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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 30  |  Issue : 3  |  Page : 935-939

Screening of Helicobacter pylori in alopecia areata patients


1 Department of Dermatology, Andrology and STIs, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Dermatology, Andrology and STIs, El-Bagour Central Hospital, Menoufia, Egypt

Date of Submission25-Sep-2016
Date of Acceptance02-Dec-2016
Date of Web Publication15-Nov-2017

Correspondence Address:
Heba Rashad
Department of Dermatology, Andrology and STIs, El-Bagour Central Hospital, Shebin El-Kom, Menoufia, 32511
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.218293

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  Abstract 

Objectives
The aim of the present study was to clarify whether Helicobacter pylori plays a role in the pathogenesis of alopecic areata or not.
Background
Alopecia areata (AA) is an immune-mediated form of hair loss that occurs in all ethnic groups, ages, and both sexes. H. pylori has been associated with many extradigestive dermatological conditions. The causal relation between AA and H. pylori is discussed in this study.
Patients and methods
We screened patients with AA for the presence of H. pylori to determine any potential role in its pathophysiology. We prospectively studied 30 patients with AA and 20 healthy volunteers (control group) of similar sex for the presence of H. pylori stool antigen (HpSAg) (which is available according to the protocol) from February 2015 to January 2016 at El-Bagour Central Hospital.
Results
The values for H. pylori infection were positive in 25 of the 30 (83.3%) patients evaluated, whereas in five (16.7%) patients, the values did not support H. pylori infection. In the control group, seven out of 20 (35%) had positive results. There was a high significant difference between the patients (83.3%) and control (35%) groups as regards positivity of HpSAg. Furthermore, as per the quantitative estimation of the level of HpSAg. In the two groups, it was found to be significantly elevated with mean ± SD 1.73 ± 0.88 U/ml for patients and 1.04 ± 0.85 for controls (P = 0.009).
Conclusion
H. pylori infection may play a role in the pathogenesis of AA.

Keywords: alopecia areata, etiology, Helicobacter pylori


How to cite this article:
El-Farargy SM, El-Hamied Yasien HA, El-Mohsen Montaser BA, Rashad H. Screening of Helicobacter pylori in alopecia areata patients. Menoufia Med J 2017;30:935-9

How to cite this URL:
El-Farargy SM, El-Hamied Yasien HA, El-Mohsen Montaser BA, Rashad H. Screening of Helicobacter pylori in alopecia areata patients. Menoufia Med J [serial online] 2017 [cited 2019 Dec 7];30:935-9. Available from: http://www.mmj.eg.net/text.asp?2017/30/3/935/218293


  Introduction Top


Alopecia areata (AA) is a complex, nonscarring hair loss disease that affects ~1–2% of the population [1]. It is characterized by the loss of hair in patches, total loss of scalp hair (alopecia totalis), or total loss of body hair (alopecia universalis) [2].

Hair loss can have significant effects on patients' quality of life, and a prompt diagnosis of the different types of alopecias and early intervention are needed [3].

The exact pathogenesis of the disease is not fully understood [4]. It is considered to be an organ-specific autoimmune disease caused by the activation of autoreactive T-helper 1 and autoreactive T-cytotoxic lymphocytes [5]. A predominance of CD8+ T-cells has been demonstrated intrafollicularly whereas CD4+ cells are predominant peribulbarly in anagen follicles [6] or follicles in early catagen, in addition to the presence of eosinophils, and therefore it appears to be mediated by T-helper 1-cell response [7].

Helicobacter pylori is a microaerophilic gram-negative bacterium that colonizes the gastric mucosa and is present in around 50% of the world's population. Prevalence of H. pylori infection in children under12 years is 60.9% and in adults it is 77.2% [8].

Recent evidence suggests that H. pylori infections play a role in the pathogenesis of a variety of skin diseases. The best evidence for such a link is found for chronic urticaria, rosacea, and immune thrombocytopenic purpura [9].

Other diseases that have a purported, but not yet, proven link to H. pylori include AA, cutaneous pruritus, Behçet's disease, nodular prurigo, and lichen planus [10].

