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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 34  |  Issue : 2  |  Page : 107-113

Evaluation of serum level of visfatin among psoriatic patients


1 Department of Dermatology, Venereology and Andrology, Alexandria University, Alexandria, Egypt
2 Department of Clinical Pathology, Alexandria University, Alexandria, Egypt
3 Faculty of Medicine, University of Baghdad, Baghdad, Iraq

Date of Submission20-Oct-2014
Date of Acceptance01-Nov-2014
Date of Web Publication29-Jan-2015

Correspondence Address:
Rasha Mahmoud Genedy
No. 9, 10th Floor, University Buildings, Smouha, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-6530.150264

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  Abstract 

Introduction
Psoriasis is a common chronic inflammatory skin condition that varies in severity. Psoriasis is associated with the complex disorder of metabolic syndrome, which incorporates hypertension, dyslipidemia, obesity, and impaired glucose tolerance, and the association is stronger for severe psoriasis compared with mild psoriasis. Adipose tissue is an important endocrine organ; it secretes several hormones and cytokines that are involved in the metabolic syndrome. Visfatin is a 52-kDa protein secreted primarily by visceral fat. Various cells such as neutrophils, monocytes, macrophages as well as epithelial and endothelial cells might be a source of visfatin after induction with inflammatory stimuli.
Aim
The aim of this work was to evaluate the serum levels of visfatin in psoriatic patients and its relation to the duration, severity of psoriasis, and BMI.
Patients and methods
This study was carried out on 40 psoriatic patients and 40 normal healthy control participants. Venous samples were obtained to measure the serum visfatin level using the ELISA technique.
Results
The serum level of visfatin in the patient group was statistically significantly higher than the serum level of visfatin in the control group. In addition, there was a positive significant correlation between the serum level of visfatin and the PASI score (R = 0.951, P = 0.0001). There was a positive significant correlation between the serum level of visfatin and the duration of psoriasis (R = 0.942, P = 0.0001).
Conclusion
This study concluded that visfatin is one of the adipokines that may play a role in the pathogenesis of psoriasis and its severity in addition to its role in diseases of the cardiovascular system, which could also explain the relation between psoriasis and cardiovascular complications and their severity in psoriatic patients.

Keywords: Obesity, psoriasis, visfatin


How to cite this article:
Badran FK, Genedy RM, Swelem RS, Al-Rawi MZ. Evaluation of serum level of visfatin among psoriatic patients. Egypt J Dermatol Venerol 2014;34:107-13

How to cite this URL:
Badran FK, Genedy RM, Swelem RS, Al-Rawi MZ. Evaluation of serum level of visfatin among psoriatic patients. Egypt J Dermatol Venerol [serial online] 2014 [cited 2020 May 28];34:107-13. Available from: http://www.ejdv.eg.net/text.asp?2014/34/2/107/150264


  Introduction Top


Psoriasis is a common chronic inflammatory skin condition that varies in severity [1]. It is prevalent worldwide. However, the estimates of its prevalence vary by geographic location, but generally, it affects 2-3% of populations [2]. The mean age of onset for the first presentation of psoriasis can range from 15 to 20 years of age, with a second peak occurring at 55-60 years [3].

Psoriasis is characterized by hyperproliferation and abnormal differentiation of epidermal keratinocytes, lymphocyte infiltration consisting mostly of T lymphocytes, and various endothelial vascular changes in the dermal layer [4].

It is known that there are two clinical presentations of psoriasis, type I and II, distinguished by a bimodal age at onset. Type I begins on or before the age of 40 years; type II begins after the age of 40 years. Type I disease accounts for more than 75% of cases [5]. Patients with early onset, or type I psoriasis, tend to have more relatives affected and more severe disease than patients who have a later onset of disease or type II psoriasis. In addition, strong associations have been reported with HLA-Cw6 in patients with early onset compared with patients with later onset of psoriasis. The course and progress of psoriasis are unpredictable. Chronic plaque psoriasis is the most common variety of psoriasis, found in about 70-80% of psoriatic patients. Psoriasis affects male and female patients equally, although females and genetically predisposed individuals tend to have earlier ages of onset [6].

Approximately 80% of patients who have psoriasis have mild disease [7]. The psychological impact of their psoriasis may be significant. Psoriasis is associated with a greater incidence of depression and suicidal ideation [8,9], and the burden of psoriasis is reported to be comparable with other chronic diseases such as diabetes and heart disease [10].

