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Non-Steroidal Anti-Inflammatory Drugs and Gastrointestinal Damage

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Non-Steroidal Anti-Inflammatory Drugs and Gastrointestinal Damage 82 Postgrad Med J 2001;77:82–88 Postgrad Med J: first published as 10.1136/pmj.77.904.82 on 1 February 2001. Downloaded from Non-steroidal anti-inflammatory drugs and gastrointestinal damage—problems and solutions R I Russell Non-steroidal anti-inflammatory drugs (NSAIDs) have been used for many years for Box 1: Areas of the gastrointestinal analgesic, anti-inflammatory, and more re- tract that may be damaged by NSAIDs cently in the case of aspirin, antithrombotic x Oesophagus: oesophagitis, ulceration, purposes. The use of NSAIDs continues to stricture increase; over 22 million prescriptions are writ- x Stomach: ulcers, erosions ten every year in the UK, and over 70 million in x Duodenum: ulcers, erosions the US. These figures underestimate their full x Small intestine: ulcers, erosions, protein use as aspirin and other NSAIDs are widely loss, strictures available as “over-the-counter” preparations. x Colon: non-specific colitis, exacerbation The use of these drugs can also be expected of ulcerative colitis and Crohn’s disease to increase in the years to come, partly because of the increasing age of the population and intestinal bleed is between 1/100 and 1/500 partly because of possible new and developing patient years; the risk of a gastrointestinal indications, particularly in vascular disease and related death is between 1/1000 and 1/5000 cancer prevention. It is therefore of importance patient years. to assess the safety and side eVects of NSAIDs, The risk of serious ulcer complications in and to consider how their safety may be patients on NSAIDs has been calculated in improved. It has long been known that various studies, the relative risk (RR) for a seri- NSAIDs may have a range of side eVects, of ous gastrointestinal event overall being re- which the commonest are gastrointestinal. ported as 2.74 in a large meta-analysis, upper It is the purpose of this paper to examine the gastrointestinal bleeding RR 3.09, perforation nature, range, and causation of the gastro- RR 5.93, and ulcer related death RR 7.62.3 intestinal side eVects associated with the use of NSAIDs may have adverse eVects in all parts NSAIDs, and to consider how these may be of the gastrointestinal tract, not only the stom- reduced or modified. NSAIDs may also be ach or duodenum; the oesophagus, small intes- associated with other adverse eVects, although tine and colon may also be aVected (box 1). these are much rarer than gastrointestinal A recent necropsy study of 713 patients has problems; these include nephropathies, skin been reported, of whom 244 had NSAIDs pre- rashes, and hepatitis. NSAIDs may also scribed during the six months before death and http://pmj.bmj.com/ interact with other drugs such as antihypergly- 464 had not; death in all patients was unrelated caemic or antihypertensive agents. to NSAID use. Ulcers of the stomach or duodenum were found in 21.7% of patients on Gastrointestinal problems NSAIDs and 12.3% of those not on NSAIDs NSAIDs may be associated with many gastro- (p<0.001), and small intestinal ulceration was intestinal problems, ranging from mild to found in 8.4% of NSAID users and 0.6% of severe dyspeptic symptoms, the development patients not on NSAIDs (p<0.001).4 Damage on September 30, 2021 by guest. Protected copyright. of gastric or duodenal ulceration, haemorrhage to the small intestine in NSAID users has also or perforation, and other events which may been demonstrated at enteroscopy. Patients lead to hospitalisation or death. with small intestinal damage associated with Endoscopic studies have shown a prevalence chronic NSAID use may present with chronic rate of 14%–25% of gastric and duodenal iron deficiency anaemia or hypoalbuminaemia ulcers in NSAID users,1 although the diYculty due to blood or protein loss, and may develop of having accurate control groups makes exact overt bleeding, perforation, or strictures. figures diYcult to obtain. Although endoscopic In the oesophagus, chronic NSAID use may studies tend to show more gastric than duode- be associated, although rarely, with oesoph- nal ulcers associated with NSAID use, patients agitis, ulceration, or stricture formation.5 presenting with gastrointestinal bleeding on In the large bowel, NSAID use may lead to NSAIDs may have a similar frequency of the development of a non-specific colitis (with University of Glasgow gastric and duodenal ulceration. Dyspeptic and Department of abdominal discomfort, bloody diarrhoea, and Gastroenterology, symptoms occur in up to 60% of patients tak- weight loss). NSAIDs may also cause an exac- Royal Infirmary, ing NSAIDs and there is a poor correlation erbation of ulcerative colitis or Crohn’s disease, Glasgow between symptoms and