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Contact Name
Murdani Abdullah
Contact Email
ina.jghe@gmail.com
Phone
+6285891498517
Journal Mail Official
ina.jghe@gmail.com
Editorial Address
Divisi Gastroenterologi, Departemen Ilmu Penyakit Dalam, FKUI/RSUPN Dr. Cipto Mangunkusumo, Jl. Diponegoro No. 71 Jakarta 10430 Indonesia
Location
Kota adm. jakarta pusat,
Dki jakarta
INDONESIA
The Indonesian Journal of Gastroenterology, Hepatology and Digestive Endoscopy
ISSN : 14114801     EISSN : 23028181     DOI : -
Core Subject : Health,
The Indonesian Journal of Gastroenterology, Hepatology and Digestive Endoscopy is an academic journal which has been published since 2000 and owned by 3 Societies: The Indonesian Society of Gastroenterology; Indonesian Association for the Study of the Liver; The Indonesian Society for Digestive Endoscopy. The aim of our journal is to advance knowledge in Gastroenterology, Hepatology, and Digestive Endoscopy fields. We welcome authors for original articles, review articles, and case reports in the fields of Gastroenterology, Hepatology, and Digestive Endoscopy.
Articles 6 Documents
Search results for , issue "VOLUME 5, ISSUE 3, December 2004" : 6 Documents clear
Pathogenesis in Portal Hypertensive Gastropathy Due to Liver Cirrhosis Loli J Simanjuntak; Chudahman Manan; Marcellus Simadibrata; Rino A Gani
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/53200495-101

Abstract

The recent advances of endoscopic examination had proven that source of upper gastrointestinal bleeding in liver cirrhosis is not always caused by esophageal varices rupture but also gastric mucosal lesion. The prevalence of gastric ulcer in patients with liver cirrhosis is higher than healthy individuals. Imbalance of defensive and aggressive factors of gastric mucosa may involve in development of portal hypertensive gastropathy (PHG). Several studies reported hemodynamic changes associated wuth portal hypertension causing decreased mucus layer thickness as one of mechanism of PHG. Other etiologic factors of PHG were hypoacidity, hypergastrinemia, reduced hexosamin concentration, mucus metabolic function associated with decreased prostaglandin E2 (PGE2), and increased nitric oxyde (NO) which had caused mucus wall thickness changes. Gastric mucus damage induced by portal hypertension has important role in the pathogenesis of gastric ulcer in liver cirrhosis. Keywords: Pathogenesis, PHG, liver cirrhosis
Risk Factors for Recurrent Upper Gastrointestinal Tract Bleeding after Esophageal Varices Ligation on Patients with Liver Cirrhosis Syarif Hidayat; Dharmika Djojoningrat; Nurul Akbar; Nanang Sukmana; Sabarinah Prasetyo
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/53200479-88

Abstract

Background: Upper gastrointestinal tract (GIT) bleeding on liver cirrhosis patients will increase morbidity and mortality. Recurrent bleeding’s risk rise after the first episode of variceal bleeding. The mortality risk also rises on each bleeding. Purpose: This study was done in order to identify the risk factors for the first episode of recurrent bleeding of upper GIT on liver cirrhosis patient. Evaluation of risk factors was based on preliminary data prior to ligation. Method: Evaluation of the upper GIT bleeding was done using anamnesis on the patients or their relatives by letter, home visits or telephone. The data on recurrent bleeding was obtained from medical records. They were evaluated on the 3rd month then 1st year after ligation. This study was a cross sectional study with retrospective data and a consecutive sampling method. Result: Bivariate analysis revealed the 3rd month’s risk factors for first episode of upper GIT bleeding were ascites, total bilirubin level of 2 mg/dL, hepatoma, Child-Pugh C classification of the liver function and red color sign on esophageal varices. The risk factors for the first episode of upper GIT bleeding on first year were age £ 60 years old, hepatoma, and red color sign (RCS) on esophageal varices. The differences between risk factors on upper GIT bleeding on the 3rd month and 1st year were likely due to intervention, collateral para-esophageal varices, medication that irritated GIT, physical activities, and differences on variceal obliteration rate related to variceal ligation. Conclusion: Risk factors for recurrent upper GIT bleeding that could be minimized were ascites, total bilirubin level, Child-Pugh classification and RCS. It was expected with parascentesis, diuretics, hepatoprotector medications and drugs that lowers portal hypertension (such as propranolol and isosorbid mononitrate), might improve those risk factors thus decreasing the risk for recurrent upper GIT bleeding. Keywords: Upper gastrointestinal tract, esophageal varices, liver cirrhotic
Helicobacter pylori, Induced Gastric Cells Apoptosis Putut Bayupurnama
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/532004102-104

