Major UGI bleeding and gastric ulcer on the greater curvature are both independent clues to NSAID use in patients with peptic ulcer regardless of H. Pylori status

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4–6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the “gold standard” for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).

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PEPTIC ULCER FREQUENCY DIFFERENCES RELATED TO H. PYLORI OR AINES

Arquivos de Gastroenterologia ◽

10.1590/s0004-28032015000100010 ◽

2015 ◽

Vol 52 (1) ◽

pp. 46-49 ◽

Cited By ~ 4

Author(s):

Diego Michelon de CARLI ◽

Rafael Cardoso PIRES ◽

Sofia Laura ROHDE ◽

Caroline Mayara KAVALCO ◽

Renato Borges FAGUNDES

Keyword(s):

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

H Pylori ◽

Second Period

Background Peptic ulcer etiology has been changing because of H. pylori decline. Objectives To estimate peptic ulcer prevalence in 10 years-interval and compare the association with H. pylori and use of non-steroidal anti-inflammatory drugs. Methods Records assessment in two periods: A (1997-2000) and B (2007-2010), searching for peptic ulcer, H. pylori infection and non-steroidal anti-inflammatory drugs use. Results Peptic ulcer occurred in 30.35% in A and in 20.19% in B. H. pylori infection occurred in 73.3% cases in A and in 46.4% in B. Non-steroidal anti-inflammatory drugs use was 3.5% in A and 13.3% in B. Neither condition occurred in 10.4% and 20.5% in A and B respectively. Comparing both periods, we observed reduction of peptic ulcer associated to H. pylori (P=0.000), increase of peptic ulcer related to non-steroidal anti-inflammatory drugs (P=0.000) and idiopathic peptic ulcer (P=0.002). The concurrent association of H. pylori and non-steroidal anti-inflammatory drugs was also higher in B (P=0.002). Rates of gastric ulcer were higher and duodenal ulcer lower in the second period. Conclusions After 10 years, the prevalence of peptic ulcer decreased, as well as ulcers related to H. pylori whereas ulcers associated to non-steroidal anti-inflammatory drugs increased. There was an inversion in the pattern of gastric and duodenal ulcer and a rise of idiopathic peptic ulcer.

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CLINICAL PROFILE AND RISK FACTORS FOR BENIGN PEPTIC ULCER DISEASE IN A TERTIARY CARE CENTRE IN THE SUBHIMALAYAN RANGES OF NORTH INDIA

10.36106/paripex/5002629 ◽

2020 ◽

pp. 1-3

Author(s):

Vishal Bodh ◽

Rajesh Sharma ◽

Brij Sharma

Keyword(s):

Risk Factors ◽

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Peptic Ulcer Disease ◽

Low Socioeconomic Status ◽

Low Socioeconomic ◽

Ulcer Disease ◽

H Pylori ◽

Upper Gastrointestinal

Background: To study the clinical profile and risk factors for benign peptic ulcer disease. Material and Methods: A total of 200 patients of peptic ulcer disease (PUD) diagnosed on upper gastrointestinal endoscopy were included. The socio-demographic profile, risk factors, clinical and endoscopic findings were recorded. Results: A total of 200 patients of peptic ulcer disease were included, out of which 168(84%) were males, while 32 (16%) were females. Most of the patients (61%) were between age 31-60 years with mean age of 47 years. Most of patients were farmers from rural areas and belonged to low socioeconomic status. History of smoking and alcohol intake was present in 106(53%) and 70( 35 %) patients respectively.Most common presenting complaints were epigastric pain and/or burning in 72 (36%) , followed by upper abdomen discomfort 70(35%) and upper gastrointestinal bleed 58(29%). Duodenal ulcer (DU) was present in 152 (76%), gastric ulcer(GU) in 30 (15%) while 18 (9%) had both DU and GU. Most of the patients had Forrest III ulcer 167 (83.5%) followed by Forrest IIc ulcer 13 (6.5%). H. pylori was detected by rapid urease test on endoscopic biopsy specimen in 156 (78 % ) of the total 200 patients of peptic ulcer disease. H. pylori was detected in 78.94 % case of DU, 60% case of GU and 100% cases of both DU and GU. Conclusion: PUD is a multifactorial health problem affecting almost all populations worldwide. . The major risk factors associated with PUD included tobacco and alcohol consumption besides low socioeconomic status, rural background and occupation of farming. Our findings indicate the substantial role of H. pylori and painkiller ingestion in the pathogenesis of PUD. Duodenal ulcer is most common type followed by gastric ulcer. Most had Forrest III ulcer followed by Forrest IIc.

