ASSESSMENT OF THE RELATION BETWEEN SERUM-ASCITES ALBUMIN
CONCENTRATION GRADIENT WITH ESOPHAGEAL VARICES AND ITS
COMPLICATION
Entesar H El-Sharqawy MD, Reda El-Badawy MD, Eman M Fathy MD,
Ibrahim El Attar MD and Hosam Amin MD.
Department of Hepatology, Gastroenterology and Infectious Diseases,
Faculty of Medicine, Benha University, EGYPT.
ABSTRACT
OBJECTIVE: We aimed to evaluate the correlation between serum-ascites albumin concentration gradient (SAAG)
with esophageal varices (EV) presence and grading, and to assess the relationship between SAAG measurements and the
occurrence of gastrointestinal hemorrhage in cirrhotic patients with ascites. METHODS: Our study included 45 nonalcoholic cirrhotic cases with ascites. They had routine clinical, ultrasonographic and laboratory investigations including
ascitic fluid analysis. They had measurement of SAAG computed. An upper gastrointestinal endoscopy was done in all
cases to assess the presence and size of EV. RESULTS: 36 of our patients (80%) had EV. The mean SAAG level was
1.46 ± 0.27 gm/dL for all cases. No correlation was found between SAAG and any of the studied clinical or biochemical
parameters. By using the ROC Curve, a SAAG value at a level of (>1.55gm/dL), was a good predictor of the presence of
EV with 100% sensitivity and 71.4% specificity. The presence of EV was positively correlated with serum bilirubin,
prothrombin time (PT), and spleen size. Meanwhile, it was negatively correlated with serum albumin, serum total protein,
platelet count and total protein in ascetic fluid. On univariate analysis of variants associated with the presence of large
esophageal varices, only the presence of splenomegaly could predict high grade varices. On comparing patients with and
without bleeding varices, the EV grade, portal vein diameter (PVD), spleen size and creatinine level were significantly
higher in the group of bleeding varices [p values were 0.002, 0.006, 0.01 and 0.012 respectively]. CONCLUSION: A
SAAG score (≥1.55 gm/dL) is a useful predictor of the presence of EV in cirrhotic patients with ascites. This finding can
assist clinicians in determining the urgency of care and referral for upper gastro-intestinal endoscopy in cases with
ascites. Meanwhile, SAAG was not valuable in screening and predicting complications, such as bleeding from
esophageal varices.
Keywords: Ascites, Serum-ascites albumin concentration gradient (SAAG), Hematemesis, Esophageal varices (EV),
Portal Hypertension (PHTN).
Introduction and Aim of the Work
SAAG is a good biochemical marker and a
better discriminator of portal hypertension (PHTN) than
ascites protein concentration. Patients with gradients of
>1.1 gm/dL have PHTN, while those with gradients of
<1.1 gm/dL do not, with accuracy rate 97% (Runyon et
al 1992). Indeed, SAAG is now considered a useful
physiological and clinical tool in the work-up of ascites.
"High-albumin gradient" (>1.1 gm/dL) or "low-albumin
gradient" (<1.1 gm/dL) have replaced the terms
"transudative" or "exudative" in the description of
ascites in all recent publications (Babu et al 2004 & Jain
et al 2004). The correlation between SAAG and EV was
emphasized. Additionally, SAAG was proposed to be a
factor determining the degree of PHTN and the
prognosis in the patients with cirrhosis due to alcohol
(Torres et al; 1998). Despite that, such a correlation
could not be proven in non-alcoholic cirrhosis.
It has been reported that most of the nonalcoholic cirrhotic patients presenting with ascites and
all of the patients with SAAG values greater than 2.0
had esophageal varices (Demirel et al., 2003). Another
research group found that SAAG in patients with PHTN
and ascites was correlated significantly with
gastrointestinal bleeding and splenomegaly. They
concluded that SAAG had a sensitivity of 100% and
specificity of 33.33% for prediction of bleeding EV
(Mene et al., 2003).
