

Abdominal obesity, which is caused by excess accu-mulation of visceral adipose tissue (VAT), is associated with increased risk for cardiovascular disease and diabe-tes mellitus [6, 7] . The visceral component of abdominal fat is the most prevalent form in insulin resistance and metabolic syndrome [8] . Studies have clearly shown that viscerally obese patients have the most disturbed meta-bolic risk profile. An excess and disproportionate accu-mulation of VAT is responsible for metabolic and athero-sclerotic diseases more frequently than the excess accu-mulation of subcutaneous or total body fat [6–9] . The accumulation of VAT is a risk factor for carotid and coro-nary atherosclerosis, irrespective of body weight [10, 11] . Anthropometric measurements such as the waist-to-hip ratio (WHR) and sagittal abdominal diameter are simple and useful indicators of VAT accumulation, but these in-dices do not always accurately reflect visceral adiposity [12–14] . Computed tomography (CT) is an optimal, re-producible, and reliable technique for accurately assess-

Key Words Psoriasis � Visceral fat � Metabolic syndrome

Abstract Background: Psoriasis is associated with obesity and meta-bolic syndrome. Metabolic syndrome is associated with vis-ceral fat accumulation. There is no study on the accumula-tion of visceral fat in patients with psoriasis. Objective: The aim of this study was to compare the visceral fat accumula-tion in patients with psoriasis and controls. Subjects and Methods: 46 patients with psoriasis and 46 sex- and age-matched control patients were included in this study. The abdominal fat area [visceral fat area (VFA), subcutaneous fat area (SFA) and total fat area (TFA)] at the level of the umbili-cus was evaluated by computed tomography. Results: The mean VFA value and VFA/SFA ratio of the psoriasis patients were significantly higher compared with the control patients (123.4 8 80.3 vs. 81.2 8 59.8 cm 2 and 0.734 8 0.593 vs. 0.491 8 0.336; p = 0.005 and p = 0.017, respectively). Fasting blood sugar levels were also found to be significantly higher in pso-riasis patients, compared with the control patients (101.8 8 43.5 vs. 83.4 8 9.1 mg/dl; p = 0.005). Multiple linear regres-sion analysis indicated that waist-to-hip ratio, age, body weight, the presence of psoriasis and metabolic syndrome were significantly associated with VFA. Conclusion: Psoriasis patients had a higher amount of VFA, compared with the control patients. Copyright © 2009 S. Karger AG, Basel

Received: May 28, 2009 Accepted after revision: August 4, 2009 Published online: October 29, 2009

Didem Didar Balci Department of Dermatology, Faculty of Medicine Mustafa Kemal University TR–31100 Antakya (Turkey) Tel. +90 326 214 0649, Fax +90 326 214 4977, E-Mail didemaltiner @ yahoo.com

© 2009 S. Karger AG, Basel1018–8665/10/2201–0032$26.00/0

Accessible online at:www.karger.com/drm

Increased Visceral Fat in Psoriasis Dermatology 2010;220:32–37 33

ing visceral fat accumulation. Using CT, visceral and sub-cutaneous fat can be accurately quantified, with small intra- and interobserver variation, allowing the determi-nation of their relationships with biochemical and an-thropometric measurements [15, 16] .

This study is the first to determine visceral fat accu-mulation in psoriasis patients compared with controls. We also investigated the association of visceral fat accu-mulation with metabolic syndrome and anthropometric measurements in patients with psoriasis.

Subjects and Methods

Study Patients 46 consecutive patients with psoriasis vulgaris and 46 gender-

and age-matched control patients attending our dermatology out-patient clinic were included in this study. Informed consent was obtained from all patients, and the study protocol was approved by the ethics committee of our institution. The diagnosis of pso-riasis vulgaris was based on a clinical or histopathological exam-ination of all patients. Controls were recruited among the patients referred for dermatological conditions other than psoriasis. The diagnoses of the controls were skin neoplasm (5 patients, 10.9%: e.g. squamous cell carcinoma, basal cell carcinoma), superficial fungal infections (17 patients, 37.0%), contact dermatitis (8 pa-tients, 17.4%), lichen planus (3 patients, 7.0%), vitiligo (4 patients, 8.7%), and urticaria (9 patients, 20.0%). The psoriasis and control patients were of the same ethnic origin. A known endocrine, kid-ney, or metabolic disease other than obesity or diabetes mellitus and age younger than 18 years were exclusion criteria. Subjects who were receiving lipid-lowering therapy were also excluded from the study.

