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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 15  |  Issue : 2  |  Page : 122-126

Serum levels of adiponectin and visfatin in patients with lichen planus: a case-controlled study


1 Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Assiut University, Egypt
2 Department of Oral Medicine and Periodontology Diagnosis and Oral Radiology, Al-Azhar University Assiut Branch, Egypt
3 Department of Public Health, Faculty of V. Medicine, Assiut University, Assiut, Egypt

Date of Submission14-Aug-2017
Date of Acceptance12-Sep-2017
Date of Web Publication21-Nov-2017

Correspondence Address:
Sahar A Ismail
Department of Dermatology, Venereology and Andrology, Assiut University Hospital, Assiut University, 71515 Assiut
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AZMJ.AZMJ_45_17

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  Abstract 

Background The association of adipokines with lichen planus (LP) is still obscure. Data regarding their effect on other immunological and inflammatory disorders suggest a probable role of adipokines in the pathophysiology of LP.
Objective The objective of the study was to investigate serum levels of adiponectin and visfatin in patients with LP compared with healthy controls and to consider their relation to disease duration and obesity markers.
Patients and methods A case-controlled study was conducted, which included 49 patients with LP and 40 healthy controls. Adiponectin and visfatin serum levels were measured using enzyme-linked immunosorbent assays.
Results Patients with LP showed lower serum levels of adiponectin than healthy controls, with significant inverse correlation with disease duration, BMI, and waist circumference. Cutaneous and mucocutaneous LP showed lower serum levels of adiponectin than oral LP. Visfatin serum level was higher in patients with LP compared with healthy controls, with significant positive correlation with BMI and waist circumference.
Conclusion Our data suggested that adiponectin and visfatin act together through modulation of the inflammatory setting of patients with LP. Because of the significant correlations of adiponectin and visfatin with obesity markers, the physical complications of obesity should be emphasized to patients with LP.

Keywords: adiponectin, lichen planus, visfatin


How to cite this article:
Ismail SA, Mwafey I, Mohamed SA. Serum levels of adiponectin and visfatin in patients with lichen planus: a case-controlled study. Al-Azhar Assiut Med J 2017;15:122-6

How to cite this URL:
Ismail SA, Mwafey I, Mohamed SA. Serum levels of adiponectin and visfatin in patients with lichen planus: a case-controlled study. Al-Azhar Assiut Med J [serial online] 2017 [cited 2018 Jun 25];15:122-6. Available from: http://www.azmj.eg.net/text.asp?2017/15/2/122/218856




  Introduction Top


Lichen planus (LP) is a chronic T-cell-mediated inflammatory disease affecting skin and mucous membrane [1]. It has been linked to a growing threat of cardiovascular risk factors including obesity, diabetes, dyslipidemia, hypertension, and metabolic syndrome [2],[3],[4]. Chronic inflammation is the eventual pathological process that causes both skin manifestations and the associated comorbidities [2].

Adipokines are key players in the pathogenesis of metabolic syndrome through their effect on vascular function, immune regulation, and adipocyte metabolism [5]. A single study exists on adiponectin in the context of LP [6] but none on visfatin. However, data from other inflammatory diseases suggest a possible role of these adipokines in LP pathophysiology [7].

Adiponectin is a protein produced by adipocytes. It has a wide variety of immunological and inflammatory tasks in several disorders such as metabolic syndrome, diabetes, and cardiovascular disorder [7]. It affects immunity and suppresses macrophage function, leading to reduction of phagocyte activity, interleukin-6 (IL-6), and tumor necrosis factor (TNF) production. It also decreases T-cell response and stimulates production of anti-inflammatory cytokines including IL-1 and IL-10 [6],[7],[8].