Several mechanisms have been suggested to mediate the systemic effects of H. pylori infection, including the development of antigen–antibody complexes and cross-reactive antibodies (by molecular mimicry), where antibodies developed against H. pylori cross-react with auto antigens to cause tissue damage [10].

On the basis of these studies and considering the fact that AA is a disease of unknown origin, we screened for the presence of H. pylori in patients with AA to clarify whether H pylori plays a role in the pathogenesis of alopecic areata or not.


  Materials and Methods Top


This study was designed to determine the incidence of H. pylori infection among AA patients and in healthy controls from February 2015 to January 2016 at El-Bagour Central Hospital, after receiving the approval of the Dermatology Research Ethics Committee. All participants signed an informed written consent.

Inclusion criteria

  1. Patients with AA
  2. Age ranging between 15 and 45 years.


Exclusion criteria

  1. Intake of drugs that cause hair fall such as antikeratinizing (etretinate), anticoagulant, anti-thyroid, anticonvalsant, and hormones
  2. Pregnancy, lactation, anemia, abnormalities of the thyroid function, or other causes of telogen effluvium
  3. Patients under treatment for H. pylori
  4. Patients receiving phototherapy
  5. Chronic liver, renal, heart, or autoimmune diseases.


We prospectively evaluated patients with AA and healthy subjects (control group, with comparable age and sex) without clinical evidence of any skin disorder or any history of dermatological problems. Patients or healthy subjects who had in past received treatment for H. pylori infection were excluded from the study. A clinical history and a thorough physical examination were obtained for all participants. Those who accepted to participate in the study were referred to undergo a stool antigen test for H. pylori (HpSAg).

A total of 30 patients with AA were enrolled in the study. Twenty healthy volunteers of similar gender and age distribution were selected as the control group.

H. pylori antigens were detected using a kit supplied by Premier Platinum HpSAg, manufactured by DRG International Inc. (Mountain Ave, Springfield Township, NJ 07081, USA), based on enzyme immunoassay for in-vitro qualitative and quantitative detection of H. pylori antigens in human stool. The samples were collected on the same day of diagnosis and were stored and frozen at −20°C. According to the manufacturer's instructions, HpSAg value less than or equal 0.9 U/ml were considered to be negative and HpSAg value greater than 0.9 U/ml were considered to be positive.

Data management

Data were collected, tabulated, and statistically analyzed using computer program statistical package for the social science (version 15; SPSS Inc., Chicago, Illinois, USA) for Microsoft Windows.

Descriptive statistics

Quantitative data were presented in the form of mean (), SD, and range. Qualitative data were presented in the form numbers and percentages.

Analytical statistics

Analytical statistics were used to find out the possible association between studied factors and the targeted disease. The used tests of significance included the χ2) (for parametric data) and the Mann–Whitney test (for nonparametric data). Correlations between various variables were determined using the Spearman rank correlation equation (for non-normal variables). A P-value of less than 0.05 was considered statistically significant.


  Results Top


Thirty patients with AA were compared with 20 healthy volunteers of the control group. AA patients included 21 (70%) males and nine (30%) females, their ages ranging from 15 to 45 years with mean ± SD of 30.63 ± 9.29 years. The duration of their disease was a minimum of 1 m and maximum of 18 m with mean ± SD 8.13 ± 5.61 m.

The control group included 20 age-matched and sex-matched apparently healthy individuals – 15 (75%) males and five (25%) females – their ages ranging from 15 to 45 years with mean ± SD of 27.30 ± 9.45 years.

There was a highly significant difference between the patient (83.3%) and control (35%) groups as regards positivity for HpSAg [Table 1]. In addition, the quantitative estimation of the level of HpSAg in the two groups revealed it to be significantly elevated with a mean ± SD of 1.73 ± 0.88 U/ml for patients and 1.04 ± 0.85 for controls (P = 0.009) [Table 2].
Table 1: Comparison between the two studied groups according to the qualitative level of Helicobacter pylori stool antigen

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Table 2: Comparison between the two studied groups according to the quantitative level of Helicobacter pylori stool antigen

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There was a significant relation between nail changes and disease duration in the studied group: with the increase in disease duration, nail changes increased as well (P < 0.05) [Figure 1].
Figure 1: Relation between disease duration and associated nail changes.

