Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: CZEŚNIKIEWICZ
Liczba odnalezionych rekordów: 4



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Tytuł oryginału: Oral cavity as a potential source of gastric reinfection by Helicobacter pylori.
Autorzy: Karczewska Elżbieta, Konturek Joanna E., Konturek Peter C., Cześnikiewicz Marta, Sito Edward, Bielański Władysław, Kwiecień Nina, Obtułowicz Wojciech, Ziemniak Witold, Majka Jolanta, Hahn Eckhart G., Konturek Stanisław J.
Źródło: Dig. Dis. Sci. 2002: 47 (5) s.978-986, il., tab., bibliogr. 24 poz.
Sygnatura GBL: 310,037

Hasła klasyfikacyjne GBL:
  • stomatologia
  • mikrobiologia
  • gastroenterologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Helicobacter pylori (Hp) is a common pathogen colonizing the a gastric mucosa, but some reports indicated that it may also be found in the oral cavity, which could serve as a reservoir of the bacteria and a source of gastric reinfection. Accordingly, we aimed to study whether the oral cavity, particularly gingival pockets, are colonized by Hp and whether it could be the source of gastric reinfection. We studied 329 patients with dyspeptic symptoms (257 with chronic gastritis, 15 with gastric ulcer. and 57 with duodenal ulcer). The [**13C]urea breath test (UBT), gastroscopy, and Hp culture from gastric biopsies were carried out, and material was collected from the oral cavity (gingival pocket) for bacteriological culture and genomic DNA studies. The serum was obtained for anti-Hp IgG and anti-CagA assays and saliva for anti-Hp IgA determination using the ELISA technique. bacteria in material from gingival pockets and biopsies from the corpus and antrum of stomach of 30 DU patients before and after Hp eradication were also examined by PCR technique, using primers specific for 16S rNA. All Hp-positive patients (276) were subjected to one week of triple therapy (omeprazole 2 x 20 mg twice a day, clarithromycin 2 = 500 mg twice a day, and metronidazole 2 x 500 mg twice a day). The measurements descrived above were then repeated at four weeks and six months. Bacterkilogical culture showed the prsence of Hp in the material from oral cavity in about 50 p.c. of patients, whereas UBT, used as a gold standard, revealed gastric Hp infection in about 84 p.c. of these patients...

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    Tytuł oryginału: Impact of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on gastric ulcerogenesis in experimental animals and in humans.
    Autorzy: Pawlik Teresa, Konturek Peter C., Konturek Jan W., Konturek Stanisław J., Brzozowski Tomasz, Cześnikiewicz Marta, Płonka Małgorzata, Bielański Władysław, Areny Hany
    Źródło: Eur. J. Pharmacol. 2002: 449 (1/2) s.1-15, il., bibliogr. s. 13-15
    Sygnatura GBL: 312,088

    Hasła klasyfikacyjne GBL:
  • gastroenterologia

    Typ dokumentu:
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • zwierzęta

    Streszczenie angielskie: 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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    Tytuł oryginału: Effects of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on gastric mucosa and risk of gastro-duodenal ulcerations in men.
    Autorzy: Bielański Władysław, Konturek Stanisław J., Płonka Małgorzata, Cześnikiewicz Marta, Penar Agnieszka, Jędrychowski Wiesław
    Źródło: Prz. Epidemiol. 2002: 56 supl.: Conference on molecular epidemiology in preventive medicine - achievements and new challenges s.139-162, il., bibliogr. 59 poz. - Konferencja pt. Molekularna epidemiologia w medycynie prewencyjnej - osiągnięcia i nowe wyzwania Kraków 20-22.06. 2002
    Sygnatura GBL: 301,250

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • mikrobiologia
  • gastroenterologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Background: Helicobacter pylori (Hp) and nonsteroidal anti-inflammatory drugs (NSAID) are the most common pathogens in the stomach, but their interaction on gastro-duodenal mucosa has been little studied. Hp infection in humans does not interfere with NSAID-induced gastric ulcer healing by omeprazole, therefore, there is no rationale to eradicate the germ under these conditions. Hp infection induces COX-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandin (PG), which should in turn counteract NSAID-induced gastropathy and contribute to healing of existing ulcers. Some investigators claim that Hp infection acts synergistically with NSAID on ulcergenesis and propose that Hp should be eradicated, particularly at the onset of long-term NSAID therapy but this is the subject of controversy. Material and methods: Our studies on 6515 dyspeptic patients undergoing upper endoscopy and 13C-urea breath test (UBT) revealed that about 70 p.c. of these patients are Hp positive and 31 p.c. of them develop gastro-duodenal ulcers. Of these ulcers, 66 p.c. were Hp positive non NSAID users, 3 p.c. were Hp negative and NSAID users, 8 p.c. were both Hp positive and NSAID users, while 23 p.c. ulcers were both Hp and NSAID negative. An evidence was obtained for negative interaction between Hp infection and NSADI on risk of gastro-duodenal ulcers suggesting that Hp may attenuate the peptic ulcerogenesis. Conclusions: Our results support the concept that 1) the interaction between Hp infection ...

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    Tytuł oryginału: Interaction of Helicobacter pylori (Hp) and nonsteroidal anti-inflammatory drugs (NSAID) on gastric mucosa and risk of ulcerations.
    Autorzy: Konturek Peter C., Konturek Stanisław J., Cześnikiewicz Marta, Płonka Małgorzata, Bielański Władysław
    Źródło: Med. Sci. Monitor 2002: 8 (9) s.RA197-RA209, il., bibliogr. 57 poz.
    Sygnatura GBL: 313,278

    Hasła klasyfikacyjne GBL:
  • mikrobiologia
  • gastroenterologia
  • toksykologia

    Typ dokumentu:
  • tytuł obcojęzyczny

    Streszczenie angielskie: Hp and NSAID are the most common pathogens in the stomach, but their interaction on gastro-duodenal mucosa has been little studies. Hp infection in humans does not interfere with NSAID-induced gastric ulcer healing by omeprazole, therefore, there is no rationale to eradicate the germ. Hp infection induces COX-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandin (PG), which should in turn counteract NSAID-induced gastropathy and contribute to healing of existing ulcers. Some investigators claim that Hp infection acts synergistically with NSAID on ulcerogenesis and propose that Hp should be eradicated, particularly at the onset of long-term NSAID therapy. Our studies in about 6500 dyspeptic patients undergoing upper endoscopy and 13C-urea breath test revealed that about 70 p.c. of these patients are Hp positivie and 31 p.c. of these develop gastro-duodenal ulcers. Of these ulcers, 66 p.c. were Hp positive and NSAID negative, 3 p.c. - NSAID positive and Hp negative, 8 p.c. were both Hp positive and NSAID positive, while 23 p.c. ulcers were Hp and NSAID negative. An evidence was obtained for negative interaction between Hp infectio and NSAID on risk of gastro-duodenal ulcers suggesting that Hp may attenuate the peptic ulcerogenesis. Our results support the concept 1) the interaction between Hp infection and NSAID on gastro-duodenal ulcerations is antagonistic, 2) the Hp and NSAID are independent risk factors for peptic ulcerations in humans, 3) there is no need for the Hp eradication in NSAID-treated patients, and 4) the rate of ulcer complications (hemorrhage and perforation) remains constant despite the decrease in Hp and ulcer prevalence.

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