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Are there differences in the harms of statins or fixed-dose combination products containing a statin and another lipid lowering drug when used in the general population of children? Summary of findings • Adverse events were variably reported; methods of detection and assessment of adverse events were often not specified buy sucralfate 1000mg visa gastritis diet . Detailed assessment Information on harms of statins and fixed-dose combination products in children was obtained from randomized-controlled trials cheap sucralfate 1000 mg fast delivery the gastritis diet, controlled clinical trials buy sucralfate 1000mg line diet chart for gastritis patient, non-controlled case series, and case reports. Data on adverse events from clinical trials is variably reported; methods for detection and assessment of the adverse events were often not specified. Several studies reported that aspartate aminotransferase and alanine aminotransferase remained below twice or 3 times the upper limit of normal. This was true for 24-48 weeks of 286, 287 291 treatment lovastatin, 28 weeks of simvastatin, and 12 weeks to 2 years of treatment with 288, 289, 297 285 pravastatin. Reports of elevations in transaminases occurred with atorvastatin, 295 simvastatin-ezetimibe combinations, and rosuvastatin (in a trial that included both adults and 293 children with homozygous familial hypercholesterolemia). In studies that reported increased transaminase levels during statin treatment, these levels returned to normal with treatment 285, 291, 295 interruption or discontinuation of the statin. Similarly, multiple studies reported no significant elevations in creatine kinase over the 285-287, 289, 293 study period. Another study reported a single child with creatine kinase elevation (>10 times the upper limit of normal) without muscled symptoms, which occurred with concomitant administration of simvastatin and erythromycin and returned to normal after completion of the antibiotics, and 2 children with increases in creatine kinase (>5- 292 fold the upper limit of normal) that returned to normal in repeat tests. Several studies also cited “no significant” or “no serious” adverse events, or even “no 286, 291, 298 adverse events”. Such statements in these studies lack rigorous definitions of the methods used to monitor for and detect adverse events. Other studies stated that the incidence of 287, reporting any adverse events was equal between the treatment and control (placebo) groups 288, 291 285, 292, 295 or reported the incidence of adverse events to demonstrate that point. Treatment- 286 related adverse effects were reported as 8. Are there differences in the harms of statins or fixed-dose combination products containing a statin and another lipid lowering drug when used in special populations or with other medications (drug-drug interactions)? Summary of findings • One study of fluvastatin in children with minimal change glomerulonephritis demonstrated decrease in total cholesterol and reported no side effects. Detailed assessment One study of children with minimal change glomerulonephritis (MCGN) assigned 36 patients to 299 20 mg of fluvastatin or dipyridamole for 2 years. The main study outcome was bone mineral density, for which there was no change over the course of the study. Hematuria decreased significantly, and creatinine clearance, total protein, and albumin increased compared to baseline in the statin group, but not the dipyridamole group. The authors observed no side effects in any of the patients over the treatment period. SUMMARY Table 15 summarizes the level and direction of evidence for each key question. Summary of the evidence by key question Strength of Key question evidence Conclusion ADULTS 1. How do statins and fixed-dose Fair The ideal study would be a double-blind, intention-to-treat combination products containing a randomized trial in which equipotent doses of different statin and another lipid-lowering statins were compared with regard to low-density drug compare in their ability to lipoprotein-lowering, withdrawals, and adverse effects. No reduce low-density lipoprotein studies met these stringent criteria. Are their doses for each statin or Fair-to-good Results of a large number of trials are generally consistent fixed-dose combination product with information from the manufacturer. When statins are containing a statin and another lipid- provided in doses that are approximately equipotent, a lowering drug that produce similar similar percent reduction in low-density lipoprotein percent reduction in low-density cholesterol can be achieved. Is there a difference in the ability Good for most For patients who require low-density