|Year : 2017 | Volume
| Issue : 3 | Page : 935-939
Screening of Helicobacter pylori in alopecia areata patients
Shawky M El-Farargy1, Hossam Abd El-Hamied Yasien1, Belal Abd El-Mohsen Montaser2, Heba Rashad MBBCh 3
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 Submission||25-Sep-2016|
|Date of Acceptance||02-Dec-2016|
|Date of Web Publication||15-Nov-2017|
Department of Dermatology, Andrology and STIs, El-Bagour Central Hospital, Shebin El-Kom, Menoufia, 32511
Source of Support: None, Conflict of Interest: None
The aim of the present study was to clarify whether Helicobacter pylori plays a role in the pathogenesis of alopecic areata or not.
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.
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).
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 2020 Sep 25];30:935-9. Available from: http://www.mmj.eg.net/text.asp?2017/30/3/935/218293
| Introduction|| |
Alopecia areata (AA) is a complex, nonscarring hair loss disease that affects ~1–2% of the population . 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) .
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 .
The exact pathogenesis of the disease is not fully understood . It is considered to be an organ-specific autoimmune disease caused by the activation of autoreactive T-helper 1 and autoreactive T-cytotoxic lymphocytes . A predominance of CD8+ T-cells has been demonstrated intrafollicularly whereas CD4+ cells are predominant peribulbarly in anagen follicles  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 .
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% .
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 .
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 .
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 .
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|| |
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.
- Patients with AA
- Age ranging between 15 and 45 years.
- Intake of drugs that cause hair fall such as antikeratinizing (etretinate), anticoagulant, anti-thyroid, anticonvalsant, and hormones
- Pregnancy, lactation, anemia, abnormalities of the thyroid function, or other causes of telogen effluvium
- Patients under treatment for H. pylori
- Patients receiving phototherapy
- 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 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.
Quantitative data were presented in the form of mean (), SD, and range. Qualitative data were presented in the form numbers and percentages.
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|| |
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|
Click here to view
|Table 2: Comparison between the two studied groups according to the quantitative level of Helicobacter pylori stool antigen|
Click here to view
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.|
Click here to view
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].
|Table 3: Correlation between Helicobacter pylori ntigen, disease duration, and size of the lesion (n=30|
Click here to view
| Discussion|| |
H. pylori infection has been associated with numerous immune and nonimmune disorders including dermatological conditions, such as chronic urticarial , rosacea, psoriasis, Schönlein–Henoch purpura, Behçet's disease, prurigo nodularis, chronic cutaneous pruritus, progressive systemic sclerosis, Sjögren's syndrome, and Sweet's syndrome  – 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 , as has been reported in atrophic gastritis , chronic gastritis , chronic idiopathic thrombocytopenic purpura , Hashimoto's thyroiditis , atherosclerosis , arterial hypertension , unstable angina pectoris , ischemic heart disease , Alzheimer's disease , systemic sclerosis , central serous chorioretinopathy , iron deficiency , autoimmune pancreatitis , and chronic urticarial .
AA has been described to be of autoimmune origin , 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.  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.  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. , 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  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 .
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|| |
- An increased prevalence of H. pylori infection was found in association with AA
- High positive results of HPSA were obtained for AA patients
- Therefore, H. pylori infection may play a role in the pathogenesis of AA.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Dudda-Subramanya R, Alexis AF, Siu K. Alopecia areata: genetic complexity underlies clinical heterogenecity. Eur J Dermatol 2007; 17
McDonagh AJ, Tazi-Ahnini R. Epidemiology and genetics of alopecia areata. Clin Exp Dermatol 2002; 27
Seleit IA, El-Bakry OA, El-Sherif RM. Dermoscopy in hair disorders. Menouf Med J 2014; 27
Duncan FJ, Silva KA, Johnson C, King B, Szatkiewicz JP, Kamdar S, et al.
Serum chemokines in alopecia areata. Br J Dermatol 2007; 157
Zhao M, Liang G, Wu X, Wang S, Zhang P, Su Y, et al.
