Role of h.pylori in congestive gastropathy with pepsinogen,doc

Prognostic value of serum pepsinogen isoenzymes in H pylori
eradication and other treatment modalities on the course
of congestive gastropathy.
Naema Al-Ashry*, Shindy Mohammed Shendy**
Clinical Chemistry Department. Theodor Bilharz Research Institute (TBRI), Tropical
medicine, Hepatology and gastroenterology department (TBRI).
Journal:-The New Egyptian Journal of Medicine, vol 37; No. 2(S), Aug. 2007; 60-68
ISSN:1110-1946
Conference: 7th International Annual Congress of the Egyptian Society of Tropical
Medicine, Infectious and Parasitic diseases (ESTIP) in collaboration with the Egyptian
Society of Hepatology, Gastroenterology and Infectious Diseases (ESHGID), Sheraton
El Montaza Hotel, Alexandria, Egypt, Sept 21-23, 2005
.
Abstract:
Portal hypertensive gastropathy (PHG) is a common finding in patients with liver cirrhosis.
Reduced gastric mucosal defense caused by H pylori may account for the pathogenesis of GI
lesions in liver cirrhosis. Most of the studies showed no relationship between H. pylori
infection and congestive gastropathy in liver cirrhosis. The aim of this work is to investigate
the role and the eradication of H. pylori and estimate the prognostic value of serum levels of
pepsinogen isoenzymes I and II and their ratio in the treatment of portal hypertensive
gastropathy in comparison with other suggested treatments such as Daflon, sucralfait,
propranolol and verapamil. Our intimate aim is to find a simple treatment; if possible; for such
common gastro-intestinal disease. Patients and methods: This study included 64 cirrhotic
patients divided into three groups: Group I: included 21 patients with congestive gastropathy
and H. pylori infection and were treated with eradication therapy for H. pylori Group II:
included 20 patients without H. pylori infection and without history of injection sclerotherapy
are treated with sucralfait and Daflon. Group III: 23 patients without H. pylori infection and
with history of injection sclerotherapy are treated with propranolol and verapamil. Upper
endoscopy and gastric biopsies for histopathology and H. pylori staining before and after
treatment were done in all patients in addition to pepsinogen isoenzymes I and II, serology and
other routine tests. Results: The three types of therapy showed significant clinical
improvement in these patients. Most of these patients are suffering from dyspeptic symptoms
in the form of epigastric discomfort and pain after meals, flatulence and distension. This was
more marked in patients with H pylori infection. . Serum Pepsinogen I levels and PG I/II ratio
were significantly less in group I with H pylori infection than groups II and III (P<0.001).
There is substantial improvement after treatment in all patients that was most marked in
patients of group I after eradication of H pylori. Serum Pepsinogen I levels and PG I/II ratio in
group I showed significant increase after eradication of H pylori (P<0.001). PHG was improved
significantly in all groups. Also, there were no differences in the response of PHG in the three
groups. Comparison of the response of oesophageal varices to therapy between the three
groups found that oesophageal varices improved significantly in group I in comparison to
group II. Conclusion: It is concluded from this study that H pylori may aggravate this disease
process and its eradication may be beneficial in patients with liver cirrhosis and portal
hypertension. In addition, improvement in the serum levels of pepsinogens after eradication of
infection may be a prognostic marker of chronic gastritis. Also, other treatment modalities
were effective in decreasing the severity of this disease, which means that this disease process
may be aggravated by other factors than H pylori.

Introduction:
Gastric mucosal lesions that were described with liver cirrhosis and portal hypertension
include acute gastric lesions, hemorrhagic gastritis, erosive gastritis or acute gastric erosions
(Franco et al., 1977). McCormick and his colleagues postulated congestive gastropathy rather
than gastritis in 1985. These lesions were classified into mild gastropathy when mosaic pattern
of multiple erythematous areas outlined by a white reticular network or a scarlatina- like
pattern of fine pink speckling was detected and severe gastropathy of cherry red spots on a
finely granular mucosa (D’Amico et al., 1990). In these studies, the prevalence of mild
gastropathy ranged from 20% – to- 94% and of severe gastropathy from 7% – to – 41% in
patients with cirrhosis and portal hypertension.
