|Year : 2017 | Volume
| Issue : 4 | Page : 223-227
Evaluation of serum periostin level in atopic dermatitis patients
Afaf H Ghanem1, Fathia M Khattab1, Amal Zidan2
1 Dermatology, Venereology and Andrology and Departments, Faculty of Medicine, Zagazig University, Egypt
2 Clinical Pathology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt
|Date of Submission||20-Jan-2018|
|Date of Acceptance||22-May-2018|
|Date of Web Publication||19-Jul-2018|
Fathia M Khattab
Lecturer of Dermatology, Venereology and Andrology Department, Faculty of Medicine, Zagazig University, 44519
Source of Support: None, Conflict of Interest: None
Background Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease. Periostin is an intrinsic mediator induced by T helper-2 cytokines. It has been reported to play a critical role in the pathogenesis of AD.
Objective The objective of this study was to estimate the serum periostin level in AD patients and to determine its correlation with the severity and chronicity of the disease.
Patients and methods This study included 36 AD patients and 36 healthy controls, matched for age and sex. Three millimeters of venous blood was collected from each patient. Serum periostin level was determined by enzyme-linked immunosorbent assay. We determined the correlation between serum periostin level, duration of disease, severity, type of atopy, and SCORAD score.
Results There were highly significant differences between patients and controls as regards serum periostin level (P<0.001). There were significant differences between severe AD patients in serum periostin level, with an increased level among those with severe degree (P<0.001). There were significant differences in serum periostin level among the widespread type (P=0.03). Furthermore, there were significant positive correlations between periostin level and both duration and SCORAD score of the patient group.
Conclusion Serum periostin level may correlate with disease severity and chronicity in patients with AD.
Keywords: atopic dermatitis, periostin, severity
|How to cite this article:|
Ghanem AH, Khattab FM, Zidan A. Evaluation of serum periostin level in atopic dermatitis patients. Al-Azhar Assiut Med J 2017;15:223-7
|How to cite this URL:|
Ghanem AH, Khattab FM, Zidan A. Evaluation of serum periostin level in atopic dermatitis patients. Al-Azhar Assiut Med J [serial online] 2017 [cited 2018 Dec 17];15:223-7. Available from: http://www.azmj.eg.net/text.asp?2017/15/4/223/237131
| Introduction|| |
Atopic dermatitis (AD) is a chronic, inflammatory skin disease characterized by defective skin barrier and allergic skin inflammation with dominant T helper-2 (Th2) type immune response. The etiology of AD is not fully understood, but evidence has revealed a complex involvement of both innate, adaptive immune responses and environmental factors with activation of keratinocytes .
Periostin is a matricellular protein, which has emerged as a novel mediator in allergic diseases such as AD. It is induced by interleukin-4 and interleukin-13 (Th2-related cytokines) ,. Periostin provides signals for tissue remodeling through its interaction with integrin − a cell surface molecule ,. Periostin has a role in wound repair, cardiac development, and tumorigenesis. Periostin is expressed in various tissues. It is highly expressed in the skin more than in other organs, as the skin is an environment rich in fibroblasts, which is a major source of periostin ,,. It has been hypothesized that periostin acts as an intrinsic mediator in amplifying and maintaining allergic skin inflammation ,,. Previous studies have suggested that periostin can serve as a biomarker for asthma diagnosis, and it is correlated with asthma severity. Periostin has a unique function as an inflammatory mediator linking immune cells and resident cells in inflamed lesions ,,,. The aim of this study was to estimate the serum periostin level in AD patients and to determine the correlation between this level and severity and chronicity of AD.
| Patients and methods|| |
This is a case–control study that included 36 (14 male and 22 female) patients with AD, with age ranging from 3 to 18 years, and 36 healthy age-matched and sex-matchedcontrols. Patients were recruited from the Dermatology Outpatient’s Clinics at Zagazig University Hospital during the period from December 2014 to December 2015 after approval of the Institutional Review Board. Diagnosis in each patient will be made on the basis of history and clinical examination according to criteria of Hanifen and Rajk.