Although the exact cause of psoriasis remains unknown, the evidence suggests that psoriasis is a complex disorder caused by the interaction of multiple genes, the immune system, and environmental factors [11]. In psoriasis, the cutaneous and systemic overexpression of various proinflammatory cytokines, such as interleukins (ILs), tumor necrosis factor (TNF), and interferon-γ, has been identified [12]. Mechanical, chemical, or microbial stress to the skin seems to initiate psoriasis on the basis of a genetic predisposition [13],[14].

Complex cellular interactions among epidermal keratinocytes, mononuclear leukocytes, neutrophils, dendritic cells, and activated T cells, together with growth factors, chemokines, and cytokines, are involved in the development of psoriasis [15].

Psoriasis belongs to a group of complex diseases, the inheritance being multifactorial - genetic variants in multiple genes interact both with each other and with the environment. Several disease susceptibility loci have been suggested as predisposing factors [16],[17]. Advanced studies in understanding the immunopathogenesis and genetics of psoriasis have shifted focus from a single-organ disease confined to dermal structures to a systemic inflammatory condition [18].

Psoriasis is associated with the complex disorder of metabolic syndrome, which incorporates hypertension, dyslipidemia, obesity, and impaired glucose tolerance, and the association is stronger for severe psoriasis compared with mild psoriasis. Similar to psoriasis, the metabolic syndrome is characterized by increases in the immunological activity of Th1, which suggests the hypothesis that psoriasis may be associated with the metabolic syndrome because of shared inflammatory pathways [19].

Therefore, it is possible that the association of the metabolic syndrome and psoriasis is explained by dysregulation of Th1 pathways shared by these diseases. Another explanation for the predisposition of psoriasis patients toward developing metabolic syndrome may be that certain behaviors or the psychological impact of psoriasis itself (e.g. poor eating habits, alcohol consumption, stress, and decreased exercise because of psoriasis symptoms or stigmatization) may lead to the development of increased body weight and the metabolic syndrome. Finally, the metabolic syndrome itself could predispose an individual toward developing psoriasis [20]. However, the close association between psoriasis and the metabolic syndrome could be explained by shared genetic risk loci. Moreover, genetic associations have been established between psoriasis and both type 1 and type 2 diabetes mellitus [21].

Central obesity is associated with abnormal levels of various inflammatory markers, including TNF-α and IL-6 [22],[23]. It is conceivable that this factor may contribute toward the pathogenesis of psoriasis. Indeed, studies found that obesity is associated with the future development of psoriasis [24].

Adipose tissue is an important endocrine organ; it secretes several hormones and cytokines that are involved in the metabolic syndrome [25]. Adipokines, signaling proteins secreted by adipose tissue, have an important regulatory function throughout the body; they include leptin, TNF-α, IL-6, resistin, and adiponectin. Lower serum adiponectin levels have been reported in patients with coronary heart disease [26],[27], and have been shown to be a risk factor for cardiovascular events [28]. In addition, it has been suggested recently that IL-6, TNF-α, leptin, and adiponectin may not just be markers of inflammation and CV risk, but are also likely to play a pathogenic role in atheromatous plaque [29],[30].

Recently, the adipocytokine family has been extended by a novel member - visfatin [31]. Visfatin, initially described as pre-B-colony enhancing factor, [32] dose dependently upregulated the production of many cytokines such as IL-1, IL-6, IL-10, and TNF in human monocytes. These cytokines play a major role in a wide range of infectious and inflammatory diseases [33],[34]. Visfatin is a 52-kDa protein secreted primarily by visceral fat. Various cells such as neutrophils, monocytes, macrophages as well as epithelial and endothelial cells might be a source of visfatin after induction with inflammatory stimuli [35].

The synthesis of visfatin is regulated by several factors, including glucocorticoids, TNF, and IL-6. It has several proinflammatory and immune-modulating properties as visfatin promotes T-cell activation by inducing costimulatory molecules such as CD80, CD40, and intercellular adhesion molecule-1 [36].

Recently, visfatin was described to be a highly expressed protein with insulin-like functions and was predominantly found in visceral adipose tissue, from which the name visfatin was derived. Injection of visfatin in mice lowered blood glucose, and mice with a mutation in visfatin had higher glucose levels [31]. Although these initial studies were promising, subsequent studies of visfatin in humans have generally not confirmed the initial study [37]. A subsequent study did not confirm the insulin mimetic action of visfatin, but instead showed that visfatin has nicotinamide adenine dinucleotide biosynthetic activity, which is essential for B-cell function [38].

