EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Fouad et al
ANTICARDIOLIPIN ANTIBODIES IN PATIENTS
WITH CHRONIC LIVER DISEASES
By
Yasser M Fouad* MD, Ashraf M Osman** MD, Hamdy Mokarrab*** MD,
Taha Hasanain*** MD, Mahmoud Saad*** MD and Waffa Abdelhameed
Departments of *Tropical Medicine, **Clinical Pathology and ***Internal medicine
El-Minia Faculty of Medicine
ABSTRACT:
Anticardiolipin antibodies (aCL) are frequently found in patients with
systemic lupus erythematosus and other autoimmune disorders as well as in both
chronic hepatitis B and chronic hepatitis C.
Aim: To study the anticardiolipin antibodies in patients with chronic liver disease and
correlate its presence with clinical features in these patients.
Patients and methods: This study included 60 patients with chronic liver disease (10
patients with chronic hepatitis (group A), 30 patients with liver cirrhosis (group B),
20 patients with hepatocellular carcinoma (groupC). Ten healthy persons matched to
age and sex were taken as control. All patients and subjects were subjected to the
following : history taking ,thorough clinical examination, abdominal Ultrasonography
and -Collection of serum blood samples: for liver function tests, serological markers,
alpha fetoprotein and anticardiolipin antibodies.
Results: there was no statistical significant influence of age, sex, PT, PC, alphafetoprotein, or Child class on the incidence of positive aCL antibodies. The incidence
of portal vein thrombosis (PVT) was lower (10.3%) in patients with positive aCL
antibodies than in patients with negative aCL antibodies (12.9%). However, the
incidence of positive aCL antibodies was higher in patients with positive aCL
antibodies and HCC (50%) than in patients with negative aCL antibodies and HCC
(28.6%).
Conclusion: The aCL antibodies are commonly found in patients with chronic liver
disease . The prevalent concept is that, in the majority of cases, aCL antibodies are
non-pathogenic and therefore their routine determination is not justified
INTRODUCTION:
Antiphospholipid (aPL) antibodies are a heterogenous family of
immunoglobulins that include lupus
anticoagulant and anticardiolipin antibodies. The presence of these antibodies characterises primary antiphospholipid syndrome consisting of
recurrent vascular thrombosis, fetal
losses,
and
thrombocytopenia.
(Hughes GRV, 1993)
HCV have anti-smooth muscle
antibodies, rheumatoid factor, antiliver-kidney-microsomal
(ALKM)
antibodies, anticaridolipin antibodies
(acl), and antinuclear antibodies
(ANA). (De-larranaga et al., 1996).
Infection with hepatitis C virus
(HCV) may lead to autoantibody
response. It has been reported that
chronically infected patients with
Zachou et al., (2003), found no
significance association between (acl)
antibodies and clinical features of
antiphospholipid syndrome (APS) in
Biron et al., (1998), Found a
high frequency of (aCL) antibodies in
patients with HCV related liver
cirrhosis and alcoholic liver disease.
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
patients with HCV infection. And
concluded that (aCL) antibodies might
not be pathogenic rather than being cofactor dependant. But a study
conducted in patients with chronic
HCV infection showed a high
prevalence of immunological G (IgG)
and/or (IgM) acl associated with
clinical manifestations of APS. (Prieto
et al., 1996).
Fouad et al
were separated under laminar airflow
cabinet with built-ii UV lamp that
provided a suitable dust- free
environment. Separated sera were
divided into 3 screw capped plastic
tubes 2 of them will be used for
deteremination of routine investigations and the other was kept frozen
at minus 20 till the time of serological
assay for anticardiolipin antibodies by
ELISA.
Aim of the Work:
To study the anticardiolipin
antibodies in patients with chronic
liver disease and correlate its presence
with clinical features in these patients.
It was done in Clinical
Pathology
laboratory,
El-Minia
University Hospital.
