scholarly journals Pengaruh Kecepatan Pembentukan Tukak Lambung Terhadap Pemberian Berbagai Golongan NSAID Pada Tikus Jantan

2019 ◽  
Vol 1 (2) ◽  
pp. 8-17
Author(s):  
Parhan Parhan ◽  
Aliman Yafarugi Gulo

Background : Gastric ulcer is wound to the mucosal layer (epithelial layer) of the stomach and mucosal irritation of 5 mm or more in diameter with depth down to submucosa. The basic pathogenesis of gastric ulcers in when there is an imbalance of aggressive factor enhancement. Non-steroidal antiinflammantory drug can cause stomach ulcers in two ways, either directly or topical irritation of the epithelial tissue and inhibit the endogeneous system of gastrointestinal mucosa of prostaglandins. In this case inhibition of prostaglandin systhesis is the dominant factor of peptic ulcers by NSAIDs. Objectives : The purpose of this study was to determine the effct of NSAID drug administration on the formation of peptic ulcers and to know the difference in the rate of formation of peptic ulcers from each class. Method : Sampel method mice performed surgery on the stomach is done in Pharmacology Laboratory of Pharmacy Institute Deli Husada Deli Tua. Results : The results of this study indicate that faster drugs cause gastric ulcers with a degree of redness are Aspirin 4.03 mm, 2.01 mm mefenamat and 1.02 mm Diclofenac Sodium while Ibuprofen mwdication does not cause peptic ulcers. Conclusion : The results of this study it can be concluded that Aspirin administration with doses of 21 mg/kg faster causes gastric ulcers from other NSAID groups such as Mefenamat with a dose of 21 mg/kg BW, Diclofenac sodium at a dose of 2 mg/kg while administration, Ibuprofen for ten days does not couse ulcers in the stomach of experimetal animals.

2019 ◽  
Vol 1 (2) ◽  
pp. 18-24
Author(s):  
Christica Ilsannas Surbakti ◽  
Nadiya Nadiya Nadiya

Background : Gastric ulcer is wound to the mucosal layer (epithelial layer) of the stomach and mucosal irritation of 5 mm or more in diameter with depth down to submucosa. The basic pathogenesis of gastric ulcers in when there is an imbalance of aggressive factor enhancement. Non-steroidal antiinflammantory drug can cause stomach ulcers in two ways, either directly or topical irritation of the epithelial tissue and inhibit the endogeneous system of gastrointestinal mucosa of prostaglandins. In this case inhibition of prostaglandin systhesis is the dominant factor of peptic ulcers by NSAIDs. Objectives : The purpose of this study was to determine the effct of NSAID drug administration on the formation of peptic ulcers and to know the difference in the rate of formation of peptic ulcers from each class. Method : Sampel method mice performed surgery on the stomach is done in Pharmacology Laboratory of Pharmacy Institute Deli Husada Deli Tua. Results : The results of this study indicate that faster drugs cause gastric ulcers with a degree of redness are Aspirin 4.03 mm, 2.01 mm mefenamat and 1.02 mm Diclofenac Sodium while Ibuprofen mwdication does not cause peptic ulcers. Conclusion : The results of this study it can be concluded that Aspirin administration with doses of 21 mg/kg faster causes gastric ulcers from other NSAID groups such as Mefenamat with a dose of 21 mg/kg BW, Diclofenac sodium at a dose of 2 mg/kg while administration, Ibuprofen for ten days does not couse ulcers in the stomach of experimetal animals.


2006 ◽  
Vol 290 (5) ◽  
pp. G1041-G1050 ◽  
Author(s):  
Tsutomu Nishida ◽  
Shingo Tsuji ◽  
Arata Kimura ◽  
Masahiko Tsujii ◽  
Syuji Ishii ◽  
...  

Endothelin (ET)-1 is a potent inducer of peptic ulcers. The roles of ET-1 in ulcer healing, however, have remained unclear, and these were investigated in mice. Gastric ulcers were induced in mice by serosal application of acetic acid. Three days later, mice were given a neutralizing ET-1 antibody or nonimmunized serum. The ulcer size, amount of fibrosis and myofibroblasts, and localization of ET-1 and ETA/B receptors were analyzed. To elucidate the mechanisms underlying the effects of ET-1, we examined the proliferation, migration, and release of growth and angiogenic factors in gastric myofibroblasts with or without ET-1. The expression of prepro-ET-1 (an ET-1 precursor) and ET-converting enzyme-1 was examined in gastric myofibroblasts using RT-PCR. Immunoneutralization of ET-1 delayed gastric ulcer healing. The areas of fibrosis and myofibroblasts were smaller in the anti-ET-1 antibody group than in the control. ET-1 was expressed in the gastric epithelium, myofibroblasts, and other cell types. ETA receptors, but not ETB receptors, were present in myofibroblasts. ET-1 increased proliferation and migration of gastric myofibroblasts. ET-1 stimulated the release of hepatocyte growth factor, VEGF, PGE2, and IL-6 from gastric myofibroblasts. mRNA for prepro-ET-1 and ET-converting enzyme-1 was also expressed. ET-1 promotes the accumulation of gastric myofibroblasts and collagen fibrils at gastric ulcers. ET-1 also stimulates migration and proliferation of gastric myofibroblasts and enhances the release of growth factors, angiogenic factors, and PGE2. Thus ET-1 has important roles not only in ulcer formation but also in ulcer healing via mobilizing myofibroblasts and inducing production of stroma-derived factors.


