|Year : 2017 | Volume
| Issue : 2 | Page : 122-126
Serum levels of adiponectin and visfatin in patients with lichen planus: a case-controlled study
Sahar A Ismail1, Ibrahim Mwafey2, Sotohy A Mohamed3
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 Submission||14-Aug-2017|
|Date of Acceptance||12-Sep-2017|
|Date of Web Publication||21-Nov-2017|
Sahar A Ismail
Department of Dermatology, Venereology and Andrology, Assiut University Hospital, Assiut University, 71515 Assiut
Source of Support: None, Conflict of Interest: None
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 Mar 22];15:122-6. Available from: http://www.azmj.eg.net/text.asp?2017/15/2/122/218856
| Introduction|| |
Lichen planus (LP) is a chronic T-cell-mediated inflammatory disease affecting skin and mucous membrane . It has been linked to a growing threat of cardiovascular risk factors including obesity, diabetes, dyslipidemia, hypertension, and metabolic syndrome ,,. Chronic inflammation is the eventual pathological process that causes both skin manifestations and the associated comorbidities .
Adipokines are key players in the pathogenesis of metabolic syndrome through their effect on vascular function, immune regulation, and adipocyte metabolism . A single study exists on adiponectin in the context of LP  but none on visfatin. However, data from other inflammatory diseases suggest a possible role of these adipokines in LP pathophysiology .
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 . 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 ,,.
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 . 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 .
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|| |
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 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|| |
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.
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|| |
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.  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, atopic dermatitis , and allergic rhinitis , whereas elevated adiponectin levels was reported in rheumatoid arthritis  and SLE.
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 . 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 . 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.  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 . Obesity is associated with low levels of chronic inflammation; thus, inflammatory factors may regulate adiponectin levels . Previous studies suggested that adiponectin may play a protecting role in coronary atherosclerosis and other obesity-related cardiovascular disorders ,. 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 , rheumatoid arthritis , and inflammatory bowel disease . However, decreased visfatin level was reported in atopic children .
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 . 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 . 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 .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 .
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.
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
Conflicts of interest
There are no conflicts of interest.
| References|| |
Manolsche L, Seceleanu-Petrescu D, Benea V, Manolache DV. Lichen planus patients and stressful events. J Eur Acad Dermatol Venereol 2008; 22:437–441.
Arias-Santiago S, Buendía-Eisman A, Aneiros-Fernández J, Girón-Prieto MS, Gutiérrez-Salmerón MT, Mellado VG, Naranjo-Sintes R. Cardiovascular risk factors in patients with lichen planus. Am J Med 2011; 124:543–548.
Dreiher J, Shapiro J, Cohen AD. Lichen planus and dyslipidaemia: a case–control study. Br J Dermatol 2009; 161:626–629.
Saleh N, Samir N, Megahed H, Farid E. Homocysteine and other cardiovascular risk factors in patients with lichen planus. J Eur Acad Dermatol Venereol 2014; 28:1507–1513.
Blüher M, Mantzoros CS. From leptin to other adipokines in health and disease: facts and expectations at the beginning of the 21st century. Metabolism 2015; 64:131–145.
Lopez-Jornet P, Cayuela CA, Tvarijonaviciute A, Parra-Perez F, Escribano D, Ceron J. Oral lichen planus: salival biomarkers cortisol, immunoglobulin A, adiponectin. J Oral Pathol Med 2016; 45:211–217.
Gerdes S, Rostami-Yanzdi M, Mrowietz U. Adipokines and psoriasis. Exp Dermatol 2011; 20:81–87.
Mamali I, Roupas ND, Armeni AK, Theodoropoulou A, Markou KB, Georgopoulos NA. Measurement of salivary resistin, visfatin and adiponectin levels. Peptides 2012; 33:120–124.
Luk T, Malam Z, Marshall JC. Pre-B cell colony enhancing factor (PBEF)/visfatin: a novel mediator of innate immunity. J Leukoc Biol 2008; 83:804–816.