Before conducting the study, a power analysis was performed based on the results of a pilot study (n = 20). Using a sample size calculator (DSS Research, Fort Worth, Tex., USA), it was estimat-ed that 43 subjects for each group were needed to give this study a power of 90% for showing a relevant change in visceral fat area (VFA) with a 95% confidence interval.

Anthropometric characteristics, including age, gender, weight, height, body mass index (BMI), and WHR, and clinical charac-teristics, including duration of disease, type and severity of dis-ease, medications, blood pressure, and smoking habits, were re-corded. The WHR was calculated as the ratio of the waist and hip circumferences. BMI was calculated as the ratio of the weight (kg) to the square of the height (m) (kg/m 2 ). Morning blood pressure was measured using a mercury sphygmomanometer, after a 15-min rest with the patient in the sitting position. Blood pressure was recorded as the average of two consecutive measurements. Disease severity was quantified using the Psoriasis Area and Se-verity Index (PASI).

Laboratory Measurements To measure serum total cholesterol, high-density lipoprotein

(HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, tri-glyceride, uric acid, and glucose levels, blood samples were ob-tained in the morning after an overnight fast of at least 8 h. Serum

total cholesterol, HDL and LDL cholesterol, triglyceride, uric acid, and glucose levels were determined spectrophotometrically using an autoanalyser (Synchron LX20; Beckman Coulter, Ful-lerton, Calif., USA). To diagnose diabetes mellitus, subjects who had a fasting blood sugar in the range of 110–126 mg/dl under-went a standard (75 g glucose) oral glucose tolerance test, as pro-posed by the World Health Organization, between 8 and 11 a.m. [17] . The number of diagnostic criteria for metabolic syndrome in each study subject was recorded. The criteria of the National Cho-lesterol Education Program’s Adult Panel III for metabolic syn-drome were used: waist circumference 1 102 cm in men or 1 88 cm in women; hypertriglyceridaemia 1 150 mg/dl; HDL cholesterol ! 40 mg/dl in men or ! 50 mg/dl in women; blood pressure 1 130/85 mm Hg or antihypertensive medication; fasting plasma glucose 1 110 mg/dl or known diabetes mellitus. Subjects who had three or more criteria were diagnosed with metabolic syndrome [18] .

Measurement of Abdominal Fat Distribution Abdominal fat distribution was examined on one cross-sec-

tional CT (Toshiba Aquilion 64 scanner, Tokyo, Japan) scan (120 kV, 200 mA, 5-mm section thickness) at the level of the umbilicus (fourth lumbar vertebra) with the patient in the supine position, using a previously described procedure [16] . A region of interest in the subcutaneous fat layer was defined by tracing its contour on each scan, and the attenuation range of CT numbers for fat tis-sue was calculated and expressed as the mean 8 2 standard de-viations (SD). Intraperitoneal tissue was defined by tracing its contour on each scan; within that region of interest, tissue with attenuation within the attenuation mean 8 2 SD for fat tissue was considered VFA ( fig. 1 ). VFA was measured as the fat tissues lo-cated in the intraperitoneal, omental, and retroperitoneal areas. Total abdominal tissue with attenuation within the mean 8 2 SD for fat tissue was considered as the total fat area (TFA) ( fig. 2 ). The subcutaneous fat area (SFA) was calculated as TFA minus VFA. The measurements were extrapolated by one of the authors (I.K.), using a previously described procedure [16] . The subjects had fast-ed overnight and were studied in the morning, between 8 and 12 a.m. All laboratory parameters and anthropometric measure-ments were obtained on the same day as the CT examination.

Statistical Analysis Continuous data are expressed as the mean 8 SD, and cate-

gorical variables are expressed as percentages. The normality of the variables was tested using the Kolmogorov-Smirnov test. Comparisons between two groups were assessed using Student’s t test for continuous variables and a � 2 test for categorical vari-ables. The Mann-Whitney U test was used for continuous vari-ables that were not distributed normally. Correlations between variables were analyzed using the Pearson correlation analysis. Multiple linear regression analysis was used to assess indepen-dent associations between VFA and other variables. The variables significantly associated with VFA (p ! 0.05) in the Pearson cor-relation analysis were included as independent variables in mul-tiple linear regression analysis models. A stepwise selection meth-od was used in the multiple linear regression analysis. Two-sided p values of less than 0.05 were considered statistically significant. The statistical analysis was carried out using the Statistical Pack-age for the Social Sciences (SPSS) version 16 (SPSS, Chicago, Ill., USA).

