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Case presentation of gastrinoma combined with gastric carcinoid with the longest survival record - Zollinger-Ellison syndrome: pathophysiology, diagnosis and therapy.
Med. Sci. Monitor 2002: 8 (6) s.CS43-CS59, il., bibliogr. 129 poz.
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dorośli = 65 r.ż.
Zollinger-Ellison syndrome is a very rare disease caused by tumor with gastrin producing cells accompanied by hypergastrinemia leading to gastirc hypersecretion and peptic ulcers and their complications. Female case of gastrinoma (Zollinger-Ellison syndrome; Z-E) with a record of 38 yrs of survival. Acute gastro-duodenal ulcers started at 28 yr of age and Z-E was diagnosed by using gastrin assays. Basal and maximal acid outputs and ratio of basal/maximal outputs were away over normal limits. Because of ulcer recurrence and complications, patients was subjected to several gastric surgeries but refused total gastrectomy. She was also treataed with many H2-receptor (R) antagonists and proton-pump inhibitors (PPI), each new drug being initially highlyt effective but then showing declinig efficacy except when PPI, lansoprazole was used. The gastrin level rose in the course of disease from initial high value of 2000 pg/mL to the extreme 4500 ng/mL at present. During the last 2 yrs, metastasis mainly to liver developed and they were successfully treated by synthetic octapeptided derivative of somatostatin and, as a result, metastatis partly reduced and plasma gastrin drasticly decreased. Biopsy taken from liver metastasis showed the presence of typical gastrinoma cells with gastrin and chromogranin, while that from oxyntic mucosa revealed the ECL-cell hyperplasia with corcinoid tumors and unexpected gastric atrophy. This phenomenal case described in this article might be the new proven evidence needed by gastroenterologists to overturn the traditional treatemnt using total gastrectomy as a treatment of choice to the partial gastrectomy combined with proton pump inhibitors.
Impact of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on gastric ulcerogenesis in experimental animals and in humans.
Eur. J. Pharmacol. 2002: 449 (1/2) s.1-15, il., bibliogr. s. 13-15
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Helicobacter pylori (H. pylori) and nonsteroid anti-flammatory drugs (NSAID) are the most common pathogens in the gastroduodenal mucosa in animals and humans, but their relationship in ulcerogenesis has been little studied. Acording to some authors, H. pylori infections in humans does not act synergistically with NSAID on ulcer healing, therefore, there is no need to eradicate the germ. This notion is supported by the finding that the eradication of H. pylori does not affect NSAID-induced gastropatyhy treated with omeprazole and that H. pylori inferction induced a strong cyclooxygenase-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandins, which should in turn counteract NSAID-induced gastropathy and heal existing ulcer. Other investigators claim that H. pylori infection acts synergistically with NSAID on ulcer development, therefore, H. pylori should be eradicated, particularly at the start of long-term NSAID therapy. Maastricht 2-2000 consensus also recommends eradication prior to NSAID treatment, but this eradication does not appear to accelerate ulcer healing or to prevent the recurrent ulcers in NSAID users. Our studies in almost 6000 dyspeptic patients undergoing upper endoscopy and [13C]-urea breath test (UBT) revealed that about 70 p.c. of these patients are H. pylori (+) and about 30.6 p.c. of these develop gastroduodenal ulcers. Of these ulcers, over 70 p.c. were H. pylori (+) positive, 12 p.c. NSAID (+), 8 p.c. both H. pylori (+) and NSAID (+), while 22 p.c. ulcers were H. pylori (-) and NSAID (-) or "idiopathic" ulcers...
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