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NR 1-3/2009
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Helicobacter pylori
– a risk factor for the developement of the central serous
chorioretinopathy
Helicobacter pylori jako
czynnik ryzyka rozwoju centralnej surowiczej chorioretinopatii
Misiuk-Hojło Marta, Michałowska
Magdalena, Turno-Kręcicka Anna
Department of Ophthalmology, Medical Academy of Wroclaw
Head: Ass. Professor Marta Misiuk-Hojło, MD, PhD |
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| Summary: |
Purpose: To prove
the influence of the Helicobacter pylori for the
developement of the central serous chorioretinopathy.
Material and methods: We examined 55 patients
with central serous chorioretinopathy confirmed by
fluorescein angiogram and 55 controls.Each patient
provided venous blood sample for IgG anti – bodies to
Helicobacter pylori by enzyme – linked immunosorbent
assay technique (ELISA) and a stool specimen for
Helicobacter pylori antigens.
Results: 44% in CSC patients were positive
results of stool examine and only 29% in group comtrol.
In 67% of the patients we proved the presence of the
antibodies IgG – anty Helicobacter pylori and in 47%
controls.The difference was statistically significant.
Conclusions: Helicobacter pylori infection is
statistically more frequently among the patients with
CSC diagnosis than in healthy population. |
| Słowa kluczowe: |
Helicobacter pylori,
central serous chorioretinopathy (CSC), the risk factors
for the developement of CSC. |
| Key words: |
Helicobacter pylori,
centralna surowicza chorioretinopatia (CSC), czynniki
ryzyka rozwoju CSC. |
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Introduction
Central serous chorioretinopathy (CSC) is a disease that affects
young and middleaged adults, more often men then women. It is
described as a neurosensory serous retinal detachment with
sudden visual disturbances. The disease affects the macula
region generally in the one eye. Bilateral and symetrical
presentation of the disease is reported to develop in only 10%
of patients. Patients usually have mild visual loss. A lot of
cases have a spontaneus recovery without therapy although the
disease can become chronic with decompensation of the retinal
pigment epithelium (RPE) and severe loss in visual acuity.
Unfortunatelly the treatment of CSC is still unsatisfactory,
probably becouse the pathogenesis of the disease is not clear.
The etiopathogenesis of CSC is still incompletely understood but
the correlation with emotional stress periods is recognized
probably through the way of the sympathic – parasympathic
activity leading to the development of defects in the RPE.
Doubtless, the main reason of the developement of CSC is
vascular defects in choroidal circulation.The other known risk
factors for the developement of CSC are:using corticosteroids
and sympathicomimetics, type A personality (1-6), vasomotorical
vascular defects (7).
An association between CSC and Helicobacter pylori(HP) infection
has been described.
HP is a gram – negative bacteria associated to multiple
digestive and extra – digestive pathologies.
Our study suggest that HP may possibly be involved in the
development of CSC and may be regarded as a risk factor for CSC.
Material and methods
We examined a group of 55 patients with diagnosis CSC – 19 women
(34.5%) and 36 men (65.5%), age range 34-60 years, middle age
49.2, confirmed by fluorescein angiogram and 55 controls – 22
women (40%) and 33 men (60%), age range 30-
-60 years, middle age 46.7, deriving from hospitals’ employees.
Our patients not have been treated 6 months prior to the study
with antibiotics, corticoids or sympathicomimetics drugs, they
have not suffered any severe chronic disease, and the women have
not been pregnant.
A total of individuals have been made a full ophthalmological
exploration (visual acuity, Ischihara test, Amsler test,
tonometry, eye fundus), including fluorescein angiography among
the patients with CSC. The diagnostic criteria for CSC were:
retinal pigment detachment in the fundus eye and CSC features in
fluorescein angiography.
A control group has not a CSC history, past or present and has
not a prior diagnosis of HP infection.
The HP study was with a non-invasive methods. Each patient
provided venous blood sample for IgG antibodies to HP by enzyme
– linked immunosorbent assay technique (ELISA) and a stool
specimen for HP antigens.
The resultats was estimated using Chi2 test and odds ratio.
Results
The prevelence of Helicobacter pylori active infection (positive
results of stool examine) was 44% in CSC patients and only 29%
in control group (Fig. 1, 2).
Using Chi2 test p = 0.11, p = 0.10 is statistically significant.
