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 Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 81-84

The frequency of Helicobacter pylori infection in vitiligo patients


1 Dermatology Clinic, Ankara Numune Education and Research Hospital, Ankara, Turkey
2 Dermatology Clinic, Ankara University Faculty of Medicine, Ankara, Turkey

Date of Web Publication29-Dec-2015

Correspondence Address:
Seray Külcü Çakmak
Yıldızevler Mah., 742 Sokak, Aykon Park Sitesi, A Blok No.: 14, Cankaya, Ankara
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2349-5847.172775

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  Abstract 

Background: Helicobacter pylori is a gastrointestinal infectious agent with worldwide distribution. A potential role of H. pylori infection in several extra-intestinal diseases including autoimmune and inflammatory skin diseases such as chronic urticaria, alopecia areata, psoriasis, and rosacea have been reported. Vitiligo is a common depigmenting skin disorder and autoimmunity has been suggested in the pathogenesis of vitiligo. There are few reports of association of H. pylori infection and vitiligo. Aims: The aim of our study is to evaluate the relationship between H. pylori infection and vitiligo. Methods: The study group included 40 patients with vitiligo, and the control group included 39 age- and gender-matched individuals. H. pylori stool antigen test was performed in the patient and control groups to detect the presence of H. pylori infection. Results: H. pylori stool antigen test was positive in 20 (50%) of the patients and 13 (33.3%) of the controls. No significant difference was found in H. pylori stool antigen test positivity between the patient and the control groups (P > 0.05). Also, no significant relationship was found between H. pylori stool antigen test positivity and the family history, type, duration, and activity of vitiligo. Conclusion: Our results indicate that H. pylori infection is not increased in vitiligo patients, and it is not necessary to screen vitiligo patients routinely for H. pylori infection.

Keywords: Autoimmunity, Helicobacter pylori, vitiligo


How to cite this article:
Çakmak SK, Tantoglu BH, Onan D, Yorulmaz A, Tamer E, Artüz F. The frequency of Helicobacter pylori infection in vitiligo patients. Pigment Int 2015;2:81-4

How to cite this URL:
Çakmak SK, Tantoglu BH, Onan D, Yorulmaz A, Tamer E, Artüz F. The frequency of Helicobacter pylori infection in vitiligo patients. Pigment Int [serial online] 2015 [cited 2020 Oct 21];2:81-4. Available from: https://www.pigmentinternational.com/text.asp?2015/2/2/81/172775


  Introduction Top


Vitiligo is an acquired dermatological disorder characterized by depigmented macules due to the progressive loss of melanocytes.[1] It is a commonly observed disorder with a prevalence of approximately 0.5% worldwide.[2] Though its exact pathogenesis is not clear autoimmunity is strongly implicated in the development of vitiligo.[1]

Helicobacter pylori is a Gram-negative bacillus which was first identified in gastric mucosa, and it is the main cause of chronic gastritis and a risk factor for gastric cancer.[3] There have also been a considerable amount of reports linking H. pylori infection with the development of extra-gastrointestinal autoimmune disorders including some autoimmune disorders affecting the skin.[4],[5]

There have been two studies which have been performed recently reporting increased prevalence of H. pylori infection in patients with vitiligo.[6],[7] The aim of our study was to investigate the frequency of H. pylori infection in patients with vitiligo to determine if there is an association between H. pylori infection and vitiligo with direct stool antigen test.


  Methods Top


A total of 40 consecutive vitiligo patients, who had been admitted to Ankara Numune Education and Research Hospital, were enrolled prospectively in the study between January 2014 and January 2015. The control group included 39 age- and gender-matched individuals with tinea pedis who were admitted to the dermatology outpatient clinic during the same period. Patients and controls with a history of previous H. pylori eradication therapy were not included in the study. Also patients and controls taking antibiotics and medicines containing bismuth during 1-month before the test and proton pump inhibitors for 2 weeks previously were not included in the study. Also pregnant and lactating females and patients younger than 18 years were not included in the study.

Family and personal medical history of the patients were learned. Possible precipitating factors of vitiligo including physical trauma, mental or emotional stress, and chemical or sun exposure were questioned. Dermatological examination of all the patients and controls were made, and the vitiligo involvement patterns were classified as generalized, segmental, focal, acrofacial, and mucosal. Vitiligo was considered as active in patients who had an expansion of the lesions or appearance of new lesions in the last 6 months. H. pylori stool antigen test was performed to detect the presence of H. pylori infection in the patient and control groups. Stool samples were analyzed using the ABON H. pylori antigen test device (Abon Biopharm, Hangzhou, China), that is, a lateral flow chromatographic immunoassay for detection of H. pylori antigen. A diluted stool sample was dispensed into the sample port of the test device, and the appearance of a colored line after 10 min in the test line region of the strip indicated a positive result.

The study was approved by the Ethical Committee Ankara Numune Education and Research Hospital in October 02, 2013 with the decision number 671/2013, and informed consent was taken from the patients and the controls.

