Even though it is possible to detect Helicobacter pylori in middle ear cleft in chronic otitis media, its role in the etiopathogenesis of the issue is controversial.

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-α (TNF-α) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-α and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.

It has been reported that fish oil protects the rat liver against acetaminophen (APAP) induced toxicity; however, this finding is controversial. The present study was undertaken to investigate the effects of fish oil-enriched diet on APAP-induced liver injury in Wistar rats. Rats were fed a diet supplemented with either 8% fish oil or 8% corn oil, or standard rat feed for 6 wk. After an overnight fast, rats in each group were given either 2 g/kg APAP or saline orally. Our findings showed that APAP increased serum alanine aminotransferase (ALT) and that this rise was potentiated in the presence of dietary fat. Further fish oil ingestion increased the glutathione (GSH) content in rat liver; however, this was not effective in protecting liver from APAP-induced toxicity. Data suggest that GSH may be necessary to detoxify APAP metabolites, which are known to induce hepatotoxicity but are increased by dietary fat.

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