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

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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: [email protected]

Statistical AnalysisStatistical 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. AgeSex 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:

GroupNumber of patients sufferingfrom dyspeptic manifestations

No improvement

Mild improvement

Marked improvement

Group I 20/21 0 5 15Group II 14/20 4 7 3Group 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 biopsyGrade Before ttt After ttt Degree Before ttt After ttt Degree Before ttt After ttt

Grade I : 5 5 Absent 00 3 Absent 0 6Grade II : 6 6 Mild 10 15 Mild 10 11Grade III: 9 10 Severe 11 3 Severe 11 4Grade IV : 1 0Signif: 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 6Grade II : 8 8 Mild 8 14 Mild 8 13Grade III: 4 4 Severe 13 1 Severe 13 2Grade IV : 2 2Signif: 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 14Absent 0 5 Absent 0 6

Grade I : 6 7Grade II : 2 2 Mild 8 17 Mild 8 16Grade III: 0 0 Severe 15 1 Severe 15 1Grade 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. DeviationPepsinogen I (ng/ml) 1.00 21 44.4762 21.14147 2.00 20 73.7000 19.59887Pepsinogen II(ng/ml) 1.00 21 11.5048 3.57638 2.00 20 12.6000 4.10904PGI/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

group1.00

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 الببسينواجين مججع استئصججال البكتريججا الحلزونيججة البوابيججة والعلاجججات الرخرى على سير مرض التعلل المعدى التحتقانى

شندى محمد شندى شريف* و نعيمة العشرى** معهد تيودور بلهارس للبحاث الكيمياء اللكلينيكيةقسمى المراض المتوطنة والكبد والجهاز الهضمى و**

إن مرض التعلل المعدى التحتقانى المصاتحب لرتفاع ضغط الوريد البابى لهجو شجائع فجى مرضجى التليجف الكبججدى. وان ضعف الغشاء المخاطى المعدى نتيجة الاصابة بالبكتريا الحلزونية البوابيججة قجد يكججون سججببا فجى ظهججور العلججل بهججذا الغشججاء وبالرخص فى مرضى التليف الكبدى لكما أن معظم الدراسات لم تجد علقة بين هذه البكتريا وبيجن التعلجل المعجدى التحتقجانى

فى هذه الحالت. ولذلك لكان الهدف من هذا البحجث هجو دراسجة دور هجذه البكتريجا واستئصجالها فجى عل ج هجذا التعلجل بالمقارنجة ببعجض الطرق الرخرى للعل ج مثل استخدام السكرالفات مع الدافلون والبروبرانولول مع الفيراباميل، وذلك لهججدف أهججم وهججو ايجججاد

عل ج بسيط لهذا المرض الشائع إذا ما أمكن ذلك.

مريضا مصابين بالتعلل المعدى التحتقانى مقسمين الى ثلث مجموعات: ٦٤وقد شمل هذا البحث مريضا مصابين أيضا بالبكتريا الحلزونية البوابية وقد تم علاجهم بعل ج الميكروب۲١المجموعة الولى: وتشمل مريضا غير مصابين بالبكتريا الحلزونية البوابية أو تم تحقنهم لعل ج دوالى المرئ وقد۲٠ المجموعة الثانية: وتشمل

تم علاجهم باستخدام السكرالفات مع الدافلون مريضا غير مصججابين بالبكتريججا الحلزونيججة البوابيججة ولكججن تججم تحقنهججم لستئصججال دوالججى۲٣المجموعة الثالثة وتشمل

المرئ من قبل وقد تم علاجهم بالبروبرانولول مع الفيراباميل وقد تم عمل منظار معدى وفحص نسججيجى للمعججدة وهججذا الميكججروب قبجل وبعججد العل ج بالضججافة إلججى التحاليججل الرخججرى

الروتينية وتحاليل الهيلكوبالكتر بالدم.

و قد أظهرت النتائج أن اجميع طرق العل ج الثلثة أتحدثت تحسنا إلكلينيكيا ذو دللة إتحصائية فى مججرض التعلججل المعججدى التحتقانى والتى لكانت أعراضه الهضججمية ألكججثر شججدة فججى المجموعججة الولججى المصججابة بالبكتريججا الحلزونيججة البوابيججة والججتى أظهرت تحسنا ألكثر بعد العل ج مججن المجموعججات الرخججرى مججن تحيججث هججذه العججراض و أيضججا دوالججى المججرئ. بالضججاية الججى

والججتى واجججدت منخفضججة بدللججة إتحصججائية فجى هججذهІ/П والنسججبة بينهمججا ПوІالتحسن فى معججدل مسجتوي البيبسجينواجين المجموعة عن المجموعات الرخرى.

يستنتج من هذا البحث أن البكتريا الحلزونية البوابية قد تسججبب زيججادة فججى شججدة مججرض التعلججل المعججدى التحتقججانى وأن عل ج هذا الميكروب قد يفيد هؤلء المرضى وأن العلاجات الرخرى أيضجا الجى تحسجن المجرض وذلجك يجدل أن هنجاك عوامجل

أرخرى مع هذا الميكروب تزيد من شدته.

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

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