The pathogenesis of PHG is still unclear. Elevated portal pressure can induce changes of
local hemodynamics, thus causing congestion in the upper stomach and gastric tissue damage.
These changes may then activate cytokines and growth factors, such as tumor necrosis factor
alpha, which are substances that activate endothelial constitutive nitric oxide synthase and
endothelin 1 in the portal hypertensive gastric mucosa. Overexpressed nitric oxide synthase
produces an excess of nitric oxide, which induces hyperdynamic circulation and peroxynitrite
overproduction. The overproduction of peroxynitrite, together with endothelin overproduction
may cause an increased susceptibility of gastric mucosa to damage. When combined with
impaired mucosal defense and healing, these factors may together produce PHG in patients
with portal hypertension (Ohta et al., 2002).
Reduced gastric mucosal defense caused by H pylori may account for the pathogenesis of
GI lesions in liver cirrhosis. H. pylori is strongly associated with peptic ulcer disease and
chronic gastritis, however, several studies showed no relationship between H. pylori infection
and congestive gastropathy in liver cirrhosis (Fujiwara et al., 1998). Old reports have shown
that the blood pepsinogen levels reflect the morphological and functional status of the gastric
mucosa and there is general agreement that subjects with gastric atrophy tend to have low
blood pepsinogen levels (Kawachi T, et al,1976, Bock OAA, et al., 1953 and Varis K, et al.
1979). They found also that low serum PG I is highly sensitive and specific for severe atrophic
gastritis of the fundic gland mucosa in first-degree relatives of cases of pernicious anemia
(Varis K, et al. 1979) and that low levels of serum PG I are highly specific for extensive
intestinal metaplasia of the stomach and is a good marker of increased risk for the intestinal
type of gastric cancer (Stemmermann et al 1978 and 1980 and Nomura et al., 1980). The PG
I/PG II ratio was the most reliable test for the normal fundic gland mucosa and extensive
chronic gastritis. It was found that a serum Pepsinogen I level failed to less than 20 ng/ml was
highly specific for severe atrophic gastritis. It is observed that serum Pepsinogen I levels fell
with increasing severity of mucosal damage in atrophic gastritis. On the other hand, the
decrease in serum Pepsinogen I levels in patients with pernicious anemia and atrophic gastritis
was found to be associated with normal or raised Pepsinogen II levels. Therefore, a Pepsinogen
I/Pepsinogen II ratio was significantly lower than those with superficial gastritis or normal
remnant mucosa (Kikuchi et al., 1994, Konishi et al., 1995 and Yoshuihara et al., 1998).
After oesophageal and fundal varices, portal hypertensive gastropathy (PHG) is the second
most frequent cause for bleeding in cirrhotic patients. It accounts for 1 to 8% of primary upper
gastrointestinal hemorrhage. Also, it accounts for 30 to 60% of secondary acute or chronic
bleeding, mainly after sclerosing therapy of varices. Endoscopy is diagnostic either by showing
a typical 'mosaic-pattern' in mild, and a single or confluent 'cherry red spots' in severe forms.
Helicobacter pylori or NSAID-induced gastropathy are to be distinguished by biopsies.
Secondary prophylaxis with propranolol especially after sclerosing therapy is recommended,

primary prophylaxis not (Hermann R, 1997). Evidence in the literature suggests that
hypertensive gastropathy might not represent a favorable environment for Helicobacter pylori
thus making the diagnostic sensitivity of the biopsy lower than expected (Farinati F et al,
1998).
The aim of this work is to investigate the role and the eradication of H. pylori and estimate
the prognostic value of serum levels of pepsinogen isoenzymes I and II and their ratio in the
treatment of portal hypertensive gastropathy in comparison with other suggested treatments
such as Daflon, sucralfait, propranolol and verapamil. Our intimate aim is to find a simple
treatment; if possible; for such common gastro-intestinal disease.
