***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND The diagnosis of non-steroidal anti-inflammatory drug ( NSAID ) induced enteropathy is difficult , requiring enteroscopy or the use of four day faecal excretion of 111In labelled white cells . AIMS To assess faecal calprotectin ( a non-de grade d neutrophil cytosolic protein ) as a method for diagnosing NSAID enteropathy . METHODS Single stool  faecal calprotectin concentrations were compared with the four day faecal excretion of 111In labelled white cells in 47 patients taking NSAIDs .  The prevalence and severity of NSAID enteropathy was assessed using this method in 312 patients ( 192 with rheumatoid arthritis , 65 with osteoarthritis , 55 with other conditions ) taking 18 different NSAIDs .  RESULTS The four day faecal excretion of 111In white cells correlated significantly with faecal calprotectin concentrations . In the group of 312 patients on NSAIDs faecal calprotectin concentrations were significantly higher than in controls , the prevalence of NSAID enteropathy being 44 % . The prevalence and severity of NSAID enteropathy was independent of the particular type or dose of NSAID being taken or other patient variables . CONCLUSIONS Assay of faecal calprotectin  provides a simple practical method for diagnosing NSAID enteropathy in man . Forty four per cent of patients receiving these drugs had NSAID induced enteropathy when assessed by this technique ; 20 % of these had comparable levels of inflammation to that previously reported in patients with inflammatory bowel disease BACKGROUND Non-adherence to immunosuppressants is a major cause of renal transplant failure . Interventions to improve adherence need to target modifiable risk factors . METHODS Adherence was measured using the ' gold st and ard ' measure of electronic monitoring in 58 adult renal transplant recipients from a UK transplant unit . Subjects were identified from a stratified r and om sample of 153 recipients recruited to a larger cross-sectional study comparing different measures of adherence . Inclusion criteria included age over 18 years and a functioning renal transplant , transplanted 6 - 63 months previously . Exclusion criteria included residence outside the region served by the unit and inability to give informed consent .  Health beliefs , depression and functional status were measured using st and ardized question naires ( Beliefs about Medicines Question naire , Illness Perception Question naire , Revised Clinical Interview Schedule and SF-36 ) and semi-structured interview . Transplant and demographic details were collected from the notes . RESULTS Seven [ 12 % , 95 % confidence interval ( CI ) 4 - 20 % ] subjects missed at least 20 % of days medication and 15 ( 26 % , 15 - 37 % ) missed at least 10 % of days . Lower belief in the need for medication and having a transplant from a live donor were the major factors associated with non-adherence . Depression was common , although not strongly associated with non-adherence . CONCLUSIONS Beliefs about medication are a promising target for interventions design ed to improve adherence . The lower adherence in recipients of transplants from live donors needs confirming but may be clinical ly important in light of the drive to increase live donation BACKGROUND & AIMS Conventional acidic nonsteroidal anti-inflammatory drugs frequently cause small bowel inflammation . Diagnosis is largely based on assay of surrogate markers of inflammation in stool , such as fecal calprotectin . However , stool markers are not widely available and the precise nature of this inflammation is uncertain . We used wireless capsule enteroscopy to quantitate and assess the nature of the small bowel damage caused by nonsteroidal anti-inflammatory drugs when taken on a short-term basis . METHODS Forty healthy volunteers underwent a baseline capsule enteroscopy and fecal calprotectin test .  