The clinical use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with significant adverse effects on the integrity of the gastrointestinal (GI) mucosa. A unique, double-blind, placebo-controlled, randomized, multicentre study investigated the prophylactic co-therapy with misoprostol, a novel PGE1 analog, for the prevention of the NSAID-induced gastric and duodenal mucosal lesions. The study also investigated whether the co-therapy with misoprostol could interfere with the anti-rheumatic action of the NSAIDs using detailed rheumatological assessments. Patients with osteoarthritis or rheumatoid arthritis had to be free of symptoms and significant erosive and/or haemorrhagic lesions of the upper GI tract. The patients were randomized to co-therapy with misoprostol or its matching placebo. Follow-up endoscopy and symptoms assessment were carried out within 4 weeks and compared to pre-study findings. Misoprostol significantly reduced (p less than 0.01) the incidence of erosive and/or haemorrhagic gastric and duodenal mucosal lesions. Misoprostol also reduced the proportion of patients with epigastric pain (p less than 0.01). Misoprostol was well tolerated and did not interfere with the anti-rheumatic activity of the administered NSAID. We conclude that misoprostol is safe and effective in the protection against NSAID-induced gastric and duodenal mucosal lesions and symptoms.

Anti-Inflammatory Agents, Non-Steroidal↗

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Common bile duct and sex, age and body mass index in normal humans: an ultrasonographic study.

A probable relationship between Common Bile Duct (CBD) size and sex, age and Body Mass Index (BMI) was investigated in healthy volunteers. Real-time ultrasonography was employed to visualize gallbladder and CBD. No change of CBD size related to sex and BMI was found. A significant increase of CBD related to age was recorded.

Adult↗

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Non-ulcer dyspepsia.

Non-ulcer dyspepsia (NUD) includes functional forms, related to secretory and/or motor disorders, but also refers to forms with gastritis and/or duodenitis (erosive or not, Helicobacter pylori positive or not), as well as to idiopathic forms. NUD pathophysiology is multifactorial. Secretory abnormalities, H. pylori infection and in particular digestive and interdigestive disorders of gastrointestinal motility are often detected in NUD patients, but psychological, social and environmental factors can be also involved in NUD pathogenesis. With regard to symptom genesis, there is still no convincing evidence as to whether and to what extent pathogenetic factors have a causal relationship with dyspeptic symptoms. Upper gastro-intestinal endoscopy with biopsies and abdominal ultrasonography must be performed in patients over 45 years complaining of sudden symptoms, in patients under 45 years suffering from symptoms suggestive of severe organic disease and in patients with unexplained worsening of chronic symptoms. Ex adjuvantibus therapy may be employed in the remainder of dyspeptics. Oligosymptomatic dyspepsia needs no pharmacological treatment and in most cases it is enough to advise modifications of dietary habits and life style. Many drugs are usually employed in the pharmacological treatment of severe NUD but only H2-antagonists, pirenzepine and prokinetics are reported to be more effective than placebo. Efficacy of therapy should be checked after 4 weeks of treatment. If no improvement occurs, combined or different therapy might be employed. Treatment should be checked again after 8 weeks: therapeutic failure at this time indicates the need for endoscopic examination.

Dyspepsia↗

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