In the current work, we aimed to evaluate
whether such a correlation exists between SAAG values
and esophageal varices, presence and grading, and to
assess the relationship between SAAG measurements
and the occurrence of gastrointestinal bleeding in a
group of non-alcoholic cirrhotic patients with ascites.
Patients and Methods
Patients:
Fourty five patients with ascites due to liver
cirrhosis were chosen between July 2004 and June 2005
from the inpatients of the department of Hepatology,
Gastroenterology and Infectious diseases, Benha
University Hospital. Diagnosis of the cases was based
on history taking including past history of
schistosomiasis and/or viral hepatitis, clinical
examination, laboratory investigations, plus ultrasound
or previous liver biopsy. None
of our cases was
alcoholic. Exclusion criteria included the presence of
spontaneous bacterial peritonitis, hepatic or extrahepatic metastasis, portal or splenic vein thrombosis,
medical
contraindications
for
gastrointestinal
endoscopy, other etiologies of ascites, and hematemesis
due to other causes than portal hypertension
complications.
separated by normal mucosa; (GIII): the varices are
confluent around the circumference of the esophagus
and cannot be depressed by the endoscope.
Statistical Analysis:
SPSS software (version 10) was used for
statistical analysis. Descriptive values were expressed
as mean ± standard deviation. Unpaired t-test was used
to compare the mean values between 2 groups.
Spearman correlation (r) test and univariate analysis of
variants were used for analysis of correlations. P values
<0.05 were considered as significant.
The diagnostic value of SAAG for prediction
of EV presence was assessed using receiver operating
characteristics (ROC) curve. Overall, diagnostic value
was given by the area under the curve (AUROC); where
an AUROC from 0.9-1.0 describes an excellent test,
from 0.8-0.9 a good test and from 0.7-0.8 is a fair test.
Then sensitivity and specificity for a given cut off were
calculated.
Methods:
During the first 24 hours of hospital admission,
ascitic fluid paracentesis was done under aseptic
conditions. Blood samples were taken simultaneously or
within 30 minutes of paracentesis. Ascitic fluid and
blood samples were immediately sent to the laboratory
to be analyzed for albumin concentration. Smears of
ascitic fluid were fixed and stained by hematoxylineosin and microscopically examined for their cellular
content. Routine laboratory investigations included
CBC and liver profile tests were done. Detection of
anti-schistosomal antibodies in serum was done by
indirect hemagglutination assay using Schistosomiasis
Fumouse Kit. Hepatitis viral markers; Anti-HCV-Ab,
HBsAg, HBsAb and HBcAb, were done using ELISA
technique. Ultrasound examination of the patients was
performed by Toshiba Eccocee machine using a convex
sector probe (3.75 MHz). The biochemical and
serological and ultrasonographic measures were done in
the departments of Clinical Pathology and Radiology at
Benha university hospital as a part of the routine
workup of the cases after admission to the department
of Hepatology, Gastroenterology and Infectious
diseases.
Sigmoidoscopy was done, and rectal snips
were taken and examined for schistosomal infection. All
patients had upper gastrointestinal endoscopy
performed by GIF 230 Olymbus esophago-gastroduodenoscope. Esophageal varices were graded
according to the Japanese classification in North Italian
Endoscopic Club (1988) as follows: Grade I (GI): the
varices can be depressed by the endoscope; (GII): the
varices cannot be depressed by the endoscope and are
Results
Eighteen males and 27 females (45 patients) with
hepatic ascites were included in our work. The mean
age of our patients was 49.84 ± 7.28 (range: 37-67)
years. The causes of liver cirrhosis were: hepatitis C
virus in 33 (73.33%) and hepatitis B virus in 6 (13.33%)
cases. The etiology could not be determined in the
remaining 6 patients (13.33%). Serum was positive for
anti-schistosomiasis antibodies in 37 cases (82.3%)
while rectal snips were positive in 25 (55.96%) of all
patients.