The inclusion criteria were as follows:
- Patients had AD through at least 2 years before the start of the study.
- Patients of any age and sex.
- Patients may have a history of asthma but not active during the study.
The exclusion criteria were as follows:
- Patients with active asthma.
- Patients with other chronic dermatological diseases.
- Patients with AD less than 2 years before the start of the study.
- Patients with bleeding tendency.
- Patients with fever.
- Patients with active viral, bacterial, or fungal infections.
- The present study included 36 AD patients and 36 healthy age-matched and sex-matched controls. Complete history taking, general examination of body systems, and detailed dermatological examination were performed for all patients.
- Three millimeters of venous blood was collected from each patient. Serum periostin level was determined by enzyme-linked immunosorbent assay (ELISA). We determined the correlation between serum periostin level, duration of disease, severity, type of atopy, and SCORAD score.
- Measurement of AD severity by SCORAD score. The SCORAD index consists of the interpretation of the extent of the disorder, that is, the intensity, composed of six items (erythema, edema/papules, effect of scratching, oozing/crust formation, lichenification, and dryness), and two subjective symptoms (itch and sleeplessness);  the maximum score is 103 points. Classification of the severity of AD for the SCORAD index is as follows: mild, 0–24; moderate, 25–50; and severe, 51–103.
- Measurement of serum periostin level by ELISA. Three milliliters of blood samples were collected and immediately centrifuged at 2000g for 15 min at −4°C. The serum was collected and stored at −80°C. Human Periostin ELISA Kit (RAB1075; Sigma, St. Louis, MO, United States) was used to detect serum level of periostin
The collected data were computerized and statistically analyzed using statistical package for the social sciences program (SPSS) version 18.0 (SPSS Inc. Released 2009, PASW Statistics for Windows, Version 18.0, Chicago: SPSS Inc.).
Qualitative data were represented as frequencies and relative percentages. Quantitative data were expressed as mean±SD.
χ2-Test was used to calculate the difference between qualitative variables. Independent t-test was used to calculate the difference between quantitative variables in two groups in normally distributed data.
Mann–Whitney test was used to calculate the difference between quantitative variables in two groups in non-normally distributed data. Analysis of variance F-test test was used to calculate the difference between quantitative variables in more than two groups in normally distributed data.
Pearson’s correlation coefficient used to calculate the correlation between quantitative variables. A P value less than 0.05 was considered to be significant.
| Results|| |
This study included 36 AD patients with a mean of 9.64±6.24. Among the patients, 22 (61.1%) were female and 14 (38.9%) were male. Controls were 36 individuals with a mean of 7.03±3.33. Among the controls, 18 (50%) were female and 18 (50%) were male. There were no significant differences between patients and controls in age or in sex distribution ([Table 1]). The mean duration of the disease among the patient group was 7.36±3.67. The SCORAD score was 43.1±19.24 ([Table 2]). Localized type was present in 29 (80.6%) patients, whereas widespread type was present in seven (19.4%) patients. Type of disease and site of lesions are shown in [Table 3].
Mean serum periostin level of the patients was 170.14±38.23, whereas in controls it was 60.39±13.76. There was a highly significant difference between patients and controls in serum periostin level (P<0.001) ([Table 4]). There was no significant difference between male and female individuals of the patient group in serum periostin level (P=0.27) ([Table 5]). According to SCORAD score of disease severity, there were highly significant differences with disease severity, with an increased level among patients with severe disease (P<0.001) ([Table 6]).
|Table 5 Relation between serum periostin level and sex of the patient group|
Click here to view
|Table 6 Relation between serum periostin level and severity of atopic dermatitis of the patient group|
Click here to view
As regards the extent of the disease. There were significant differences between spread and localized AD patients in serum periostin level, with an increased level among widespread patients (P=0.03). There was no significant difference between localized types (P=0.71) ([Table 7]).
|Table 7 Relation between serum periostin level and atopic dermatitis type of the patient group|
Click here to view
There was a negative correlation between serum periostin level and age, whereas there was a highly significant positive correlation between serum periostin level and SCORAD score (P<0.001). There was a significant positive correlation between serum periostin level and duration of disease (P=0.04) ([Figure 1] and [Figure 2]).