Balci /Balci /Yonden /Korkmaz /Yenin /Celik /Okumus /Egilmez

Dermatology 2010;220:32–37 34

Results

The main demographic, clinical, and laboratory fea-tures of the subjects are shown in table 1 . The two groups were comparable in terms of age, gender, BMI, WHR, to-tal cholesterol, LDL cholesterol, HDL cholesterol, triglyc-eride, uric acid levels, TFA, and SFA. However, the mean VFA and VFA/SFA ratio of the psoriasis patients were significantly higher than those in the control patients (123.4 8 80.3 vs. 81.2 8 59.8 cm 2 and 0.734 8 0.593 vs. 0.491 8 0.336; p = 0.005 and p = 0.017, respectively) ( fig. 3 ). The fasting blood sugar level was also significant-ly higher in the psoriasis patients than in the controls (101.8 8 43.5 vs. 83.4 8 9.1 mg/dl; p = 0.005).

The presence of diabetes mellitus and smoking habit were significantly more frequent in psoriasis patients compared with controls. However, the prevalence of hy-pertension did not differ significantly between the two groups ( table 1 ).

Table 2 shows the results of multiple linear regression analyses for factors associated with VFA in the entire group of 92 study subjects and in the psoriasis patients only. Multiple linear regression analysis in all study sub-jects indicated that VFA was significantly associated with WHR, age, body weight, presence of psoriasis, and meta-bolic syndrome. Multiple linear regression analyses of the factors associated with VFA in psoriasis patients only indicated that VFA was significantly associated with WHR, age, body weight, and presence of metabolic syn-

drome ( table 2 ). BMI was not associated with VFA in the linear regression analysis.

PASI score, duration or type of disease, smoking hab-it, and therapies were not associated with VFA (p 1 0.05). None of the laboratory findings were associated with VFA (p 1 0.05). At the time of the study, 22 (47.8%) pa-tients were using topical corticoid or calcipotriol; 4 (8.7%) acitretin, 2 each (4.3% each) phototherapy and biologics,

Fig. 1. A CT scan obtained at the level of the umbilicus. The area in pink is regarded as VFA.

Fig. 2. A CT scan obtained at the level of the umbilicus. The area in pink shows TFA.

0

400V

FA

Controls

(n = 46)

244

100

200

300

Patients

(n = 46)

Fig. 3. Boxplot graph of VFA in patients with psoriasis and con-trols. The upper and lower sides of each box show the upper and lower quartile, respectively, while the horizontal line dividing each box shows the median. Circles represent outliers.

Increased Visceral Fat in Psoriasis Dermatology 2010;220:32–37 35

and 1 each (2.2% each) cyclosporine, methotrexate, and salazopyrine. The remaining 13 (28.3%) were not taking any therapy. 40 (87.0%) of the psoriasis patients had the plaque type, 5 (10.9%) had the guttate type, and the re-maining 1 (2.2%) had the erythrodermic type. 3 (6.5%) patients had psoriatic arthritis.

Discussion

This study clearly demonstrated for the first time that VFA is increased in psoriasis patients compared with control patients with similar waist circumferences. This study also clarified that VFA is independently associated with the presence of metabolic syndrome in patients with psoriasis. Several recent studies have indicated that pso-riasis patients tend to develop metabolic syndrome, which is a cluster of conditions that include increased waist cir-cumference, dyslipidaemia, hypertension, and diabetes mellitus or insulin resistance [2–5] . Other comorbidities such as smoking habit and obesity have also been report-ed more frequently in patients with psoriasis than in non-psoriatic controls [19, 20] . In the present study, diabetes mellitus and smoking habit were more common in pso-

riatic patients than in controls, whereas no significant difference was found in the prevalence of hypertension or metabolic syndrome between psoriasis patients and con-trols. However, this study did not aim to compare the prevalence of these comorbidities, and the study popula-tion was too small for an analysis of these parameters.