endoscopically proved if the associated arthropathy in inflammatory lesions; up to 50% of endoscopically confirmed bowel disease is treated with NSAIDs.67 Correspondence to: ulcers associated with NSAIDs are asympto- Professor R I Russell, High risk factors for NSAID related gastro- 28 Ralston Road, Bearsden, matic. intestinal damage include older age group Glasgow G61 3BA It has been estimated that the individual risk (especially over 70), previous history of peptic [email protected] of hospitalisation with gastrointestinal compli- ulceration, and probably the first three months Submitted 26 October 1999 cations of NSAIDs is between 1/50 and 1/150 of NSAID treatment. Other high risk factors Accepted 22 June 2000 patient years.2 The risk of an upper gastro- are smoking, underlying respiratory or cardio- www.postgradmedj.com Non-steroidal anti-inflammatory drugs and gastrointestinal damage 83 Postgrad Med J: first published as 10.1136/pmj.77.904.82 on 1 February 2001. Downloaded from Box 2: Risk factors for gastrointestinal Box 3: COX-1 and COX-2 damage due to NSAIDs COX-1 x Age: older age group, especially over 70 x Constitutively expressed in most tissues: x Previous ulcer history stomach, duodenum, kidneys, platelets x First three months of treatment x Key role in the production of x Smoking prostaglandins which regulate physi- x Underlying cardiovascular or respira- ological processes: gastrointestinal pro- tory disease tection, blood flow, adaptation, cellular x Concomitant drug use, especially recovery, maintenance of good renal corticosteroids and anticoagulants function, vascular homoeostasis impor- x Use of NSAIDs in high doses, and more tant “housekeeping” role than one NSAID COX-2 x ?Helicobacter pylori x Normally undetectable in most tissues x Can be induced rapidly and in large quantities in the presence of inflamma- vascular disease, and concomitant drug use, tion and other pathological processes particularly corticosteroids, aspirin, and anti- coagulants (box 2).8 Perioperative use is also a risk factor. Individual NSAIDs incurring high- maintenance of good renal function and in est risk include azapropazone, ketoprofen and maintaining normal physiological functions in piroxicam, and those with least risk include many other cells. This is an important “house- ibuprofen, diclofenac, and etodolac. Higher keeping” role. COX-2, on the other hand, is doses are associated with increased risk and normally undetectable in most tissues, but it also the use of more than one NSAID. There is can be induced rapidly, and in large also an increased risk of gastrointestinal quantities—to 200–300-fold—by cytokines, complications with relatively low dose prophy- growth factors, and hormones in the presence lactic aspirin, which is widely used nowadays.9 of inflammation and other pathological proc- There is debate on the possible interaction and esses (box 3). Platelets appear to contain only increased risk of Helicobacter pylori causing COX-1. ulceration with NSAIDs, and this will be Most conventional NSAIDs are non- discussed in a later section. The balance of selective in their COX inhibition, exerting their physiological association and clinical evidence anti-inflammatory eVects through the inhibi- tends to support the possibility of some tion of COX-2, but having adverse eVects interaction occurring, especially in those pa- (such as gastrointestinal mucosal damage and tients at high risk and possibly in those who nephrotoxicity) primarily due to inhibition of have bled. Well planned, prospective controlled COX-1. Some existing and longstanding studies are required to provide more infor- NSAIDs, such as etodolac, a known safer mation on this with respect to diVerent types NSAID with respect to gastrointestinal dam- and doses of NSAIDs, diVerent forms and age and which is known to have reduced http://pmj.bmj.com/ strains of H pylori, and diVerent types of adverse eVects on mucosal prostaglandins, has erosions and ulcers. been subsequently found to have a degree of COX-2 inhibition selectivity. Why do NSAIDs cause gastrointestinal Currently, a range of new and specific damage? COX-2 selective inhibitor NSAIDs have been, NSAIDs interfere with the cyclo-oxygenase and are being further developed with the hope (COX) pathways which lead to the production of reducing possible gastrointestinal side ef- on September 30, 2021 by guest. Protected copyright. of prostanoids (prostaglandins, prostacycline, fects; the preliminary clinical results, as we and thromboxane). This interferes with mu- shall see later, are encouraging. One of these, cosal protection by reducing the eVectiveness rofecoxib, is now available in this country. of the mucus-bicarbonate barrier; gastric acid, and possibly also pepsin, are thus more likely to Solutions cause damage. The fact that most NSAIDs are Treatment and prevention of NSAID related also weak acids
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