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Conceptual study of pathophysiology and pharmacological effect of Saptamrit Louha in approach to Soola

International Journal of Advances in Medicine ◽

10.18203/2349-3933.ijam20174278 ◽

2017 ◽

Vol 4 (5) ◽

pp. 1203

Author(s):

Deepak Ekka ◽

Swati Dubey ◽

S. D. Khichariya ◽

D. S. Dhruw

Keyword(s):

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Pain Relief ◽

Blood Group ◽

Modern Science ◽

Effective Role ◽

H Pylori ◽

Conceptual Study ◽

Time Of Presentation

Anndrvashoola and Parinamshoola briefly described by aacharya Vijayrakshitand Kanthdatta on Madhukosh in shoola Nidanam 26th chapter, mainly vata dosha is responsible for that disease. In Anndrvashoola continuous pain in abdomen, pain present before meal and relif in pain after vomiting in Parinamshoola, aadhman, aatop, arti, kamp and pain relief by consuming greaspy and worm food. In modern science, according to sign symptoms we correlated with peptic ulcer. Main cause is H. Pylori, NSAID, stress, smoking, steroid either duodenum or stomach ulcer in ratio of 4:1. The peak incidence of duodenal ulcer is 5th decade while for Gastric ulcer is 6th decade and “O” blood group persons are more prone to develop duodenal ulcer. To treat this disease Vranropan and Shothhara chikitsa is very important for that this drug should have properties like Dahaprashmana, Amashayakshata sandhan, Pittashamak, Amlatanashak, shothhara due to those action Saptamrit Louha play effective role in Shoola. Considering above factor SAPTAMRIT LOUHA is chosen in management of shoola. Later on, I will have explained how Sapamrit louha works on Anndrvashoola and Parinamshoola at the time of presentation.

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AMBIVALENCE OF CHRONIC INFLAMMATION IN THE MUSCULOUS STOMACH

Crimea Journal of Experimental and Clinical Medicine ◽

10.37279/2224-6444-2020-10-2-104-111 ◽

2020 ◽

Vol 10 (2) ◽

pp. 104-111

Author(s):

O. V. Shtygasheva ◽

E. S. Ageeva

Keyword(s):

Gastric Cancer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Gastric Mucosa ◽

Chronic Inflammation ◽

Morphological Changes ◽

Reference Points ◽

Gastric Epithelium ◽

H Pylori ◽

Cag A

For peptic ulcer disease, the etiological role of H. pylori infection has been proven, 60-90% of gastric cancer cases are associated with H. pylori. The bacterium is recognized as a first-order carcinogen. An association has been established between the successful elimination of H. pylori and a reduced risk of gastric cancer and relapse of peptic ulcer. In the pathogenesis of chronic inflammation in the gastric mucosa associated with H. pylori, there are reference points that determine the further path of development of the pathology. If peptic ulcer is not a consequence of the direct damaging effect of NSAIDs, it is associated with the development of gastritis. In gastric ulcer, gastritis is found in both the antrum and the fundus of the stomach Atrophy of the glands begins in the antrum, then its foci are found in the fundus on the front and back walls. Gradu- ally they increase in size, merge with each other, the acid secreting zone decreases, and the border between the fundus and pyloric glands shifts in the proximal direction. With atrophic fundus gastritis, the likelihood of developing high ulcers and stomach cancer increases. Significant increase in apoptosis processes with relative rigidity of proliferation leads to the formation of ulcer, and carcinogenesis is due to excessive proliferation and accumulation of cell mutations. One of the subjects of damage is Cag A H. pylori protein, which implements remodeling of the gastric epithelial barrier. Among its effects are modulation and impaired proliferation of gastric epithelium, leading to morphological changes. The aggressive action of Cag A protein enhances toxic doses of alcohol and smoking, supporting inflammation and causing damage to the gastric mucosa. Despite the common etiology and pathogenesis of gastric ulcer and gastric cancer, the relationship with the de- velopment of atrophic pangastritis and the similarity of convention risk factors determines that the key point in the manifestation of gastric cancer is a genetic predisposition in the form of gene polymorphism causing severe atrophy as a result of chronic inflammation.

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Peptic Ulcer Diseases

10.2310/tywc.1114 ◽

2018 ◽

Author(s):

Edward A Lew

Keyword(s):

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Peptic Ulcer Disease ◽

Clinical Manifestations ◽

Muscularis Propria ◽

Gastric Ulcers ◽

Peptic Ulcers ◽

Ulcer Disease ◽

H Pylori

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.

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Peptic Ulcer Diseases

10.2310/im.1114 ◽

2020 ◽

Author(s):

Edward A Lew

Keyword(s):

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Peptic Ulcer Disease ◽

Clinical Manifestations ◽

Muscularis Propria ◽

Gastric Ulcers ◽

Peptic Ulcers ◽

Ulcer Disease ◽

H Pylori

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.

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PREVALENCE OF H. PYLORI

The Professional Medical Journal ◽

10.29309/tpmj/2010.17.03.2536 ◽

2010 ◽

Vol 17 (03) ◽

pp. 431-439

Author(s):

MASOOD JAVED ◽

KHALID AMIN ◽

DILSHAD MUHAMMAD ◽

Aamir Husain ◽

Nasir Mahmood

Keyword(s):

Duodenal Ulcer ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Peptic Ulcer Disease ◽

Protective Mechanism ◽

Skilled Workers ◽

Ulcer Disease ◽

Peptic Disease ◽

Number Of Patients ◽

H Pylori

Background: Acid peptic disease is a world wide problem among all the age groups and both sexes. Duodenal ulcer is common as compared to gastric ulcer. Its prevalence being 4:1 in USA & UK and 5:1 in Pakistan1,2,3. Etiology of peptic ulcer is almost certainly multi-factorial. Basic paradigm for ulcer disease is the imbalance between the digestive activity of acid and pepsin and the protective mechanism in place toresist mucosal digestion. Over the past few years a new line of thought has been evolved after isolating spiral campylobacter like organism from antral biopsy specimens. H pylori is now considered to be an important if not the only causative agent of gastritis and peptic ulcer disease. The dictum; No acid – No ulcer summarized the pathogenesis of peptic ulcer disease but new dictum seems to be; No H.pylori -No ulcer4,5, as over90% of Duodenal ulcer and 70% of Gastric ulcer patients are infected byH.Pylori6. Aim of the study was to evaluate the prevalence of H.pylori among Duodenal ulcer patients at Faisalabad District and its suburbs. Study Design: Descriptive Study. Period: From Mar 2008 to Oct 2008. Materials and Methods: 50 patients (40 Males, 10 Females) belonging to Faisalabad District and surrounding areas with upper gastrointestinal symptoms of acid peptic disease and endoscopy proved duodenal ulcer were subjected to gastric antral mucosal biopsies for evaluation of the H.Pylori status with the help of unease test and histological examination of biopsy specimen. Results: Epigastric pain was the most frequent symptom 90%. (46 out of 50 patients). 92% showed evidence of H. pylori infection. Maximum incidence of H. pylori was recordedin age group IV (46—55 years). Maximum number of patients was skilled workers (35 out of 50) 70%. 80 % of the patients belonged to lower and middle class. Percentage of H.pylori positivity was 89.1 % and 84.34 %. Conclusions: Acceptance of contributory role and high prevalence rate of H.pylori instigates us for addition of antimicrobial treatment to the conventional treatment with H2 Blockers and PPIs which is cost effectiveand alter the course of the disease.

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