Curing Helicobacter pylori infection in patients with duodenal ulcer does not provoke gastroesophageal reflux disease.

BACKGROUND: It has been suggested that the incidence of gastroesophageal reflux disease (GERD) increases after successful eradication of Helicobacter pylori infection. We present data on development of GERD from a controlled study of H. pylori eradication in 165 duodenal ulcer patients. METHODS: Patients (mean age, 55 years; 102 men; current smokers; n = 74) were randomly assigned 2: 1 to receive omeprazole, 40 mg twice daily, in combination with either amoxicillin, 750 mg twice daily, or placebo. Endoscopy and dyspeptic symptoms, including heartburn, were assessed at inclusion and at 6, 12, and 24 months after treatment. In addition, symptoms were assessed at 18 months. Patients with erosive esophagitis or reflux symptoms requiring treatment at inclusion were not included in the study. RESULTS: Fifty-one of 145 (35%) evaluable patients developed heartburn, and 13 of 145 (9%) developed esophagitis during follow-up. The life-table analysis of the cumulated risk of developing heartburn showed that patients whose H. pylori infection was eradicated had a significantly lower risk for developing heartburn than those with persistent H. pylori infection. The groups did not show any difference in cumulative risk of developing esophagitis. CONCLUSION: Our data show that successful eradication of H. pylori infection does not increase the incidence of GERD in duodenal ulcer patients.

Pravastatin and gemfibrozil alone and in combination for the treatment of hypercholesterolemia.

PURPOSE: To compare the efficacy and safety of pravastatin, gemfibrozil, combined therapy, and placebo in the treatment of hypercholesterolemia. PATIENTS AND METHODS: At 5 centers in Sweden and 2 in Finland, 290 ambulatory patients were randomized to active treatment or placebo for 12 weeks following a single-blind placebo lead-in period. The study was double-blind and placebo-controlled. Patients has plasma total cholesterol levels of at least 6.0 mmol/L or in the 90th percentile by age and sex and triglycerides less than 4.0 mmol/L. Concentrations of lipids, lipoproteins, and apolipoproteins were measured, and clinical laboratory tests included liver function and creatine kinase determinations. RESULTS: Pravastatin reduced total cholesterol (26.3% versus 15.2%, p < or = 0.01), low-density lipoprotein cholesterol (LDL-C) (33.5% versus 16.8%, p < or = 0.01), and apolipoprotein B (28.8% versus 15.3%, p < or = 0.01) more than gemfibrozil. Gemfibrozil reduced very-low-density lipoprotein cholesterol (VLDL-C) (49.1% versus 21.9%, p < or = 0.01) and triglycerides (42.2% versus 14.2%, p < or = 0.01) and increased high-density lipoprotein cholesterol (HDL-C) (15.2% versus 5.9%, p < or = 0.01) more than pravastatin. Pravastatin and gemfibrozil increased apolipoprotein A-I comparably (3.3% versus 5.0%, p = NS). The combination significantly (p < or = 0.01) reduced total cholesterol (29.0%), LDL-C (37.1%), VLDL-C (49.4%), and apolipoprotein B (31.6%), and increased HDL-C (16.8%). The combination reduced the total cholesterol/HDL-C (39.3%) and LDL-C/HDL-C (45.8%) ratios significantly (p < 0.01). Adverse events and clinical laboratory abnormalities were generally mild and transient in all groups, although creatine kinase tended to be higher with combination therapy. Study drugs were withdrawn from two patients with asymptomatic creatine kinase elevations. Severe myopathy was not observed; however, the presence of subclinical musculoskeletal effects cannot be excluded. CONCLUSIONS: Co-administration of pravastatin and gemfibrozil combined the specific effects of the two drugs on lipoprotein concentrations and ratios. The incidence of side effects was low; severe myopathy did not occur. The combination may be useful in selected cases of combined hyperlipidemia; however, since myopathy at a low incidence or after long-term therapy cannot be excluded, the routine use of combination therapy is not advisable.

Gemfibrozil in familial combined hyperlipidaemia: effect of added low-dose cholestyramine on plasma and biliary lipids.

Gemfibrozil is frequently used for lipid-lowering in familial combined hyperlipidaemia (FCHL) and in other forms of combined hyperlipidaemia. This therapy increases biliary cholesterol saturation, enhancing the risk for gallstone formation. Furthermore, in hypertriglyceridaemia, LDL cholesterol levels often tend to rise. We have explored the possibility that addition of a low dose of cholestyramine to gemfibrozil therapy obliterates these phenomena. Eighteen gallstone-free patients with definite (n = 5) or probable (n = 10) FCHL, or combined hyperlipoproteinaemia (n = 3) were randomized to a 6 week treatment with gemfibrozil, 600 mg b.i.d., or gemfibrozil 600 mg b.i.d. plus 4 g cholestyramine o.d. After 6 weeks the patients were crossed over to the alternative treatment. Plasma lipoproteins and biliary lipids were determined at baseline and at the end of each period. Institution of gemfibrozil treatment resulted in a decrease in plasma cholesterol by 15% (P less than 0.05) and in plasma triglycerides by 47% (P less than 0.05); HDL cholesterol increased by 18% (P less than 0.05). Addition of cholestyramine further decreased plasma and LDL total cholesterol by 9% (P less than 0.05). Total triglycerides and HDL cholesterol did not change. Gemfibrozil treatment was associated with a rise in the relative biliary concentration of cholesterol from 5.6 +/- 0.4 to 6.9 +/- 0.5 molar percent (P less than 0.01), and a parallel decrease in the relative concentration of bile acids, resulting in an increased cholesterol saturation of the bile, from 77 +/- 5 to 90 +/- 6% (P less than 0.05). This change was not observed during the combined therapy (mean cholesterol saturation, 82 +/- 4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Decay and recovery of the acoustic stapedius reflex in humans.

The time course of decay and recovery of ipsilateral and contralateral stapedius reflex responses to 2 000 Hz pure tone stimulation was studied in 10 normal-hearing subjects. Reflex responses were found to follow a closely similar time course with respect to both decay and recovery in simultaneous bilateral recordings. The similarity is compatible with the assumption that decay and recovery originate in the afferent auditory system, and not in the muscles. Recovery was 50% complete 250 ms after the end of the stimulus and most subjects had reached their initial amplitude after 1-3 s. The individual correlation between decay and recovery was negative but weak, which is interpreted as showing that these processes have a tendency to balance each other, but are based partly on different mechanisms. The implications of the present results for diagnosis of disorders of the lower auditory system as well as for the evaluation of the protective role of the stapedius reflex against noise damage are pointed out.