lipoprotein cholesterol of a statin or fixed-dose combination comparisons reductions of up to 35% to meet their goal, any of the statins product containing a statin and (see text) are effective. In patients requiring a low-density lipoprotein another lipid-lowering drug to cholesterol reduction of 35% to 50% to meet the National achieve National Cholesterol Cholesterol Education Program goal, atorvastatin 20 mg or Education Panel goals? Atorvastatin 80 mg daily and rosuvastatin 20 mg or more can reduce low-density lipoprotein cholesterol by 50% or more. Based on fair-quality studies, atorvastatin 80 mg daily resulted in 5 to 6 additional percentage points of low-density lipoprotein reduction than simvastatin 80 mg (53% to 54% vs. In head-to-head studies rosuvastatin 40 mg had greater reduction in low-density lipoprotein cholesterol than atorvastatin 80 mg with similar frequency of adverse events. In patients requiring a low-density lipoprotein cholesterol reduction of greater than 50%, the higher doses of ezetimibe-simvastatin at 10/40 mg and 10/80 mg are more likely to meet the National Cholesterol Education Program Adult Treatment Panel III goal than an equivalent high potency statin. How do statins and fixed-dose Fair-to-good When statins are provided in doses that are approximately combination products containing a equipotent for lowering LDL-C, a similar percent increase in statin and another lipid-lowering high-density lipoprotein cholesterol can be achieved. There drug compare in their ability to raise is conflicting evidence about simvastatin vs. Some studies found greater increases in high-density lipoprotein cholesterol with rosuvastatin compared with atorvastatin, while other studies found no difference. How do statins and fixed-dose NA There are no controlled trials comparing equivalent doses of combination products containing a 2 or more statins to reduce the risk of coronary events, statin and another lipid-lowering stroke, or death. Which statins have been shown to Good Patients who have never had CHD: pravastatin (high-risk reduce all-cause mortality? Patients with CHD: simvastatin, atorvastatin Which statins have been shown to Fair-to-good Patients who have never had CHD: atorvastatin (high-risk reduce CHD events? Which statins have been shown to Good Atorvastatin, pravastatin, simvastatin, rosuvastatin (patients reduce strokes? Atorva 10 mg reduced cardiovascular events in a primary prevention trial of patients with diabetes (CARDS), and simvastatin 40 mg reduced cardiovascular events in patients with diabetes (Heart Protection Study). In a subgroup analysis of the LIPS trial, there was a reduction in coronary events (cardiac death, nonfatal MI, CABG, or repeat PCI) with fluvastatin 80 mg in patients with diabetes who had undergone successful PCI. Studies that included people with diabetes had rates of adverse effects similar to other studies. Are there differences in Good (elderly, The benefits of statins have been documented in women effectiveness of statins and fixed- women)-to- and the elderly. There are almost no data about African dose combination products Fair to Poor Americans, Hispanics, or other ethnic groups. In short-term containing a statin and another lipid- (African head-to-head trials, reductions in LDL-C and frequency of lowering drug in different Americans, adverse events with rosuvastatin 10 to 20 mg and demographic groups or in patients Hispanics, and atorvastatin 10 to 20 mg in Hispanic, South Asian, and with comorbid conditions (e.

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Hemag- glutinin (HA) and neuraminidase (NA) comprise the major surface gly- coproteins buy 1000mg sucralfate with mastercard gastritis zunge. HA and NA reactivities with antibodies define the subtypes of in- fluenza A (Cox and Subbarao 2000) sucralfate 1000mg amex gastritis diet . Fifteen different HA antigenic sub- types occur order 1000 mg sucralfate mastercard gastritis doctor, each subtype cross-reacting relatively little with the other subtypes. The designation HxNy describes an influenza subtype with HA antigenic subtype x = 1,... RNA sequences differ more between antigenic subtypes than within subtypes. Sequence similarity falls below 70% between HA subtypes and rises above 80% between isolates of the same subtype (Röhm et al. Thus, broad measures of antigenic and phylogenetic distances provide similar pictures of divergence. Much antigenic diversity also occurs between different members of an antigenic subtype. At these smaller distances, antigenic measures of differentiation become sensi- tive to the panel of antibodies and the nature of the test. A host infected with two dif- ferent viral genotypes can produce hybrid viral progeny