Search PubMed⌕ Search

Biomedical subjects

Jaap C Thijs

Publications and source records attributed to Jaap C Thijs.

2 recordsLinked to original sources

Functional dyspepsia.

PURPOSE OF REVIEW: Functional dyspepsia is a common disorder, most of the time of unknown etiology and with variable pathophysiology. Therapy has been and still is largely empirical. Data from recent studies provide new clues for targeted therapy based on knowledge of etiology and pathophysiologic mechanisms. RECENT FINDINGS: The role of Helicobacter pylori gastritis in the pathogenesis of functional dyspepsia has been defined: It is causative in a small minority of patients. Associations between (groups of) symptoms and pathophysiologic mechanisms have been established, but there is much overlap and interaction, and their relevance for the individual patient is uncertain, especially because of the variability of symptoms over time. Little progress has been made in pharmacotherapy of functional dyspepsia, but exploratory studies show interesting new options. Hypnotherapy seems a promising alternative. SUMMARY: For the time being, diagnostic strategies for patients with suspected functional dyspepsia continue to be directed at excluding other disorders, in particular peptic ulcer disease and gastroesophageal reflux disease. In the presence of reflux symptoms, acid inhibitory therapy, preferably with a proton pump inhibitor, is a rational choice; otherwise, therapy is still empirical. Hypnotherapy is an option that could be seriously considered.

Journal Article↗

Role of the rdxA and frxA genes in oxygen-dependent metronidazole resistance of Helicobacter pylori.

Almost 50 % of all Helicobacter pylori isolates are resistant to metronidazole, which reduces the efficacy of metronidazole-containing regimens, but does not make them completely ineffective. This discrepancy between in vitro metronidazole resistance and treatment outcome may partially be explained by changes in oxygen pressure in the gastric environment, as metronidazole-resistant (MtzR) H. pylori isolates become metronidazole-susceptible (MtzS) under low oxygen conditions in vitro. In H. pylori the rdxA and frxA genes encode reductases which are required for the activation of metronidazole, and inactivation of these genes results in metronidazole resistance. Here the role of inactivating mutations in these genes on the reversibility of metronidazole resistance under low oxygen conditions is established. Clinical H. pylori isolates containing mutations resulting in a truncated RdxA and/or FrxA protein were selected and incubated under anaerobic conditions, and the effect of these conditions on the MICs of metronidazole, amoxycillin, clarithromycin and tetracycline, and cell viability were determined. While anaerobiosis had no effect on amoxycillin, clarithromycin and tetracycline resistance, all isolates lost their metronidazole resistance when cultured under anaerobic conditions. This loss of metronidazole resistance also occurred in the presence of the protein synthesis inhibitor chloramphenicol. Thus, factor(s) that activate metronidazole under low oxygen tension are not specifically induced by low oxygen conditions, but are already present under microaerophilic conditions. As there were no significant differences in cell viability between the clinical isolates, it is likely that neither the rdxA nor the frxA gene participates in the reversibility of metronidazole resistance.

Amoxicillin↗