Materials and methods:
This study includes 64 patients who have liver cirrhosis and portal hypertensive
gastropathy with or without H. pylori infection. Patients were admitted to Theodor Bilharz
Research Institute and were subjected to history taking and clinical examination. Urine, stool,
sigmoidoscopy, upper endoscopy and gastric biopsies for histopathology and H. pylori staining
before and after treatment were done in all patients. Abdominal ultrasound examination was
performed to evaluate the liver disease and its manifestations. CBC, liver function tests, kidney
function tests and blood sugar were done routinely in all patients. Most of the patients were
diagnosed by previous liver biopsy during the course of their disease. H. pylori serology using
ELISA was done in all patients. Patients in this study were divided into the following groups:
Group I: included 21 patients with congestive gastropathy and H. pylori infection and were
treated with eradication therapy for H. pylori (PPI, amoxicillin and clarithromythin in the
standard doses) followed by PPI for 2 weeks.
Group II: included 20 patients without H. pylori infection and without history of injection
sclerotherapy are treated with sucralfait 2gm twice daily and Daflon 500 mg three times daily
for three months (Daflon is a purified flavinoid fraction corresponding to diosomin90% and
hesperidin flavinoid 10% tablets; Les laboratories, Servier, France).
Group III: 23 patients without H. pylori infection and with history of injection sclerotherapy
are treated with propranolol 40 mg three times daily and verapamil 80 mg three times daily for
three months.
Measurement of Human Pepsinogen I and II in Serum using microplate-based
quantitative enzyme immunoassay (ELISA): This PGI & II ELISA are based on a sandwich
enzyme immunoassay technique with a PG I or II specific capture antibody adsorbed on a microwell plate
and detection antibody labelled with horseradish peroxidase (HRP). (BIOHIT diagnostic Laippatie 1 FIN-
00880 Helsinki, Finland) (. Tel: +358-9-773 861 Fax: +358-9-773 86290. E-mail: info@biohit.com
Statistical Analysis
Statistical analysis was performed using the SPSS 12 for window statistical Package
Results are expressed as absolute values and mean ± SD. Statistical analysis of the data was
carried out using the ANOVA test. For correlation studies, the Pearson correlation coefficient
was used. A p -value of < 0.05 was considered significant.
RESULTS:
Tables 1 & 2 show the clinical characteristics and effect of therapy on such manifestations.
The three types of therapy showed significant clinical improvement in these patients. Most of
these patients are suffering from dyspeptic symptoms in the form of epigastric discomfort and
pain after meals, flatulence and distension. This was more marked in patients with H pylori

infection. There is substantial improvement after treatment in all patients that was most marked
in patients of group I after eradication of H pylori. Effect of therapy on OV and PHG in the
three groups is shown in Tables 3, 4 & 5. PHG was improved significantly in all groups. Also,
there were no differences in the response of PHG in the three groups. Comparison of the
response of oesophageal varices to therapy between the three groups using Levene's Test for
Equality of Variances for independent samples test found that oesophageal varices improved
significantly in group I in comparison to group II. Oesophageal varices were found the only
predictive variable among all studied variables for the presence and severity of PHG. Serum
levels of pepsinogens I and II and PGI/II ratios in all groups and before and after eradications
in group I are shown I in tables 6, 7, and 8.