Obesity may be accompanied by several metabolic dis-turbances, including diabetes mellitus, dyslipidaemia, insulin resistance, and atherosclerotic diseases. In gen-eral, the risk associated with obesity is proportional to the total amount of excess adipose tissue, but visceral obesity appears to be an important indicator of metabolic and atherosclerotic diseases [6–9] . In psoriasis, the chronic inflammation and persistent secretion of TNF- � and other pro-inflammatory cytokines together with comor-bidities such as metabolic syndrome and smoking habit appear to be the main cause of increased atherosclerosis [2, 3, 19, 20] .

A number of mechanisms have been proposed to ex-plain the association between visceral adiposity and met-abolic complications and atherosclerosis. First, visceral fat, owing to its anatomical location and peculiar metab-olism (enhanced lipolytic activity), releases toxic free fat-ty acids (FFAs), which are delivered in high concentration

Table 1. Demographic, clinical and laboratory features of the subjects

Psoriasis patients (n = 46) Controls (n = 46) p values

Age, years 39.5814.2 39.8813.5 0.898a

Male/female 29/17 29/17 1Disease duration, years 11.088.3PASI score 6.186.3BMI, kg/m2 26.584.2 26.884.1 0.760a

WHR, % 90.688.3 88.187.5 0.132a

Total cholesterol, mg/dl 178.8836.6 170.1839.0 0.310a

LDL cholesterol, mg/dl 107.8834.4 103.4835.6 0.542a

HDL cholesterol, mg/dl 43.6810.5 42.1811.6 0.516a

Triglyceride, mg/dl 139.78129.9 119.1874.2 0.631b

Fasting blood sugar, mg/dl 101.8843.5 83.489.1 0.005b

Uric acid, mg/dl 4.481.3 4.681.0 0.419a

Smoking 24 (52.2) 14 (30.4) 0.028c

Diabetes mellitus 7 (15.2) 1 (2.2) 0.029c

Hypertension 4 (8.7) 5 (10.9) 0.500c

Metabolic syndrome 8 (17.4) 5 (10.9) 0.275c

VFA, cm2 123.4880.3 81.2859.8 0.005a

TFA, cm2 291.88148.7 268.08126.0 0.410a

SFA, cm2 168.4891.3 186.8893.4 0.342a

VFA/SFA, % 73.4859.3 49.1833.6 0.017a

Figures in parentheses are percentages. a Student’s t test. b Mann-Whitney U test. c �2 test.

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Dermatology 2010;220:32–37 36

to the liver. An excessive accumulation of FFAs in the liver impairs hepatic insulin sensitivity, resulting in pe-ripheral hyperinsulinaemia and insulin resistance [8, 21, 22] . In addition, an increased amount of FFAs in the liver is ultimately responsible for the production of highly ath-erogenic small dense LDLs [8] . Second, adipose tissue functions as an endocrine organ, releasing pro-inflam-matory and adipocyte-derived cytokines such as TNF- � , leptin, resistin, and adiponectin, which are thought to constitute an important link between obesity and insulin resistance [8, 20, 23, 24] . These cytokines can also con-tribute to an increased risk for atherosclerotic diseases [8] . More recently, Takahashi et al. [25] reported that plasma adiponectin levels were decreased and plasma leptin levels increased in psoriasis patients compared with healthy controls. In that study, a negative correlation was also demonstrated between plasma adiponectin lev-els and both the PASI score and TNF- � level in psoriasis patients. Adiponectin is the most abundant adipocyte-specific adipokine in the circulation. This important cy-tokine has anti-inflammatory effects and functions in regulating insulin sensitivity [20, 26] . The adiponectin level is decreased in obese subjects, particularly in those viscerally obese [27] . Reduced adiponectin levels have also been found to be associated with metabolic syn-drome, atherosclerosis, and insulin resistance [20] . An-other adipocyte-specific cytokine, leptin, appears to be influenced by pro-inflammatory cytokines. It has been suggested that omental fat has more influence than sub-cutaneous fat on plasma leptin [28] . Similarly, TNF- �

and IL-6 are secreted in adipose tissue and have impor-tant roles in the pathogenesis of psoriasis. TNF- � and IL-6 promote a chronic inflammatory state, angiogene-sis, and oxidative stress, which contribute to the aetiology of insulin resistance, glucose intolerance, dyslipidaemia, hypertension, endothelial dysfunction, and atherogene-sis [20, 29] .