After taking diclofenac slow-release 75 mg twice a day ( with omeprazole 20 mg twice a day for gastroprotection ) for a total of 14 days , both investigations were repeated . RESULTS After drug treatment , 30 subjects ( 75 % ) had increased repeat fecal calprotectin concentrations above the upper limit of normal . Capsule enteroscopy showed new pathology in 27 subjects ( 68 % ) . The commonest lesions were mucosal breaks , seen in 16 ( 40 % ) , which were seen to be bleeding in 2 ( 5 % ) ; reddened folds in 14 ( 35 % ) ; petechiae or red spots in 13 ( 33 % ) ; denuded mucosa in 8 ( 20 % ) ; and blood in the lumen without a visualized source in 3 ( 8 % ) . Fifteen of the 27 subjects had more than one lesion concurrently . CONCLUSIONS This study provides both biochemical and direct evidence of macroscopic injury to the small intestine in 68%-75 % of volunteers result ing from 2 weeks ' ingestion of slow-release diclofenac CONTEXT Conventional nonsteroidal anti-inflammatory drugs ( NSAIDs ) are associated with a spectrum of toxic effects , notably gastrointestinal ( GI ) effects , because of inhibition of cyclooxygenase (COX)-1 . Whether COX-2-specific inhibitors are associated with fewer clinical GI toxic effects is unknown . OBJECTIVE To determine whether celecoxib , a COX-2-specific inhibitor , is associated with a lower incidence of significant upper GI toxic effects and other adverse effects compared with conventional NSAIDs . DESIGN The Celecoxib Long-term Arthritis Safety Study ( CLASS ) , a double-blind , r and omized controlled trial conducted from September 1998 to March 2000 . SETTING Three hundred eighty-six clinical sites in the United States and Canada . PARTICIPANTS A total of 8059 patients ( > /=18 years old ) with osteoarthritis ( OA ) or rheumatoid arthritis ( RA ) were enrolled in the study , and 7968 received at least 1 dose of study drug . A total of 4573 patients ( 57 % ) received treatment for 6 months . INTERVENTIONS Patients were r and omly assigned to receive celecoxib , 400 mg twice per day ( 2 and 4 times the maximum RA and OA dosages , respectively ; n = 3987 ) ; ibuprofen , 800 mg 3 times per day ( n = 1985 ) ; or diclofenac , 75 mg twice per day ( n = 1996 ) . Aspirin use for cardiovascular prophylaxis ( < /=325 mg/d ) was permitted . MAIN OUTCOME MEASURES Incidence of prospect ively defined symptomatic upper GI ulcers and ulcer complications ( bleeding , perforation , and obstruction ) and other adverse effects during the 6-month treatment period . RESULTS For all patients , the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib vs NSAIDs were 0.76 % vs 1.45 % ( P = .09 ) and 2 . 08 % vs 3.54 % ( P = .02 ) , respectively . For patients not taking aspirin  , the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib vs NSAIDs were 0.44 % vs 1.27 % ( P = .04 ) and 1.40 % vs 2.91 % ( P = .02 ) . For patients taking aspirin  , the annualized incidence rates of upper GI ulcer complications alone and combined with symptomatic ulcers for celecoxib vs NSAIDs were 2.01 % vs 2.12 % ( P = .92 ) and 4.70 % vs 6.00 % ( P = .49 ) . Fewer celecoxib-treated patients than NSAID-treated patients experienced chronic GI blood loss , GI intolerance , hepatotoxicity , or renal toxicity . No difference was noted in the incidence of cardiovascular events between celecoxib and NSAIDs , irrespective of aspirin use . CONCLUSIONS In this study , celecoxib , at dosages greater than those indicated clinical ly , was associated with a lower incidence of symptomatic ulcers and ulcer complications combined , as well as other clinical ly important toxic effects , compared with NSAIDs at st and ard dosages . The decrease in upper GI toxicity was strongest among patients not taking aspirin concomitantly . JAMA . 