Table 1: Some clinical features of patients in the three groups:
Group No. Age
Sex H pylori positivity Bleeding status
Male Female Serology biopsy present absent
Group I 21 48.9±13.6 13 8 21 21 0 21
Group II 20 44.85±12.8 11 9 2 0 0 20
Group III 23 44.86±14.5 14 9 5 0 23 0
Table 2: Symptomatic improvement of dyspeptic symptoms in all groups:
Group Number of patients suffering
from dyspeptic manifestations
No
improvement
Mild
improvement
Marked
improvement
Group I 20/21 0 5 15
Group II 14/20 4 7 3
Group III 17/23 3 8 6
Table 3: Oesophageal varices and portal hypertensive gastropathy in patients with H pylori
infection (group I):
OV PHG PHG, in biopsy
Grade Before ttt After ttt Degree Before ttt After ttt Degree Before ttt After ttt
Grade I : 5 5 Absent 00 3 Absent 0 6
Grade II : 6 6 Mild 10 15 Mild 10 11
Grade III: 9 10 Severe 11 3 Severe 11 4
Grade IV : 1 0
Signif: P=0.7 NS P= 0.001 sign. P=0.000 sig
Table 4: Oesophageal varices and portal hypertensive gastropathy in patients treated with
Daflon and sucralfait (group II):
Grade I : 6 6 Absent 0 6 Absent 0 6
Grade IV : 2 2
Signif: P=0.8 NS. P= 0.005 : sig. P=0.001 : sig

Table 5: Oesophageal varices and portal hypertensive gastropathy in patients with history of
injection sclerotherapy, treated with propranolol and verapamil (group III):
Grade 0: 15 14 Grade I : 6 7 Absent 0 5 Absent 0 6
Grade IV : 0 0
Signif: P= 0.6 NS P= 0.006 : Sig P= 0.003 : Sig
Table 6: Comparison of the means and SD of Pepsinogen I and II and I/II Ratio in groups I
and II
group N Mean Std. Deviation
Pepsinogen I (ng/ml) 1.00 21 44.4762 21.14147
2.00 20 73.7000 19.59887
Pepsinogen II(ng/ml) 1.00 21 11.5048 3.57638
2.00 20 12.6000 4.10904
PGI/II Ratio 1.00 21 3.9843 1.35085
2.00 20 6.1235 1.62579
Serum Pepsinogen I levels and PG I/II ratio are significantly less in group I with H pylori infection than group II
(P<0.001)
Table 7: Comparison of the means and SD of Pepsinogen I and III and I/II Ratio in groups I
and III
21 44.4762 21.14147
23 76.6957 17.98847
21 11.5048 3.57638
23 12.5217 4.03248
21 3.9843 1.35085
23 6.3657 1.25368
group
1.00
3.00
1.00
3.00
1.00
3.00
Pepsinogen I (ng/ml)
Pepsinogen II(ng/ml)
PGI/II Ratio
N Mean Std. Deviation
Serum Pepsinogen I levels and PG I/II ratio are significantly less in group I with H pylori infection than group III
(P<0.001)
Table 8: Means and SD of Pepsinogen I and II and I/II Ratio in group I before and after
eradication of H pylori.
42.9500 20.46943
68.9000 25.73938
11.3800 3.62210
14.0500 4.51285
3.9155 1.34768
5.1340 1.70606
Pepsinogen I (ng/ml) before eradication
pepsinogen I after eradication
Pepsinogen II(ng/ml) before eradication
Pepsinogen II after eradication
PGI/II Ratio before eradication
PGI/II Ratio after eradication
Mean Std. Deviation
Serum Pepsinogen I levels and PG I/II ratio in group I showed significant increase after eradication of H pylori
(P<0.001)

Discussion:
In this study, portal hypertensive gastropathy (PHG) and H pylori infection were found a
common association in Egyptian patients with liver cirrhosis. H pylori infection may be
another factor that helps in the development of PHG. This is proved in this study by the
significant improvement in such condition after eradication therapy. Such improvement was
noticed mainly in the severe cases which become mild after treatment in group I. However,
there is no significant change in the mild cases of gastropathy. Thus, H pylori may only add to
the severity of the condition but not the initiative factor. Increased expression of inducible
nitric oxide synthase (iNOS) has been reported in gastric mucosa of patients with Helicobacter
pylori infection or portal hypertensive gastropathy (PHG) but probably there is no additive or
synergistic impact between H. pylori and PHG on iNOS expression. Furthermore, It was found
that expression of iNOS was significantly higher in patients with severe PHG than in those
with mild PHG and without PHG (Arafa UA et al; 2003).