According to Child-Pugh classification ,15
patients (33.33%) were class B & 30 patients (66.66%)
were class C. Twenty four (53%) of the patients had a
history of gastrointestinal bleeding. On endoscopic
examination 36 patients (80%) had EV that was (GI) in
6 (13.33%), (GII) in 16 (35.56%) and (GIII) in 14
(31.11%) patients. Gastric varices was combined with
EV in 9 (20%) and portal gastropathy was found in 32
(71.1%) patients.
On comparing the patients' criteria in 36 cases
with EV (group I) versus 9 caeses without EV (group
II), only spleen size was statistically significant,
p<0.001 (Table 1). The presence of EV showed a
significant positive correlation with serum bilirubin,
prothrombin time (PT), and spleen size in addition to a
near significant positive correlation with Child-Pugh
grade & portal vein diameter (PVD) (r = + 0.32, p =
0.054 for both). Meanwhile, a significant negative
correlation of the presence of EV could be detected with
each of serum albumin, serum total protein, platelet
count and ascetic fluid total protein (Table 2).
SAAG between 1.5 and 1.99 gm/dL and in the only case
with SAAG value greater than 2.0 gm/dL (p>0.05;
Figure 1).
On univariate analysis of variants associated
with the presence of large esophageal varices, only the
increase in the size of the spleen size was a predictor of
high grade varices; p<0.05 (Table 3). No correlation
could be found between SAAG and any of the studied
clinical, biochemical parameters, or the presence or
grade (Table 4) of EV.
By using the ROC Curve to evaluate SAAG in
prediction of EV presence (Figure 2), a SAAG value at
a level ≥ 1.55 gm/dL, is a good predictor of the
presence of EV. The AUROC was (0.85 ± 0.09), with
100% sensitivity and 71.4% specificity.
Table (5) shows a comparison of the criteria of
24 patients with hematemesis (group A) versus 21 cases
without (group B). Each of the EV grade, PVD, spleen
size, and creatinine level was significantly higher in
those with hematemesis, with p values of 0.002, 0.006,
0.01, and 0.012 respectively.
The assessment of different cut-off values of
SAAG in relation to the presence of EV revealed that
EV was present in each of the 2 patients with SAAG
less than 1.1 gm/dL; 17 of the 22 cases with SAAG
between 1.1 and 1.49 gm/dL; 6 of the 20 patients with
Table (1): Comparison of the patients' criteria in the group (I) with
Esophageal Varices (n=36) versus the group (II) without Esophageal
Varices (n =9).
Parameter
Group
Mean
SD
Platelet Count
(Thousands/ml)
PT
(seconds)
S. Bilirubin
(mg/dL)
S. Albumin
(gm/dL)
S. Total Protein
(gm/dL)
Ascitic fluid
Protein
(gm/dL)
Ascitic fluid
Albumin
(gm/dL)
SAAG
(gm/dL)
S. creatinine
(mg/dL)
PVD
(mm)
Spleen size
(cm)
I
II
I
II
I
II
I
II
I
II
I
II
98.84
69.89
18.6
17.9
2.59
3.09
2.68
2.39
5.68
5.7
2.32
2.03
65.53
9.02
2.7
3.3
1.35
1.19
0.32
0.45
0.53
0.55
0.55
0.55
I
II
1.25
0.86
0.35
0.22
I
II
I
II
I
II
I
II
1.08
1.5
1.53
1.37
14.22
13.56
15.41
12
0.13
0.26
0.25
0.23
0.87
1.74
2.3
1.15
t
p
0.007
> 0.05
0.167
> 0.05
0.193
> 0.05
0.05
> 0.05
0.457
> 0.05
0.094
> 0.05
0.0002
> 0.05
0.294
> 0.05
0.043
> 0.05
0.156
> 0.05
5.628
< 0.001
p>0.05 [non signficant]; p<0.05 [significant]; p<0.001[highly significant]
Table (2): Correlation between the presence of EV and the studied
Clinical, Ultrasonographic and Biochemical parameters.