5- Routine laboratory investigations:
 Liver function tests: Using an automated clinical chemistery system dimension ES, Supplied
by
Dupont
Medical
products,
Wilminagton, Delaware, USA the
upper limit of normal for total
bilirubin is 1mg/dl (Moseley, 1996);
alanine transaminase (ALT) 65u/ml,
aspartate transaminase (AST) 37u/ml,
and alkaline phosphatase (ALP)
136u/ml (Hultcrantz et al., 1986),
serum albumin (3-5g/dl) and total
protein (6.4-8.2g/dl) (Tavill,1972).
 Prothrombine time &concentration
(P.T and P.C) was also assayed (Dade
behring Inc Newark, DE 19741USA
(Mammen,1994)
 Complete
blood
count
on
automated cell counter sysmex K 800.
PATIENTS AND METHODS:
This study included 60 patients
with chronic liver disease (10 patients
with chronic hepatitis, 30 patient with
liver cirrhosis, 20 patients with hepatocellular carcinoma); they were selected
from those attendants of the outpatient
clinic and/or admitted to the Tropical
Medicine
Department,
El-Minia
University Hospital.
The patients of liver cirrhosis
and hepatocellular carcinoma were
classified according to Child-Pugh
classification into group A, B and C
(Pugh et al., 1973).
Ten healthy persons matched
to age and sex were taken as control.
All patients were subjected to the
following:
1-Careful history taking :
2-Thorough clinical examination:
3-Abdominal Ultrasonography:
4-Collection of serum blood samples:
6- Serological assays:
A) Hepatitis B virus surface antigen
(HBsAg):
The Kit was supplied from
Hoechst Orient SAA, Germany.
Behring ELISA Processor II apparatus
was used for its determination.
B) Hepatitis C virus antibody (HCV ab):
The kit was supplied from
Innotest HCV-Ab III, Innogenetics,
Belgium. Behring ELISA Processor II
apparatus
was
used
for
its
determination.
About 10 ml of venous blood
sample was obtained from each patient
and control by sterile clean venpuncture and evacuated in a plain tube,
allowed to clot at 37" C for 20 min and
centrifuged at 3000r pm. The sera
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
HCV-RNA by RT-PCR:
The kit was supplied from
Promega Inc., USA. Reaction mixtures
consisted of 5 ul of target, 100 pmol of
each of the oligonucleotide primers,
1.25 U of the enzyme Taq polymerase
(Perkin-Elmer cetus, Norwalk, Conn.),
200uM
(each)
deoxynucleotide
triphosphate (Boehringer Mannheim,
Indianapolis, Ind.), 5 ul of 10x reaction
buffer (500mM KCL, 100mM tris-HCl
[PH 8.3], 15mM Mgcl2, 0.01%
gelatin), 10 ul of a50% glycerol
solution, 25 ug of isopsoralen per ml,
and high pressure liquid chromatography-grade distilled water to atotal
volume of 50ul in a microcentrifuge
tube.
C) Serum alpha-fetoprotein (AFP):
(Only for patients with HCC on top of
chronic liver disease); By ELISA
technique.
D) Anticardiolipin antibodies by
ELISA:
Fouad et al
* Assay procedure:
 One hundred uL of positive
control/calibrator, negative control and
diluted test specimens were dispensed
into wells. Then were incubated for
30-35 minutes at room temperature
(18-25`c).
 All wells were filled with diluted
wash buffer (300 UL per well), then
were shake into disposal container, it
was done for three times, the wells
were blotted thoroughly on absorbent
paper after the last wash.
 One hundred uL enzyme tracer
were pipette , then were incubated for
30-35 minutes at room temperature
(18-25`C).
 Washing step was repeated.
 One hundred of chromogen were
pipetted into all wells then were
incubated at room temperature (1825`C)for 9-10 minutes, away from
light.
 50 ul of stop solution were
dispensed into all wells in the same
order and at the same rate as for
chromogen, and were mixed by gently
tapping the plate. The color changed
from blue to yellow.