2021 ◽  
Vol 51 (3) ◽  
Author(s):  
Guillermo Rubén Fernandez ◽  
Matías Zanetti ◽  
Mariano Rubén Argüello ◽  
Liria Salomé Martínez Rejtman ◽  
Marisa Francisco ◽  
...  

Giant peptic ulcers are defined as having a diameter greater than 2 cm in the case of duodenal ulcers, and greater than 3 cm in the case of gastric ulcers. The presentation is infrequent, but raises questions about the etiological factor and the definitive treatment. The literature on its physio-pathology is scarce and the cases described are unusual. The following case is presented to review the conduct to be followed in the presence of a giant gastric ulcer. We highlight the difficulty to assess the differential diagnosis of malignant pathology, trying to emphasize the value of the predictive factors of malignancy to define the conduct to follow. Finally, we focus on the relationship between the clinical presentation of gastric giant ulcer with primary gastric lymphomas and their clinical characteristics.


2012 ◽  
Vol 2 (3) ◽  
pp. 48 ◽  
Author(s):  
Vandana Panda ◽  
Madhav Sonkamble

Background: Peptic ulcers occur in that part of the gastrointestinal tract which is exposed to gastric acid and pepsin, i.e., the stomach and duodenum. Gastric and duodenal ulcers are common pathologies that may be induced by a variety of factors such as stress, smoking and noxious agents including non-steroidal anti-inflammatory drugs. Ipomoea batatas tubers (sweet potato) contain ample amounts of antioxidants. It has been proven already by many scientific studies that antioxidants have ulcer healing properties. In reference to this, we tried assessing the ulcer healing effect of Ipomoea batatas tubers. Methods: The anti-ulcer activity of the tubers of Ipomoea batatas (sweet potato) was studied in cold stress and aspirin-induced gastric ulcers in Wistar rats. Methanolic extracts of Ipomoea batatas tubers (TE) at two doses, viz., 400 and 800 mg /kg were evaluated in cold stress and aspirin-induced gastric ulcer models using cimetidine and omeprazole respectively as standards. The standard drugs and the test drugs were administered orally for 7 days in the cold stress model and for 1 day in the aspirin-induced gastric ulcer model. Gastroprotective potential, status of the antioxidant enzymes {superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase(GR)} along with GSH, and lipid peroxidation were studied in both models. Results: The results of the present study showed that TE possessed gastroprotective activity as evidenced by its significant inhibition of mean ulcer score and ulcer index and a marked increase in GSH, SOD, CAT, GPx, and GR levels and reduction in lipid peroxidation in a dose dependant manner.Conclusion: The present experimental findings suggest that tubers of Ipomoea batatas may be useful for treating peptic ulcers.Key Words: Sweet potato tubers, cold stress, aspirin, ulcer, antioxidants.


2018 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 76 references.


2020 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 5 figures, 6 tables and 78 references.


Author(s):  
SHUBANGEE MISHRA ◽  
BALAJI O ◽  
VANISHREE RAO ◽  
SHALINI ADIGA

Objectives: Bisphosphonates are known to cause gastritis and only few studies have evaluated the use of plant extracts in the treatment of bisphosphonate induced peptic ulcers. In the present study, we examined the effect of sesame seed extract in the alendronate-induced gastric ulcer in adult Wistar rats. Methods: Thirty adult Wistar rats (180–250 g) of both sexes, divided into five groups (n=6) were used: Group 1 (vehicle control) – 0.9% saline, Group 2 (ulcer control) – alendronate 60 mg/kg, Group 3 (standard) – alendronate 60 mg/kg + pantoprazole 30 mg/kg/day, Group 4 (test groups) – alendronate 60 mg/kg + sesame 0.5 mg/kg, and Group 5 (test groups) – alendronate 60 mg/kg + sesame 1 mg/kg. All drugs were given orally once daily for 7 days except for alendronate given only on day 1. On day 8, rats were sacrificed, and stomach tissues were analyzed macroscopically for ulcers. Estimation of gastric pH, acidity, and volume was done along with mucin content measurement. One-way ANOVA followed by Tukey’s post hoc test was used for statistical analysis with p<0.05 taken as significant. Results: Our study found that sesame extract given therapeutically at doses of 0.5 and 1 mg/kg showed comparable results with that of pantoprazole 30 mg/kg. Both the doses of sesame, 0.5 and 1 mg/kg showed similar gastroprotective activity against alendronate-induced gastric ulcers in Wistar rats. Conclusion: The findings of this study clearly demonstrated the protective effects of Sesame against alendronate-induced gastric ulceration.