Presence of EV
r
p
Child-Pugh Score
S. Albumin
S. Total Protein
Ascitic fluid Protein
Ascitic fluid Albumin
SAAG
S. Bilirubin
Platelet Count
PT
PVD
+0.32
-0.39
-0.34
-0.57
-0.13
-0.28
+0.60
-0.38
+0.54
+0.32
= 0.054
< 0.05
< 0.05
< 0.0001
> 0.05
> 0.05
< 0.05
< 0.05
< 0.05
= 0.054
Spleen size
+0.43
< 0.05
Parameter
p>0.05 [non signficant]; p<0.05 [significant]; p<0.0001[highly significant]
Table (3): Comparison of the mean ± SD of different subgroups of the
group of Esophageal Varices according to the grade of EV in different
studied parameters
Variants
GI
(n=6)
G II
(n=16)
G III
(n=14)
F
Platelet Count
(Thousands/ml)
S. Bilirubin
(mg/dL)
S. Total Protein
(gm/dL)
S. Albumin
(gm/dL)
PT
(Seconds)
SAAG
(gm/dL)
PVD
(mm)
Spleen size
(cm)
74.33 ± 57.31
94.29±61.06
3.43
> 0.05
3.44±1.66
91.60±69.8
0
2.89±1.27
1.99±1.14
2.75
> 0.05
5.73 ± 0.72
5.83 ± 0.54
5.63 ± 0.55
3.42
>0.05
2.75 ± 0.32
2.67 ± 0.36
2.59 ± 0.27
1.82
> 0.05
17.6 ± 4.1
18.2 ± 3.9
18.9 ± 3.2
2.63
> 0.05
1.53 ± 0.25
1.49 ± 0.26
1.14 ± 0.053
3.83
> 0.05
14.33 ± 0.82
14.38 ±
0.89
14.89 ±
1.78
14.07 ± 0.99
1.68
> 0.05
16.99 ± 1.23
4.21
< 0.05
13.44 ± 1.37
p>0.05 [non signficant]; p<0.05 [significant]
p
Table (4): Spearman's Correlation Coefficients (r) of Serum-Ascites
Albumin Concentration Gradient (SAAG) to different Parameters:
Parameter
Child-Pugh Score
Hematemesis.
EV presence
EV Grading
S. Bilirubin
Platelet Count
PT
S. Albumin
Spleen size
PVD
r
p
-0.12
+0.35
-0.28
+0.31
+0.14
-0.08
+0.24
+0.28
+0.23
+0.18
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
> 0.05
p>0.05 [non signficant]
18
16
14
12
10
No.of Cases
8
6
4
2
0
Esophageal Varices
Presence
Esophageal Varices
Absence
<1.1
1.11.49
1.51.99
>2
SAAG(g/dl)
Figure (1): Distribution of esophageal varices in relation to
different cut–off values of SAAG.
Figure (2): ROC curve testing the ability of SAAG value
To identify the presence of Esophageal Varices.
ROC Curve
1.00
.75
.50
Sensitivity
.25
0.00
0.00
.25
.50
.75
1.00
1 - Spec if ic ity
Diagonal seg ments are produced by ties.
(The AUROC = 0.85±0.09)
Table (5): Comparison of the patients' criteria between cases of group (A)
[n =24] with the hematemesis versus those without hematemesis of group B
[n=21].