 The absorbance of each well was
measured at 450/620-690 nm.
 By special equation anti-cardiolipin
concentration was obtained.
* Principle of the assay:
The kit is a solid-phase enzyme
immunoassay. Microtitre wells are
coated with cardiolipin and B2glycoprotein (B2-GPI, apolipoprotein
H), the latter being cardiolipin cofactor, which forms complexes with
cardiolipin. The presence of cardiolipin and B2-glycoprotein l complexes
allows specific cardiolipin antibodies
to bind to the solid phase. Antigenprecoated microplate wells are incubated with controls and
serum
specimens. During the incubation,
antibody present in the test sample
binds to the coated wells. Horseadish
peroxidase-cojugated anti-human IgM
and IgG is incubated in the wells to
recognize the autoantibodies bound to
the coated wells. Chromogen is added
and autoantibodies are measured using
a spectrophotometric plate reader. At
the end of each incubation, aspirating
and washing remove the unbound
material.
STATISTICAL METHODS:
Data
were
statistically
represented in terms of range, mean,
standerd deviation (±SD), and percentage of the total number. Comparison
between different groups in the present
study was done using analysis of
variant tests (ANOVA), Chi square
tests and multiple linear regression
test. A probability values (P value) less
than 0.05 was considered significant
(S), less than 0.01considered highly
significant (HS), and less than .001
considered significant (VHS). All
statistical calculations were done using
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
computer programs Microsoft Excel
version 5 and SPSS (statistical
Package For Social Science) statistical
program.
Fouad et al
PC, alpha-fetoprotein, or Child class
on the incidence of positive aCL
antibodies. The incidence of portal
vein thrombosis (PVT) was lower
(10.3%) in patients with positive aCL
antibodies than in patients with
negative aCL antibodies (12.9%).
However, the incidence of positive
aCL antibodies was higher in patients
with positive aCL antibodies and HCC
(50%) than in patients with negative
aCL antibodies and HCC (28.6%). The
results are shown in tables (1-10) and
figures (1-2)
RESULTS:
This study included 60 patients
with chronic liver disease (10 patients
with chronic hepatitis (group A), 30
patients with liver cirrhosis (group B),
20 patients with hepatocellular carcinoma (groupC)). Ten healthy persons
matched to age and sex were taken as
control. There was no statistical
significant influence of age, sex, PT,
Table (1): The demographic data of the different groups of patients with chronic liver
disease and the control.
Demographic data
Age (mean±SD)
Male
Sex
Female
Residence
Rural
Urban
Group
A
(N=10)
49.7±7.3
4
40%
6
60%
8
80%
2
20%
Group
B
(N=30)
51.3±10.7
15
50%
15
50%
23
76.7%
7
23.3%
Group C
(N=20)
54.3±8
14
70%
6
30%
20
100%
0
0%
Controls
(N=10)
36.7±14.9
5
50%
5
50%
2
20%
8
80%
Table (2): Thrombotic complications in the studied groups of patients with chronic
liver disease.
Thrombosis
Group A
Group B
Group C
P-value
(N=10)
(N=30)
(N=20)
0
0
7
0.002**
PVT
0%
0%
35%
0
1
0
DVT
0%
3.3%
0%
10
29
13
No thrombosis
100%
96.7%
65%
(Data are expressed as number and percent (%). Kruskal-Wallis test was used. **
high significant).
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Fouad et al
Table (3): Showed the relation between the presence of aCL antibodies and the age
of patients with chronic liver disease.
Age
Median (range)
P-value
ACL antibodies
Positive patients
Negative patients
(N=29)
(N=31)
52.5
54.5
(45-67)
(35-70)
0.59 NS
(Data are expressed as median (range). Mann-Whitney test was used for comparing
positive and negative aCL antibodies s groups. NS: non significant).
Table (4): Showed the relation between the presence of aCL antibodies and the sex of
patients with chronic liver disease.
