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52
© 2009 Wiley Periodicals, Inc. •
Journal of Cosmetic Dermatology
,
8
, 52–55
Research Letter
Blackwell Publishing Inc
ORIGINAL CONTRIBUTION
Is
Helicobacter pylori
infection associated with alopecia areata?
Hisham Zayan Abdel-Hafez, MD,
1
Ayman Mohamed Mahran, MD,
1
Eman RM Hofny, MD,
1
Dalia Abdel Aziz Attallah, MD,
1
Doaa Sameer Sayed, MD
1
& Hebat-Allah G Rashed, MD
2
1
Department of Dermatology, Assiut University Hospital, Assiut, Egypt
2
Department of Clinical Pathology, Assiut University Hospital, Assiut, Egypt
Summary
Background
Alopecia areata (AA) is an immune-mediated form of hair loss that occurs
in all ethnic groups, ages, and both sexes.
Helicobacter pylori
has been associated with
certain extra-digestive dermatological conditions, including chronic urticaria, rosacea,
Schönlein-Henoch purpura, Sweet syndrome, systemic sclerosis, and atopic dermatitis.
Objective
The causal relation between alopecia areata and
H. pylori
is discussed. We have
screened for the presence of
H. pylori
in patients with AA in order to determine any potential
role in its pathophysiology.
Patients and methods
We have prospectively studied 31 patients with AA and 24 healthy
volunteers of similar gender for the presence of
H. pylori
surface antigen (HpSag) in stool.
Results
Optical density values for
H. pylori
infection were positive in 18 of all 31 patients
evaluated (58.1%), while in 13 patients, values did not support
H. pylori
infection
(41.9%). While in the control group, 10 of 24 (41.7%) had positive results. Within the group
of AA, there was no significant difference between HpSag-positive and HpSag-negative
patients.
Conclusions
Based on these results, the relation between
H. pylori
and AA is not
supported. We advise that
H. pylori
detection should not be included in the laboratory
workup of AA.
Keywords
:
alopecia areata,
Helicobacter pylori
, alopecia
Introduction
Alopecia areata (AA) is an immune-mediated form of
hair loss that occurs in all ethnic groups, ages, and both
sexes, with an estimated lifetime risk of 1.7% among the
general population.
1
Circumstantial evidence indicates
that AA may be an auto-immune disease. The most direct
evidence is provided by the histological finding that in
early stages the lower ends of hair follicles are surrounded
by an infiltrate of lymphocytes.
2
The hypothesis of the
autoimmune nature of AA is supported not only by the
coexistence with other autoimmune diseases, but also by
the presence of autoantibodies against thyroid constituents,
gastric parietal cells, and smooth muscle cells.
3,4
Further-
more, the identification of antibodies against normal
anagen scalp hair follicles in serum of patients with AA
supports this hypothesis.
5
Since
Helicobacter pylori
identification in 1983,
6
an
increasing amount of knowledge has accumulated, with
this agent having been directly involved in the pathogenesis
of several gastro-duodenal pathologies.
3
H. pylori
is con-
sidered to be a noninvasive organism that is essentially
confined to the gastric mucosa. In addition to their direct
injury to target tissues, infectious agents might exert
their deleterious effects indirectly by interfering with the
immune system.
7
This bacterium has been associated
Correspondence: Hisham Zayan Abdel Hafez, MD, Lecturer of Dermatology,
Department of Dermatology, Ninth floor, Assiut University Hospital,
Assiut, Egypt. E-mail: hishamzayan@yahoo.com
Accepted for publication August 16, 2008
Is
H. pylori
infection associated with alopecia areata? •
H Z Abdel-Hafez
et al.
© 2009 Wiley Periodicals, Inc. •
Journal of Cosmetic Dermatology
,
8
, 52–55
53
with certain extra-digestive dermatological conditions,
including chronic urticaria, rosacea, Schönlein-Henoch
purpura, Sweet syndrome, systemic sclerosis, and atopic
dermatitis.
8
On the basis of these studies, and considering the fact
that AA is a disease of unknown origin, we have screened
for the presence of
H. pylori
in patients with AA in order
to determine any potential role in its pathophysiology.
Patients and methods
This study was designed to determine the incidence of
H. pylori
infection among AA patients and in healthy
controls. From March 2006 through December 2006, we
prospectively evaluated at the Dermatology Outpatient
Clinic, Assiut University Hospital, 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 ever received treatment for
H. pylori
infection were excluded.
A clinical history and thorough physical examination
were obtained for all subjects. After that, they were
invited to participate in the study, which was conducted
according to the Declaration of Helsinki principles and
was approved by the local Ethics Committee. Those who
accepted to participate in the study were referred to
perform a stool antigen test for
H. pylori
.
A total of 31 patients with AA were enrolled in the
study (21 male and 10 female). Demographic (age, sex,
duration) and gastrointestinal symptoms were recorded
using a structural questionnaire. Twenty-four 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 HpsA manufactured by Meridian
Diagnostics Inc. USA (Cat no. 601348-045) based on
enzyme immunoassay for
in vitro
qualitative detection of
H. pylori
antigens in human stool.
9
Samples were collected
at the same day of diagnosis and were stored and frozen
at –20
°
C. According to the manufacturer’s instructions,
the cut-off optical density values used were as follows:
<
0.140, negative; 0.140–0.159, equivocal; and
>
0.160,
positive. Equivocal results were considered negative.
Statistical analysis
Statistical analysis conducted was performed using SPSS
10.0 statistical software package, with continuous
variables being presented as mean, standard deviation,
and range and discrete variables being presented as
percentage and 95% confidence interval. Statistical tests
employed in the analysis were unpaired Student’s
t
-test
and the chi-squared test.