with reassorted genotypes (Scholtissek 1998). For example, coinfection with HxNy and HwNz could produce the hybrids HxNz and HwNy in addition to the parental types. The H3N2 subtype that caused the “Hong Kong” pandemic of 1968 arose by reassortment of the human H2N2 subtype with avian genes. The reassorted genotype had the H3 subtype and the PB1 gene from the bird lineage and the other six segments from the H2N2 human lineage (Kawaoka et al. Other reassortments between the major human subtypes have been documented during the past twenty-five years (Cox and Bender 1995). Reassortment between subtypes may not occur frequently, but may be important in creating novel genotypes that have the potential to spread widely through a host population, causing pandemics. All HA and NA subtypes occur in aquatic birds, suggesting that those avian species were the original host of influenza (Webster and Bean 1998; Coxand Subbarao 2000). Widespread human epidemics have been lim- ited to H1N1, H2N2, and H3N2, although occasional transfers of other subtypes occur from birds or mammals to humans. Pigs harbor H1 and H3, whereas horses have H3 and H7. Other mammals and nonaquatic birds occasionally become infected, but do not appear to maintain stable lineages over time. Influenza HA and NA molecules mediate viral attachment and entry to host cells and release of progeny viral particles by budding through themembrane of infected cells (Lamb and Krug 2001). Current under- standing assigns adsorption and entry functions to HA (Steinhauer and Wharton 1998) and release of progeny to NA (Colman 1998). However, the HA and NA molecules may have multiple active sites and various functions, and the different subtypes of each molecule differ signifi- cantly (Lamb and Krug 2001). With those caveats, a brief summary of structure and function follows. The HA mole- cule then cleaves into two parts, the terminal HA1 and the basal HA2 fragments. Cleavage exposes on the surface of HA2 a highly conserved, hydrophobic region that mediates fusion and entry via the host mem- brane (Wilson and Cox 1990; Skehel and Wiley 2000). EXPERIMENTAL EVOLUTION: INFLUENZA 209 B Receptor binding site 155 193 188 A 133 186 126 220 144 145146 226 217 D 143 205 122 208 78 E 83 54 275 53 C 278 Figure 13. This drawing is based on structural analysis of H3 hemagglutinin. Inference about other HA subtypes depends on presumed structural similarity with H3. Labeled amino acid num- bers for HA1 are a subset of the variable sites listed in Wiley et al. The sialic acid binding site oc- curs near the tip of HA1. The letters A–E locate the major regions for 210 CHAPTER 13 Tyr 195 Leu 194 Glu 190 Thr 155 His 183 HO N OH N H H O N HO 9 OH Trp 153 7 CH 8 3 O 5 NH OH 6 OH H RO 3 4 O 2 O O O Leu 226 135 O HO 225 Ser 136 224 H Tyr 98 N 137 138 98 Y→F 5 183 H→F 12 225 G→D 53 136 S →A 30 183 H→A — 225 G→R 136 136 S →T 45 190 E →A 125 226 L →P 42 153 W→A — 194 L →A 3 228 S →G 112 153 W→F 39 195 Y→F 36 Figure 13. The listing below shows the binding affinities for sialic acid when particular amino acids are changed ex- perimentally by site-directed mutagenesis (Martín et al. The number on the left defines the amino acid site in HA1, x → y shows the original and new amino acid, and the number on the right is the binding affinity of the mutant as a percentageof the affinity of the wild type. Dashesshow cases in which the recep- torsiteisnot properly expressed. Redrawn from Skehel and Wiley (2000), with permission from the Annual Review of Biochemistry, www. The sialic acid has been displaced slightly to show the structure of the fit. The amino acids numbered within and around the binding site provide a reference for the location of important residues. The bottom of the figure shows the effect on binding affinity to sialic acid caused by experimental change of particular amino acids. This space-filling model has roughly the same orientation as the schematic diagram in figure 13. Antibodies bound to HA can neutralizeinfluenza infectivity by physi- cally obstructing the sialic acid binding site. For example, the HC19 MAb binds to HA of strain X-31 (H3 subtype),partially overlapping the sialic acid binding site (Bizebard et al. The specific antibody-epitope re- gion of direct contact covers 1250 Å2,including amino acids 134, 136, 212 CHAPTER 13 153, 155, and 194. The de- pression extends 315 Å2,ofwhichtheantibody binding region covers 167 Å2. Antibody escape mutants map to the ridge of amino acids that ring the conserved amino acids in the binding pocket. Each upper arm forms an Fab frag- ment, with the binding region on the tip of the fragment. An antibody molecule can be cleaved to release two identical Fab fragments, each containing a binding region.