2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Nitin Vashistha ◽  
Dinesh Singhal ◽  
Gurpreet Makkar ◽  
Suneel Chakravarty ◽  
Vivek Raj

Giant gastric ulcer (GGU) is defined as an ulcer more than 3 cm in diameter. Now infrequent in clinical practice, in the pre-H2 receptor antagonist (H2RA) era, the incidence of GGU varied between 12 and 24% of all gastric ulcers. Proton pump inhibitors reportedly achieve better healing rates and symptom relief in comparison to H2RA. The GGU is associated with high incidence of serious complications such as hemorrhage. A perforated GGU though rare (<2%) offers serious challenges in management. We report one such case wherein the role of multidetector CT scan (MDCT) for diagnosis and treatment planning, surgical options for GGU perforations, and factors affecting outcome are discussed.


2009 ◽  
Vol 23 (9) ◽  
pp. 604-608 ◽  
Author(s):  
Marcel JM Groenen ◽  
Ernst J Kuipers ◽  
Bettina E Hansen ◽  
Rob J Th Ouwendijk

BACKGROUND/OBJECTIVES: As recently as 40 years ago, a decline in the incidence of peptic ulcers was observed. The discovery of Helicobacter pylori had a further major impact on the incidence of ulcer disease. Our aim was to evaluate the trends in the incidence and bleeding complications of ulcer disease in the Netherlands.METHODS: From a computerized endoscopy database of a district hospital, the data of all patients who underwent upper gastrointestinal endoscopy from 1996 to 2005 were analyzed. The incidence of duodenal and gastric ulcers, with and without complications, were compared over time.RESULTS: Overall, 20,006 upper gastrointestinal endoscopies were performed. Duodenal ulcers were diagnosed in 696 (3.5%) cases, with signs of bleeding in 158 (22.7%). Forty-five (6.5%) of these ulcers were classified as Forrest I and 113 (16.2%) as Forrest II. Gastric ulcers were diagnosed in 487 cases (2.4%), with signs of bleeding in 60 (12.3%). A Forrest 1 designation was diagnosed in 19 patients (3.9%) and Forrest 2 in 41 patients (8.4%). The incidence of gastric ulcers was stable over time, while the incidence of duodenal ulcers declined.CONCLUSIONS: The incidence of duodenal ulcer disease in the Dutch population is steadily decreasing over time. Test and treatment regimens for H pylori have possibly contributed to this decline. With a further decline in the prevalence of H pylori, the incidence of gastric ulcers is likely to exceed the incidence of duodenal ulcers in the very near future, revisiting a similar situation that was present at the beginning of the previous century.


2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Xin Chen ◽  
Lijuan Hu ◽  
Huanhuan Wu ◽  
Wei Liu ◽  
Shuhe Chen ◽  
...  

Chronic gastritis and gastric ulcers are prevalent throughout the world and are considered to be a global health problem. Modified Xiaochaihutang (MXCHT) prescription is broadly used in traditional medicine hospital for the treatment of gastritis. In order to assess the anti-Helicobacter pylori (H. pylori) effect of MXCHT, agar diffusion method in vitro and fluid dilution method for the minimal inhibitory concentration (MIC) were established. The anti-inflammatory effects were then evaluated using mouse ear edema model and rat paw edema model. The ethanol-induced gastric ulcer method was employed to verify the gastroprotective effect of active extracts in MXCHT. HPLC-TOF-MS/MS was used for analyzing the possible active constituents after oral administration of effective extracts in ethanol-induced gastric ulcer models. MXCHT and 4 different extracts of the bacterial inhibition diameter and MIC were dramatically decreased compared with control group, showing anti-Helicobacter pylori effects. High dose groups of MXCHT, water extract, EtOAc extract, and n-BuOH extract displayed significant anti-inflammatory effects in xylene-induced mouse ear edema model and carrageenan-induced rat paw edema model test. MXCHT and all active extracts exhibited gastroprotective activity and prevented gastric lesions induced by ethanol in rats. 4 prototype components and 4 metabolites were identified after oral administration of EtOAc extract. In addition, 6 prototype components and 6 metabolites were identified in n-BuOH extract. MXCHT, EtOAc extract, and n-BuOH extract demonstrate gastroprotective effects through anti-Helicobacter pylori and anti-inflammatory activities. Thus, this prescription may be a suitable natural source for the prevention and treatment of chronic gastritis and gastric ulcers.


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