In human studies, a positive correlation between visceral adipose tissue visfatin gene expression and BMI was observed, in addition to a negative correlation between BMI and subcutaneous fat visfatin, suggesting that visfatin regulation in these different depots is different and adipose depot ratios are highly dependent on the extent of obesity of the patients. No difference was found in visfatin expression between fat depots of humans, and visfatin was expressed predominantly by non-macrophage cells in the adipose tissue stroma [39],[40],[41].

The aim of this work was to evaluate the serum levels of visfatin in psoriatic patients and its relation to the duration, severity of psoriasis, and the BMI.


  Patients and methods Top


This study was carried out on 40 psoriatic patients and 40 normal healthy control participants recruited from the Outpatient Clinic of the Dermatology Department of Alexandria Main University Hospital.

Inclusion criteria for patients were as follows: patients with psoriasis vulgaris diagnosed clinically who had not received systemic treatments for psoriasis within 1 month before the study, with variable duration and severity of the disease, and of both sexes. Exclusion criteria for both patients and control were as follows: acute or chronic inflammatory condition, recent myocardial infarction or revascularization (≤3 months), exertional angina or arrhythmias, atrial fibrillation, severe lung disease, severe renal insufficiency or other organ disorders significantly compromising participants' physical capacity, and diabetes mellitus as all of the above affect the serum level of visfatin in the body.

An informed consent was obtained from all the participants before the start of the study and approval from the Research Ethics Committee of Faculty of Medicine, Alexandria University, was obtained.

Participants were divided into two groups: the patient group included 40 psoriatic patients and the control group included 40 normal healthy control individuals.

Both groups were subjected to a full assessment of history including drug intake and medical history. Patients were additionally asked about age of onset, duration of psoriasis, previous treatment, and family history of psoriasis. A careful general examination was performed with measurement of body weight (kg). Height was measured as the distance (m) from the top of the head to the bottom of the feet with no shoes using a measuring tape and BMI was calculated according to the following equation [42]:



Patients were examined carefully to determine the distribution, extent, and severity of psoriasis lesions. The extent and severity of psoriasis were assessed according to the PASI score [43]. Patients were classified according to the PASI score as follows [44]: mild psoriasis: PASI less than 10, moderate psoriasis: PASI 10-20, and severe psoriasis: PASI more than 20.

Venous samples were obtained to measure the serum visfatin level using the ELISA technique after 12 h of fasting. Blood samples were collected in sterile tubes and allowed to clot at room temperature. Sera were isolated by centrifugation and stored frozen below −20 until assayed for the visfatin level.

Measurement of the serum level of visfatin

Visfatin levels were determined using EIA (RayBio_Visfatin Enzyme Immunoassay Kit Protocol; Cat#: EIA-VIS-1) [45]. The microplate in the kit was precoated with anti-rabbit secondary antibody. After a blocking step and incubation of the plate with the anti-visfatin antibody, both the biotinylated visfatin peptide and the peptide standard or targeted peptide in samples interacted competitively with the visfatin antibody. Uncompeted (bound) biotinylated visfatin peptide then interacted with streptavidin-horseradish peroxidase, which catalyzed a color development reaction. The intensity of the colorimetric signal was directly proportional to the amount of the biotinylated peptide-streptavidin-horseradish peroxidase complex and inversely proportional to the amount of visfatin peptide in the standard or samples. This was because of the competitive binding to the visfatin antibody between the biotinylated visfatin peptide and peptides in the standard or samples. A standard curve of a known concentration of the visfatin peptide was established and the concentration of the visfatin peptide in the samples was calculated accordingly.

Assay procedure summary

  1. All reagents, samples, and standards were prepared according to instructions.
  2. 100 μl anti-visfatin antibody was added to each well and incubated for 1.5 h at room temperature.
  3. 100 μl standard or sample was added to each well and incubated for 2.5 h at room temperature.
  4. 100 μl prepared streptavidin solution was added and incubated for 45 min at room temperature.
  5. 100 μl TMB one-step substrate reagent was added to each well and incubated for 30 min at room temperature.
  6. 50 μl stop solution was added to each well and read at 450 nm immediately.


The absorbance was calculated for each standard, control, and sample, and the blank optical density was subtracted. The standard curve was plotted using Sigma Plot software, with the standard concentration on the x-axis and the percentage of absorbance on the y-axis. The best-fit straight line was drawn through the standard points.