Parameter
Platelet
(Thousands/ml)
S. Bilirubin
(mg/dL)
S. Creatinine
(mg/dL)
S.Albumin
(gm/dL)
Ascitic fluid Protein
(gm/dL)
Ascitic fluid Albumin
(gm/dL)
SAAG (gm/dL)
PVD (mm)
Spleen Size (cm)
EV grading
Group
Mean
SD
A
B
A
B
A
B
A
B
A
B
A
B
A
B
A
B
A
B
A
B
89
93
2.51
2.91
1.59
1.41
2.62
2.66
2.02
2.4
1.09
1.26
1.51
1.19
15.2
13.15
16.3
14.13
2.48
1.29
67.71
49.30
1.35
1.29
0.27
0.22
0.24
0.46
0.51
0.50
0.31
0.42
0.30
0.33
1.44
2.30
1.54
2.14
1.08
1.31
Discussion
Esophageal varices may cause life-threatening
bleeding with attendant high hospital cost. Since effective
preventive modalities for variceal hemorrhage have been
established, early detection of esophageal varices is
t
p
0.21
> 0.05
0.57
> 0.05
2.76
0.012
0.41
> 0.05
2.05
> 0.05
2.03
>0.05
1.81
>0.05
3.13
0.006
2.99
0.01
3.48
0.002
critical for prevention of bleeding. Currently, endoscopic
screening is widely recommended to patients who have
the diagnosis of cirrhosis. Urgent or emergent endoscopy
is still advocated to accurately diagnose bleeding
esophageal varices. However, endoscopic screening also
burdens medical resources. An accurate non-invasive
diagnostic model to predict the presence of esophageal
varices may reduce unnecessary endoscopic procedures
and prophylactic medication and may improve costbenefit of these approaches.
A highly significant correlation was observed by
Kajani et al (1990) between SAAG and the portal pressure
in patients with alcoholic liver disease. They concluded
that, SAAG and portal pressure are statistically correlated
in individuals with alcoholic liver disease but not in those
with a non-alcoholic cause of cirrhosis. The correlation
between SAAG and esophageal varices was emphasized
and additionally, SAAG was proposed to be a factor
determining the degree of PHTN and the prognosis of the
patients with cirrhosis due to alcohol in the study of Torres
et al., (1998). In a more recent study, no correlation was
found in patients with non-alcoholic cirrhosis (Demirel et
al; 2003). Meanwhile, Mene et al (2003) found that SAAG,
in patients with PHTN and ascites, was correlated
significantly with each of gastrointestinal bleeding and
splenomegaly. In this study we have tried to propose a cutoff value for SAAG in discriminating patients with and
without esophageal varices and to assess any association
between SAAG measurements and the occurrence of
gastrointestinal hemorrhage in a group of cirrhotic patients
with EV and ascites.
In the present study, the mean SAAG was 1.46 ±
0.27 (0.9-2.1) gm/dL. Two of our cases (4.4%) had low
SAAG (<1.1 gm/dL) and 43 (95.6%) patients had high
SAAG (>1.1 gm/dL).This is in consonant with the findings
of the study of Samal and associates in 2001.They reported
the SAAG level of their cirrhotic patients was 1.33 ± 0.36
gm/dL. Among 132 cirrhotic patients, Al-Knawy (1997)
found that SAAG was 1.71 ± 0.61 gm/dL, and that five
patients had a SAAG <1.1 g / dL. The mean SAAG in the
study of Dittrich et al (2001) was 2.0 gm/dL. On the
contrary, Jain et al, (2004) found that, 19 patients with
documented PHTN had low SAAG (<1.1g/ dL), and none
of them was found to have any other cause of ascites. They
have attributed this finding to high serum globulin or low
serum albumin, and they have postulated corrected SAAG
ratio for patients with high globulin by this formula: {
corrected SAAG = SAAG [0.21 + (0.208× Serum globulin
gm/dL)}.
No correlation was detected in our work between
SAAG and the presence or grading of EV (Tables 1, 2, 3
& 4, and Figure 1). This coincides with Demirel et al,
(2003) who found no significant correlation between
SAAG and EV in patients with non-alcoholic cirrhosis.
They concluded that, most of the patients presenting with
ascites and all of the patients with a SAAG value greater
than 2.0 had EV. On the other hand, the studies of Torres
et al (1998) and Gurubacharya et al (2005) concluded
that, in patients with ascites and high SAAG, the degree
of SAAG is directly related to the presence of EV but not
to the size of the EV. This difference in the results can be
attributed to the difference in the population samples. In
these studies, most of the patients with high SAAG were
alcoholic liver cirrhosis, and there was inclusion of some
non-cirrhotic patients as acute fulminant hepatitis and
congestive heart failure, and the low SAAG ascitic
patients were non-portal hypertensive (they were
diagnosed as tuberculous and malignant ascites). In our
study, anti-HCV-Ab was positive in 73.3% of cases, and
55.96% of the patients were proven to have
schistosomiasis, by rectal snip, which aggravate the
periportal fibrosis, PHTN and development of portosystemic collaterals (Abdel Wahab et al 1993).