Zhu KJ, Shi G, Zhang C, Li M, Zhu CY, Fan YM. Adiponectin levels in patients with psoriasis: a meta-analysis. J Dermatol 2013; 40:438–442.
Han B, Wu WH, Bae JM, Son SJ, Lee JH, Han TY. Serum leptin and adiponectin levels in atopic dermatitis (AD) and their relation to disease severity. J Am Acad Dermatol 2016; 75:629–631.
Hsueh K-C, Lin Y-J, Lin HC, Lin C-Y. Serum leptin and adiponectin levels correlate with severity of allergic rhinitis. Pediatr Allergy Immunol 2010; 21:e155–e159.
Chen X, Lu J, Bao J, Guo J, Shi J, Wang Y. Adiponectin: a biomarker for rheumatoid arthritis? Cytokine Growth Factor Rev 2013; 24:83–89.
Fantuzzi G. Adiponectin and inflammation: consensus and controversy. J Allergy Clin Immunol 2008; 121:326–330.
Erdem MT, Gulec AI, Kiziltunc A, Yildirim A, Atasoy M. Increased serum levels of tumor necrosis factor alpha in lichen planus. Dermatology 2003; 207:367–370.
Abdel-Haq A, Kusnierz-Cabala B, Darczuk D, Sobuta E, Dumnicka P, Wojas-Pelc A, Chomyszyn-Gajewska M. Interleukin-6 and neopterin levels in the serum and saliva of patients with Lichen planus and oral Lichen planus. J Oral Pathol Med 2014; 43:734–739.
Sarkar M, Dayal S, Samanta S, Ghalaut VS, Malik I, Sehgal PK. Serum leptin and lipid profile in lichen planus: a case control study. Int J Health Sci Res 2015; 5:129–135.
Kaur S, Zilmer K, Leping V, Zilmer M. The levels of adiponectin and leptin and their relation to other markers of cardiovascular risk in patients with psoriasis. J Eur Acad Dermatol Venereol 2011; 25:1328–1333.
Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005; 352:1685–1695.
Li RC, Krishnamoorthy P, DerOhannessian S, Doveikis J, Wilcox M, Thomas P et al.
Psoriasis is associated with decreased plasma adiponectin levels independently of cardiometabolic risk factors. Clin Exp Dermatol 2014; 39:19–24.
Ismail SA, Mohamed SA. Serum levels of visfatin and omentin-1 in patients with psoriasis and their relation to disease severity. Br J Dermatol 2012; 167:436–439.
Otero M, Lago R, Gomez R, Lago F, Dieguez C, Gómez-Reino JJ, Gualillo O. Changes in plasma levels of fat-derived hormones adiponectin, leptin, resistin and visfatin in patients with rheumatoid arthritis. Ann Rheum Dis 2006; 65:1198–1201.
Moschen AR, Kaser A, Enrich B, Mosheimer B, Theurl M, Niederegger H, Tilg H. Visfatin, an adipocytokine with proinflammatory and immunomodulating properties. J Immunol 2007; 178:1748–1758.
Machura E, Szczepanska M, Ziora K, Ziora D, Swietochowska E, Barc-Czarnecka M, Kasperska-Zajac A. Evaluation of adipokines: apelin, visfatin, and resistin in children with atopic dermatitis. Mediators Inflamm 2013; 2013:760691.
Gerdes S, Osadtschy S, Rostami-Yazdi M, Buhles N, Weichenthal M, Mrowietz U. Leptin, adiponectin, visfatin and retinol-binding protein-4–mediators of comorbidities in patients with psoriasis? Exp Dermatol 2012; 21:43–47.
Dahl TB, Yndestad A, Skjelland M, Øie E, Dahl A, Michelsen A et al.
Increased expression of visfatin in macrophages of human unstable carotid and coronary atherosclerosis: possible role in inflammation and plaque destabilization. Circulation 2007; 115:972–980.
[Table 1], [Table 2]