  Results Top


Participants included in this study were divided into two groups.

In terms of the sex distribution, in this study, the patient group included 22 (55%) men and 18 (45%) women and the control group included 17 (42.5%) men and 23 (57.5%) women. There were no statistically significant differences between the two groups studied (P = 0.186).

Age ranged between 24 and 64 years, mean 42.63 ± 14.123 years, for the patient group and between 20 and 70 years, mean 37.35 ± 10.83 years, for the control group. There was no statistically significant difference between the two groups (P = 0.068).

BMI ranged between 20 and 45 kg/m 2 , mean 29.827 ± 7.66 kg/m 2 , for the patient group and between 22.2 and 46.2 kg/m 2 , mean 28.756 ± 4.84 kg/m 2 , for the control group. There was no statistically significant difference between the two groups (P = 0.457).

The serum level of visfatin ranged between 15 and 60 ng/ml, with a mean of 26.6 ± 10.21 ng/ml for the patient group, whereas in the control group, the serum level of visfatin ranged between 10 and 29 ng/ml, with a mean of 15.6 ± 3.38 ng/ml. In the patient group, the serum level of visfatin was statistically significantly higher than the serum level of visfatin in the control group (P = 0.0001) [Table 1] and [Figure 1].
Figure 1: Comparison between the two groups in terms of the serum level of visfatin.

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Table 1: Comparison between the two groups of the serum level of visfatin

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The serum level of visfatin ranged between 15 and 60 ng/ml, with a mean of 25.86 ± 12.009 ng/ml for men, and between 17 and 42 ng/ml, with a mean of 27.5 ± 7.71 ng/ml for women; there were no statistically significant differences between men and women in the serum level of visfatin (P = 0.62).

The PASI score in the patient group indicated that 13 (32.5%) patients had mild psoriasis, six (15.0%) patients had moderate psoriasis, and 21 (52.5%) patients had severe psoriasis. Descriptive statistics of the PASI and duration of psoriasis in the patient group indicated that the PASI score in the patient group ranged between 2 and 56, mean 21.48 ± 15.65, and the duration of psoriasis ranged between 0.2 and 32.0 years, mean 10.002 ± 9.105 years.

Correlations in the patient group showed that there was a positive, but nonsignificant correlation between the serum level of visfatin and BMI, where R = 0.221 and P = 0.170. There was a positive significant correlation between the PASI score and the serum level of visfatin (R = 0.951, P = 0.0001), but there was no correlation between the PASI score and BMI (R = 0.159, P = 0.327). There was a positive significant correlation between the duration of psoriasis and the serum level of visfatin (R = 0.942, P = 0.0001), but there was no correlation between the duration of psoriasis and BMI (R = 0.116, P = 0.478). There was a negative but nonsignificant correlation between age and the serum level of visfatin (R = −0.133, P = 0.413), but there was a positive significant correlation between age and BMI (R = 0.430, P = 0.006) [Table 2].
Table 2: Correlations in the serum level of visfatin, BMI, PASI, duration of psoriasis, and age in the patient group

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Correlations in the control group showed that there was a positive significant correlation between the serum level of visfatin and BMI, where R = 0.566 and P = 0.000, whereas there was a negative correlation between age and BMI, but this was not significant (R = −0.058, P = 0.723). There was a positive correlation between age and the serum level of visfatin, but this was not significant (R = 0.092, P = 0.573) [Table 3].
Table 3: Correlation between the serum level of visfatin and BMI in the control group

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  Discussion Top


The aim of this work was to evaluate the serum levels of visfatin in psoriatic patient and its relation to the duration, severity of psoriasis, and BMI. The present study included 80 participants divided into two groups: the patient group included 40 psoriatic patients and the control group included 40 age-matched and sex-matched controls.

BMI ranged between 20 and 45 kg/m 2 , mean 29.827 ± 7.66 kg/m 2 , in the patient group and between 22.2 and 46.2 kg/m 2 , mean 28.756 ± 4.84 kg/m 2 , in the control group. There was no statistically significant difference between the two groups. The PASI score in the patient group showed that 13 (32.5%) patients had mild psoriasis, six (15.0%) patients had moderate psoriasis, and 21 (52.5%) patients had severe psoriasis. The PASI score in the patient group ranged between 2 and 56, mean 21.48 ± 15.65. There was no correlation between BMI and the PASI score (R = 0.159, P = 0.327), whereas the duration of psoriasis ranged between 0.2 and 32.0 years, mean 10.002 ± 9.105 years. Thus, there was also no correlation between BMI and the duration of psoriasis (R = 0.116, P = 0.478).