Sex
aCL antibodies
Positive patients
(N=29)
17
Male
Female
Negative patients
(N=31)
16
58.6%
51.6%
12
15
41.4%
P-value
48.4%
0.58 NS
(Data are expressed as number and percent (%). Chi-square test was used. NS: non
significant).
Table (5): Relation between Child's classification of patients with positive and
patients with negative aCL antibodies.
Child class.
Child A
Child B
Child C
aCL antibodies
Positive patients
Negative patients
(N=29)
(N=31)
6
3
20.7%
9.7%
13
11
44.8%
35.5%
10
17
34.5%
54.8%
P-value
0.23 NS
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Fouad et al
Table (6): Relation between PC% and PT of patients with positive and patients with
negative aCL antibodies.
Coagulation profile
PC (%)
P-value
PT (sec.)
aCL antibodies
Positive patients
Negative patients
(N=29)
(N=31)
63
53.5
(40-67)
(32-66)
0.06 NS
15.7
(15.1-20)
P-value
16.6
(15.3-30)
0.20 NS
(Data are expressed as median (range). Mann-Whitney test was used for comparing
positive and negative aCL antibodies groups. NS: non significant).
Table (7): Relation between aCL antibodies and alpha-fetoprotein in patients with
HCC (n=20).
Alpha-fetoprotein
Median (range)
P-value
aCL antibodies
Positive patients
Negative patients
(N=29)
(N=31)
306.5
235.5
(111-499)
(44.4-3584)
0.32 NS
(Data are expressed as median (range). Mann-Whitney test was used for comparing
positive and negative aCL antibodies groups. NS: non significant).
Table (8): Incidence of thrombotic events (PVT) in relation to aCL antibodies in
patients with HCC (n=20).
PVT
No PVT
HCC+Positive aCL
antibodies
(N=6)
3
50%
3
50%
P-value
HCC+Negative aCL antibodies
(N=14)
4
28.6%
10
71.4%
0.35 NS
(Data are expressed as number and percent (%). Chi-square test was used. NS: non significant).
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Fouad et al
Table (9): Comparison of median of aCL antibodies in patients with HCC with and
without PVT.
aCL antibodies
HCC with PVT
(N=7)
6.1
(4.6-15.4)
Median (range)
HCC without PVT
(N=13)
5.6
(2.3-18.9)
P-value
0.241 NS
(Mann-Whitney test was used. NS: non significant).
Table (10): Independent risk factors for Anticardiolipin antibodies.
Risk factors
Beta
Age
.170
Child classification
.018
Portal vein thrombosis
-.079
Platelets
-.087
ALT
-.098
Sex
-.15
AST
-.161
PT
-.162
PC
-.325
Beta (multiple linear regression analysis)
P value
.174(NS)
.922(NS)
.551(NS)
.592(NS)
.542(NS)
.961(NS)
.337(NS)
.513(NS)
.283(NS)
100%
90%
80.00%
80%
70%
70%
60%
50%
50%
50%
40%
30%
30%
20.00%
20%
10%
0%
Positive ACAs
Group I
Negative
Group II
Group III
Fig. 1: Percentage of patients with positive or negative aCL antibodies in the studied patients.
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Fouad et al
35%
65%
HCC and PVT
HCC w ithout PVT
Fig. 2: Incidence of PVT in-group III (HCC).
protein cofactors (Roubey et al., 1995;
Arvieux et al., 1995).
DISCUSSION:
Infection with HCV tends to
induce nonspecific autoimmune reactions, as demonstrated by the high
prevalence of various non-organspecific autoantibodies, usually in low
titers. The non-organ-specific antibodies include the antinuclear, smooth
muscle, antineutrophil, and liverkidney microsomal antibodies (Cacoub
et al., 2000). Anticardiolipin antibodies (aCL) have also been reported
in patients with HCV infection (OrdiRos et al., 2000).
Goldberg et al., (1995) suggest
that aCL-related illnesses may be
familial.
