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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 34  |  Issue : 2  |  Page : 130-134

Serum level of celiac disease-associated antigliadin antibodies in psoriatic patients


1 Department of Dermatology & Venereology, Tanta University, Tanta, Egypt
2 Department of Clinical Pathology, Tanta University, Tanta, Egypt

Date of Submission16-Jun-2014
Date of Acceptance14-Dec-2014
Date of Web Publication29-Jan-2015

Correspondence Address:
Nashwa N Elfar
MD, Department of Dermatology & Venereology, Faculty of Medicine, Tanta University, Tanta
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-6530.150274

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  Abstract 

Background
Antigliadin antibodies (AGA) are markers of celiac disease (CD). Elevated levels of these antibodies are also seen in many other autoimmune, neurological, hematological, collagen vascular, and cutaneous disorders, even in the absence of clinically overt gastrointestinal disease. The possible relationship between psoriasis and CD has been attributed to the common pathogenic mechanisms of the two diseases.
Aim of work
The aim of the study was to assess the prevalence of serum level of immunoglobulin A [(IgA); AGA] in psoriatic patients and its correlation with disease severity.
Patients and methods
This study included 60 patients with psoriasis in whom severity was assessed with the Psoriasis Area and Severity Index (PASI) score, in addition to 30 healthy individuals who served as controls. Blood samples were taken from all patients and controls for detection of serum IgA (AGA) level by means of the enzyme-linked immunosorbent assay.
Results
A highly significant increase was found in the mean serum level of IgA (AGA) in psoriatic patients compared with controls. The serum level of IgA (AGA) was significantly correlated with the severity of psoriasis and with a history for food intolerance.
Conclusion
A high serum IgA (AGA) positivity rate was detected in severe psoriatic patients, and therefore these patients are at risk for latent and/or overt CD. Serological evaluation for serum level of IgA (AGA) should be considered in patients with severe psoriasis and a gluten-free diet must be prescribed.

Keywords: Antigliadin antibodies, celiac disease, psoriasis


How to cite this article:
Elfar NN, Elbandari AS. Serum level of celiac disease-associated antigliadin antibodies in psoriatic patients. Egypt J Dermatol Venerol 2014;34:130-4

How to cite this URL:
Elfar NN, Elbandari AS. Serum level of celiac disease-associated antigliadin antibodies in psoriatic patients. Egypt J Dermatol Venerol [serial online] 2014 [cited 2020 May 28];34:130-4. Available from: http://www.ejdv.eg.net/text.asp?2014/34/2/130/150274


  Introduction Top


Psoriasis (PS) is a common, chronic, disfiguring inflammatory disease of the skin characterized in most cases by well-defined scaly, red, and indurated plaques mainly over extensor surfaces but also often involving other areas of the body [1]. It is considered to be a genetically programmed disease of dysregulated inflammation, which is driven and maintained by multiple components of the immune system [2]. Celiac disease (CD) is an immunomediated enteropathy caused by permanent intolerance to dietary wheat gliadin in predisposed individuals [3]. It is characterized clinically by malabsorption and histologically by villous atrophy and crypt hyperplasia [4]. Many autoimmune disorders, such as dermatitis herpetiformis, thyroiditis, and diabetes mellitus, are associated with CD [5]. Previous studies have shown a high prevalence of immunoglobulin A (IgA) antibodies to gliadin (AGA) in patients affected by PS and showed that a gluten-free diet (GFD) significantly improved the psoriatic lesions [6],[7].

It is not easy to explain the possible links between PS and gluten-sensitive enteropathy, especially CD. Keratinocyte hyperproliferation in PS produces a broad spectrum of cytokines, in particular interleukin (IL)-1 and IL-18. These two potent inductors of interferon-g, tumor necrosis factor, and other mediators play an important role in inducing a T-helper 1 response [8]. The mucosal inflammation of the small bowel in CD is also caused by Th1 activation, in response to dietary gluten. IL-18 is capable of promoting T-cell interferon-g production and facilitating T-helper 1 cell polarization. These results are suggestive of an interplay between skin, intestinal cells, and lymphocyte activation, the mechanism of which is unknown [9]. The relationship between CD and PS remains controversial as there are few and contrasting data on this topic, with some authors maintaining that the association between CD and PS is coincidental [10].

Hence, this work aimed to assess the prevalence of serum level of IgA (AGA) in psoriatic patients and study its correlation with disease severity.


  Patients and methods Top


This study included 60 psoriatic patients in active phase (36 male and 24 female), their ages ranging from 8 to 85 years, with a mean of 42.32 ± 17.34 years, and 30 healthy individuals as controls, who were sex and age matched with the studied patients. The control group comprised 16 male and 14 female individuals, their ages ranging from 15 to 58 years, with a mean of 38.63 ± 14.22 years. They were recruited from the Outpatient Clinic of Dermatology and Venereology Department, Tanta University Hospital, during January 2012 to December 2012. The study was approved by the Research Ethics Committee. All participants signed an informed consent form before participating in the study.