2000;284:1247 - Renal prostagl and in inhibition by nonsteroidal antiinflammatory drugs ( NSAIDs ) may decrease renal function , especially under conditions of low effective circulating volume . To evaluate the risk of important deterioration of renal function due to this effect , the authors performed a nested case-control study using Tennessee Medicaid enrollees aged > or = 65 years in 1987 - 1991 . Cases were patients who had been hospitalized with community-acquired acute renal failure ; they were selected on the basis of medical record review of Medicaid enrollees with selected discharge diagnoses . Information on the timing , duration , and dose of prescription NSAIDs used , demographic factors , and comorbidity was gathered from computerized Medicaid-Medicare data files . Of the 1,799 patients with acute renal failure ( 4.51 hospitalizations per 1,000 person-years ) , 18.1 % were current users of prescription NSAIDs  as compared with 11.3 % of 9,899 r and omly selected population controls . After control for demographic factors and comorbidity , use of NSAIDs increased the risk of acute renal failure 58 % ( adjusted odds ratio = 1.58 ; 95 % confidence interval ( CI ) : 1.34 , 1.86 ) . For ibuprofen , which accounted for 35 % of NSAID use , odds ratios associated with dosages of < or = 1,200 mg/day , > 1,200-<2,400 mg/day , and > or = 2,400 mg/day were 0.94 ( 95 % CI : 0.58 , 1.51 ) , 1.89 ( 95 % CI : 1.34 , 2.67 ) , and 2.32 ( 95 % CI : 1.45 , 3.71 ) , respectively ( test for linear trend : p = 0.009 ) . Prescription NSAID use result ed in an estimated 25 excess hospitalizations associated with renal failure per 10,000 years of use . Thus , NSAIDs represent a relatively uncommon but avoidable cause of acute renal failure in frail elderly persons BACKGROUND Cyclo-oxygenase 2 (COX2)-selective inhibitors should reduce ulcer complications compared with non-selective non-steroidal anti-inflammatory drugs , but evidence is limited , and the possibility that these inhibitors increase cardiovascular events has been raised . The Therapeutic Arthritis Research and Gastrointestinal Event Trial ( TARGET ) aim ed to assess gastrointestinal and cardiovascular safety of the COX2 inhibitor lumiracoxib compared with two non-steroidal anti-inflammatory drugs , naproxen and ibuprofen . METHODS 18325 patients age 50 years or older with osteoarthritis were r and omised to lumiracoxib 400 mg once daily ( n=9156 ) , naproxen 500 mg twice daily ( 4754 ) , or ibuprofen 800 mg three times daily ( 4415 ) for 52 weeks , in two sub studies of identical design ( lumiracoxib vs ibuprofen or naproxen ) . R and omisation was stratified for low-dose aspirin use and age . The primary endpoint was the difference in time-to-event distribution of upper gastrointestinal ulcer complications ( bleeding , perforation , or obstruction ) ; analysis was by modified intention to treat . The principle measure of adverse cardiovascular events was the Antiplatelet Trialists ' Collaboration endpoint ( myocardial infa rct ion , stroke , or cardiovascular death ) ; this analysis was intention to treat . FINDINGS 81 ( 0.44 % ) patients did not start treatment and 7120 ( 39 % ) did not complete the study . In patients not taking aspirin , the cumulative 1-year incidence of ulcer complications was 1.09 % ( 95 % CI 0.82 - 1.36 ) with non-steroidal anti-inflammatory drugs ( 64 events ) versus 0.25 % ( 95 % CI 0.12 - 0.39 ) with lumiracoxib ( 14 events ; hazard ratio 0.21 [ 95 % CI 0.12 - 0.37 ] , p<0.0001 ) . Reductions in ulcer complications were also significant in the overall population ( 0.34 [ 0.22 - 0.52 ] , p<0.0001 ) but not in those taking aspirin ( 0.79 [ 0.40 - 1.55 ] , p=0.4876 ) . In the overall population , 0.55 % ( 5 
    Output:
    
Evidence on the efficacy of NSAID plus gastroprotection  with acid suppressants ( proton pump inhibitors , PPIs , and histamine antagonists , H2As ) was based mainly on the surrogate measure of endoscopic ulcers .
The limited information on damage to the bowel suggested that NSAID plus PPI was more damaging than coxibs .
When gastroprotection was prescribed , it was often described as inadequate .
Conclusion Evidence for efficacy of gastroprotection strategies with NSAIDs is limited .
In clinical practice few patients who need gastroprotection get it , and those who get it may not take it .
For coxibs , gastroprotection is inherent , although probably not complete