They
determined
the
frequency of anticardiolipin antibodies
(aCL) and their clinical sequelae in
family members of aCL-positive
patients,
and
concluded
that
antinuclear antibodies (ANA), aCL,
and clinical events associated with
antiphospholipid antibodies occur with
increased frequency in relatives, but
not spouses of aCL-positive probands.
Both chronic HBV and chronic
HDV infections are considered potent
stimulants for the production of ACAs.
The presence of ACAs in a great
proportion of HBV-cirrhosis-related
HCC patients with PVT suggests their
possible participation in thrombotic
mechanisms and in the hypercoagulable state that occurs in advanced
liver disease and HCC (Elefsiniotis et
al., 2003). The mechanism by which
anticardiolipin antibodies serve their
role in chronic infectious diseases is
explained in different studies indicated
that, as well as cardiolipin, the
phospholipid binding proteins ß2glycoprotein I and prothrombin can
behave as real antigens as well as
Similarly, several reports have
described a high prevalence of acl
antibodies in chronic hepatitis C virus
(Matsuda et al., 1995, Prieto et al.,
1996, Violi et al., 1997, Mangia et al.,
1999, Harada et al., 2000, and OrdiRos et al., 2000).
It has been proposed that the
release from HCV-infected cells of
pro-coagulant products consisting of
membrane fragments and negatively
charged
macromolecules
might
stimulate the synthesis of ACA. In
most cases these antibodies are
cofactor independent and of nonpathogenic type (Dalekos et al., 2000,
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EL-MINIA MED., BULL., VOL. 18, NO. 1, JAN., 2007
Harada et al., 2000, and Ordi-Ros et
al.,
2000).
However,
cofactor
dependency of aCL antibodies has
been described in some patients with
chronic HCV as reported by Alric et
al., (1998) and Leroy et al., (1998).
Fouad et al
Further, sera from all but one
anticardiolipin antibody-positive HCV
patient
were
negative
for
phospholipid-dependent
anti-beta2
glycoprotein I antibodies. These
results suggest that anticardiolipin
antibodies are frequently found in
patients with chronic HCV infection,
but they do not appear to be of clinical
importance.
In the present study, there was
no statistical significant influence of
age, sex, AST, ALT, PT, PC, alphafetoprotein, or Child class on increase
the incidence of positive aCL
antibodies. Thus, the positive aCL
antibodies levels might not have a
major clinical significance in patients
with chronic liver diseases infected by
HCV.
Harada et al., (2000) reported
that, immunologic disturbances induced by HCV or prolonged tissue
damage in systemic organs as a result
of the extra hepatic manifestations of
HCV infection may induce the
production of antibodies to various
cardiolipin-binding
proteins
or
phospholipids. Nevertheless, Prieto et
al., (1996) showed a high prevalence
of portal hypertension, thrombotic
events, and thrombocytopenia. Biron
et al., (1998) found more liver fibrosis
in patients with HCV and aCL
antibodies.
In agreement with our study,
most of published reports did not find
a clinical significance for the presence
of aCL antibodies as such reported by
Matsuda et al., (1995) and Cacoub et
al., (1997).
Similarly, and in order to
evaluate
the
prevalence
and
importance
of
antiphospholipid
antibodies in various chronic liver
diseases, Harada et al., (2000)
determined the levels of anticardiolipin antibodies, platelet numbers, and
levels of platelet-associated immunoglobulin G (PA-IgG) and thrombinantithrombin III complex (TAT) in
patients with chronic HCV infection,
chronic hepatitis B virus (HBV)
infection, and primary biliary cirrhosis
(PBC). The prevalence of anticardiolipin antibodies in patients with HCV
infection was significantly higher than
that in control subjects or individuals
with the other liver diseases examined.
However, there was no significant
correlation between anticardiolipin
antibodies and platelet counts or TAT.
The frequency of thrombotic complications was similar in anticardiolipin
antibody-positive
and
-negative
patients with chronic HCV infection.
