scholarly journals A Case of H. pylori-associated Granulomatous Gastritis with Hypertrophic Gastropathy

Gut and Liver ◽  
2009 ◽  
Vol 3 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Yeon Soo Kim ◽  
Hye Kyung Lee ◽  
Jong Ok Kim ◽  
Seung Woo Lee ◽  
Sang Beom Kang ◽  
...  
2018 ◽  
Vol 1 (2) ◽  
pp. 10-15
Author(s):  
Jouini Raja ◽  
Meriam Sabbah ◽  
Naija Meriam ◽  
Fatma Khanchel ◽  
Wafa Koubaa ◽  
...  

Introduction: Granulomas in gastric biopsy specimens are extremely rare. The final diagnosis of granulomatous gastritis is based on morphological findings, clinical and laboratory data. The aim of our study is to evaluate the clinical fields and to determine the etiology of gastric granulomatosis in our experience Patients and Methods: Thirty nine patients were reviewed retrospectively in the department of pathology of Habib Thameur between 2000 and 2018. Slides from all cases were stained by hematoxylin and eosin. The clinic-pathologic findings and the associated lesions were analyzed and the final etiology of the gastric granulomatosis was noted. Results: Biopsies from the 39 patients diagnosed as having granulomatous gastritis were reviewed. Mean age was 49 years (24 – 96) and sex ratio was 0,25 (M/F=8/31). Indication of endoscopy was gastric pain in 12 cases, chronic diarrhea in 6 cases, anemia in 2 cases, vomiting in 4 cases. Other symptoms were rare. Upper endoscopy was normal in 8 cases, showed antral gastropathy in 20 cases (erythematous in 6 cases, nodular in 8 cases and ulcerated in 6 cases). In four cases, fundic lesions were observed. Granuloma was unique in 14 cases and multiple in 25 cases. Localisation of granuloma was the antrum in 25 cases, the fundus in 7 cases, and both of them in 7 cases. An associated chronic gastritis was noted in 25 cases. Concerning the etiology, 10 of our patients had Crohn's disease while 6 of them had gastric tuberculosis. In five cases, H Pylori was the retained cause of gastric granulomatosis. In the other patients, the final diagnosis was sarcoidosis (n=3), foreign body reaction (n=1), yersiniosis (n=1). In our series, thirteen cases were unclassifiable. Conclusion: Although many cases remain unclassified, in most cases of granulomatous gastritis, a diagnosis of Crohn's disease or tuberculosis could be established. If this cases are excluded, an association between H. pylori and granulomatous gastritis cannot be ruled out. The others causes are extremely rare.


2008 ◽  
Vol 73 (2) ◽  
pp. 142-143
Author(s):  
Yasumasa Matsuo ◽  
Yuichi Morohoshi ◽  
Natsuko Mori ◽  
Yusuke Horiuchi ◽  
Shuichi Nagakubo ◽  
...  

Author(s):  
A. R. Crooker ◽  
W. G. Kraft ◽  
T. L. Beard ◽  
M. C. Myers

Helicobacter pylori is a microaerophilic, gram-negative bacterium found in the upper gastrointestinal tract of humans. There is strong evidence that H. pylori is important in the etiology of gastritis; the bacterium may also be a major predisposing cause of peptic ulceration. On the gastric mucosa, the organism exists as a spiral form with one to seven sheathed flagella at one (usually) or both poles. Short spirals were seen in the first successful culture of the organism in 1983. In 1984, Marshall and Warren reported a coccoid form in older cultures. Since that time, other workers have observed rod and coccal forms in vitro; coccoid forms predominate in cultures 3-7 days old. We sought to examine the growth cycle of H. pylori in prolonged culture and the mode of coccoid body formation.


Author(s):  
M. H. Chestnut ◽  
C. E. Catrenich

Helicobacter pylori is a non-invasive, Gram-negative spiral bacterium first identified in 1983, and subsequently implicated in the pathogenesis of gastroduodenal disease including gastritis and peptic ulcer disease. Cytotoxic activity, manifested by intracytoplasmic vacuolation of mammalian cells in vitro, was identified in 55% of H. pylori strains examined. The vacuoles increase in number and size during extended incubation, resulting in vacuolar and cellular degeneration after 24 h to 48 h. Vacuolation of gastric epithelial cells is also observed in vivo during infection by H. pylori. A high molecular weight, heat labile protein is believed to be responsible for vacuolation and to significantly contribute to the development of gastroduodenal disease in humans. The mechanism by which the cytotoxin exerts its effect is unknown, as is the intracellular origin of the vacuolar membrane and contents. Acridine orange is a membrane-permeant weak base that initially accumulates in low-pH compartments. We have used acridine orange accumulation in conjunction with confocal laser scanning microscopy of toxin-treated cells to begin probing the nature and origin of these vacuoles.


2000 ◽  
Vol 15 (12) ◽  
pp. H29-H29
Author(s):  
Vera D. Yoewono ◽  
E. Krinuhoni ◽  
W Marwoto ◽  
S.O. Sri Widodo

2001 ◽  
Vol 120 (5) ◽  
pp. A81-A81
Author(s):  
J MARTIN ◽  
A POTTHOFF ◽  
M COMBERG ◽  
I SOBEKKLOCKE ◽  
S LEDIG ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A81-A81
Author(s):  
B NEU ◽  
R RAD ◽  
M NEUHOFER ◽  
C TRAUTWEIN ◽  
M GERHARD ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A55-A55
Author(s):  
N KIM ◽  
D WEEKS ◽  
J SHIN ◽  
D SCOTT ◽  
G SACHS
Keyword(s):  

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