Abstract

Gastric epithelial cells apoptosis induced by Helicobacter pylori depends on microbial and host factors. Apoptosis on mitochondrial level by Bcl2 family protein is the main pathway for Helicobacter pylori induced gastric epithelial cells apoptosis, though there are roles for apoptosis through Fas receptors or TNF. Imbalance between proliferation and apoptosis gastric epithelial cells determines the risk for neoplastic transformation. Increase of gastric epithelial cells apoptosis seems to have an obligation for initiating secondary hyperproliferative response. If altruistic cellular death fails to oppose this process, uncontrollable cellular growth leading to neoplastic transformation will occur. Keywords: Helicobacter pylori, gastric cells, apoptosis
A Comparison of Efficacy between Rebamipide and Omeprazole in the Treatment of NSAIDs Gastropathy Suyata Suyata; Erita Bustami; Syadra Bardiman; Fuad Bakry
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/53200489-94

Abstract

Background: Gastropathy represent a disparity of gastric mucosal characterized by sub-epithelial bleeding and erosion. Gastropathy can be induced by non steroidal anti-inflammatory drugs (NSAIDs), alcohol, stressor, and chemical agents with various sign and symptoms. NSAIDs-induced gastropathy is the second most common etiology of gastric ulcer and variceal haemorrhages. Aims: To investigate the effectivity of rebamipide compare with omeprazole in treatment of NSAIDs- induced gastropathy. Method: This triple blind randomized study was enrolled from January to June 2004 with 38 subjects who were recruited from outpatient and inpatient clinic in M Hoesin Hospital in Palembang. Subject was divided into two groups. Endoscopic examination was performed in every patients. Results: There was an improvement of symptom in rebamipide group (78.9%) and omeprazole group (79.0%) after treatment but it didn’t have significant difference statistically. Improvement of NSAIDs induced gastropathy after treatment between two groups have significant difference (P = 0.02), and improvement of gradation of gastropathy after treatment has significant difference (P = 0.007).There was no side effect of administration of rebamipide and omeprazole in each group. Conclusion: Rebamipide as effective as omeprazole in improvement of symptom. Omeprazole is more effective than rebamipide in improvement of NSAIDs induced gastropathy and is as safe as rebamipide in the treatment of NSAIDs induced gastropathy. Keywords: Gastropathy, NSAIDs, rebamipide, omeprazole
Paralytic Ileus in Vegetarian with Pneumonia Infection Khaira Utia Yusrie
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/532004109-114

Abstract

Paralytic ileus which is commonly found in clinical practice is referred to clinical syndrome of transportation disturbance of the intestinal lumen content due to various etiology and underlying condition. It has been considered a transient gastrointestinal syndrome with good prognosis. Most cases respond well to conservative management. However, inappropriate diagnostic approach and management will result in severe complication leading to death such as septicemia and perforation. We reported a case of paralytic ileus in young male who is vegetarian with pneumonia infection as the suspected underlying etiology. Radiological examination of the abdomen in three position (upright, supine and lateral) showed dilated gaster and duodenum with minimal air fluid level, no herring bone appearance and absent of free intraperitoneal air. The laboratory result also showed low level of vitamin B12 which might be due to his lactovegetarian diet habit. Management including supportive therapy such as decompression, fasting, adequate parenteral nutrition, fluid balance and treatment of pneumonia as the underlying cause of paralytic ileus had been resulted in good clinical response. Keywords: Paralytic ileus, pneumonia, treatment
Gastrointestinal Bleeding, Jejunum Perforation and Intussusceptions Ileo-Jejunal Segment with Multiple Polyposis Due to Metastasic Melanoma with Out Primary Cutaneus Melanoma? Lianda Siregar; Mangalindung Ompusunggu
The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy VOLUME 5, ISSUE 3, December 2004
Publisher : The Indonesian Society for Digestive Endoscopy

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24871/532004105-108

Abstract

Approximately 60% of patients who die due to melanoma have gastrointestinal metastases at autopsy, yet ante mortem diagnosis is uncommon. The small bowel is the most frequent intestinal site of metastasis and prognosis is very poor with a median survival after operation was 6.2 months (range: 1–42 months). Bowel metastases may appear radiologically as polypoid mucosal lesions, submucosal nodules, diffuse infiltration with thickening of the intestinal wall, or serosal implants. Bowel obstruction due into intussusceptions is common clinical presentation of gastrointestinal metastasis; other presentation include gastrointestinal bleeding, perforation and large masses.We reported a case of metastatic melanoma to small bowel, whose had hematemesis melena, abdominal pain, diarrhea and weight loss without primary cutaneus melanoma. Gastroduodenoscopy appeared normal. The ultrasonography of bowel showed a”doughnut” configuration with concentric rings of bowel wall. Left lateral decubitus abdominal radiographies showed free air appearances. Laparatomy reported three location of invagination (intussuception) with multiple polyposis at ileo–jejunal segment (29 pieces of polyp) and jejunum perforation. Resection and end–to end anastomosis of the affected segment had been performed with no serious complication after this. Miscroscopical examination of specimen showed metastatic melanoma malignant in 3 lymph nodes. Eight weeks later patients died with distant metastases to brain. Keywords:  Intussesception and perforation, multiple polyposis, metastase melanoma without primary cutaneus melanoma

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