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  1. Ian Forgacs
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A paper in this journal two years ago caused quite a stir in the media as it highlighted the alarming increase in mortality from cholangiocarcinoma in the UK. The associated rise in incidence is not explained by enhanced diagnosis—it's real. The group from St Mary's that made the earlier observation now speculate that an environmental carcinogen is to blame. They studied DNA adduct formation as a marker of DNA damage and as a primary event in chemical carcinogenesis. In cholangiocarcinomas, they found that there were more DNA adducts than in controls. Maybe this will initiate the search for the causative agent(s). Gut wishes them well in the hunt but don't bet against the epidemiologists getting there first. See 586


Examples of countries where intrahepatic cholangiocarcinoma is rising (see 586).


If you take the “it's not in your mind, it's in your guts” approach to explaining irritable bowel syndrome to newly-diagnosed patients, it can be quite tricky to explain why you then wish to prescibe an antidepressant drug. Nevertheless it is an evidence based treatment option as this month's Therapy Update reminds us. The author writes of the therapeutic armamentarium but there are often not that many items left in the arsenal for the patient with IBS by the time they have reached secondary care. Clouse reminds us that 85% of the patients in his published series have at least a moderate response to low dose tricyclic antidepressants. That's impressive but even sceptics may find some helpful information which they could usefully offer to their (maybe) equally sceptical patients. See 598


The bones of patients with coeliac disease are subject to a double whammy. The risk of osteomalacia has been appreciated for decades. Only in recent years has the high prevalence of osteoporosis been fully recognised. This sounds like bad news for patients and guidelines for screening and drug treatment have emerged from authoritative sources. Yet the clinical importance of metabolic bone disease has not been clarified. Two large databases from Nottingham and Derby have been interrogated in the search for patients with coeliac disease having reported a fracture. By comparison with controls, coeliac patients showed no overall increase in fracture risk. The authors of this paper and of the accompanying commentary raise interesting questions about the appropriateness of regular bone density assessment for all patients. See 518


As with other factors that are independently noxious to the stomach, the interaction between aspirin and H pylori on the gastric mucosa (both in vivo and in vitro) might reasonably be said to be unclear. Results of clinical studies give conflicting results on the frequency of mucosal lesions in patients taking aspirin with or without H pylori infection. Wong and colleagues wished to study the interaction by looking at the effect of aspirin on the growth of H pylori and its susceptibility to antibiotics. They conclude that aspirin inhibited the growth of H pylori and increases its susceptibility to antimicrobial agents. These experiments were done in vitro but do offer a potential mechanism of improving clearance rates by modifying the efficacy of antibiotics. See 490


Two titans of therapeutics offer their current thinking on NSAID toxicity and its prevention in this era of COX-2 inhibitors and PPIs. What becomes totally clear is that there is no “one size fits all” answer to how NSAIDs may be most safely used in the various at risk groups. Hawkey and Langman write authoritatively if, in places, didactically. This is a stimulating article. Readers will find it a refreshing contrast to the mind-numbingly dull ex cathedra guidelines neutered by endless consensual drafting and re-drafting. See 600


The natural history of HCV infection continues to intrigue. At diagnosis, it is not possible to stratify patients into those who will have a slow, moderate or rapid transition to fibrosis. Wright and colleagues studied factors which were likely to influence disease progression. As in earlier studies, fibrosis was more rapid in men and in those who acquire infection later in life. However, demographic factors account for only 30% of the variability in the rate of development of fibrosis. Evaluation of liver fibrosis by separate scoring systems in two serial biopsies was unable to assess the linearity of progression of fibrosis. There are still very important but as yet unidentified factors in play. What odds are offered against at least one key factor being genetic? See 574

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