Viscerally obese patients are more susceptible to thrombosis and are more likely to show evidence of a chronic inflammatory state [8] . Obesity has also been suggested as a risk factor for the development of psoriasis in a large cohort study [30] . In our study, mean BMI did not differ significantly between the groups. However, our study found that the patients with psoriasis had more vis-ceral fat than controls, even when BMI and waist circum-ference were similar between the two groups. Further-more, the linear regression model showed that the pres-ence of psoriasis was independently associated with VFA, suggesting that visceral fat is linked to the chronic in-flammatory state. We failed to detect any association be-tween VFA and PASI score or disease duration. The fact that PASI is not a stable parameter and may change over time, mainly due to therapy, may explain our failure to detect a significant association between VFA and PASI score.

The therapies, particularly systemic steroids, used in psoriasis may affect the metabolic state of patients. How-ever, no significant association was found between VFA and the therapies. None of the patients with psoriasis were receiving systemic steroids. In addition, the study

Table 2. Multiple linear regression analysis factors associated with VFA in the entire group and psoriasispatients only

Independent variables Standard regression coefficients (�)

VFA in psoriasispatients only (n = 46)

VFA in all studysubjects (n = 92)

WHR 0.412*** 0.343***Age 0.282** 0.293***Body weight 0.219* 0.278***Presence of metabolic syndrome 0.245** 0.182**Presence of psoriasis – 0.222***R2 (multiple coefficient of determination) 0.787*** 0.773***

* p < 0.05; ** p < 0.01; *** p < 0.001.VFA is significantly associated with WHR (p < 0.001), age (p < 0.01), body weight (p < 0.05) and presence of

metabolic syndrome (p < 0.01) in psoriasis patients only. VFA is significantly associated with WHR (p < 0.001), age (p < 0.001), body weight (p < 0.001), presence of metabolic syndrome (p < 0.01) and presence of psoriasis(p < 0.001) in all study subjects.

Increased Visceral Fat in Psoriasis Dermatology 2010;220:32–37 37

References

1 van de Kerkhof PCM, Schalkwijk J: Psoria-sis; in Bolognia JL, Jorizzo JL, Rapini RP (eds): Dermatology, ed 2. Philadelphia, Mos-by Elsevier, 2008, pp 115–135.

2 Gisondi P, Tessari G, Conti A, et al: Prev-alence of metabolic syndrome in patients with psoriasis: a hospital-based case-con-trol study. Br J Dermatol 2007; 157: 68–73.

3 Wakkee M, Thio HB, Prens EP, et al: Unfa-vorable cardiovascular risk profiles in un-treated and treated psoriasis patients. Ath-erosclerosis 2007; 190: 1–9.

4 Sommer DM, Jenisch S, Suchan M, et al: In-creased prevalence of the metabolic syn-drome in patients with moderate to severe psoriasis. Arch Dermatol Res 2006; 298: 321–328.

5 Cohen AD, Sherf M, Vidavsky L, Vardy DA, Shapiro J, Meyerovitch J: Association be-tween psoriasis and the metabolic syndrome. A cross-sectional study. Dermatology 2008; 216: 152–155.

6 Bays HE: ‘Sick fat’, metabolic disease, and atherosclerosis. Am J Med 2009; 122: 26–37.

7 Bays HE, González-Campoy JM, Bray GA, et al: Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hyper-trophy and increased visceral adiposity. Ex-pert Rev Cardiovasc Ther 2008; 6: 343–368.

8 Després JP: Is visceral obesity the cause of the metabolic syndrome? Ann Med 2006; 38: 52–63.

9 Després JP, Lemieux I, Bergeron J, et al: Ab-dominal obesity and the metabolic syn-drome: contribution to global cardiometa-bolic risk. Arterioscler Thromb Vasc Biol 2008; 28: 1039–1049.

10 Kobayashi H, Nakamura T, Miyaoka K, etal: Visceral fat accumulation contributes to insulin resistance, small-sized low-density lipoprotein, and progression of coronaryartery disease in middle-aged non-obese Japanese men. Jpn Circ J 2001; 65: 193–199.

11 Yamamoto M, Egusa G, Hara H, Yamakido M: Association of intraabdominal fat and ca-rotid atherosclerosis in non-obese middle-aged men with normal glucose tolerance. Int J Obes Relat Metab Disord 1997; 21: 948–951.

12 Ashwell M, Cole TJ, Dixon AK: Obesity: new insight into the anthropometric classifica-tion of fat distribution shown by computed tomography. Br Med J 1985; 290: 1692–1694.