Visfatin is a 52 kDa protein secreted mostly by visceral fat. A variety of cells were reported to be a source of visfatin, including neutrophils, macrophages, and monocytes, in addition to epithelial and endothelial cells [9]. Visfatin synthesis is induced with different inflammatory stimuli and regulated by several factors, such as TNF, IL-6, and glucocorticoids. It has several proinflammatory and immune-modulating characteristic, as visfatin promotes activation of T cell through induction of costimulatory molecules such as ICAM-1, CD40, and CD80 [7].

The aim of this work was to investigate the serum levels of adiponectin and visfatin in patients with LP compared with healthy controls and to consider their relation to the disease duration and markers of obesity.


  Patients and methods Top


A total of 49 patients with LP attending the Dermatology Outpatient Clinic at Assiut University Hospital and the dental clinic at Al-Azhar University Dental Hospital, Assiut, Egypt, and 40 healthy controls were enrolled in this case-controlled study (2016–2017). None of the patients were on systemic therapy, and they were off topical therapy for 4 weeks. Participants provided informed consent before enrollment in this study, which was approved by the institutional review board.

On enrollment, waist circumference, weight, and height of all participants were measured. Waist circumference was measured at the middle point between the lower rim of the rib cage and iliac crest. The BMI was calculated as weight/height2 (kg/m2), and participants were classified into normal weight (BMI: 18–25 kg/m2), overweight (BMI: >25–30 kg/m2), or obese (BMI: >30 kg/m2).

Smokers and patients with metabolic syndrome, diabetes mellitus, autoimmune disorders acute or chronic infections, malignancies, pregnancy, polycystic ovary syndrome, renal, cardiac, or hepatic disorders were excluded. Patients on medications known to affect lipid metabolism (systemic retinoids, steroids) were also excluded.

Blood samples were drawn in the morning (9–11 a.m.) after a 12-h overnight fast. Serum was kept at −80°C for subsequent assay. Serum adiponectin levels and serum visfatin levels were assessed by enzyme-linked immunosorbent assay kits (Phoenix Pharmaceuticals Inc., Burlingame, California, USA) following the manufacturer’s instructions.

Statistical analysis

Statistical analysis of the data was done using SPSS version 21 program (SPSS Inc., Chicago, Illinois, USA). Data were expressed as mean and SD. Kruskal-Wallis test, t-test, and Pearson’s correlation coefficient test were used in the analysis. P value of less than 0.05 was considered significant.


  Results Top


Of 57 recruited patients with LP, 49 (85.9%) were enrolled in the study. They included 24 patients with cutaneous LP, 16 patients with mucocutaneous LP, and nine patients with oral LP. No statistically significant differences were detected between patients and controls regarding age, sex, BMI, and waist circumference (P>0.05) ([Table 1]). The mean±SD disease duration was 12.08±8.4 months.
Table 1 Characteristics of patients and controls

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Serum adiponectin level in patients with LP was significantly lower than that of the controls (<0.0001) ([Table 1]). It was also significantly lower in patients with cutaneous and mucocutaneous LP than those with oral LP (P=0.002) ([Figure 1]). Moreover, the serum adiponectin level was significantly lower in obese and overweight patients compared with normal weight patients (P=0.006).
Figure 1 Mean serum adiponectin (a) and visfatin (b) levels in different types of lichen planus compared with control.

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Serum visfatin level in patients with LP was significantly higher than that in the controls (P<0.0001) ([Table 1]). There was no statistically significant difference between cutaneous, mucocutaneous, and oral LP regarding serum visfatin level (P=0.123) ([Figure 1]). The serum visfatin level was significantly higher in obese and overweight patients compared with normal weight patients (P=0.241).