Statistical analysis

Data analysis was performed by using for SPSS 15.0 (SPSS Inc. 233 South Wacker Drive, 11th Floor Chicago, IL 60606-6412). Quantitative variables were described as mean ± standard deviation and qualitative variables were presented as frequency distribution and percentages. Mann–Whitney, Chi-square, and t-tests were used for statistical analysis and a P ≤ 0.05 was considered to be significant.


  Results Top


The study included 40 patients with vitiligo and 39 patients with tinea pedis as a control group. The patients were aged between 20 and 70 years (mean: 42.4 ± 15.6 years) and the control group was aged between 19 and 69 years (mean: 42.4359 ± 14.5 years). There was no significant difference in the ages of the patient and control groups (t-test, P: 0.577). 16 (40%) of the patients were female, and 24 (60%) of them were male. 20 (51.3%) of the controls were female, and 19 (48.7%) of them were male. There was no significant difference in the genders of the patient and control groups (Chi-square test, P = 0.370).

The mean duration of the vitiligo lesions was 95.6 ± 17.9 months. The lesions were active in 29 (24.1%) of the patients. 21 (52.5%) of the patients had generalized, 11 (27.5%) had acrofacial, and 8 (20%) of them had focal vitiligo. 21 (52.5%) had mentioned triggering factors in the initiation of vitiligo lesions. 7 (17.5%) of them had a family history of vitiligo.

H. pylori stool antigen test was positive in 20 (50%) of the patients and 13 (33.3%) of the controls. No significant difference was found in H. pylori stool antigen test positivity between the patient and the control groups (Chi-square test, P = 0.173). Also no significant relationship was found between H. pylori stool antigen positivity and the family history of vitiligo (Chi-square test, P = 1.0), presence of triggering factors (Chi-square test, P = 1.0), type (Chi-square test, P = 0.933), duration (Mann–Whitney test, P = 0.914), and activity of vitiligo (Chi-square test, P = 0.205) [Table 1].
Table 1: The relation of Helicobacter pylori infection and clinical parameters

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  Discussion Top


Vitiligo is a multifactorial polygenic disorder with a complex interaction between genetic, environmental, biochemical, and immunological factors.[8] The exact etiopathogenesis of vitiligo is not clear; however, several findings suggest that autoimmunity is strongly linked to vitiligo etiopathogenesis. Circulating antimelanocyte and antikeratinocyte antibodies have been shown in vitiligo patients and also it is associated with other autoimmune diseases and the use of topical or systemic immunosuppressive therapy results in clinical improvement of the disease.[8],[9],[10],[11],[12] Autoimmune reactivity toward melanocyte antigens are thought to be T-cell dependent and antigen-driven in vitiligo.[9]

Autoimmune diseases are thought to arise from the interaction of genetic susceptibility and environmental exposures. Infectious triggers have been implicated among environmental exposures.[4]H. pylori is a widely prevalent microorganism affecting 50–80% of the population worldwide. As H. pylori infection can affect host immune responses, a possible role of H. pylori in the development of several autoimmune diseases have been investigated.[13] The inflammatory response to H. pylori is thought to lead to the development of antigen-antibody complexes or cross-reactive antibodies resulting in autoimmunity.[14]

Sjören's syndrome, rheumatoid arthritis, and immune thrombocytopenic purpura are among the autoimmune diseases in which the role of H. pylori infection as a pathogenetic factor has been investigated. The results of these reports vary, and the role of H. pylori in autoimmune disorders is inconclusive.[4],[13] Several studies have also studied the association of H. pylori infection and immune-mediated skin disorders such as psoriasis, chronic urticaria, and Behçet's disease. Increased prevalence of H. pylori infection and benefit of H. pylori eradication therapy to skin symptoms have been reported in some of these studies.[5],[14]

The relation between H. pylori infection and vitiligo has been recently studied in two prospective studies in Turkey.[6],[7] Dogan et al. studied 68 patients with vitiligo and 65 with telogen effluvium. All were tested for H. pylori IgG and cytotoxin-associated gene A (CagA) and urea breath test (UBT) was performed to detect the presence of H. pylori infection. Significantly higher rates of H. pylori positivity, H. pylori CagA and IgG was found in serum in the vitiligo group but no statistically significant relationship was found between H. pylori positivity, CagA, H. pylori IgG, and vitiligo activity score and vitiligo involvement pattern.[6]

Rifaioglu et al. investigated 34 patients with vitiligo and 30 age- and sex-matched healthy controls for H. pylori infection using UBT and reported the significantly higher frequency of H. pylori infection in patients with vitiligo.[7]

The reason for the different results from our study might be because of the geographic locations of the above studies. Socioeconomic statuses and ethical factors may affect the prevalence of H. pylori infection.[15] The study of Rifaioglu is performed in Hatay, which is in the Southeast of Turkey which houses Syrian immigrants and also has a population with Arabic origins. Also, the socioeconomic status of the people in this region is lower than the middle part of Turkey.

Dogan et al. performed their study in Ankara; the same city as in our study, but the hospital which the study is performed generally receives patients with lower socioeconomic statuses than ours.

