Evolution of Pediatric Gastrointestinal Ulcer Disease: Is Acute Surgical Intervention Relevant?

Author(s):  
Alyssa D. Brown ◽  
Michael D. Traynor ◽  
Jr D. Dean Potter ◽  
Michael B. Ishitani ◽  
Christopher R. Moir ◽  
...  
Author(s):  
Oladayo E. Apalowo ◽  
Oladayo J. Areola ◽  
Gbenga S. Ogunleye ◽  
Ayodeji S. Odukoya ◽  
Olusegun O. Babalola

Aim: The study investigated the possible risks associated with gastrointestinal ulcer disease by evaluating the biochemical response of three body organs; heart, kidney and liver, in gastric ulcerated rats. Methodology: Twenty male wistar albino rats were used in the study. Gastric ulcer was induced in rats with single oral dose of 400 mg/kg body weight (b.w.) aspirin, 80 mg/kg b.w. indomethacin and 5 ml/kg b.w. acidified ethanol (40:60 v/v). Blood samples were collected into heparinized bottle and centrifuged at 4000 rpm for 10 mins to obtain the plasma. Gastric tissue, liver, kidney and heart were also collected. Results: Oral administration of 400 mg/kg b.w. aspirin, 80 mg/kg b.w. indomethacin and 5 ml/kg b.w. acidified ethanol caused a remarkable increase in ulcer index. There was observed a significant (p<0.05) reduction in AST and ALT activities in gastric ulceration caused by aspirin (Asp), with no significant (p<0.05) change in total protein (TP) concentration, lactate dehydrogenase and creatine kinase activity. However, there was increase in creatinine and urea concentration. Acidified ethanol and Indomethacin-induced ulcerated rats showed significant (p<0.05) reduction in all other parameters except ALT and lactate dehydrogenase activities which did not show any significant (p<0.05) change. There was also observed a significant (p<0.05) increase in creatine kinase activity in indomethacin-induced ulcerated rats. Conclusion: Overall, the result indicates a link between gastric ulcer and organ toxicity. The use of NSAIDs above the therapeutic doses in the treatment of pains and related illness as well as excess consumption of alcohol is shown to negatively impact the stomach and cause serious damage to different body organs of wistar rats.


1996 ◽  
Vol 43 (4) ◽  
pp. 348
Author(s):  
J. Steven Burdick ◽  
M. Aiyer ◽  
J. Aldag ◽  
Medicine R. Bertino ◽  
T. Brady ◽  
...  

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.


2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A491-A491
Author(s):  
G GONZALEZSTAWINSKI ◽  
J ROVAK ◽  
H SEIGLER ◽  
J GRANT ◽  
T PAPPAS

1953 ◽  
Vol 25 (2) ◽  
pp. 173-201 ◽  
Author(s):  
William S. Haubbich ◽  
James L.A. Roth ◽  
H.L. Bockus

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