Fourteen patients with Helicobacter pylori infection were treated with 20 mg omeprazole, 1 g amoxycillin and 400 mg metronidazole bd for 7 days (OAM), and 16 patients were treated with 20 mg omeprazole, 250 mg clarithromycin and 400 mg metronidazole bd for 7 days (OCM). Saliva, gastric biopsies and faecal samples were collected before, during (day 7) and 4 weeks after treatment in order to analyse alterations of the normal microflora and to determine antimicrobial susceptibility. Both treatment regimens resulted in marked quantitative and qualitative alterations. A selection of resistant streptococcal strains were noticed in both treatment groups, most apparent in the OCM group where a shift from susceptible to resistant strains was recorded. In the OAM group, six patients had overgrowth of resistant enterobacteriaceae during treatment compared with none in the OCM group, in the gastric microflora. The MICs for Enterococcus spp. and Enterobacteriaceae in faeces increased significantly during treatment in both groups. Nine patients in the OAM group became intestinally colonized by yeasts during treatment. The total anaerobic microflora was strongly suppressed in both treatment groups, although most pronounced in the OCM group, where the frequency of clarithromycin-resistant bacteroides strains increased from 2 to 76% during treatment, and remained at 59% 4 weeks post-treatment. Even if the treatment outcome was better in the OCM group (100%) than in the OAM group (71%), the amoxycillin-based treatment might be preferable from an ecological point of view, since the qualitative alterations in terms of emergence and persistence of resistant strains seemed to be most pronounced in the clarithromycin-treated group.

In addition to cholelithiasis, smoking and heavy alcohol use, drugs may be an important risk factor for acute pancreatitis.

Our data show that successful eradication of H. pylori infection does not increase the incidence of GERD in duodenal ulcer patients.

SUMMARYBackground: On-demand therapy with esomeprazole is effective for long-term treatment of non-erosive gastrooesophageal reflux disease, but it has not been evaluated in erosive gastro-oesophageal reflux disease. Aims: To compare endoscopic and symptomatic remission over a 6-month period when patients with healed erosive gastro-oesophageal reflux disease are treated with esomeprazole 20 mg, either once daily or on-demand. Methods: Patients with verified erosive reflux oesophagitis of Los Angeles grades A-D were enrolled. Following 4-8 weeks treatment with esomeprazole 40 mg daily, those who were endoscopically healed and had symptom control during the last week were randomized to maintenance therapy for 6 months with esomeprazole 20 mg, taken either once daily or on-demand.

Thirty healthy volunteers in three groups participated in a study of the effect on the intestinal microflora of oral supplementation with Bifidobacterium longum, Lactobacillus acidophilus and oligofructose, an indigestible oligosaccharide, during oral administration of cefpodoxime proxetil bd for 7 days. Those in group A also received an oral supplement with c.1011 cfu of B. longum BB 536 and L. acidophilus NCFB 1748 and 15 g oligofructose daily, those in group B received a supplement with oligofructose only and those in group C received placebo, for 21 days. In all three groups there was a marked decrease in aerobic microorganisms, involving mainly a rapid and almost complete disappearance of Escherichia coli (P: < 0.05) during antimicrobial administration and, thereafter, an overgrowth of enterococci (P: < 0.05). The number of intestinal yeasts also increased significantly (P: < 0.05) in groups A and B over the same period. There was a dramatic decrease in anaerobic microorganisms on day 4 of administration, mainly caused by loss of bifidobacteria (P: < 0.05) in all groups. The number of lactobacilli also decreased but was significantly higher in group A than in group C at the end of cefpodoxime proxetil administration. Clostridium difficile was found in only one person from group A, but six persons each in groups B and C. Of the bifidobacterial strains isolated from the faecal samples in group A, one was similar to the strain of B. longum administered, but most volunteers were colonized by several different strains of B. longum during the investigation period. The administered strain of L. acidophilus was recovered from six patients in group A.