Differences in demographic
and genetic background, HCV
subtypes, and lengths of follow up
periods may explain the differences
between the various studies.
In the present study, the
incidence of portal vein thrombosis
(PVT) was 10.3% (3/29) in patients
with positive aCL antibodies that were
lower than its incidence in patients
with negative aCL antibodies (12.9%;
4/31). However, the incidence of was
higher in patients with positive aCL
antibodies and HCC (50%) than in
patients with negative aCL antibodies
and HCC (28.6%).
Some authors have found a
higher prevalence of thrombotic events
in aCL antibodies-positive patients
than in aCL antibodies -negative
patients as stated by Prieto et al.,
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(1996), who found that thrombotic
processes occurred in 45.5% of aCL
antibodies-positive chronic hepatitis C
patients and in only 15.3% of those
who were aCL antibodies-negative.
Interestingly, some of aCL antibodies positive patients suffered from
repeated thrombotic processes (myocardial infarction and retinal central
vein thrombosis in one case and
ischaemic stroke plus deep vein
thrombosis in another case).
Fouad et al
It should also be recognized
that antiphospholipid antibodies with
pro-coagulant activity might occur in
isolated cases of HCV infection (Josi
and Prieto, 2003).
In this respect, Alric et al.,
(1998) described an interesting case of
a patient with HCV infection who
presented with cofactor-dependent
aCL antibodies and associated thrombotic disorder. In this case, interferon
therapy induced elimination of the
virus and negativization of cofactordependent aCL antibodies together
with improvement of the thrombotic
disease. Discontinuation of the therapy
and a subsequent relapse of viral
infection were accompanied by the
reappearance of cofactor-dependent
aCL antibodies and recrudescence of
the thrombotic process.
Oksuzoglu et al., (2003) found
that anticardiolipin antibody concentrations were significantly higher in
cirrhotics with portal vein thrombosis.
Thus, they concluded that anticardiolipin antibodies might play a role in
the development of portal vein thrombosis in cirrhosis.
In a study by Elefsiniotis et al.,
(2003), the presence of aCL antibodies
in a great proportion of HCC patients
with PVT suggests their possible
participation in thrombotic mechanisms and in the hypercoagulable state
that occurs in advanced liver disease
and HCC.
The present study clearly
revealed that, aCL antibodies are one
of the most common autoantibodies
found in patients with chronic liver
disease (mainly in chronic viral hepatitis). The prevalent concept is that, in
the majority of cases, aCL antibodies
are non-pathogenic and therefore their
routine determination is not justified.
However, in particular patients with
special immune reactivity or with
abnormal haemostatic regulation, they
may exert a pro-coagulant effect and
be involved in the genesis of
thrombotic events. The question as to
whether aCL antibodies are purely
neutral epiphenomenic autoantibodies
or whether they have a role in disease
progression or in the pathogenesis of
extrahepatic manifestations of viral
hepatitis, as yet, an unresolved issue.
Most reports clearly indicate
that, in chronic HCV, aCL antibodies
are a mere epiphenomenon of the
disease
possibly
secondary
to
activation of the clotting system in this
infection as reported by Violi et al.,.
(1997).
Also, Mangia et al., (1999)
found that, in patients with nonautoimmune liver disease, aCL
production is an epiphenomenon of the
liver damage and is not associated
with thrombotic complications. These
data do not support the hypothesis that
HCV is a cause of the antiphospholipid syndrome.