No correlation was found between SAAG values
and Child-Pugh score, platelet count, PT, bilirubin, PVD
and spleen size in our study as in table (4). This is
coincident with Torres et al (1996) who demonstrated that
the degree of high SAAG does not have any association
with PT, serum bilirubin, degree of encephalopathy or the
grade of ascites but weakly associated with serum
albumin.
By using the ROC Curve (Figure 2), for evaluation
of SAAG as predictor of EV presence, the area under
ROC was (0.85 ± 0.093), which indicates that SAAG can
be a good test for prediction of the presence of EV.
SAAG at cut-off value of 1.55 gm/dL is an accurate
indicator of the presence of EV, with 100% sensitivity
and 71.4% specificity. This is in agreement with Torres
and associates (1998) who found that a SAAG value of ≥
1.435 gm/dL is an accurate indicator of the presence of
EV (positive predictive value = 87.5% and negative
predictive value = 66.7%). In a study on 26 cirrhotic
pediatric patients, Das et al (2001), concluded that SAAG
can differentiate cirrhosis with EV from those without EV
with sensitivity 91%, specificity 50%, positive predictive
value 91%, negative predictive value 50% and efficacy
85%. Bjelakovic et al (2003) found that the cut-off value
for SAAG of 11 gm/L had high sensitivity (97.56%) but
low specificity (46.34%). They used ROC curve analysis
to determine a new cut-off value, and it was 15.86 gm/L.
So, they concluded that the cut-off value for SAAG has to
be corrected to a higher level to achieve the maximal
sensitivity and specificity, and they proposed the new cutoff value of 16 gm/L for discriminating the patients with
and without PHTN, as this value seems to have higher
sensitivity and specificity, than the previous value of 11
gm/L.
In the current study, patients were classified
according to the varix size on endoscopic examination.
Out of 36 patients (80%) with EV, (GI) EV was found in
6 (13.33%), (GII) EV in 16 and (GIII) EV in 14 (31.11%)
patients. Gastric varices were found in nine 9 (20%) and
portal gastropathy was found in 32 (71.1%) patients.
Prevalence of EV in cirrhosis varies among studies from
85.29% (Adrover et al., 2004); 76.6% (Prihatini et al.,
2005) to 50% (Thombolus et al., 2003).
In this study, a significant positive correlation was
found between EV presence and bilirubin, PT & spleen size
(p < 0.05). The positive correlation with Child-Pugh score
and PVD just failed to reach statistical significance (r =
0.324, p = 0.054). A significant negative association of EV
was found with each of serum albumin, serum total protein,
total ascetic fluid protein & platelet count (Table 2). This is
in agreement with Madhorta et al (2002) who concluded
that the prevalence of EV in cirrhosis increases with the
severity of liver disease, and Thombolus et al (2003) who
found that esophageal varices presence is directly
correlated
with
hyperbilirubinemia
(p=0.01),
thrombocytopenia
(p<0.0001),
and
splenomegaly
(p<0.0001) and that these factors are independent
predictors of large EV in cirrhosis.
The study of Serwar et al (2005) documented that
serum albumin less than 2.95 gm/dL, platelet count less
than 88,000 /µL and PVD more than 11 mm were
associated with presence of varices and they concluded that
these patients are candidates for surveillance endoscopy. In
the study of Prihatini et al (2005), it was reported that a
platelet count of 82,000/µL( 90.9% sensitivity ; 41.7%
specificity), PVD of 1.15 cm (75% sensitivity; 54.5%
specificity) and an anteroposterior splenic measurement of
10.3 cm (83.3% sensitivity; 63.6% specificity) were
predictive factors for esophageal varices in liver cirrhosis.