The aim of the study was to study the ecological effects of levofloxacin, compared to that of ofloxacin, on the oral and intestinal human microflora. 10 healthy volunteers received levofloxacin (500 mg) and 10 subjects were given ofloxacin (400 mg) perorally, once daily for 7 days. Saliva and stool samples were obtained prior to drug administration, during administration (days 2, 4 and 7), and after withdrawal of the agents (days 9, 11, 14 and 21). The concentrations of levofloxacin and ofloxacin in the saliva and faecal samples, respectively, were assayed, and quantitative and qualitative microbiological analyses were performed. Oral administration of levofloxacin and ofloxacin led to low drug concentrations in the saliva, which corresponded with mild disturbances in the oral microflora. High drug levels were obtained in the intestinal tract, and both agents caused a selective reduction in the normal microflora, mainly directed towards aerobic Gram-negative bacteria. There was no significant difference between levofloxacin and ofloxacin, regarding ecological effects on the normal oral and intestinal microflora. From an ecological point of view, these agents acted favourably, since no major selection of resistant strains occurred in the normal microflora during administration.

We have investigated various modes of adherence of Helicobacter pylori to the human gastric epithelium, using transmission electron microscopy, in biopsies from nine patients with peptic ulcer disease and from four patients with chronic active gastritis. H. pylori was demonstrated in abundance in all cases within the surface mucous layer. In all ulcer‐ and in one out of four gastritis patients H. pylori was shown in close proximity to the gastric epithelium, with concurrent alterations in the configuration of microvilli and the apical cytoplasmic region of gastric cells. Previously described modes of H. pylori adherence were confirmed, such as loose attachment with fibrillar‐like strands, firm attachment with pedestal formation, invasion in the intercellular spaces, and invagination with “cup” formation. Moreover, in many cases a fusion between the bacterial outer layer and gastric cell membranes was evident. In four cases (31%; three with active and one with past ulcer disease) viable H. pylori was found in the cytoplasm of gastric mucous cells. Our results support the hypothesis that the different modes of adherence of H. pylori represent a stepwise, possibly sequential, process which in a significant number of cases leads to internalisation of the organism. The invariable occurrence of adhesion and more frequent internalisation of H. pylori in ulcer patients may suggest a link with the pathogenesis of peptic ulcer disease.

HOFFSTEDT, JOHAN, MANABU SHIMIZU, SVANTE SJOSTEDT AND FREDRIK LONNQVIST. Determination of B3-adrenoceptor mediated lipolysis in human fat cells. Obes Res. 1995;3:447-457. The existence and relative importance of Bradrenoceptors in man is still controversial. The aim of the present study was 1) to find further evidence for the existence of functional B3-adrenoceptors in human fat, and 2) to investigate factors that may influence this 03-adrenoceptor function. Fifty individuals were examined. Lipolysis mediated by the selective Il3-adrenoceptor agonist CGP 12177 in omental fat cells correlated with the response in subcutaneous fat cells. However, lipolysis was more pronounced in omental as compared to subcutaneous adipocytes, the intrinsic activity for CGP 12177 was 41% and 33%, respectively, while dobutamine, terbutaline and norepinephrine were full agonists. Both the lipolytic response and the sensitivity to CGP 12177 correlated with the effects of norepinephrine in the omental fat cells (r2= 0.68 and 0.50, respectively, p=O.OOOl). The D3-adrenoceptor mediated lipolytic response did also correlate with the responses induced by l31-and B2-agonists and by postreceptor acting agents. The antagonistic properties (PA$ of the D-adrenoceptor subtypes were also investigated. The pA2 for the selective " 1 -and 02-adrenoceptor antagonists versus CGP 12177-induced lipolysis were 2 to 3 log units lower than those for the Ill-antagonist versus dobutamine or for the Il2-antagonist versus terbutaline. Furthermore, bupranolol had a significantly better antagonistic effect (pA2 7.17, p