The patients were subjected to the following: (a) full history taking, including personal history, past history of food intolerance (e.g. for wheat or milk products), malabsorption and other skin or systemic diseases, previous treatment and the date of stoppage of the last treatment modality, history of drug intake (e.g. lithium, antimalarial medication, β-blockers, angiotensin-converting-enzyme inhibitors, corticosteroids, and tetracycline), and family history of PS. Patients who received medical treatment or phototherapy in the last 6 weeks, as well as pregnant and lactating women, were excluded from the study. (b) Full clinical examination, including a complete dermatological examination for each patient to determine the extent and distribution of the disease. Clinical severity of PS was assessed by using the Psoriasis Area and Severity Index (PASI) score [11]. (c) Estimation of serum level of IgA (AGA) [12].

Sample collection

Venous blood of 2 ml were drawn from each patient. The blood sample was left to clot for 30 min at room temperature and then subjected to centrifugation for 15 min at Ნ1000 × g to separate the serum. The serum samples were removed using a sterile pipette and stored at −20°C until use, avoiding repeated freeze-thaw cycles.

Principles of the procedure

Solid-phase enzyme-linked immunosorbent assay is based on the sandwich principle. The wells are coated with antigen. Specific antibodies of the sample binding to the antigen-coated wells are detected with a secondary enzyme-conjugated antibody (E-Ab) specific for human IgA. After the substrate reaction the intensity of the color developed is proportional to the amount of IgA-specific antibodies detected.

The data obtained are quantitatively evaluated with a standard curve using a conventional enzyme-linked immunosorbent assay evaluation program. A good fit is provided with a 4-parameter function or spline approximation. The obtained absorbance value (ODs) of the calibrators (y-axis, linear) is plotted against their concentration (x-axis, logarithmic). The concentration of the samples can be read directly from the standard curve. The initial dilution has been taken into consideration when reading the results from the graph. Results of samples of higher predilution have to be multiplied with the dilution factor.

Elevated values indicate the presence of IgA (AGA) and suggest the possibility of certain gluten-sensitive enteropathies such as CD. Values less than 120 U/ml are interpreted as normal and those more than or equal to 320 U/ml are interpreted as elevated IgA (AGA).

Statistical analysis was conducted using the statistical package for social sciences for Windows, V. 20. The range, mean, SD, median, and the χ2 -test were used for statistical analysis. Correction for χ2 was carried out with Fisher's exact test or the Monte Carlo test. The Kolmogorov - Smirnov test, the Shapiro - Wilk test, the D'Agstino test, histograms, and Q - Q plots were used for vision test. The Mann - Whitney test, Kruskal - Wallis test, and Spearman's coefficient correlation were also used.


  Results Top


Regarding the severity of disease according to the PASI score in the studied psoriatic patients, 37 patients (61.66%) were classified as having mild PS; of them 16 patients (59.3%) had a positive history for food intolerance and 21 patients (63.6%) were negative. Moderate PS was found in 18 patients (30%); of them six patients (22.2%) had a positive history for food intolerance and 12 patients (36.4%) were negative. Severe PS was seen in five patients (8.33%), and all of them (18.5%) had a positive history for food intolerance. There was a statistically positive relation between severity of disease and history of food intolerance in the studied patients: higher the severity of PS, higher the positivity rate for history of food intolerance [Table 1].
Table 1: Relation between history of food intolerance and PASI score in patients

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The serum level of IgA (AGA) in psoriatic patients was elevated, ranging from 0.0 to 2600.0 U, with a mean of 481.31 ± 462.5, in comparison with the control group, in which it ranged from 0.0 to 730.0 U, with a mean of 200.26 ± 192.3. The mean serum levels of IgA (AGA) in psoriatic patients were markedly higher than that in the control group, with a highly statistically significant difference (P < 0.001) [Table 2].
Table 2: Comparison between the studied psoriatic patients and control groups as regards serum level of IgA (AGA)

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With regard to the serum level of IgA (AGA) in relation to the PASI score of the studied patients, in mild PS patients it ranged from 0.0 to 1250.0 U, with a mean of 372.9 ± 274.4; in moderate PS patients, it ranged from 0.0 to 1200.0 U, with a mean of 409.2 ± 331.6; and in severe PS patients it ranged from 867.0 to 2600.0 U, with a mean of 1543.4 ± 684.4. There was a highly statistically significant positive relation between IgA (AGA) serum level and severity of the studied patients (P = 0.002). There was statistically positive significance between the mild and severe groups and also between the moderate and severe groups, whereas no significance was detected between the mild and moderate groups, revealing that the serum level of IgA (AGA) was much higher in severe PS patients than in both mild and moderate PS patients [Table 3].
Table 3: Relation between serum IgA (AGA) and severity in psoriatic patients