In the current study, using univariate analysis of variables
associated with the presence of large esophageal varices,
only splenomegaly was associated with high grade varices
(Table 3). This is consistent with the study of Adrover et al
(2004) which reported that the presence of large EV was
associated only with splenic volume index ≥ 45 (p=0.02).
bleeding, SAAG had a sensitivity of 100% and specificity
of 33.33%, positive predictive value of 71.4% and
negative predictive value of 100%. This variability of the
results may be due to the difference in the study
population. In the Mene et al study (2003), patients were
diagnosed as PHTN with and without cirrhosis, and they
were Child-Pugh grades A and B. They did not exclude
cases with non-variceal bleeding as endoscopy was not
done in their study.
CONCLUSION: A high SAAG score (≥1.55 gm/dL)
is a useful predictor of the presence of esophageal varices
in cirrhotic patients with ascites, and it can assist
clinicians in determining the urgency of care, and can
help identify patients who need early referral for upper
gastro-intestinal endoscopy. Meanwhile, SAAG was not
valuable in screening and predicting complications, such
as bleeding from esophageal varices. Further prospective
studies might result in a discriminating algorithm to
predict which patients with cirrhosis would benefit from
early or regular endoscopy to detect clinically significant
varices, and may help in optimizing prophylactic therapy
and where available, improving the cost effectiveness of
screening endoscopy.
REFERENCES
1-Abdel-Wahab M.F., Esmat G., Farrag A., et al.; (1993):
Ultrasonographic prediction of esophageal varices in
Schistosomiasis mansoni. Am. J. Gastroenterol.; 88:
560-563.
2-Adrover R., Coccozzella D., Borzi S., et al.; (2004):
{When is the best time to perform upper digestive
endoscopy to detect the presence of esophageal varices
in patients with cirrhosis?}. Gastroenterol. Hepatol. ;
27: 353-356.
3-Al-Knawy B. A. (1997): Etiology of ascites and the
diagnostic value of serum-ascites albumin gradient in
non-alcohol liver disease. Ann. Saudi Med.; 17: 26-28.
Comparing the criteria of our patients with and
without hematemesis, the EV grade, PVD, spleen size and
creatinine level were significantly higher in the group
4-Babu B.R., Sankaranaraynan V.S., Raju B.B. et al.;
with hematemesis (Table 5), and no correlation was
(2004): Ascitic fluid total protein (AFTP) and serum
existing between SAAG and occurrence of hematemesis
ascites albumin gradient (SAAG) in childhood ascites.
(Table 4 & 5). This is in agreement with the group of Goa
J. Gastro. Hepatol.; 19 (Suppl.): 788.
and
associates
(2005)
who
concluded
that,
thrombocytopenia, splenomegaly, and ascites are 5-Bjelaković G., Nagorni A., Stamenković I., et al.; (2003):
unreliable predictors of bleeding in EV. The study of
The value of serum –ascites albumin gradient in
Mbengue et al (2003) stated that clinical and biological
differential diagnosis of ascites and the proposal for the
parameters did not seem predictive of bleeding, and that
new cut-off value .Acta Fac. Med. Naiss. 20: 209-212.
the risk of hemorrhage was positively correlated with the
[Abstract]
presence of esophageal varices and their stage, the gastric
varices and the portal gastropathy, while the Child-Pugh 6-Das B.B., Purohit A., Acharya U., and Utreskova E.
score was a poor predictor of either first hemorrhage or
(2001): Serum-ascites albumin gradient: a predictor of
re-bleeding. On the contrary, Mene et al (2003) found that
esophageal varices with ascites. Indian J. Pediatrics; 68:
SAAG values correlated significantly with bleeding and
511-514.
splenomegaly. They concluded that, for prediction of
7-Demirel U., Karincaoglu M., Hapuiluoglu M., et al.;
(2003): Two findings of portal hypertension: Evaluation
of correlation between serum-ascites concentration
gradient and esophageal varices in non-alcoholic
cirrhosis. Turkish J. Gastroenterol. ; 14: 219-222.