A difference of the frequency of antibodies IgG – anty HP in the
patients with CSC and in the control group was higher – 67% in
th patients group and 47% in the control (Fig. 3, 4). In the
Chi2 test p = 0.03 and odds ratio = 2.29 it means that HP
antybodies are over twice frequent among CSC patients than in
controls. The difference is statistically significant.
Discussion
Typical CSC is a common disease that usually resolves with good
vision after acute episodes. However in some cases reccurent of
persistent disease may lead to permanent damage to the RPE and
retina causing visual loss. The pathogenesis of CSC is unknown,
but may be due to alterations in choroidal permeability with
subsequent focal damage to the RPE. Risk factors of CSC are male
gender, psychological stress, type A – personality,
corticoid-steroid treatment and pregnancy.
A correlation between CSC and HP infection has recently been
hypothesized. This association is still unclear. A possible
explanation might arise from correlation between the HP
infection and the development of atherosclerosis. Although the
etiology of atherosclerosis is multifactorial, it has been
documented that HP – cytotoxin – associated – gene A (CagA) may
significantly increase the risk of its development. Anti – CagA
antibodies may cross react with vascular wall antigens and begin
an immunological cascade that causes arterial cell wall damage
and leads to the developement of atherosclerosis. Anti – CagA
antibodies may destroy vascular endothelial cells and lead to
the imbalance in vascular reactivity and permeability. Heat
shock proteins (HSP) produced by HP make similar reaction with
vascular wall antigens and have similar significance in making
inflammation.
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An inflammation leads to defects in
choroidal perfusion and to the ischaemia. Otherwise, the
immunoglobulin – G (IgG) antibody response to the infection, can
be a risk factor leading to the endothelial disfunction. This
theory of „molecular mimicry” might be an explanation of the
prolonging the disease`s process, although the bacteria is
eliminated (8-12).
Vascular endothelium regulates walls’ permeability, hormones
activations, coagulation and produces the factors regulating
vascular spasm (7). The disturbances of endothelial cells’
function may determine vasostenosis and ischaemical defects.
This process is probably responsable for changes in the retinal
and choroidal tissue leading to the developement of the CSC.The
most probably is the focal occlusion of the choroidal
microcirculation leading to the local ischaemia and local RPE
damage.
If an auto-inflammatory etiology was solely responsible for the
development of CSC, steroids would probably have been needed to
suppress the inflammation. But it is documented that use of
corticosteroid may cause the developement of CSC (2).
However, independently of the kind of the pathogenesis of CSC,
an association between HP infection and CSC has recently been
documented and CSC could be an extra digestive expression of HP.
Otherwise HP infection could be a risk factor of transformation
the acute CSC in chronic and progresive process with
decompensation of RPE and severe vision loss.
Conclusions
The results of this study show that the prevalence of
Helicobacter pylori infection seems to be significantly higher
in patients with CSC than in control group, and the difference
is statistically important.
Helicobacter pylori infection may represent a risk factor for
incidence of CSC.
CSC patients with accompanied HP infection have statistically
more often a chronic form of CSC than other.
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The study was originally received 11.12.2008 (1091)/
Praca wpłynęła do redakcji 11.12.2008 (1091)
Accepted for publication 20.01.2009/
Zakwalifikowano do druku 20.01.2009 r.Adres do
korespondencji (Reprint requests to):
Katedra i Klinika Okulistyki AM
dr n. med. Magdalena Michałowska
ul. Chałubińskiego 2a
55-035 Wrocław
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Fig. 1. Presence of HP antigens in the
patients with CSC and in the control group.
Ryc. 1. Obecność antygenów HP u pacjentów z CSC i w grupie
kontrolnej.
Fig. 2. A frequency of HP antigen in patients
with CSC and in the control group.
Ryc. 2. Częstość występowania antygenu HP u pacjentów z CSC I
w grupie kontrolnej.
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Fig. 3. Presence of IGg anti – HP in the
patients with CSC and in the control group.
Ryc. 3. Obecność IG anty HP u pacjentów z CSC i w grupie
kontrolnej.
Fig. 4. A frequency of IGg anti – HP in
patients with CSC and in the control group.
Ryc. 4. Częstość występowania IG anty HP u pacjentów z CSC
i w grupie kontrolnej.
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