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With regard to the serum level of IgA (AGA) in relation to the history of food intolerance in psoriatic patients, in the positive group (27 patients) it ranged from 220.0 to 2600.0 U, with a mean of 785.0 ± 536.6, whereas in the negative group (33 patients) it ranged from 0.0 to 600.0 U, with a mean of 232.8 ± 138.0. There was high statistically positive significance between IgA (AGA) serum level and history of food intolerance in psoriatic patients (P ≤ 0.001) [Table 4].
Table 4: Relation between serum IgA (AGA) and history of food intolerance in psoriatic patients group

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  Discussion Top


PS is a chronic, relapsing form of dermatosis, with immune mechanisms having an important role in its pathogenesis [13]. CD is a chronic autoimmune enteropathy occurring in genetically predisposed individuals following ingestion of wheat gluten and related protein fractions of other grains [14]. Some reports have appeared about a probable association of PS with enteropathy, and about a contribution of intestinal processes to skin lesions [12],[15]. Hence, this study was undertaken to assess the prevalence of serum AGA in psoriatic patients and its correlation with disease severity.

Our results revealed that the serum level of IgA (AGA) was significantly higher in psoriatic patients as compared with controls. These results were in agreement with previous studies conducted in Europe, which found positive AGA levels in 16% of included patients with PS [7],[16]. These results are also consistent with those of Michaelsson et al. [17], who reported a positivity for IgA (AGA) and/or IgG in 302 cases of PS. Also, Nagui et al. [18] found a significantly higher level of AGA in patients with PS compared with controls, with significant statistical difference. In addition, a study conducted by Danesh-Pajouh et al. [19] has reported positivity for IgA (AGA) in 10 psoriatic patients.

However, a study conducted in the USA found no significant difference in the prevalence of AGA between patients with PS and controls. This may reflect epidemiological differences in the underlying prevalence of CD between these populations. Kia et al. [20] found no significant difference in their levels among psoriatic patients, psoriatic arthritic patients, and controls. In a study of palmoplantar pustulosis, it was found that 24% of patients had IgA (AGA) [21]. They reported that palmoplantar pustulosis may be an autoimmune disease in which autoantigen(s) are localized to the dermal papillary endothelium and which is associated with both nicotinic acetylcholine receptor antibodies and antibodies to gliadin and thyroglobulin [22].

Our results revealed significant correlation between the serum level of IgA (AGA) and PASI score; all severe psoriatic patients in the present study were positive for IgA (AGA), which agrees with the results of a previous study where in psoriatic patients correlated with greater disease severity (increase in PASI score) [12]. The numbers of CD3+ and CD8+ lymphocytes in the epithelium were found to be increased in patients with AGA, which led to increased severity of PS and increased PASI scores and after a period of GFD led to significant decrease in PASI score [23]. An improvement in PS skin lesions was seen after 3-6 months of GFD without other pharmacological approaches [7].

With regard to the relation between history of food intolerance and serum level of IgA (AGA), a statistically significant positive correlation was found. These results are in accordance with those of Lindqvist and colleagues, who reported that 16% of their AGA‐positive and 11% of their AGA‐negative patients were intolerant of gluten and/or milk. Four of the patients with milk intolerance had abnormal results on a lactose tolerance test; in the other patients no attempts were made to verify food intolerance [6]. This could be explained by the fact that lactose is a sugar found in dairy products, and to be digested it must be broken down by an enzyme called lactase. Lactase is produced on the tips of villi in the small intestine. As gluten damages the villi, it is common for untreated celiac patients to have problems with milk and milk products. A GFD will usually eliminate lactose intolerance [24].

The pathogenetic mechanism responsible for the association between PS and gluten sensitivity may be the increased risk of vitamin D deficiency that influences T-cell activation and modulates the phenotype and function of antigen-presenting cells and dendritic cells. Moreover, exposure to gliadin will trigger a CD4 T-cell response. The increased number of T cells in the blood may also affect the dermis and epidermis, thereby stimulating the development of PS. In addition, it has been shown that the gliadin fraction of wheat gluten is strongly associated with the development of intestinal damage, as preformed zonulin is released in the presence of gliadin, leading to barrier dysfunction (increased intestinal permeability) and passage of gliadin into the subepithelial compartment [25].


  Conclusion Top


A high serum IgA (AGA) positivity rate was detected in severe psoriatic patients, and therefore these patients are at risk for latent and/or overt CD. Serological evaluation for serum level of IgA (AGA) should be considered in severe PS and a GFD must be prescribed.


  Acknowledgements Top


Conflicts of interest

None declared.

 
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  [Table 1], [Table 2], [Table 3], [Table 4]



 

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