|Figure 1 Correlation between serum periostin level of the patient group and SCORAD score.|
Click here to view
|Figure 2 Correlation between serum periostin level of the patient group and duration.|
Click here to view
| Discussion|| |
AD is chronic inflammatory skin disease characterized by remission and exacerbation; the underlying mechanism for this unstable course is not fully elucidated . It has been reported that persistence of allergic skin inflammation in AD results from Th2 cytokine, which induces periostin. Moreover, periostin is an intrinsic mediator that has a role in keratinocyte activation and in amplifying the inflammation ,,,. It was discovered as a novel mediator in allergic diseases.
The aim of this study was to estimate the serum periostin level in AD patients and to determine the correlation between this level and severity and chronicity of AD.
In this study, mean serum periostin level of the patients was 170.14±38.23 compared with 60.39±13.76 in the controls. There was a highly statistically significant difference in serum periostin level between patients and controls (P<0.001).
In agreement with these results, Masuoka et al.  found in their study that serum levels of periostin were highly significantly elevated in AD patients (P<0.001). In addition, periostin is highly expressed in skin tissues of AD patients.
Kou et al.  found that the level of periostin in patients with the AD ranged from 96 to 224, with a mean of 144 ng/ml; periostin level in healthy controls ranged from 49 to 63, with a mean of 56 ng/ml. There was a highly significant elevation in serum periostin level in patients with AD compared with healthy controls (P<0.0001). These results were similar to our study results.
In this study, the mean serum periostin level in mild patients was 115.6±12.31 ng/ml, in moderate AD patients it was 153.12±20.28 ng/ml, and in severe AD patients it was 206.47±19.06 ng/ml. There were highly significant differences in serum periostin level between mild, moderate, and severe patients (P<0.001).
In agreement with the current study, Masuoka et al.  grouped AD patients into mild (11.1%), moderate (40.7%), and marked (48.1%). They concluded that serum periostin level is correlated with disease severity (P<0.01).
In contrast to the results of the present study, Kou et al.  showed that there was no significant difference in serum periostin level between patients with mild and moderate disease, whereas patients with severe or very severe disease had considerably higher levels of serum periostin than those with mild or moderate diseases, and thus level of serum periostin was significantly elevated in patients with severe or very severe disease (P<0.01).
Kou et al.  classified their patients into mild (16.3%), moderate (36.9%), severe (28.7%), and very severe (17.8%). The mean of serum level of periostin was 104.0 ng/ml in mild patients, 122.0 ng/ml in moderate patients, 157.5 ng/ml in severe patients, and 241.0 ng/ml in very severe patients.
These findings may be because the determination of disease severity in our study was based on SCORAD score, whereas in the study by Kou et al.  disease severity was based on a simple classification system following Japanese guidelines for the AD as mild, moderate, severe, and very severe. In addition, in the present study, we included 36 AD patients of any age, whereas Kou et al.  included a large number of adult atopic patients.
In this study, mean serum periostin level in the widespread type was 198 ng/ml compared with 163.41 in the localized type; there were significant differences between widespread and localized patients in serum periostin level (P=0.03), with an increased level among widespread patients.
Kou et al.  found that serum periostin level is significantly higher in patients with erythroderma type followed by widespread type compared with other clinical types (P<0.01). However, patients with AD with lesions that were not distributed systemically, such as limbs type, had lower level of periostin. Kou et al.  found that level of serum periostin was correlated with clinical types of AD.
In the present study, there were highly significant positive correlations between serum periostin level and SCORAD score (P<0.001). There were significant positive correlations between serum periostin level and duration of the disease (P=0.04). Another study  found a positive correlation between the periostin serum level and SCORAD score (P=0.001), which was consistent with our results.
Discovering the role of periostin in the mechanisms underlying tissue remodeling may lead to novel therapeutic strategies against chronic allergic inflammatory diseases in the near future.