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There was a significant positive relation between the quantitative level of HpSAg and disease duration [Figure 2]. There was an insignificant relation between the quantitative level of HpSAg and size of the lesion [Table 3].
Figure 2: Correlation between disease index and disease duration.

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Table 3: Correlation between  Helicobacter pylori Scientific Name Search ntigen, disease duration, and size of the lesion (n=30

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  Discussion Top


H. pylori infection has been associated with numerous immune and nonimmune disorders including dermatological conditions, such as chronic urticarial [2], rosacea, psoriasis, Schönlein–Henoch purpura, Behçet's disease, prurigo nodularis, chronic cutaneous pruritus, progressive systemic sclerosis, Sjögren's syndrome, and Sweet's syndrome [11] – many of them improving or going into remission after eradication of H. pylori infection. Several mechanisms have been suggested to mediate the systemic effects of H. pylori infection, including the development of antigen–antibody complexes and cross-reactive antibodies (by molecular mimicry), where antibodies developed against H. pylori cross-react with auto antigens to cause tissue damage [10], as has been reported in atrophic gastritis [12], chronic gastritis [13], chronic idiopathic thrombocytopenic purpura [14], Hashimoto's thyroiditis [15], atherosclerosis [16], arterial hypertension [17], unstable angina pectoris [18], ischemic heart disease [19], Alzheimer's disease [20], systemic sclerosis [21], central serous chorioretinopathy [22], iron deficiency [23], autoimmune pancreatitis [24], and chronic urticarial [25].

AA has been described to be of autoimmune origin [26], with the presence of inflammatory cells around and within the human hair follicles.

After reviewing the medical literature, an association between H. pylori infection and AA has not been clearly demonstrated; few reports have explored such associations whereas others have reported contrasting results. Abdel Hafez et al. [27] compared 31 patients with AA with 24 healthy controls for in-vitro qualitative detection of HpSAg and found no significant difference in the H. pylori status, but in our study we carried out qualitative and quantitative estimation of H. pylori antigen in human stool.

Rigopouloset al. [28] compared H. pylori seroprevalence for only immunoglobulin G (IgG) in 30 patients with AA and 30 healthy controls, and found no significant difference between the groups, but in our study, given the high reliability of stool testing for the verification of H. pylori, we found an association between H. pylori infection and AA, supporting the findings of a previous study by Tawfik et al. [29], which was conducted on 44 Egyptian patients with different types of AA (localized patches, alopecia universalis, and alopecia totalis) and 30 age-matched and sex-matched healthy controls by qualitative estimation through positive, equivocal, or negative cases and quantitative estimation of titer of IgG, IgM, and IgA and which showed insignificant difference in the prevalence of H. pylori infection between the two groups as regards IgM and IgA whether qualitative or quantitative. As regards IgG (which denotes old infection), the qualitative estimation showed no significant difference between the two groups but the quantitative estimation of the titer showed significant higher titer in patients than in control groups.

Campuzano-Maya [30] presented a case of a 43-year-old man with patchy AA and H. pylori infection. The patient had hair regrowth and AA was cured after bacterial eradication by proton pump inhibitor (omeprazole) 20 mg twice daily, amoxicillin 1000 mg twice daily, and clarithromycin 500 mg twice daily for 14 days according to the recommendations from the Maastricht III Consensus Report and was followed photographically every 2 weeks. He was instructed not to take or apply any medications for AA. H. pylori eradication was confirmed 6 weeks after treatment with a negative result.

Furthermore, a significant relation was found between disease duration and nail changes (ridges, striations, redness of lunula, and pitting) that increased as disease duration prolonged; this is may be attributed to immunologic disturbances as lymphocytes, initially active against chondroitin sulfate in the hair follicle, later on attack chondroitin sulfate and proteoglycan in ear cartilage, nails, and perhaps other tissues on long-standing disease [31].

Although our study supports a causal role of H. pylori in the pathogenesis of AA, a large-scale study is needed to confirm our findings.


  Conclusion Top


  1. An increased prevalence of H. pylori infection was found in association with AA
  2. High positive results of HPSA were obtained for AA patients
  3. Therefore, H. pylori infection may play a role in the pathogenesis of AA.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3]



 

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