13 Seidell JC, Oosterlee A, Deurenberg P, et al: Abdominal fat depots measured with com-puted tomography: effects of degree of obe-sity, sex, and age. Eur J Clin Nutr 1988; 42: 805–815.

14 Kvist H, Chowdhury B, Grangård U, et al: Total and visceral adipose-tissue volumes derived from measurements with computed tomography in adult men and women: pre-dictive equations. Am J Clin Nutr 1988; 48: 1351–1361.

15 Tokunaga K, Matsuzawa Y, Ishikawa K, Ta-rui S: A novel technique for the determina-tion of body fat by computed tomography. Int J Obes 1983; 7: 437–445.

16 Yoshizumi T, Nakamura T, Yamane M, et al: Abdominal fat: standardized technique for measurement at CT. Radiology 1999; 211: 283–286.

17 World Health Organization: Diabetes Mel-litus: Report of a WHO Study Group. Tech-nical Report Series No 727. Geneva, World Health Organization, 1985.

18 National Institutes of Health: Third Report of the National Cholesterol Education Pro-gram (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Pan-el III). Executive Summary. NIH publ. No01-3670. Bethesda, National Institutes of Health, National Heart, Lung and Blood In-stitute, 2001.

19 Naldi L, Chatenoud L, Linder D, et al: Ciga-rette smoking, body mass index, and stress-ful life events as risk factors for psoriasis: re-sults from an Italian case-control study. J Invest Dermatol 2005; 125: 61–67.

20 Sterry W, Strober BE, Menter A, Internation-al Psoriasis Council: Obesity in psoriasis: the metabolic, clinical and therapeutic implica-tions. Report of an interdisciplinary confer-ence and review. Br J Dermatol 2007; 157: 649–655.

21 Bergman RN, Kim SP, Catalano KJ, et al: Why visceral fat is bad: mechanisms of the metabolic syndrome. Obesity (Silver Spring) 2006; 14(suppl 1):16–19.

22 Lafontan M, Berlan M: Do regional differ-ences in adipocyte biology provide new pathophysiological insights? Trends Phar-macol Sci 2003; 24: 276–283.

23 Trayhurn P, Wood IS: Adipokines: inflam-mation and the pleiotropic role of white adi-pose tissue. Br J Nutr 2004; 92: 347–355.

24 Chen YJ, Wu CY, Shen JL, et al: Psoriasisindependently associated with hyperlepti-nemia contributing to metabolic syndrome. Arch Dermatol 2008; 144: 1571–1575.

25 Takahashi H, Tsuji H, Takahashi I, et al: Plas-ma adiponectin and leptin levels in Japanese patients with psoriasis. Br J Dermatol 2008; 159: 1207–1208.

26 Pajvani UB, Scherer PE: Adiponectin: sys-temic contributor to insulin sensitivity. Curr Diab Rep 2003; 3: 207–213.

27 Lihn AS, Bruun JM, He G, et al: Lower ex-pression of adiponectin mRNA in visceral adipose tissue in lean and obese subjects. Mol Cell Endocrinol 2004; 219: 9–15.

28 Moses AG, Dowidar N, Holloway B, et al: Leptin and its relation to weight loss, ob gene expression and the acute-phase response in surgical patients. Br J Surg 2001; 88: 588–593.

29 Sonnenberg GE, Krakower GR, Kissebah AH: A novel pathway to the manifestations of metabolic syndrome. Obes Res 2004; 12: 180–186.

30 Setty AR, Curhan G, Choi HK: Obesity, waist circumference, weight change, and the risk of psoriasis in women: Nurses’ Health Study II. Arch Intern Med 2007; 167: 1670–1675.

included few patients receiving systemic therapies such as cyclosporine, methotrexate, or biologics.

In conclusion, for the first time, we demonstrated that VFA is increased in psoriasis patients and is indepen-dently associated with the presence of psoriasis. We also demonstrated that VFA is independently associated with the presence of metabolic syndrome in patients with pso-

riasis. Therefore, the increased accumulation of VAT, which releases pro-inflammatory cytokines, is a poten-tial mechanism linking psoriasis and its metabolic co-morbidities and may be a major contributor to the unfa-vourable cardiovascular risk in psoriasis. Visceral obesity may be an important target for future interventions in metabolic comorbidities of psoriasis.