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‫‪Fouad et al‬‬
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‫األجسام المضادة للكارديوليبين فى أمراض الكبد المزمنة‬
‫ياسر فؤاد* – أشرف عثمان** – حمدى مقرب* – طه حسانين* –‬
‫محمود سعد** – وفاء عبد الحميد**‬
‫أقسام *طب المناطق الحارة و**الباطنة العامة و***الباثولوجيا األكلينيكية‬
‫كلية طب المنيا‬
‫دلت العديد من الدراسات التى أجريت علي األجسام المضادة للكارديوليبين على مصااببتاا‬
‫للعديد من األمراض الفيروسية مثل االلتااب الكبدي الفيروسي (سى) وبعض باالت مرض‬
‫تليف الكبد الناتج عن إدمان الكبوليات‬
‫ومنذ وقت طويل كانت أصابع االتاام تشير الى ان الفيروسات قد تسبب اإلصابة بالعديد من‬
‫األمراض المناعية و ذلك عن طريق التشابه الجزيئى مع االنتيجينات الذاتية او بالتفاعل مع‬
‫بروتينات الجسم ذاته إلبداث مولدات اجسام مناعية‪0‬‬
‫وماان التعااارف عليااه أن االلتااااب الكباادي الفيروسي(سااي) يصاااببه العديااد ماان األجسااام‬
‫المضادة الذاتية إال أن هذه األجسام المضاد الذاتية وعالقتاا باذا المرض غير مبددة بتاى‬
‫اآلن‪ .‬و فى الوقت الراهن أصبح فيارو االلتاااب الكباد (ساى) موضاع اتااام مان بعاض‬
‫الدراسات بأنه قد يسبب مرضاى متالزماة الفوسافات الشابمى ولااذا كاان ال ارض مان هاذه‬
‫الرسااالة هااوا مباولااة معرفااة الااربط بااين اإلصااابة بماارض الكبااد وأرتفااا نساابة األجسااام‬
‫المضادة للكارديوليبين ومد إمكانية وجود أعراض مرض متالزمة الفوسفات الشبمي في‬
‫هذه الباالت‪.‬‬
‫و قد اشتملت الدراسة على ‪ 00‬مريضا‪ ,‬تراوبت اعماار المرضاى باين ‪ 00-00‬سانة وكاان‬
‫عدد الذكور ‪ 23‬وعدد اإلناث ‪ 23‬ومنام ‪ 23‬من الريف و‪ 2‬من البضر وقد تم تقسيمام الى‬
‫ثالث مجموعاتا‬
‫‪ - 1‬مرضى مصابون بالتااب كبدي فيروسي مزمن‪.‬‬
‫‪-3‬مرضى مصابون بتليف بالكبد‪.‬‬
‫‪-2‬مرضى مصابون بأورام كبدية‬
‫باالضافة الى ‪ 10‬أشخاص كمجموعة اختبار‪.‬‬
‫وقد تم إجراء االتى لكل مريضا‬
‫‪-1‬التعرف على التاريخ المرضى الكامل‪.‬‬
‫‪ -3‬إجراء فبص اكلينيكى دقيق وشامل‪.‬‬
‫‪-2‬عمل أشعة تليفزيونية على البطن بالموجات فوق الصوتية‪.‬‬
‫‪-0‬عمل تباليل كاملة لوظائف الكبد‪.‬‬
‫‪-2‬عول اختبار لوجود الجسام المضادة للكارديوليبين ‪.‬‬
‫ثم بساب نتائج الدراسة وجدولتاا وتبليلاا إبصائيا‪ .‬وقاد أوضابت النتاائج وجاود األجساام‬
‫المضاااادة للكاااارديوليبين فاااي نسااابة غيااار قليلاااة (‪ )%0282‬مااان مرضاااى االلتاااااب الكبااادي‬
‫الفيروسي‪.‬‬
‫كمااا لااوبظ عاادم وجااود عالقااة بااين تواجااد مثاال هااذه األجسااام المضااادة وباادوث التجلطااات‬
‫الدموية أو جلطة الوريد البابي الكبدي ‪ ,‬كما نفت الدراسة بدوث مرض متالزمة الفوسافات‬
‫ألشبمي في مثل هؤالء المرضى ‪.‬‬
‫وبذلك القول ال توجد عالقة إبصائية دالة على ابتمال وجود صلة تالزم بين المرضين‬
‫وفي النااية ينصح باالستمرار في الدراسات واألبباث في مثل هذا المجال ‪.‬‬
‫‪225‬‬