Sucralfait and the venotonic medication; Daflon; also produced significant improvement in
PHG, even in mild cases. Sucralfait being a cytoprotective agent to the gastric mucosa added to
daflon produced such effect in these patients despite no effect on the large vessels; esophageal
varices. These simple and safe medications can be added to the management of these patients
particularly those with dyspeptic symptoms from PHG.
After injection sclerotherapy and band ligation, the development of PHG increases
(Primignant M et al 2000 and Dong L et al 2003). The use of propranolol and calcium channel
blocker; verapamil as secondary prophylaxis for both esophageal varices and PHG seems
effective. In this study they produced significant improvement in PHG with changing of most
severe cases to mild and complete disappearance of 6 mild lesions. In spite of this marked
improved; some cases still have milder grades of varices on treatment (recurrent or not
completely eradicated by previous endoscopic therapy).
In this study, esophageal varices were found the only predictive variable for the presence
and severity of PHG. This finding is similar to the finding of Dong L. et al. (2003) who found
that gastroesophageal varicosity was closely related to PHG, but their degrees are not related.
In some studies, H. pylori was found less frequently in congestive gastropathy patients than
in the control group and presence and severity of congestive gastropathy is independent of the
H. pylori status (Dai L and Wu X; 1999, Dong L et al 2003, and Batmanabane et al 2004).
These researchers suggested that there might be no need for its routine eradication in patients
with PHG and it was concluded that portal hypertensive gastropathy does not provide a
favorable environment for the colonization of H. pylori.
The prevalence of gastropathy in different studies (and this study) was correlated with the
duration of disease, presence and size of esophagogastric varices, and a previous history of
endoscopic variceal sclerotherapy (Primignant M et al 2000).
The lower levels of pepsinogen I and the pepsinogen I/II ratio in the patient group with H
pylori infection than other two groups mean that this infection is long lasting and already has
caused chronic atrophic gastritis of the corpus of the stomach in many patients. Also the return
of these levels and ratio towards the normal value after eradication of infection is an indication
and a good prognostic marker of such therapy. It was suggested that the measurement of serum
pepsinogens served as a “serological biopsy” for predicting the presence of atrophic gastritis or
superficial gastritis. These levels in addition to the PG I.II may also identify persons at

increased risk for intestinal types of stomach cancer. In a previous study of 3 population-based
family samples from Finland (Varis et al., 1991), SPGI was <25 mg/l in 80% of subjects with
severe atrophic corpus gastritis, but in only 2.1% of those without atrophic gastritis. In a recent
investigation from the UK (Knight et al., 1996), SPGI levels <80 ng/ml and the presence of
Helicobacter positivity disclosed corpus atrophy with a sensitivity and specificity of 89% and
92%, respectively. In another study, using the SPGI/SPGII ratio as an additional screening
criterion (cut-off level 2.5) resulted in a slight increase in specificity, but a reduction of the
sensitivity to 78% (Varis et al., 2000). In a Swedish study (Borch et al., 1989), the SPGI/SPGII
ratio (cut-off level 5.5) was found to be the most sensitive test for corpus atrophy, the
sensitivity and specificity being 99% and 94%, respectively. The prevalence of atrophic
gastritis varied in these studies; thus, sensitivity and specificity figures are not fully
comparable
In this study, there is substantial improvement in all patients that was most marked in
patients having additional H pylori infection (group I), after eradication therapy. Thus, gastritis
due to H pylori adds more loads on the symptomatology of these patients and it is advised to
eradicate this infection in patients with cirrhosis. Also the improvement in the serum levels of
pepsinogens after eradication of infection is a marker of improvement of chronic gastritis in
many patients with its all manifestations.
It is concluded from this study that H pylori may aggravate this disease process and its
eradication may be beneficial in patients with liver cirrhosis and portal hypertension. In
addition, improvement in the serum levels of pepsinogens after eradication of infection may be
a prognostic marker of chronic gastritis. Also, other treatment modalities were effective in
decreasing the severity of this disease, which means that this disease process may be
aggravated by other factors than H pylori i.e. multifactorial. Such treatment can be used in
combination with or after eradication therapy. More prolonged studies are recommended to
prove that such effect is long lasting and is not due to other factors.
