Duodenal diverticulum causing obstructive jaundice - Lemmel's syndrome.

The duodenum is the second most common location of intestinal diverticula. Periampullary duodenal diverticulum rarely causes obstructive jaundice and this condition was first described by German surgeon Gerhard Lemmel in 1934. Lemmel's syndrome is defined as obstructive jaundice due to a periampullary duodenal diverticulum in the absence of choledocholithiasis or a neoplasm.

Therapy of the rat hemorrhagic cystitis induced by cyclophosphamide. Stable gastric pentadecapeptide BPC 157, L-arginine, L-NAME.

We focused on the cyclophosphamide-induced hemorrhagic cystitis (100 mg/kg/day intraperitoneally throughout three days) as a particular NO-system disturbance, and therapy possibilities. We demonstrated that it may be attenuated by subsequent administration of the NOS substrate L-arginine (100 mg/kg/day intraperitoneally), aggravated by NOS-blocker L-NAME (5 mg/kg/day intraperitoneally), all influenced by the stable gastric pentadecapeptide BPC 157 (10 µg/kg/day, 10 ng/kg/day, intraperitoneally or perorally, in drinking water). Regularly, cyclophosphamide dose- and time-dependently induced severe hemorrhagic cystitis lesions, gross lesions, and corresponding urothelial necrosis, vesical edema, erosion, hemorrhage, inflammation, and ulceration, microscopically. The bladder wet weight dramatically increased. Functionally, already after first cyclophosphamide administration, there is an increased leak point pressure. Until the second cyclophosphamide administration, L-arginine consistently attenuated regular cyclophosphamide-induced severe hemorrhagic cystitis lesions, grossly and microscopically, but not functionally. L-NAME aggravated these lesions and eradicated beneficial effect of L-arginine when combined. BPC 157 administration after cyclophosphamide, given in either dose or in either regimen markedly attenuated all cyclophosphamide lesions, grossly, microscopically. The increase of the bladder wet weight was consistently attenuated. Functionally, increased leak point pressure was reversed to the values noted in normal rats. The similar findings were noted in rats that received BPC 157 together with L-NAME or L-arginine, given alone or combined. Thus, the lesions are NO-related based on the administration of L-NAME as well as administration of L-arginine, and their mutual interaction, and counteraction by BPC 157 application. Likewise, we reveal new therapeutic possibilities, emphasizing stable gastric pentadecapeptide BPC 157 and L-arginine, versus L-NAME in rats underwent cyclophosphamide-induced cystitis.

Cyclophosphamide induced stomach and duodenal lesions as a NO-system disturbance in rats: L-NAME, L-arginine, stable gastric pentadecapeptide BPC 157.

We revealed a new point with cyclophosphamide (150 mg/kg/day intraperitoneally for 7 days): we counteracted both rat stomach and duodenal ulcers and increased NO- and MDA-levels in these tissues. As a NO-system effect, BPC 157 therapy (10 µg/kg, 10 ng/kg, intraperitoneally once a day or in drinking water, till the sacrifice) attenuated the increased NO- and MDA-levels and nullified, in rats, severe cyclophosphamide-ulcers and even stronger stomach and duodenal lesions after cyclophosphamide + L-NAME (5 mg/kg intraperitoneally once a day). L-arginine (100 mg/kg intraperitoneally once a day not effective alone) led L-NAME-values only to the control values (cyclophosphamide + L-NAME + L-arginine-rats). Briefly, rats were sacrificed at 24 h after last administration on days 1, 2, 3, or 7, and assessment included sum of longest lesions diameters (mm) in the stomach and duodenum, oxidative stress by quantifying thiobarbituric acid reactivity as malondialdehyde equivalents (MDA), NO in stomach and duodenal tissue samples using the Griess reaction. All these parameters were highly exaggerated in rats who underwent cyclophosphamide treatment. We identified high MDA-tissue values, high NO-tissue values, ulcerogenic and beneficial potential in cyclophosphamide-L-NAME-L-arginine-BPC 157 relationships. This suggests that in cyclophosphamide damaged rats, NO excessive release generated by the inducible isozyme, damages the vascular wall and other tissue cells, especially in combination with reactive oxygen intermediates, while failing endothelial production and resulting in further aggravation by L-NAME which was inhibited by L-arginine. Finally, BPC 157, due to its special relations with NO-system, may both lessen increased MDA- and NO-tissues values and counteract effects of both cyclophosphamide and L-NAME on stomach and duodenal lesions.

The impact of primary antibiotic resistance on the efficacy of ranitidine bismuth citrate- vs. omeprazole-based one-week triple therapies in H. pylori eradication--a randomised controlled trial.

AIMS: To compare ranitidine bismuth citrate with omeprazole as to their efficacy to eradicate H. pylori in two different treatment schedules both consisting of a combination of either of above with two antibiotics for 1 week, and to relate these treatment results to primary antibiotic resistance. METHODS: 256 H. pylori positive patients with non-ulcer dyspepsia were randomised to one of the following four treatment groups: omeprazole 20 mg + clarithromycin 500 mg + amoxycillin 1000 mg (OCA); ranitidine bismuth citrate 400 mg + clarithromycin 500 mg + amoxycillin 1000 mg (RBCCA); omeprazole 20 mg + clarithromycin 500 mg + metronidazole 500 mg (OCM); ranitidine bismuth citrate 400 mg + clarithromycin 500 mg + metronidazole 500 mg (RBCCM). All drugs were given twice daily for one week. The patients were assessed for prevalence of H. pylori by CLO test, histology and culture on gastric biopsy samples obtained during upper gastrointestinal endoscopy before randomisation and 4-6 weeks after completion of therapy. Bacterial sensitivity to clarithromycin, metronidazole and amoxycillin was determined by E-test. RESULTS: On per-protocol analysis, overall eradication rates were 96% for RBCCA vs. 85% for OCA (p = 0.03), and 95% for RBCCM vs. 79% for OCM (p = 0.01). Amongst the 196 patients (77% of the entire study group) in whom antibiotic sensitivity testing was technically feasible, primary resistance was found in 8% for clarithromycin, in 33% for metronidazole, and in 0% for amoxycillin. Eradication of clarithromycin sensitive/resistant strains was 89%/40% for OCA (p = 0.0042) and 98%/80% for RBCCA (p = 0.0428). When strains were sensitive to both antibiotics, cure rates with OCM/RBCCM were 87%/96% respectively (p = 0.39), for strains resistant to clarithromycin only, eradication was achieved in 82% with OCM vs. 94% with RBCCM (p = 0.2), and in the case of metronidazole resistance in 85% with OCM vs. 94% with RBCCM (p = 0.09). CONCLUSIONS: Ranitidine bismuth citrate in combination with clarithromycin and either metronidazole or amoxycillin produced higher eradication rates than omeprazole co-administered with the same antibiotics. This appeared especially prominent in the subgroups with clarithromycin resistance without, however, reaching statistical significance. Efficacy of neither eradication regimen was influenced by metronidazole sensitivity to a significant degree.