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Clinical progression of HIV-1 infection according to the viral response during the first year of antiretroviral treatment purchase 1000 mg sucralfate amex gastritis cats. High exposure to nevirapine in plasma is associated with an improved virological response in HIV-1-infected individuals discount 1000mg sucralfate gastritis causas. Impact of 5 years of maximally successful highly active antiretroviral therapy on CD4 cell count and HIV-1 DNA level buy 1000mg sucralfate visa gastritis prevention. Influence of age on CD4 cell recovery in HIV-infected patients receiving HAART: evidence from the EuroSIDA study. Clinical implications of identifying non-B subtypes of HIV type 1 infec- tion. Stop routine CD4 monitoring in HIV-infected patients with fully suppressed virus and CD4> = 350 cells/ml. Characterization of viral dynamics in HIV type 1-infected patients treated with combination antiretroviral therapy: relationships to host factors, cellular restoration, and virologic end points. Prevention of HIV infection CHRISTIAN HOFFMANN Approximately 35 years after AIDS was first described, a prophylactic vaccination remains a distant prospect. In 2007 two highly promising vaccine studies were prematurely halted. It seems doubtful now that a vaccine to effectively prevent HIV infection will be discovered anytime soon – the moderate but surprisingly successful RV144 vaccine study will not change that (Rerks- Ngarm 2009, see chapter on Preventive Vaccination). Several experts believe that a promising vaccine candidate does not exist currently. The finding that HIV superinfection occurs at approximately the same rate as primary HIV incidence (Redd 2013) has significant implications for HIV vaccine research. When HIV itself does not provide any protection from re-infection – how can a pro- tective vaccine for uninfected persons be found? Neither blind hope nor overambitious time schedules have proved very helpful. Some vaccine studies up until now can in fact be regarded as counter- productive, fatiguing both sponsors and the community. Considering all this, prevention will continue to be the central means of control- ling the HIV epidemic. However, common prevention strategies focused on the ABC guidelines (abstinence, be faithful, condom use) have reached their limits. Despite significant efforts – according to UNAIDS, the incidence has dropped from 3. In every major city in the US or in Europe syphilis outbreaks in HIV-infected patients have been reported. It seems clear that advertisements and brochures alone are not the solution, especially when these simple publicity mechanisms are not maintained. Prevention remains an arduous business and success is not imme- diately visible nor is it profitable in economic terms, although the savings in people needing treatment, i. In any case, sexual behavior is not easily modified by a few advertisements or brochures. For some time, preventive medicine in HIV has been taking completely new and sometimes unusual paths to reach focus groups. Terms such as serosorting, seropo- sitioning, dipping or strategic positioning show that the medical world is learning to face sexual reality. People have sex and not everyone cares about, follows, or can follow the ABC guidelines. Recent studies with serosorting, choosing sexual partners according to perceived HIV serostatus, show that new prevention strategies can be developed (Morin 2008). The following focuses mainly on medical prevention strategies. In 2010 there were groundbreaking new findings in this area regarding PrEP and microbicides. In 2011, the protective effect of ART, which had been expected for a while, finally became evident and now may have a substantial impact on HIV prevention. Treatment as prevention (TasP) Little in HIV medicine of the last few years has met with such wide response as the results of the HTPN 052 trial. Spontaneous, standing ovations as seen during the International AIDS Conference in Rome in July 2011 are seldom seen in the world of science. The reputable journal “Science” described the results as “the breakthrough in 2011” and “The Economist” even wrote about the “end of AIDS”. Results of a trial were published in the summer of 2011, which had investigated the protective effect of ART (Cohen 2011). HTPN-052 was a trial with 1763 HIV-discordant couples in the US, India, Brazil, Thailand and five African coun- tries. The HIV-infected partners were treatment-naïve and had CD4 T cell counts between 350 and 550/µl. Approximately 97% of the couples were heterosexual and most of the volunteers were between 26 and 40 years. The couples received thor- ough instructions and the use of condoms was counselled at monthly sessions. Then the HIV-infected partners were randomized to start ART, either immediately or when CD4 T cells fell to below 250/µl or when AIDS had manifested. The primary end- point was defined as new infections of the HIV-negative partners that clearly origi- nated from the infected partners (“linked infections”). In a first evaluation in February 2011 after a follow-up of 1. There was only one infection in the arm in which infected partners had received ART immediately. Later investigations showed that the infection was probably caused before or just after the infected partner had started ART. Even when counting this case, the results gave evidence for a 96% protection with ART, a result unachieved up to then by any of the other prevention strategies, including PrEP or vaccination (Karim 2011).