Serum adiponectin level showed a statistically significant inverse correlation with disease duration (P=0.005), whereas serum visfatin did not show a significant correlation with disease duration (P=0.343) ([Table 2]). In relation to obesity, serum adiponectin level showed a statistically significant inverse correlation with BMI and waist circumference in patients (P=0.001 and 0.003, respectively) and controls (P=0.001 and 0.012, respectively). Serum visfatin level showed a statistically significant positive correlation with BMI in patients and controls (P<0.0001, 0.032, respectively) and statistically significant positive correlation with waist circumference in patients only (P=0.018).
Table 2 Correlations between adipokines and disease duration, BMI, and waist circumference for patients and controls

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  Discussion Top


We have shown for the first time that adiponectin serum level decreased significantly in patients with LP compared with control and that it correlated inversely with disease duration, proposing adiponectin as a marker of LP chronicity. No data were found on serum adiponectin in patients with LP; however, Lopez-Jornet et al. [6] measured adiponectin in the saliva of patients with oral LP and reported no significant differences compared with the healthy controls. Low serum adiponectin level was reported in several inflammatory states, such as psoriasis[10], atopic dermatitis [11], and allergic rhinitis [12], whereas elevated adiponectin levels was reported in rheumatoid arthritis [13] and SLE[14].

Elevated serum TNF-α and IL-6 levels have been observed in patients with LP. TNF-α was reported to play a major role in the pathogenesis of LP [15]. Moreover, IL-6 has been suggested to promote the proliferation of keratinocytes and has been related to the process of epithelial hyperplasia seen in LP [16]. Given that adiponectin is reported to decrease TNF-α and IL-6 production, a protective function of adiponectin in LP may be suggested.

Cutaneous and mucocutaneous forms of LP had significantly lower adiponectin level compared with oral LP. As oral LP is a localized form of the disease, the levels of inflammation, immunological process, and cytokine release are limited, compared with the widely spread forms of LP. This is in concurrence with Sarkar et al. [17] study in which they reported higher serum leptin level in mucocutaneous LP than other forms.

In agreement with our results, adiponectin was found to be inversely correlated with markers of obesity, that is, BMI, waist circumference, and circulating leptin [18]. Obesity is associated with low levels of chronic inflammation; thus, inflammatory factors may regulate adiponectin levels [7]. Previous studies suggested that adiponectin may play a protecting role in coronary atherosclerosis and other obesity-related cardiovascular disorders [19],[20]. Therefore, decreased adiponectin level in patients with LP may represent a contributing factor for the increased prevalence of cardiovascular disease.

We have also shown for the first time that serum visfatin level is elevated in patients with LP.

No data were found on serum visfatin in the context of LP; however, increased visfatin plasma concentrations have been observed in various chronic inflammatory diseases such as psoriasis [21], rheumatoid arthritis [22], and inflammatory bowel disease [23]. However, decreased visfatin level was reported in atopic children [24].

The role of visfatin in LP pathogenesis may include alteration of the inflammatory or immunological response as it stimulates chemotaxis and enhances the production of IL-1, TNF, and IL-6. This enhances their capability to promote the proliferation of keratinocytes [25]. Visfatin is produced by cells involved in LP pathology; moreover, its serum level might be upregulated in response to the proinflammatory cytokines released during inflammation [7]. Visfatin may possibly present a link between LP and cardiovascular morbidity as it was proven to be increased in the atherosclerotic plaques in myocardial infarction [26].There are conflicting reported relations between visfatin and obesity. We did find significant positive correlation between serum visfatin level and obesity markers in patients with LP. In the literature, multiple studies reporting increased, unaffected, and decreased levels of visfatin. Weight loss was reported to either increase or decrease visfatin levels [9].

The novelty of the present study lies in the fact that it is the first to evaluate the relation between adiponectin, visfatin, and LP. These adipokines may represent a potential pharmacotherapeautic target against LP and its cardiovascular comorbidities.

In conclusion, our data suggested that adiponectin and visfatin act together through modulation of the inflammatory setting of patients with LP and that their irregularities may be one of the mechanisms behind the reported association between LP and cardiovascular disorders. Because of the significant correlations of adiponectin and visfatin with obesity markers, the complications of obesity should be emphasized to patients with LP.

Acknowledgements

A preliminary version of this work has been presented in the 2nd International Conference of Dermatology Department, Al-Azhar Assiut Faculty of Medicine (3 August 2017).

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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