Results
Thirty-one patients with AA were compared with 24
healthy volunteers of the control group. At the time of
initial visit, 48.4% were presented with AA at the front of
the scalp, 45.2% at the back of scalp, 9.7% at the beard,
12.9% at temporal area, 6.5% at the eye brows, and 3.2%
at the moustache. 77.4% of the patients presented with a
single lesion of AA, while 22.6% presented with multiple
lesions. The size of the lesions ranged from 0.2 to
11.8 cm
2
. The duration of the disease ranged from 2 days
to 1 year with 71% had a progressive course and 29%
had a stationary one. AA clinical characteristics are
summarized in Table 1. Both groups were comparable in
terms of age (mean, 24.48 vs. 27.50 years) and sex (67.7%
vs. 58.3% males in both). Optical density values for
H. pylori
infection were positive in 18 of all 31 patients evaluated
(58.1%), while in 13 patients, optical density values were
negative (41.9%). In the control group, 10 of 24 (41.7%)
yielded positive results (Fig. 1). Although the mean of
H. pylori
surface antigen (HpSag) was higher in the AA group, the
difference was not statistically significant.
Within the group of AA, there were no significant
differences noticed for the age, gender, duration, course,
size, and multiplicity between HpSag-positive and HpSag-
negative patients as shown in Table 2.
Discussion
AA is an immune-mediated form of hair loss
characterized by extreme variability not only in the time
Table 1 AA clinical characteristics.
Descriptive statistics
Duration Mean ± SD: 2.35 ± 2.90 (months)
Range: 2 days to 1 years
Course Progressive: 22 (71.0%)
Stationary: 9 (29.0%)
Site Front of Scalp: 15 (48.4%)
Back of Scalp: 14 (45.2%)
Beard: 3 (9.7%)
Temporal: 4 (12.9%)
Eye brows: 2 (6.5%)
Moustache: 1 (3.2%)
Size Mean ± SD: 4.74
±
2.77 (cm2)
Range: 0.8–11.8
Sites multiplicity Single: 24 (77.4%)
Multiple: 7 (22.6%)
Is
H. pylori
infection associated with alopecia areata? •
H Z Abdel-Hafez
et al.
54
© 2009 Wiley Periodicals, Inc. •
Journal of Cosmetic Dermatology
,
8
, 52–55
of initial onset of hair loss but also in the duration, extent,
and pattern of hair loss during any given episode as well
as in the unpredictable nature of spontaneous re-g rowth.
10
Circumstantial evidence indicates that AA may be an
autoimmune disease. The familial predisposition to
develop autoimmune diseases and the association with
autoantibodies in patients with AA is analogous to
findings in other autoimmune diseases and strengthens
the possibility that AA is itself an autoimmune disease.
2
It is not clear, however, whether specific antifollicle
auto-reactivity occurs although antibodies have not been
found by direct immunofluorescence in affected scalp.
11
Since
H. pylori
identification in 1983, a putative patho-
genetic role has been ascribed to this bacterium in several
extra-digestive diseases including rosacea, ischemic
heart disease, and diabetes mellitus.
8
In addition to their
direct injury to target tissues, infectious agents might
exert their deleterious effects indirectly by interfering
with the immune system. Antigens from this bacterium
might show cross-reactivity with thyroidal antigens.
7
De Luis
et al
. have published two articles showing that
the seroprevalence of
H. pylori
is significantly higher in
patients with insulin-dependent diabetes mellitus
4
and
autoimmune atrophic thyroiditis.
7
They express the
hypothesis that
H. pylori
antigens might be involved in
the development of these two autoimmune diseases or
that autoimmune function in these diseases may increase
the likelihood of an
H. pylori
infection. On the basis of these
studies, and considering the fact that AA is a disease of
unknown origin, we tried to determine whether there
might be an association of
H. pylori
infection with AA.
A single study has searched for an association between
this bacterium and AA. This trial has shown no signifi-
cant difference in the seroprevalence of
H. pylori
infection
between patients with AA and healthy controls.
12
In our study, we have found no evidence for an increased
association between
H. pylori
infection and AA, supporting
the previous study by Rigopouos
et al
.
12
Given the high
reliability of stool testing for the verification of
H. pylori
,
we believe that
H. pylori
cannot be incriminated in the
pathogenesis of AA.
Conclusions
Our results revealed no causal link between
H. pylori
infection and AA. Based on these information, we advise
that
H. pylori
detection should not be included in the
laboratory workup of AA.
References
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2 Friedmann PS. Alopecia areata and autoimmunity.
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Figure 1 Scatterogram for HpSA among both groups of the study.
Table 2 Characteristics of AA patients in relation to presence of
H. pylori.
Characteristics
Presence of
H. pylori (N = 18)
Absence of
H. pylori (N = 13) P
Age (years):
Mean ± SD 25.28 ± 12.17 23.38 ± 7.81 NS
Sex incidence: No. (%)
Males 12 (66.7%) 9 (69.2%) NS
Females 6 (33.3%) 4 (30.8%)
Duration (months):
Mean ± SD 2.44 ± 2.74 2.23 ± 3.23 NS
Course:
Progressive 12 (66.7%) 10 (76.9%) NS
Stationary 6 (33.3%) 3 (23.1%)
Size (cm2):
Mean ± SD 4.89 ± 2.76 4.53 ± 2.89 NS
Sites multiplicity:
Single 13 (72.2%) 11 (84.6%) NS
Multiple 5 (27.8%) 2 (15.4%)
Is
H. pylori
infection associated with alopecia areata? •
H Z Abdel-Hafez
et al.
© 2009 Wiley Periodicals, Inc. •
Journal of Cosmetic Dermatology
,
8
, 52–55
55
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60: 33–7.
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Rokkas T. No increased prevalence of Helicobacter pylori in
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