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N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or Y ear W ith drawals Due to (Q uality rating) A dverse Events F ocketal cheap sucralfate 1000 mg amex gastritis pediatric symptoms. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberscreened/ Y ear Population eligible/ (Q uality rating) Setting Inclusioncriteria Exclusioncriteria enrolled M onikesetal sucralfate 1000mg amex gastritis diet 8 jam. Proton pump inhibitors Page 108 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 3 safe 1000 mg sucralfate gastritis diabetes diet. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberwith drawn/ Y ear lostto followup/ (Q uality rating) analyzed Results Results M onikesetal. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or Y ear W ith drawals Due to (Q uality rating) A dverse Events M onikesetal. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberscreened/ Y ear Population eligible/ (Q uality rating) Setting Inclusioncriteria Exclusioncriteria enrolled Placebo- controlled trials Peuraetal. E x cludedthosewithanactivegastric parallelgroup during the3monthsbeforethestudy. Proton pump inhibitors Page 111 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 3. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberwith drawn/ Y ear lostto followup/ (Q uality rating) analyzed Results Results Peuraetal. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or Y ear W ith drawals Due to (Q uality rating) A dverse Events Peuraetal. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberscreened/ Y ear Population eligible/ (Q uality rating) Setting Inclusioncriteria Exclusioncriteria enrolled A ctive-controlled trials vanZyletal. Historyof keyGE RD andpatientswhohadrecentlytakenorwerestillreceiving symptoms(oneepisode/monthforatleast3 PPI therapyoragentslikelytoaffectgastricacidsecretionor months)priortoentryintothestudy. Proton pump inhibitors Page 114 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 3. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or N umberwith drawn/ Y ear lostto followup/ (Q uality rating) analyzed Results Results vanZyletal. N onerosive gastroesoph agealreflux disease sh ort-term trials A uth or Y ear W ith drawals Due to (Q uality rating) A dverse Events vanZyletal. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup Caos O f 497enrolledpatients,261patientscom pleted(Phase N R N R /N R /497/236(Phase1)/N R 2005 1)and205patientscom pleted(Phase2. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup D evault2007 IntheU S at143centers;twogroupsincluded-patients L A classification,% 4015screened,1026random iz edtotrm t, with healedE E from atrialof patientswith L A gradesC or GradeA 37% 1001ITT D E E whoweretreatedwith esom epraz ole40m g once GradeB38% dailyorlansopraz ole30m g oncedailyforup to8weeks. GradeC 20% Thesecondgroup of patientsincludedthosewith L A GradeD 4. Theyreceivedopen-labeltreatm entwith esom epraz ole40m g oncedailyforup to8weeks. Those whoseE E wasconsideredhealedonthebasisof an esophagogastroduodenoscopy(E GD )atweek4andwho reportednoheartburnoracidregurgitationsym ptom s during theprevious7dayswereeligibleforrandom iz ation intothism aintenancetrial. M eanage48years 41% fem ale 78% white 6% black 16% other J asperson 30patientsinGerm anywhoseesophagitishealedafter6- AllGrade4(Savary-M iller) 36treated,6didnotheal,30included. Proton pump inhibitors Page 118 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup L abenz etal2005 2766patients(63% m en;m eanage50years)were L A grade D iscontinuationsduetoadverseevents requiredtohaveE E [photographicallydocum entedat A:32. Proton pump inhibitors Page 119 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup L auritsenetal. A:38% (89%)random iz edform aintenance B:45% treatm ent. ITT = 1224(615 M eanage:49 C:14% esom epraz ole,609lansopraz ole). Proton pump inhibitors Page 120 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup R ichteretal. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or Esoph agitis G rade (grading criteria),oth er N um berscreened,eligible,enrolled, Y ear Population,setting ch aracteristics with drawn,lostto followup Thjodleifssonet 243patientsat21centersinE uropewith aprevious Grade0:77% 210/243com pletedoneyear;13 al. Proton pump inhibitors Page 122 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or F unding source Y ear R esults Q uality rating and role offunder Caos Primary endpoint: R elapseratesat5yrswere F air SupportedbyE isaiInc and 2005 11% forrabepraz ole20m g,23% forrabepraz ole J anssenPharm aceuticals 10m g and63% forplacebo(p<0. Secondary endpoints: D aytim eheartburnrelapse lowerwith both dosesof rabepraz olevplacebo (p<0. Symptomaticrelapse by 48 weeks: lansopraz ole30m g:0. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or F unding source Y ear R esults Q uality rating and role offunder D evault2007 E stim atedrem issionratesthrough 6m onths,% F air SupportedbyAstraZeneca (95% CI) esom epraz olevslansapraz ole E ndoscopic/sym ptom atic rem issionrate 84. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or F unding source Y ear R esults Q uality rating and role offunder L abenz etal2005 Primary endpoint: E ndoscopic plussym ptom atic Supportedbyagrantfrom rem issionforallpatientsat6m oswas74. Secondary endpoint: E som epraz ole20m g was significantlym oreeffectivethanpantopraz ole20 m g form aintaining pureendoscopic healing of E E (6-m onth lifetableestim ates:88. Proton pump inhibitors Page 125 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or F unding source Y ear R esults Q uality rating and role offunder L auritsenetal. F air:sm alldifferencesatbaseline(slightly>m aleson SponsoredbyAstraZeneca 2003 esom epraz ole84% vs. Proton pump inhibitors Page 126 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 4. H ead-to-h ead trials ofprotonpum pinh ibitors forpreventionofesoph agitis relapse A uth or F unding source Y ear R esults Q uality rating and role offunder R ichteretal. Secondary endpoints: N oSS differenceof healing m aintenancebasedonh.