Lansoprazole quadruple therapy is effective in curing Helicobacter pylori infection.

BACKGROUND: Quadruple therapy using omeprazole combined with classic bismuth triple therapy has been advocated as optimal therapy for the cure of Helicobacter pylori (H. pylori) infection. We investigated the efficacy of substituting lansoprazole for omeprazole in proton pump quadruple therapy. MATERIALS AND METHODS: In a prospective open study, 219 consecutive patients, with either peptic ulcer disease or biopsy-proven H. pylori-associated gastritis, received seven days of lansoprazole, bismuth, tetracycline and metronidazole after three days of lansoprazole pretreatment. Cure of infection was judged by 14C urea breath test at six weeks after completion of therapy. RESULTS: On an intention to treat basis, 198 of the 219 patients (90%) were confirmed to be cured of H. pylori infection. Compliance was excellent and minimal side effects reported. CONCLUSION: Lansoprazole-based quadruple therapy achieves a very high cure rate in an unselected population of either peptic ulcer patients or those with H. pylori-associated gastritis. Recommended regimens should achieve at least 90% cure of infection. Lansoprazole quadruple therapy is effective and compares favorably with other H. pylori treatment regimens.

Sucralfate as an alternative to bismuth in quadruple therapy for Helicobacter pylori eradication.

BACKGROUND: There are persuasive arguments for treating all patients with Helicobacter pylori-associated peptic ulcer disease. However, the choice of therapeutic regimen remains problematical. Bismuth triple therapy produces greater than 80% cure of H. pylori infection, whereas omeprazole and bismuth quadruple therapy has produced cure rates in excess of 90%. Colloidal bismuth is not available in many countries, hence limiting the use of bismuth-based therapeutic regimens. We substituted widely available sucralfate for bismuth in a quadruple-therapy regimen. METHOD: We studied 223 consecutive patients with gastritis or peptic ulcer disease in whom H. pyori infection was confirmed by CLOtest (Delta West Ltd., Bentley, WA, Australia) or histological assessment. Successful therapy was validated by the 14C urea breath test 4 to 6 weeks after therapy. Omeprazole, 20 mg was given twice daily for 10 days. After 3 days of omeprazole sucralfate (1 gm qid), tetracycline (500 mg qid) and metronidazole (400 mg tid) were added for 7 days. RESULTS: Therapy was successful in 194 of 223 patients (87%). Compliance was excellent, with only two patients being unable to tolerate therapy. Side effects were minimal and included nausea, vomiting, headache, and vaginal moniliasis. At 6 months' follow-up, 10 of 210 patients (5%) who were previously documented as "cured" had a positive breath test. CONCLUSIONS: The wide availability of sucralfate in many countries makes it a possible alternative to bismuth for use in proton pump quadruple-therapy regimens, achieving a reasonable cure rate for H. pylori infection.

Plasma arachidonic acid-rich phospholipids in Crohn's disease: response to treatment.

1. Increased concentrations of plasma polyunsaturated fatty acids have been implicated in the pathogenesis of Crohn's disease. However, it is not known whether there are corresponding changes in circulating phospholipids--the major source of fatty acids in the plasma. 2. Fasting plasma samples were obtained from 17 control subjects and 13 patients with active Crohn's disease [Simple Index of Crohn's Disease Activity (SICDA) > 6] before, and 2 and 8 weeks after, treatment with either a peptide diet or oral prednisolone. 3. Before treatment, the Crohn's disease patients had mildly active disease (SICDA 9.9 +/- 0.8, erythrocyte sedimentation rate 26.4 +/- 6.5 mm/h, serum C-reactive protein 2.8 +/- 0.4 mg/l). The proportions of the polyunsaturated phosphatidylcholine species, 16:0-20:4 (10.0 +/- 0.7%) and 16:0-22:6 (7.1 +/- 0.8%), were both significantly higher than those in healthy controls (7.6 +/- 0.5%, P < 0.01 and 5.3 +/- 0.5%, P < 0.05 respectively). 4. After 2 weeks treatment, the SICDA in the Crohn's disease patients decreased to 3.2 +/- 0.6 (P < 0.0001 compared with the pretreatment value), and there were corresponding falls in the erythrocyte sedimentation rate (to 12.6 +/- 2.7 mm/h, P < 0.05) and C-reactive protein concentration (to 1.7 +/- 0.3 mg/l, P < 0.05)--these improvements being maintained at 8 weeks. There was also a fall to normal values in 16:0-20:4 (to 7.7 +/- 0.6%, P < 0.01 compared with the pretreatment value) and in 16:0-22:6 (to 5.7 +/- 0.5%, P not significant), by week 8. 5. The proportions of polyunsaturated phosphatidylcholine molecular species were increased in the plasma of patients with active Crohn's disease, but fell to normal levels during disease remission. These observations are consistent with the theory that, in active Crohn's disease, the mucosal phospholipids containing polyunsaturated fatty acids are increased, contribute to eicosanoid synthesis and 'spill' into the plasma.

Measurement of androgen receptor expression in adult liver, fetal liver, and Hep-G2 cells by the polymerase chain reaction.

Hepatocellular carcinoma is the most commonly fatal malignant tumour worldwide. The role of androgen receptors, which have been found in hepatocellular carcinoma, is controversial. Sequence specific polymerase chain reaction (PCR) was used to quantify, for the first time, the expression of androgen receptor in four adult liver biopsy specimens (HL-A to HL-D), fetal liver, and Hep-G2 cells. The measurement of androgen receptor is expressed as a ratio (androgen receptor: beta-actin) of the value of androgen receptor to the value of a control gene, beta-actin. The value of the androgen receptor: beta-actin ratios for HL-A, HL-B, HL-C, HL-D, fetal liver, and Hep-G2 were 0.37, 0.86, 0.37, 0.44, 0.87, and 0.66 respectively. To verify sequence specific amplification of the androgen receptor, the PCR androgen receptor fragment was sequenced. The resultant sequence data for both strands of the double stranded PCR androgen receptor fragment had 100% similarity with the published androgen receptor mRNA sequence (complete codons).