The stool antigen test has been shown to be highly sensitive and specific in the diagnosis of H. pylori infection.[16] By using stool antigen test

no significant difference was found in H. pylori infection between the patient and the control groups. Also, no significant relation was found between H. pylori stool antigen positivity and the presence of family history, triggering factors, type, duration and activity of vitiligo. Our results indicate that H. pylori infection does not play a significant role in the pathogenesis of vitiligo, but it does not exclude the probability that H. pylori infection may play a triggering role in at least some of the patients.

In our opinion, one of the limitations of our study is the relatively small number of patients and controls. In addition, we could only use one method to detect H. pylori infection. One of the other limitations was that we did not give eradication therapy for H. pylori infection and follow-up the patients to see the effect of the treatment on vitiligo lesions.

Our results are conflicting with the previous results of the studies performed in our country which might be because of the methods used in the detection of H. pylori infection and the geographic and socioeconomic differences.

Our study does not confirm the role of H. pylori infection in the pathogenesis of vitiligo. It indicates that H. pylori infection is not increased in vitiligo patients, and it is not necessary to screen vitiligo patients routinely for H. pylori infection.

Further studies with larger number of patients from different countries and ethnicity are required to investigate whether H. pylori infection is associated with vitiligo and H. pylori eradication therapy has a favorable effect on the clinical course of vitiligo.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Colucci R, Dragoni F, Moretti S. Oxidative stress and immune system in vitiligo and thyroid diseases. Oxid Med Cell Longev 2015;2015:631927.  Back to cited text no. 1
    
2.
Park JH, Jung MY, Lee JH, Yang JM, Lee DY, Park KK. Clinical course of segmental vitiligo: A retrospective study of eighty-seven patients. Ann Dermatol 2014;26:61-5.  Back to cited text no. 2
    
3.
Hussain SA, Hamid S. Helicobacter pylori in humans: Where are we now? Adv Biomed Res 2014;3:63.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.
Smyk DS, Koutsoumpas AL, Mytilinaiou MG, Rigopoulou EI, Sakkas LI, Bogdanos DP. Helicobacter pylori and autoimmune disease: Cause or bystander. World J Gastroenterol 2014;20:613-29.  Back to cited text no. 4
    
5.
Shiotani A, Okada K, Yanaoka K, Itoh H, Nishioka S, Sakurane M, et al. Beneficial effect of Helicobacter pylori eradication in dermatologic diseases. Helicobacter 2001;6:60-5.  Back to cited text no. 5
    
6.
Dogan Z, Özdemir P, Eksioglu M, Filik L. Relationship between Helicobacter pylori infection and vitiligo: A prospective study. Am J Clin Dermatol 2014;15:457-62.  Back to cited text no. 6
    
7.
Rifaioglu EN, Aydogan F, Bülbül Sen B, Sen T, Ekiz Ö. Investigation into the frequency of Helicobacter pylori infection with carbon 14 urea breath test in patients with vitiligo. Turk J Med Sci 2014;44:1051-4.  Back to cited text no. 7
    
8.
Laddha NC, Dwivedi M, Mansuri MS, Singh M, Gani AR, Yeola AP, et al. Role of oxidative stress and autoimmunity in onset and progression of vitiligo. Exp Dermatol 2014;23:352-3.  Back to cited text no. 8
    
9.
Sanchez-Sosa S, Aguirre-Lombardo M, Jimenez-Brito G, Ruiz-Argüelles A. Immunophenotypic characterization of lymphoid cell infiltrates in vitiligo. Clin Exp Immunol 2013;173:179-83.  Back to cited text no. 9
    
10.
Gopal KV, Rao GR, Kumar YH. Increased prevalence of thyroid dysfunction and diabetes mellitus in Indian vitiligo patients: A case-control study. Indian Dermatol Online J 2014;5:456-60.  Back to cited text no. 10
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11.
Shankar DS, Shashikala K, Madala R. Clinical patterns of vitiligo and its associated co morbidities: A prospective controlled cross-sectional study in South India. Indian Dermatol Online J 2012;3:114-8.  Back to cited text no. 11
    
12.
Laddha NC, Dwivedi M, Mansuri MS, Gani AR, Ansarullah M, Ramachandran AV, et al. Vitiligo: Interplay between oxidative stress and immune system. Exp Dermatol 2013;22:245-50.  Back to cited text no. 12
    
13.
Hasni S, Ippolito A, Illei GG. Helicobacter pylori and autoimmune diseases. Oral Dis 2011;17:621-7.  Back to cited text no. 13
    
14.
Magen E, Delgado JS. Helicobacter pylori and skin autoimmune diseases. World J Gastroenterol 2014;20:1510-6.  Back to cited text no. 14
    
15.
Malnick SD, Melzer E, Attali M, Duek G, Yahav J. Helicobacter pylori: Friend or foe? World J Gastroenterol 2014;20:8979-85.  Back to cited text no. 15
    
16.
Patel SK, Pratap CB, Jain AK, Gulati AK, Nath G. Diagnosis of Helicobacter pylori: What should be the gold standard? World J Gastroenterol 2014;20:12847-59.  Back to cited text no. 16
    



 
 
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