Abnormal epigenetic modifications in peripheral blood mononuclear cells from patients with alopecia areata. Br J Dermatol 2012; 166
Chan LS, Vanderlugt CJ, Hshimooto T. Lessons from autoimmune skin diseases. J Invest Dermatol 1998; 110
Arca E1, Muşabak U, Akar A, Erbil AH, Taştan HB. Interferon-gamma in alopecia areata. Eur J Dermatol 2004; 14
Ford AC, Axon AT. Epidemiology of Helicobacter pylori
infection and public health implications. Helicobacter 2010; 15 (Suppl 1):
Suzuki H, Matsuzaki J, Hibi T. Lifestyle related diseases and H. pylori
. Nihon Rinsho 2009; 67
Hernando-Harder AC, Booken N, Goerdt S, Singer MV, Harder H. Helicobacter pylori
infection and dermatologic diseases. Eur J Dermatol 2009; 19
Magen E, Delgado JS. Helicobacter pylori
and skin autoimmune diseases. World J Gastroenterol 2014; 20
Negrini R, Savio A, Poiesi C, Appelmelk BJ, Buffoli F, Paterlini A. Antigenic mimicry between Helicobacter pylori
and gastric mucosa in the pathogenesis of body atrophic gastritis. Gastroenterology 1996; 111
Negrini R, Savio A, Appelmelk BJ. Autoantibodies to gastric mucosa in Helicobacter pylori
infection. Helicobacter 1997; 2 (Suppl 1):
Stasi R, Provan D. Helicobacter pylori
and chronic ITP. Hematology Am Soc Hematol Educ Program 2008; 2008:206–211.
Franceschi F, Satta MA, Mentella MC, et al. Helicobacter pylori
infection in patients with Hashimoto's thyroiditis. Helicobacter 2004; 9
Lamb DJ, El-Sankary W, Ferns GA. Molecular mimicry in atherosclerosis: a role for heat shock proteins in immunization. Atherosclerosis 2003; 167
Migneco A1, Ojetti V, Specchia L, Franceschi F, Candelli M, Mettimano M, et al.
Eradication of Helicobacter pylori
infection improves blood pressure values in patients affected by hypertension. Helicobacter 2003; 8
Rechcinski T, Kasprzak JD, Chmiela M, Krzeminska-Pakula M, Rudnicka W. Patients with unstable angina pectoris present increased humoral response against Helicobacter pylori
in comparison with patients with aggravated dyspepsia. Acta Microbiol Pol 2002; 51
Franceschi F1, Leo D, Fini L, Santoliquido A, Flore R, Tondi P, et al. Helicobacter pylori
infection and ischaemic heart disease: an overview of the general literature. Dig Liver Dis 2005; 37
Kountouras J, Gavalas E, Zavos C, Stergiopoulos C, Chatzopoulos D, Kapetanakis N, et al.
Alzheimer's disease and Helicobacter pylori
infection: defective immune regulation and apoptosis as proposed common links. Med Hypotheses 2007; 68
Radic M, Kaliterna DM, Radic J. Helicobacter pylori
infection and systemic sclerosis-is there a link? Joint Bone Spine 2011; 78:337–340.
Giusti C. Association of Helicobacter pylori
with central serous chorioretinopathy: hypotheses regarding pathogenesis. Med Hypotheses 2004; 63
Hershko C, Ronson A. Iron deficiency, Helicobacter infection and gastritis. Acta Haematol 2009; 122
Kountouras J, Zavos C, Chatzopoulos D. A concept on the role of Helicobacter pylori
infection in autoimmune pancreatitis. J Cell Mol Med 2005; 9
Greaves MW. Pathophysiology of chronic urticaria. Int Arch Allergy Immunol 2002; 127
Alkhalifah A, Alsantali A, Wang E, et al.
Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol 2010; 62
:177–188; quiz 189–190.
Abdel-Hafez HZ1, Mahran AM, Hofny ER, Attallah DA, Sayed DS, Rashed HA. Alopecia areata is not associated with Helicobacter pylori
. Indian J Dermatol 2009; 54
Rigopoulos D, Katsambas A, Karalexis A, Papatheodorou G, Rokkas T. No increased prevalence of Helicobacter pylori
in patients with alopecia areata. J Am Acad Dermatol 1992; 46
Tawfik OS, Ezzat AN, Mohammed AE. Serology of Helicobacter pylori
in alopecia areata patients [thesis]. Cairo, Egypt: Faculty of Medicine Cairo University; 2013.
Campuzano-Maya G. Cure of alopecia areata after eradication of Helicobacter pylori
: anew association? World J Gastroenterol 2011; 17
Starr JC, Taneja N, Brasher GW. Relapsing polychondritis following alopecia areata, Academic Microsoft J 2010; 2010
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]