8-Dittrich S., Yordi L.M., and de-Mattos A.A. (2001): The
value of serum-ascites albumin gradient for the
determination of portal hypertension in the diagnosis of
ascites. Hepatogastroenterology; 48: 166-168
9-Giannini E., Botta F., Borro P., et al. (2003); Platelet
count/spleen diameter ratio: proposal and validation of a
non invasive parameter to predict the presence of
oesophageal varices in patients with liver cirrhosis. Gut;
52:1200-1205.
17-Mbengue M., Diouf M.L., Pouye A., et al.; (2003):
Gastrointestinal hemorrhage in cirrhosis at Dakar:
predictive factors study. Dakar Med. J.; 48:213-218.
[Abstract].
18-Mene A.; Sharma D.; and Raina V.K. (2003):
Correlation
between
serum-ascites
albumin
concentration gradient with gastrointestinal bleeding in
patients of portal hypertension. Trop. Doct.; .33:39-41.
19-North Italian Endoscopic Club for the study and
treatment of esophageal varices; (1988): Prediction of
the first variceal hemorrhage in patients with cirrhosis
of the liver and esophageal varices. N. Engl. J. Med.;
319: 983-989.
10-Goa S.H., Tan W.P., and Lee S.W. (2005): Clinical
predictors of bleeding esophageal varices in the ED.
Am. J. Emerg. Med.; 23: 53.
20-Prihatini J., Lesmana L.A., Manan C., and Gani R.A.
(2005): Detection of esophageal varices in liver
cirrhosis using non invasive parameters. Acta Med.
Indones. ; 37:126-131. [Abstract].
11-Gue C.S., Yap C.K., and Ng H.S. (2004): The
correlation between cytopenia and esophageal varices in
patients with liver cirrhosis. Med. J. Malaysia. ; 59:604608. [Abstract]
21-Runyon B.A., Montano A.A., Acaridiasis E.A., et al;
(1992): The serum-ascites albumin gradient is superior
to exudate-transudate concept in differential diagnosis
of ascites. Ann. Intern. Med.; 117:215-220.
12-Gurubacharya D.L., Mathura K.C. and Karki D.B.
(2005): Correlation between serum-ascites albumin
concentration gradient and endoscopic parameters of
portal hypertension. Kathmandu University Med. J.;
3:327-333 [Abstract].
22-Samal K.K., Sahu K.C., Bag S., et al.; (2001):
Seroascitic Gradient of Albumin in Ascites of Various
Aetiologies. Annual Association of Physicians of India
Conference (APICON); Jan 23. [Abstract]
13-Hoefs, J.C. (1990): Diagnostic paracentesis: A potent
clinical tool. Gastroenterology; 98: 230-236.
23-Sarwar S., Khan A., Alam A., et al; (2005): Nonendoscopic prediction of presence of esophageal
varices. J. Coll. Physicians Surg. Pak.; 15: 528-531.
14-Jain R.K., Dasaraty S., and Achaya S.K. (2004): Serum
ascites albumin gradient: Correction for high serum
globulin & very low serum albumin: more rational
approach. J. Gastroenterol. Hepatol. ; 19 (Suppl.): 676.
24-Thompoulos K.C., Labropoulou-Karatza C., Mimidis
K.P. et al.; (2003): Non-invasive predictors of large
esophageal varices in patients with cirrhosis. Dig. Liver
Dis.; 35: 473-478.
15-Kajani M.A., Young Y.K., Alexander J.A. et al;
(1990):
Serum-ascites
albumin
gradients
in
nonalcoholic liver disease. Dig. Dis. Sci.; 35: 33-37.
25-Torres E., Barros P., Calmet F. (1998): Correlation
between serum-ascites albumin concentration gradient
and endoscopic parameters of portal hypertension. Am J
Gastroenterol.; 93: 2172-2178
16-Madhotra R., Mulchay H.E., Willner I., and Reuben
A. (2002): Prediction of esophageal varices in cirrhosis.
J. Clin. Gastroentrol.; 34 : 4-5.