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قيمة قياس انزيمات الببسينوجاين مججع استئصجال البكتريجا الحلزونيجة البوابيجة والعلجاجات
الخررى على سير مرض التعلل المعدى الحتتقانى
شندى محمد شندى شريف* و نعيمة العشرى**
قسمى المراض المتوطنة والكبد والجهاز الهضمى و** الكيمياء الكللينيكية معهد تيودور بلهارس للبحاث
إن مرض التعلل المعدى الحتتقانى المصاحتب لرتفاع ضغط الوريد البابى لهجو شجائع فجى مرضجى التليجف الكبججدى. وان
ضعف الغشاء المخاطى المعدى نتيجة الصاابة بالبكتريا الحلزونية البوابيجة قجد يكجون سجببا فجى ظهجور العلجل بهججذا الغشجاء
وبالخرص فى مرضى التليف الكبدى كلما أن معظم الدراسات لم تجد علقة بين هذه البكتريا وبيجن التعلجل المعجدى الحتتقجانى
فى هذه الحالت.
ولذلك كلان الهدف من هذا البحجث هجو دراسجة دور هجذه البكتريجا واستئصجالها فجى علج هجذا التعلجل بالمقارنجة ببعجض
الطرق الخررى للعلج مثل استخدام السكرالفات مع الدافلون والبروبرانولول مع الفيراباميل، وذلك لهججدف أهجم وهجو ايججاد
علج بسيط لهذا المرض الشائع إذا ما أمكن ذلك.
وقد شمل هذا البحث ٦٤ مريضا مصابين بالتعلل المعدى الحتتقانى مقسمين الى ثلث مجموعات:
المجموعة الولى: وتشمل ۲١ مريضا مصابين أيضا بالبكتريا الحلزونية البوابية وقد تم علجاهم بعلج الميكروب
المجموعة الثانية: وتشمل ۲٠ مريضا غير مصابين بالبكتريا الحلزونية البوابية أو تم حتقنهم لعلج دوالى المرئ وقد
تم علجاهم باستخدام السكرالفات مع الدافلون
المجموعة الثالثة وتشمل ۲٣ مريضا غير مصجابين بالبكتريجا الحلزونيجة البوابيجة ولكججن تجم حتقنهجم لستئصجال دوالجى
المرئ من قبل وقد تم علجاهم بالبروبرانولول مع الفيراباميل
وقد تم عمل منظار معدى وفحص نسجيجى للمعججدة وهججذا الميكججروب قبجل وبعججد العلج بالضجافة إلجى التحاليجل الخرججرى
الروتينية وتحاليل الهيلكوباكلتر بالدم.
و قد أظهرت النتائج أن جاميع طرق العلج الثلثة أحتدثت تحسنا إكللينيكيا ذو دللة إحتصائية فى مججرض التعلججل المعججدى
الحتتقانى والتى كلانت أعراضه الهضجمية أكلجثر شججدة فجى المجموعجة الولجى المصجابة بالبكتريجا الحلزونيجة البوابيجة والجتى
أظهرت تحسنا أكلثر بعد العلج مججن المجموعجات الخرججرى مججن حتيججث هججذه العججراض و أيضجا دوالجى المججرئ. بالضجاية الجى
والجتى وجاججدت منخفضجة بدللجة إحتصجائية فجى هججذه І/П والنسجبة بينهمجا П وІ التحسن فى معججدل مسجتوي البيبسجينوجاين
المجموعة عن المجموعات الخررى.
يستنتج من هذا البحث أن البكتريا الحلزونية البوابية قد تسجبب زيجادة فجى شججدة مججرض التعلجل المعججدى الحتتقجانى وأن
علج هذا الميكروب قد يفيد هؤلء المرضى وأن العلجاات الخررى أيضجا الجى تحسجن المجرض وذلجك يجدل أن هنجاك عوامجل
أخررى مع هذا الميكروب تزيد من شدته.

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