Helicobacter pylori - Az ujrafelfedezes elso 15 eve

Translated title of the contribution: Helicobacter pylori - The first 15 years of rediscovery

J. Lonovics, I. Rácz, L. Simon, I. Szekely, L. Szikra, L. Ujszaszy

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The etiopathogenetic role of H. pylori in gastroduodenal ulcer is widely accepted in the medical community. H. pylori exerts its pathologic effects through its so called virulence factors. The outcome of the infection is mainly determined by the characteristics of gastritis and host genetics. Depending upon the relationship of these factors the outcome may be peptic ulcer, malignant disease or symptom free carrier status. In the latest classification H. pylori negative ulcers include non-steroidal antiinflammatory drug-induced ulcers (the most frequent manifestations) and idiopathic/hyperacid ulcers (a 'new' clinical entity). The mechanism of extra-gastrointestinal manifestations may be explained at least partially by inflammatory mediators, mainly cytokines activated during the H. pylori- induced gastritis. Based upon international guidelines and the recommendation of the National Board of Gastroenterology clear therapeutic guidelines are provided: 'triple therapy' is a combination of either proton pump inhibitors (omeprazole, pantoprazole, lansoprazole) or ranitidine bismuth citrate with two antimicrobial agents, while 'dual therapy' consists of ranitidine bismuth citrate and clarithromycin. The microbiologist has got an important role in the planning of the eradication strategy for the fast growing metronidazol and gradually increasing clarithromycin resistance of the bacteria. If the first eradication attempt was unsuccessful (the most frequent causes of this include inadequate first-line therapy, antimicrobial resistance, poor patient compliance etc.), a modified one is needed. The association between H. pylori infection and the risk of gastric cancer is supported by numerous data of epidemiological, molecular biological and experimental studies. In this respect the CagA gene positive H. pylori strains are studied. Hungarian data of cost effectiveness are provided using a modified Markov chain model proving that a proper eradication package substantially reduce the costs of peptic ulcer treatment.

Original languageHungarian
Pages (from-to)358-379
Number of pages22
JournalLege Artis Medicinae
Volume9
Issue number5
Publication statusPublished - 1999

Fingerprint

Helicobacter pylori
Peptic Ulcer
Ulcer
Clarithromycin
Gastritis
Guidelines
Lansoprazole
Markov Chains
Omeprazole
Proton Pump Inhibitors
Helicobacter Infections
Virulence Factors
Gastroenterology
Therapeutics
Patient Compliance
Anti-Infective Agents
Stomach Neoplasms
Cost-Benefit Analysis
Anti-Inflammatory Agents
Cytokines

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Lonovics, J., Rácz, I., Simon, L., Szekely, I., Szikra, L., & Ujszaszy, L. (1999). Helicobacter pylori - Az ujrafelfedezes elso 15 eve. Lege Artis Medicinae, 9(5), 358-379.

Helicobacter pylori - Az ujrafelfedezes elso 15 eve. / Lonovics, J.; Rácz, I.; Simon, L.; Szekely, I.; Szikra, L.; Ujszaszy, L.

In: Lege Artis Medicinae, Vol. 9, No. 5, 1999, p. 358-379.

Research output: Contribution to journalArticle

Lonovics, J, Rácz, I, Simon, L, Szekely, I, Szikra, L & Ujszaszy, L 1999, 'Helicobacter pylori - Az ujrafelfedezes elso 15 eve', Lege Artis Medicinae, vol. 9, no. 5, pp. 358-379.
Lonovics J, Rácz I, Simon L, Szekely I, Szikra L, Ujszaszy L. Helicobacter pylori - Az ujrafelfedezes elso 15 eve. Lege Artis Medicinae. 1999;9(5):358-379.
Lonovics, J. ; Rácz, I. ; Simon, L. ; Szekely, I. ; Szikra, L. ; Ujszaszy, L. / Helicobacter pylori - Az ujrafelfedezes elso 15 eve. In: Lege Artis Medicinae. 1999 ; Vol. 9, No. 5. pp. 358-379.
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