Serum periostin levels appear to be novel potential clinical biomarkers that can predict the efficacy of treatment in AD disease and in asthma patients with inadequately controlled disease despite glucocorticoid therapy .
This study was limited by the small number of patients. Further large studies are recommended to confirm that serum periostin level could be used as a biomarker in the pathogenesis of AD.
| Conclusion|| |
Serum periostin level is correlated with disease severity and chronicity in patients with AD, suggesting that periostin may play an important role in the pathogenesis of AD.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Leung DY, Boguniewicz M, Howell MD et al.
New insights into atopic dermatitis. J Clin Invest 2004; 113:651–657.
Conway SJ, Izuhara K, Kudo Y et al.
The role of periostin in tissue remodeling across health and disease. Cell Mol Life Sci 2014; 71:1279–1288.
Kou K, Okawa T, Yamaguchi Y et al.
Periostin levels correlate with disease severity and chronicity in patients with atopic dermatitis. Br J Dermatol 2014; 171:283–291.
Yamaguchi Y, Ono J, Masuoka M et al.
Serum periostin levels are correlated with progressive skin sclerosis in patients with systemicsclerosis. Br J Dermatol 2013; 168:717–725.
Tilman G, Mattiussi M, Brasseur F et al.
Human periostin gene expression in normal tissues, tumors and melanoma: evidences for periostin production by both stromal and melanoma cells. Mol Cancer 2007; 17:80.
Masuoka M, Shiraishi H, Ohta S et al.
Periostin promotes chronic allergic inflammation in response to Th2 cytokines. J Clin Invest 2012; 122:2590–2600.
Izuhara K, Arima K, Ohta S et al.
Periostin in allergic inflammation. Allergol Int 2014; 63:143–151.
Kudo A. Periostin in fibrillogenesis for tissue regeneration: periostin actions inside and outside the cell. Cell Mol Life Sci 2011; 68:3201–3207.
Nishiyama T, Kii I, Kashima TG et al.
Delayed re-epithelialization in periostin-deficient mice during cutaneous wound healing. PLoS One 2011; 6:e18410.
Ontsuka K, Kotobuki Y, Shiraishi H et al.
Periostin, a matricellular protein, accelerates cutaneous wound repair by activating dermal fibroblasts. Exp Dermatol 2012; 21:331–336.
Ohta S, Taniguchi K, Arima K et al.
Establishment of novel biomarkers for personalized medication for atopic dermatitis. Rinsho Byori 2013; 61:247–255.
Ohta S, Okamoto M, Fujimoto K et al.
The usefulness of monomeric periostin as a biomarker for idiopathic pulmonary fibrosis. PLoS One 2017; 12:e0174547.
Shiraishi H, Masuoka M, Ohta S et al.
Periostin contributes to the pathogenesis of atopic dermatitis by inducing TSLP production from keratinocytes. Allergol Int 2012; 61:563–572.
Oyoshi MK, He R, Kumar L. Cellular and molecular mechanisms in atopic dermatitis. Adv Immunol 2009; 102:135–226.
Takayama G, Arima K, Kanaji T et al.
Periostin: a novel component of subepithelial fibrosis of bronchial asthma downstream of IL-4 and IL-13 signals. J Allergy Clin Immunol 2006; 118:98–104.
Kii I, Nishiyama T, Li M et al.
Incorporation of tenascin-C into the extracellular matrix by periostin underlies an extracellular meshwork architecture. J Biol Chem 2010; 285:2028–2039.
Norris RA, Damon B, Mironov V et al.
Periostin regulates collagen fibrillogenesis and the biomechanical properties of connective tissues. J Cell Biochem 2007; 101:695–711.
Maruhashi T, Kii I, Saito M et al.
Interaction between periostin and BMP-1 promotes proteolytic activation of lysyl oxidase. J Biol Chem 2010; 285:13294–13303.
Sung MS, Lee KS, Ha EG. An association of periostin levels with the severity and chronicity of atopic dermatitis in children. Pediatr Allergy Immunol 2017; 28:543–550.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]