In agreement with this study, Ilkin et al. [46] did not find BMI and waist circumference to be significantly higher in psoriasis patients. However, they observed a higher prevalence of metabolic syndrome among psoriatic patients than the controls. This was explained in the literature, which concluded that the association between psoriasis and metabolic syndrome is independent of the tendency of psoriatic patients to be obese.

In contrast, Wolk et al. [47] observed that one unit increment in BMI was statistically significantly associated with a 7% higher risk of increased psoriasis activity measured by the PASI score at the onset of psoriasis, explaining that excessive adipose tissue in obese patients produces proinflammatory cytokines such as TNF-α, which is involved in psoriasis.

However, Lara et al. [48] observed that there were more statistically significant correlations between overweight and normoweight patients with PASI score than between obese and normoweight patients with PASI score.

In the present study, the serum level of visfatin ranged between 15 and 60 ng/ml, mean 26.6 ± 10.21 ng/ml, in the patient group, whereas in the control group, the serum level of visfatin ranged between 10 and 29 ng/ml, mean 15.6 ± 3.38 ng/ml. The serum level of visfatin was statistically significantly higher in the patient group than in the control group. In addition, there was a significant positive correlation between the serum level of visfatin and the PASI score (R = 0.951, P = 0.0001); also, there was a significant positive correlation between the serum level of visfatin and the duration of psoriasis (R = 0.942, P = 0.0001). Moreover, there was a positive, but nonsignificant correlation between the serum level of visfatin and BMI, where R = 0.221 and P = 0.170.

In agreement with our study, Ismail et al. [49] found that the serum level of visfatin in patients with psoriasis was significantly higher than that of the controls. It was also significantly higher in patients with severe psoriasis than those with mild and moderate psoriasis. Also, there was a significant correlation with the duration of psoriasis, but there was no statistically significant difference between normal weight, overweight, and obese patients in the serum level of visfatin.

Gerdes et al. [50] also found that serum visfatin is increased in patients with psoriasis independent of other factors such as BMI.

In the last few years, visfatin has been proposed as a marker of endothelial dysfunction, an initial and crucial step in the progression of the atherosclerotic process [51]. It seems that visfatin levels are associated positively with a series of inflammatory conditions, independent of other potential metabolic implications. The role of visfatin in psoriasis might include modulation of the inflammatory or immune response as it induces chemotaxis and increases the production of IL-1, TNF, IL-6, and costimulatory molecules by CD14 + monocytes. This enhances their ability to induce proliferative responses [50]. Another explanation is that visfatin levels might be upregulated during inflammation and in response to proinflammatory cytokines [52]. Also, as visfatin is produced by cells involved in psoriasis, increased visfatin values could be attributed to this. Visfatin could provide a link between psoriasis and cardiovascular morbidity as it was shown to be upregulated in atherosclerotic plaques in myocardial infarction [53].

Summary

This study found that the serum level of visfatin in psoriatic patients was statistically significantly higher than the serum level of visfatin in the control group. In addition, there was a positive significant correlation between the serum level of visfatin with the PASI score and with the duration of psoriasis. Moreover, there was a positive, but nonsignificant correlation between the serum level of visfatin and BMI and no correlation between BMI with the PASI score and duration of psoriasis.

This study concluded that visfatin may play a role in the pathogenesis of psoriasis and its severity in addition to its role in diseases of the cardiovascular system, which could also explain the relation between psoriasis and cardiovascular complications and their severity in psoriatic patients.


  Conclusion and recommendations Top


After interpretation of the results of this study, the following were obtained:

  1. Several adipokines may play a role in the pathogenesis of psoriasis, which may or may not be related to obesity.
  2. Visfatin is one of the adipokines that may exert effects on the pathogenesis and activity of psoriasis, which in turn may be one of the contributory factors in the cardiovascular effects of psoriasis.
  3. More attention should be paid to psoriatic patients with follow-up of vital systems in the body as psoriasis is a multisystemic disorder, especially in severe cases with a long duration.
  4. Further studies are required to prove whether there is an association between the serum level of visfatin and obesity.
  5. Further studies on the serum level of visfatin should be carried out on psoriatic patients with and without metabolic syndrome, with evaluation of correlations between the two groups.
  6. Studies are required to determine the effect of treatment of psoriasis on the serum level of visfatin and its level after improvement in the PASI score.



  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
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