摘要:

AbstractThere are several interesting approaches to augmenting defence or repair mechanisms that can be used already or may find a place in therapy for ulcer disease. Factors such as epidermal growth factor and basic fibroblast growth factor show potential. Alternative strategies might be to stimulate mucosal blood flow with agents that release nitric oxide (NO), or to scavenge free radicals in the inflamed or ischaemic mucosa.If such approaches are to find a role in therapy, it is likely that it will be restricted: perhaps for the treatment of refractory ulcers, or for prophylaxis of stress ulceration. This is because most ulcers in future are likely to be healed with tolerable and high efficacy acid‐inhibiting drugs then have their recurrence prevented by regimens that eradicateHelicobacter pylori.The most important current indication for concentrating on enhancing mucosal defences is for managing non‐steroidal anti‐inflammatory drug (NSAID)‐induced ulcers. There is no clear advantage in using a defence‐enhancing agent (rather than an acid suppressant) to heal an NSAID ulcer if the NSAID can be stopped. The main value of prostaglandins is for prophylaxis of NSAID ulcers in those patients who need ongoing treatment with NSAID. For cost‐benefit reasons, prostaglandins should probably be used mainly for those at high risk of NSAID complications, and there has been progress in identifying these. Another interesting approach is aimed at clarifying mechanisms of gastric adaptation to NSAID, so that we might be able to design drugs and dosing regimens to maximize this

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01312.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractTherapy of acid/peptic disease has evolved since the 1970s with development of: (i) more accurate endoscopes which permit precise examination and documentation of upper gastrointestinal lesions; and (ii) the histamine H2‐receptor antagonists. As well, refined standards for clinical investigation have contributed to the clinical study of acid/peptic diseases. Initially, ulcer diseases were considered to be principally secondary to increased ‘aggressive’ factors (acid, pepsin) and the therapeutic focus was directed at antacids, the progressive evolution of additional histamine H2‐receptor antagonists and recently the H+/K+‐ATPase inhibitors. Later studies indicated efficacy of sucralfate, low dose antacids and prostaglandin analogues, drugs with either no or only modest antisecretory effect. This led to studies on the role of gastroduodenal mucosal defensive factors (mucus and bicarbonate secretion, blood flow, leucocyte adherence, cytokines, reactive oxygen radicals). The prominent role played by aspirin and other non‐steroidal anti‐inflammatory drugs (NSAID) in initiating and causing recurrence of peptic ulcer disease has been increasingly realized. Recognition of those most at risk for NSAID‐induced complication has led to newer approaches to treatment and prevention. Since 1983,Helicobacter pylorihas been incriminated as a major factor in the pathogenesis of ulcer disease, particularly ulcer recurrences. Treatment of such ulcers now includes antibiotics and bismuth compounds in order to eradicateH. pylori.This therapeutic regimen is in a state of flux (‘triple therapy’vsa H+/K+‐ATPase inhibitor plus antibiotic) as is the question of how to work up and treat patients initially presentin

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01313.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY