STATEMENT O; >NTENTEvidence"based best practice guidelines are produce - PDF document

STATEMENT O; >NTENTEvidence"based best practice guidelines are produced to help health practitioners and consumers ma`e decisions about health care in speciÄc clinical circumstances. Research has shown that if properly developed! communicated and implemented! guidelines can improve care. The advice on dyspepsia and heartburn given in this guideline is based on epidemiological and other research evidence! supplemented where necessary by the Lhile guidelines represent a statement of best practice based on the latest available evidence at the time of publishing! they are not intended to replace the health practitioner¼s COPYR>GHTThe New Zealand Guidelines Group encourages the free emchange and sharing of evidence and guidelines! and the adaptation of the guidelines for local conditions. However! please note that the guidelines are sub_ect to copyright. >f you wish to replicate or reproduce this guideline! in part or in full! please obtain agreement from the New Zealand Guidelines Group. The New Zealand Guidelines Group as`s people wanting to reproduce guidelines Lhere guidelines are modiÄed for local circumstances! signiÄcant departures from the national guidelines should be fully documented and the reasons for the differences emplicitly Purpose ................................................................................................viiAbout the Guideline .............................................................................im>ntroduction ........................................................................................mviiSummary and Recommendations .........................................................mim @ey Messages .................................................................................mim Recommendations ............................................................................mm Algorithms ...................................................................................mmviiiCHAPTERS1 Bac`ground ....................................................................................... ' Undifferentiated Dyspepsia ............................................................... 3 Gastro"oesophageal ReÅum Disease GORD .....................................',4 Helicobacter Pylori and Peptic Ulceration ..........................................43* NSA>Ds and G> Complications ..........................................................+*+ Using the Guideline in General Practice ............................................,., >mplementation ................................................................................818 Evaluation ........................................................................................8*APPEND>CES A. Fuestionnaire for people with gastro"oesophageal reÅum disease ..............................................................................88 B. Recommended Medication for Heartburn and$or Dyspepsia ..........% C. Patient >nformation Sheet/ > Have Dyspepsia >ndigestion – Lhat Does This Mean4 ................................................................1Glossary and Abbreviations ..................................................................*References ..........................................................................................., The Core Committee of the Dyspepsia and GORD Lor`ing Party established four regional committees! each including general practitioner! gastroenterology and surgical input! to develop the guidelines for speciÄc areas/ Dunedin$Christchurch for GORD0 Lellington for undifferentiated dyspepsia and non"ulcer dyspepsia NUD0 Lai`ato$Rotorua$Bay of Plenty The four regional wor`ing groups each established a systematic search of the literature. Each developed their evidence tables from which their recommendations were made. Lhen the core committee convened they made a decision that the evidence tables would not be published nor would they include the level of evidence for each study in the guideline temt. Rather! the committee would put its emphasis on producing a wor`boo` style guideline with detailed references for those who wish to delve into the original research. Their drafts were developed between 1..8 and '%%1 by which time they had been submitted to the Core Committee for review. Decisions were made by consensus of the various groups! and the Core Committee and a professional editor$writer. The edited copies were returned to the four wor`ing groups to ensure they had maintained their original interpretation. Opportunity was given to update the information with the Änal drafts being returned in mid '%%'. The Änal draft was again reviewed by the Core Committee and further corrections were made. The draft was then sent to the NZGG for circulation to reviewers as part of the AGREE process. The results of the AGREE review were circulated to the leaders of the Regional Lor`ing groups and members of the Core Committee. Most of the suggestions ;low diagrams were constructed from the recommendations agreed in the Guideline. They were discussed with representatives of the Best Practice Advocacy Centre >nc who reviewed the draft Åow diagrams in association with some of their representatives and general practitioners.Other dyspepsia guidelines published between 1..8 and ?une '%%3 were perused to ensure appropriate information was considered in developing the New Zealand version of the Guideline. As updates of Cochrane Reviews became available! they were also included A. Cochrane reviews1. Soo S! Moayyedi P! Dee`s ?! Delaney B! Aewis M! ;orman D. '. Moayyedi P! Soo S! Dee`s ?! Delaney M! >nnes M! ;orman D. 3. van Pinmteren B! Numans ME! Bonis PA! Aau ?. Short"term treatment with proton pump inhibitors! H' receptor antagonists and pro`inetics for gastro"oesophageal reÅum disease"li`e symptoms and endoscopy negative reÅum disease. Cochrane Database Health Economist! Health Outcomes Associates Atd  Associate Professor! School of Epidemiologist! Department of Public Health and General Practice! Christchurch School of REG>ONAA COMM>TTEES ;UND>NG;unding for this guideline was initiated by an independent grant from Astra Pharmaceuticals NZ Atd! which also provided secretarial assistance. A second ma_or grant was received from the Health ;unding Authority! and supportive grants from ?anssen"Cilag Pty Atd and PHARMAC. The New Zealand Guidelines Group too` over administration of funds from EK>DENCE AND RECOMMENDAT>ON GRAD>NG SYSTEM USED ;OR TH>S GU>DEA>NEGroups developing the guideline conducted literature searches! including current computer searches Medline! EMBASE and surveys of review publications Cochrane Aibrary! Bandolier. There are a number of systems for grading the evidence. The method adopted AEKEAS O; EK>DENCE Dyspepsia is a `ey but not a speciÄc symptom indicating upper gastrointestinal G> malfunction or disease. Only a minority of people with dyspepsia have speciÄc abnormalities eg! erosive oesophagitis! peptic ulcer or cancer. The challenge of this guideline is to present an approach that helps the doctor to choose which people to treat empirically and whom to investigate when and how! and to guide This guideline is designed to be a practical! wor`ing document. The Ärst encounter between the person with dyspepsia and the practitioner starts with the undifferentiated symptoms of dyspepsia or heartburn. The choice is then between empiric management and investigation. Alarm signals are clearly deÄned to channel the individual for early investigation. >ndividuals with heartburn often have GORD about ,* and respond well to appropriate treatment. Others refuire more information! emercising both the art and science of medical practice! ;or those in whom investigation has established a speciÄc diagnosis! there are now treatments that! although having the common features of acid inhibition! differ widely in their details and application. There is now good evidence for optimum but different regimens for the main diagnostic groups/ GORD! H. pylori related peptic ulcers and gastric cancer. Problems related to NSA>D use have a separate origin and often run a different clinical course! which must be recognised and treated speciÄcally. GORD! H. pylori"related peptic ulcers! and NSA>D"induced problems are addressed in separate sections in the guideline! while gastric cancer A large group of individuals remain with non"ulcer or functional dyspepsia. Management approaches for these individuals are varied and have a high placebo NSA>Ds! particularly aspirin! have a very useful part to play in the treatment of a variety of non"gastrointestinal conditions eg! arthritis! and prevention of ischaemic heart disease and stro`e. >ndividual evaluation of the ris`s and beneÄts is refuired! preferably by the medical practitioner responsible for that person¼s care! although team consultation with other practitioners involved may be necessary. Ris` factors for G> complications are deÄned! and potential adverse effects of NSA>Ds are described. Lhere there is an increased ris` of NSA>D"induced G> complications! or any adverse effects! NSA>D treatment may be able to be stopped. However! if he beneÄt of continued treatment outweighs the ris`s! treatment can be continued! providing appropriate steps are ta`en as described in this Guideline! to minimise the degree of ris`. An alternative medication could also be considered. Lhile this Guideline provides evidence"based advice on best management! it cannot replace SUMMARY AND RECOMMENDAT>ONS@EY MESSAGES>nitial Evaluation >dentify ris` factors for organic pathology. >f there are alarm signals! or if age 3*% years >f a NSA>D is being used! evaluate ris` of G> complications! as well as potenitial beneÄt Undifferentiated Dyspepsia >f prevalence of H. pylori 33%! treat empirically domperidone or H RA for 4 – 1' wee`s test for H. pylori and treat if positive. >f there is no response to test"and"treat! or if prevalence of H. pylori 13%! treat empirically. >f there is no response to either strategy! GORD >f there is no response or early recurrence after cessation of treatment! refer for OGD! H. pylori Management Test for H. pylori in those with past history of peptic ulcer! family history of gastric cancer! or where the prevalence of H. pylori is 33%. Urea breath test is recommended. Serology can be used where the prevalence of H. pylori is 33%. ;aecal antigen test is also recommended! and is becoming increasingly available in New Zealand. >f testing is Chec` eradication of H. pylori in those with a peptic ulcer complication! important comorbidity factors! symptom recurrence or those living in isolated areas. Re"treat if Peptic Ulcer >f peptic ulcer is identiÄed! test for H. pylori! treat if positive! and start a PP> or H Treat gastric ulcers for 8 – 1' wee`s! and chec` healing with OGD. Treat duodenal ulcers NSA>D Use >f there is no dyspepsia! consider a safer alternative! or a less tomic NSA>D eg! ibuprofen. >f continued use is refuired! and there is increased ris` of G> complications! consider a >f there is dyspepsia and increased ris` of G> complications! refer for OGD. Eradicate >f there is dyspepsia and no increase in ris`! stop NSA>D! use a safer alternative! reduce the dose! or use a less tomic NSA>D. >f symptoms continue! refer for OGD. Eradicate >f an ulcer is identiÄed! and continued NSA>D use is refuired! treat with a PP>! and consider RECOMMENDAT>ONSUND>;;ERENT>ATED DYSPEPS>A>nitial management of undifferentiated dyspepsia ™ ;or people with heartburn! manage as GORD see recommendations for ™ ;or people with dyspepsia but no heartburn reÄum symptoms! either/¶ treat initially with domperidone or H ¶ test"and"treat for >f there is heartburn and dyspepsia! treat as GORD in the Ãrst instance.  Although data regarding the prevalence of H. pylori infection in New Zealand are patchy! the following statements can ™ ™ economic status ™ rates in adults living in Auc`land have generally been found to be 33%. Management of recurring undifferentiated dyspepsia Management of functional dyspepsia 1. pro`inetics domperidone NNT '.8 NNT based on total pro`inetics '. H 3. PP>s NNT211.1. ™ does not have heartburn™ is not ta`ing NSA>Ds™ has normal blood tests ;BC! ESR! CRP™ has normal OGD. Treatment of GORD diagnosed after OGD ™ Treat with a step"down drug regimen see ™ >f symptoms recur at stepped"down dosage! continue on lowest effective ™ Treat with ongoing continuous full"dose PP> treatment. ™ age 1*% years™ age *% years and over and there is no comorbidity™ there is inability or unwillingness to ta`e medications™ there is inadefuate control with medical therapy. H. pylori treatment failure ™ an alternative triple therapy regimen PP> plus two of the following/ ™ fuadruple therapy standard triple therapy plus bismuth. ™ review compliance factors and consider testing for bacterial resistance™ consider retreatment for ' wee`s. ConÄrmation of H. pylori eradication ™ UBT is the recommended non"invasive test serology should not be used ™ ;or people having OGD to chec` for healing of gastric ulcer! conÃrm ™ Perform at least one month after completion of eradication regimen™ ;or people ta`ing PP>s! perform at least one wee` after cessation of PP>. Management of H. pylori"negative peptic ulcers ™ ulcer recurrences are frefuent eg! more than once per 1' months or ™ there is a previous peptic ulcer complication™ there are comorbid factors that might ma`e any complications life" NSA>DS AND G> COMPA>CAT>ONS>ndividuals at increased ris` Of NSA>D"induced G> complications ™ misoprostol at doses of '%% mcg$day. >ncrease dose over two wee`s as ™ standard doses of PP> once daily. AAGOR>THM GORD AAGOR>THM PEPT>C UACER Note/ >f H. pylori treated! and there are The word »dyspepsia¼ comes from the Gree` »dys¼ meaning »bad¼ and »pepsia¼ meaning »digestion¼. Dyspepsia is a common symptom complem with epigastric pain and other associated features. Dyspepsia may have an organic cause such as peptic ulcer! but is more frefuently associated with normal or near"normal Ändings on gastroscopy ie! functional or non"ulcer >n Britain it has been estimated that more money is spent on drugs for dyspepsia than on any other treatment for a symptom. >t is li`ely a similar situation emists in New Zealand. About '* of people with dyspepsia in Britain consult their general practitioner for the problem0 the remainder either use no medication or self"medicate. Self"medication is common amongst Management of dyspepsia is variable! and a number of possible strategies have been recommended in different guidelines. This evidence"based guideline attempts to provide a framewor` that is appropriate for New LHAT >S DYSPEPS>A4Dyspepsia! or indigestion! is a common symptom complem! deÄned as pain or discomfort centred in the upper abdomen epigastrium. Dyspepsia may have a number of associated symptoms! including fullness after meals! bloating! belching! early satiety! anoremia! nausea and vomiting. Heartburn! retrosternal pain and acid regurgitation! although commonly included with dyspepsia! relate more to lower oesophageal dysfunction! which is treated separately in this guideline. Heartburn is also lin`ed with some dyspepsia subgroups and with cardiac disease. Some people may have both symptom Symptoms of dyspepsia may be episodic! recurrent or chronic. Many but not all symptoms are related to food. Symptoms connected with the process of defaecation are emcluded from a deÄnition of dyspepsia as they relate more to bowel function in the lower part of the G> tract. However! a number of Dyspepsia is not a diagnosis. >t is a symptom complem associated with upper gastrointestinal G> tract conditions eg! peptic ulcer or gastric cancer! other upper abdominal pathology eg! gallstones! or disorders related to other systems eg! cardiovascular. People with dyspeptic symptoms and no Attempts have been made to lin` particular symptoms with speciÄc pathological entities. Heartburn¸deÄned as a burning sensation starting in the epigastrium and radiating towards the nec`¸is classiÄed as a reÅum"li`e symptom. Heartburn is the most reproducible and sensitive indicator of gastro"oesophageal reÅum disease GORD with a speciÄcity the probability of correctly emcluding those without the disease of about ,*! but it may also be lin`ed with some dyspepsia subgroups and with cardiac disease. Heartburn may also Dyspepsia has been sub"classiÄed into ulcer"li`e localised epigastric pain! either aggravated or relieved by meals and relieved by antacids and dysmotility"li`e fullness after meals! bloating! belching! early satiety! anoremia! nausea and vomiting. Although these sub"categories have some use in directing initial approaches to empiric treatments for non"ulcer dyspepsia! and are still favoured by some! the sensitivity and speciÄcity of these are very ™ epigastric pain or discomfort™ pain relieved by food™ pain relieved by antacids or ulcer"reducing drugs™ pain occurring before meals or when hungry™ pain that at times wa`ens the person from sleep™ periodic pain with remission and relapse. ™ early satiety™ post"prandial fullness™ nausea™ retching and$or vomiting ™ bloating in upper abdomen not accompanied by visible distension™ upper abdominal discomfort often aggravated by food. POPUAAT>ON SEE@>NG MED>CAA ADK>CEBesides the severity and persistence of dyspepsia! many other factors including psychosocial issues are important in determining who see`s medical consultation! although these factors are not well understood. Studies such as a postal survey conducted by ?ones et al have shown that only about '* of people with dyspepsia actually see` medical advice. Nevertheless! because dyspepsia symptoms are so common! this accounts for between 3 and 1% of the adult population and for between ' and , of visits to general practitioners.One British study estimated that 4 to * of general practice consultations are for dyspepsia.13 Results obtained by McAvoy et al in the New Zealand"based LaiMedCa study showed that +.4 of general practice consults were for digestive problems both upper and lower G> symptoms and resulted in a higher referral rate for secondary investigation 1' of consults FUAA>TY O; A>;E L>TH DYSPEPS>AA number of studies have shown an association between dyspepsia and reduced fuality of life. >n general! people with functional dyspepsia score higher on measures of anmiety! neuroticism! depression and hypochondriasis compared with healthy controls. These personality proÄles are similar to people with other pain syndromes! both organic and functional in nature. Haug et al compared 1%% people with functional dyspepsia! 1%% with duodenal ulcer! and 1%% controls!18 and found that those with functional dyspepsia had more anmiety and depression! and a lower general level of functioning than people in the other two groups. >n addition! those with functional dyspepsia had more frefuent dyspepsia symptoms and longer duration of symptoms than those with duodenal ulcer. However! it was more difÄcult to recruit people with functional dyspepsia! which may have >nterestingly! fuality"of"life scores as _udged by total symptoms improve with improvement of dyspepsia! suggesting that anmiety and stress"related symptoms may be the result of The fuality of life of people with GORD has been shown to be similar to that of people CAUSES O; DYSPEPS>AThe causes of dyspepsia are shown in Table 1.'. The prevalence Ägures given are derived from the small minority of people who are referred to gastroenterologists for investigation and deÄnitive diagnosis. >t can be reasonably assumed that more people with functional dyspepsia will be treated at the general practice level and that those with organic disorders will be more li`ely to be referred to specialists. However! reliable data to support this are oesophagus Sources/ Auc`land data. ;raser AG! Ali MR! McCullough S! Yeates N?! Haystead A. Diagnostic tests for Dunedin data/ Barbeoat GO. Unpublished data. ;irst *%% endoscopies of '%%10 total 1%+.8! as some with Gastro"oesophageal ReÅum Disease GORDThis condition is common in OECD countries but rare in the rest of the world. >t encompasses a broad range of clinical disorders! from simple acid reÅum without inÅammation of the oesophagus to severe oesophagitis and its complications. Besides typical heartburn and acid regurgitation symptoms! people may present with atypical chest pain! and respiratory Unfortunately! there is a poor correlation between endoscopically demonstrable oesophageal inÅammation and the severity of symptoms! as at least half the people with symptomatic gastro"oesophageal reÅum will have a normal OGD. >t has been demonstrated that it is emceedingly rare for OGD"negative and minor grades of oesophagitis to progress to the severe complicated forms.'+!', Treatment is aimed not only at relieving symptoms but at treating or preventing inÅammatory changes and complications in the more severe grades. with appropriate medical treatment! including acid inhibition and H. pylori eradication. Ulcer recurrence is common up to 88 by 1 year! unless H. pylori is eradicated. Recurrence CancerGastric cancerCancer of the stomach accounts for a small minority of people with dyspepsia 1 – ' of OGDs. >t is uncommon in the European population in New Zealand and is emtremely rare below the 4+ to ** age group. However! it is more prevalent among certain ethnic groups! including Maori! PaciÄc and East Asian people. One Maori family cohort with a genetic predisposition to gastric cancer has been identiÄed0 these individuals can present at a very H. pylori has been shown to be a carcinogen see pages *' – *3. >n the early stage of gastric cancer! dyspepsia may be the only symptom. >n later stages! presenting symptoms include weight loss! anaemia! early satiety and! in some cases! pyloric obstruction. Because gastric cancers can masfuerade as! or coemist with! gastric ulcers! healing of gastric ulcers Cure of gastric cancer usually depends on early diagnosis and appropriate surgical intervention. The cure rate is generally poor! with recent Ägures varying from * to 3% in most OECD countries! although better results have been obtained where surgical resection has been possible. Different forms of early gastric cancers may emist in ?apan! ma`ing Gastric lymphomasOther gastric malignant conditions include lymphomas. Some lymphomas involving the stomach are related to H. pylori infection mucosa"associated lymphoid tissue! or MAAT lymphoma and can now be treated medically see Chapter 4/ Helicobacter pylori and peptic ulceration. Overall! gastric lymphomas are less common than cancers about 1% Oesophageal cancerAlthough some people with oesophageal cancer will present with symptoms of reÅum or dyspepsia! most will have dysphagia as their presenting symptom. This will not be pursued Non"Ulcer Dyspepsia NUDOther common organic causes of dyspepsia include symptomatic cholelithiasis ie! gallstones and ingestion of drugs eg! NSA>Ds! aspirin! iron! digomin! theophylline! antibiotics! and potassium. Aess common causes include gastric dysmotility eg! with diabetic gastroparesis! chronic mesenteric ischaemia! chronic pancreatitis! pancreatic malignancy! gastric surgery! lower G> tract disorders! partial small bowel obstruction! Crohn¼s disease! coeliac disease! liver cancer! and malabsorption syndromes. Non"gastrointestinal causes include cardiac pain! metabolic disturbances! collagen vascular disorders and abdominal Although conditions such as cholecystitis with gallstones! lactose intolerance! pancreatitis and achalasia of the oesophagus usually present with their own! often typical! constellation of symptoms! many people with these conditions present in a non"speciÄc way with dyspepsia. Certain aspects of the person¼s history or emamination may offer clues for a correct diagnosis! and where necessary be confirmed by the appropriate choice of ;unctional dyspepsiaThis term includes all deÄned cases of dyspepsia in which ulceration! GORD! malignancy and other deÄned conditions have been emcluded. »;unctional¼ dyspepsia is deÄned as dyspepsia of at least several wee`s¼ duration for which no focal or structural lesions can be found using upper OGD! and which cannot be emplained by any other obvious structural or biochemical abnormalities on ultrasound emamination or screening blood tests. This large group of conditions includes common! sometimes stress"related! G> symptoms and The pathogenesis of functional dyspepsia has been the sub_ect of considerable study! but remains unclear. >f deÄned pathology can be demonstrated for any identiÄable subgroup! RANGE O; MANAGEMENT OPT>ONSThe range of management options is great! particularly if it is accepted that dyspepsia has a wide variety of causes. >n addition! many people with dyspepsia will decide that their symptoms are minor or transient enough to ignore! or they will prefer to treat themselves with proprietary antacids or over"the"counter acid inhibitors rather than consult Lhen consulted! the general practitioner must decide whether the person refuires reassurance only! empiric treatment! simple investigation! or referral to a gastroenterologist for deÄnitive diagnosis. Appropriate treatment includes the care of the whole person. >t is an opportunity to review personal and lifestyle factors eg! diet! weight control! smo`ing! alcohol abuse! drug use and! in a number of cases! this may be all that is refuired. Most people can be treated by simple medical means with satisfactory outcomes. However! symptomatic recurrence is common! so that repeated courses and sometimes continuous Once a deÄnitive diagnosis has been made! further follow"up can be deÄned more precisely. However! for functional dyspepsia! follow"up is often dictated by symptoms. Aong"term continuing medication for functional dyspepsia is discouraged. Care needs to be emercised to achieve a balance between not »overmedicalising¼ and offering rational long"term follow" MANAGEMENT O; RECURR>NG UND>;;ERENT>ATED DYSPEPS>A MANAGEMENT O; ;UNCT>ONAA DYSPEPS>A ™ does not have heartburn™ is not ta`ing NSA>Ds™ has normal blood tests ;BC! ESR! CRP™ has normal OGD. 1. pro`inetics domperidone NNT '.8 NNT based on total pro`inetics studied '. H 3. PP>s NNT211.1. PROBAEMS ASSOC>ATED L>TH STUD>ES O; DYSPEPS>AThere are a number of problems associated with clinical trials of therapy for dyspepsia! and this is reÅected in the number of poor fuality trials in the literature. Clinical trials in secondary and tertiary care centres are usually performed on carefully selected people with deÄned speciÄc diagnoses! usually supported by endoscopic evidence. Treatment groups are thus generally similar and the information provided not necessarily directly relevant to people presenting to general practitioners. ;urthermore! individuals who have been referred to secondary and tertiary care centres from primary care may well represent those who fail to respond to simple initial therapy eg! H RAs or antacids! and now often also PP>s. On the other hand! it could also be argued that if these difÄcult cases respond to treatment! ™ The placebo effect is very high mean *+0 range * – .%! which means that any gains from medication are difÄcult to measure. The placebo effect is generally so consistent that any study with a placebo effect lower than '% should be interpreted ™ Many trials have inadefuate controls.™ Crossover trials are li`ely to be inaccurate because the duration of beneÄt may ™ Many different deÄnitions of dyspepsia have been used ¸ for instance! some studies ™ Some studies use a washout period with antacid treatment prior to the study proper ™ Some studies have used treatment phases as short as two wee`s which may not allow ™ ;ew studies have loo`ed at long"term management.™ Most medication studies have been in the secondary health care setting where the person¼s characteristics are potentially different from those of people seen in the ™ Different endpoints for beneÄt are used! from complete resolution of symptoms to reduction in symptom scores! for which different scoring systems have been AGA MANAGEMENT OPT>ONSThe American Gastroenterological Association AGA position statement! published in 1. Empiric medical therapy antisecretory or pro`inetic! with any subsefuent investigation Although these studies do not directly address the strategy of empiric medical therapy! they provide the most relevant information on li`ely response rates for people presenting in primary care. The Cochrane review authors commented that there are no long"term treatment trials. This is an important deÄciency because dyspepsia is a chronic relapsing condition! and that intermittent use of medication may be effective. PP>s seem more effective in the treatment of reÅum symptoms in the non"differentiated group! but between * and + individuals would have to be treated for one to gain some beneÄt. ;or the symptom of heartburn! the number needed to treat NNT for PP>s to gain advantage over antacids and RAs was 3.* and 3.1! respectively. The effect on those with no reÅum symptoms is less clear. The effectiveness and cost implications of early investigation versus acid inhibition were emamined in four trials. No difference was shown in global improvement! and the economic data were also inconclusive. However! several studies are currently under way emamining COCHRANE REK>ELS O; PHARMACOAOG>CAA >NTERKENT>ONS>n the Cochrane review by Soo et al! on pharmacological intervention in non"ulcer dyspepsia NUD! trials with people presenting primarily with heartburn were speciÄcally emcluded. The authors felt this would lead to a »purer¼ cohort with NUD. Their review clearly showed a treatment preference for pro`inetic agents! with the important proviso that the results could have been inÅuenced by publication selection bias. Compared with placebo! H were shown to be signiÄcantly more effective! and PP>s and bismuth salts only marginally superior. This is compatible with results reÅecting the emclusion of individuals with heartburn. This review was based on trials of people referred to hospital clinics! and not on presentation Source/ Soo S! Moayyedi P! Dee`s ?! et al. Pharmacological interventions for non"ulcer dyspepsia. The Cochrane >n a meta"analysis! Keldhuyoen van Zanten et al showed that cisapride produced a global improvement of functional dyspepsia symptoms as assessed by the investigator or individual with dyspepsia0 odds ratio OR '..! .* C> 1.* – *.8. The corresponding Ägure for domperidone! based on a smaller number of individuals n2'11! was OR ,.% .* C> 3.+ – 1+! which clearly demonstrates its efÄcacy as a pro`inetic agent. Cisapride also improved epigastric pain OR %.1.! .* C> %.%* – %.,! early satiety OR %.3'! .* C> Cisapride is no longer a Ärst"line treatment for dyspepsia because of the ris` of cardiac arrhythmias which is very rare but can prove fatal. Cisapride refuires specialist >n an open trial in general practice! Heyse et al showed that at sim months! after a four"wee` course of cisapride! there was a ', relapse rate in people previously »cured¼ as _udged by symptom control at the end of the treatment period. Of those who relapsed! 88 responded well to a repeat treatment. Despite the obvious limitations of an open trial! this result raises the possibility that repeat courses of therapy on demand! rather than This conclusion is further supported by ;arup! who was involved in an RCT comparing those who responded to acid inhibition therapy with those who did not. A multi"crossover design was used to identify people who consistently responded to ranitidine compared with This group of responders was then entered into a double"blind parallel study with placebo! and their responses compared with those of the non"responders from the initial study. Responders again improved signiÄcantly with ranitidine! while non"responders >n practice! intermittent therapy may be what people choose anyway! as noted in the study by Hungin et al! who analysed the prescribing patterns for PP>s over a calendar year. >t was found that of '.. individuals on long"term PP>s for a variety of reasons! including dyspepsia and reÅum! '1 refuested sufÄcient prescriptions for the entire year! 44 refuested enough for less than . months total! and '% refuested more than 1 year¼s Although one study showed that smo`ing and aspirin were both independent ris` factors for dyspepsia smo`ing OR '.1! .* C> 1.3 – 3.+0 aspirin OR '.'! .* C> 1.3 – 3., among *.' healthy blood donors! other studies! including the Lellington survey! did not support the association with smo`ing. To date! there are no consistent data showing >N>T>AA MANAGEMENT O; UND>;;ERENT>ATED DYSPEPS>AThe initial management of a person presenting for the Ärst time with dyspepsia needs to 1. >s there a signiÄcant underlying pathology that needs to be treated4'. Lhy has the person presented with this problem at this time4The organic causes of dyspepsia are described in Chapter 1/ Bac`ground. SpeciÄc alarm signals are indicative of speciÄc pathology. Heartburn as a primary presenting complaint gives at least a ,* chance of the person having GORD.1+!1,!18 Symptoms may be associated with recent medication inta`e! particularly NSA>Ds and aspirin! and the person¼s drug history should be reviewed. Aess common causes of dyspepsia may have other features on AAARM S>GNAASThe following features increase the li`elihood of signiÄcant organic disease/™ family history of gastric cancer onset age 1*% years™ severe or persistent dyspeptic symptoms™ previous peptic ulcer disease! particularly if complicated™ ingestion of NSA>Ds in those at ris`™ unemplained weight loss™ G> bleeding™ anaemia™ dysphagia difÄculty swallowing™ coughing spells or nocturnal aspiration™ protracted vomiting™ palpable abdominal mass.NB/ All symptoms should be regarded as more serious in people who are aged 3*% years when presenting for the Ärst time. Gastric cancer tends to occur a decade earlier in people Besides addressing these issues! the fears that precipitate the initial visit for dyspepsia should only about one"fuarter of people with dyspepsia consult their general practitioner for the problem. Aydeard and ?ones compared a group of +. consulters with a group of ++ non"consulters identiÄed by postal fuestionnaire! and found no differences in the frefuency or duration of symptoms between consulters and non"consulters , – 1% years. Consulters tended to be older **.4 vs 48.+ years! had more severe symptoms p1%.%*! and had greater concerns that their symptoms may be indicators of underlying serious or potentially of age *% years. >n addition! Delaney et al have produced evidence that initial OGD in However! each case needs to be _udged not only on biological age but also on past history and ethnicity. Maori and PaciÄc people have an incidence of gastric cancer that is up to Äve times higher than European New Zealanders! and their cancers often occur 1% years earlier! as do those of people from East Asia. New Zealand cancer registrations for 1..8 show that stomach cancer accounts for 3 of cancer deaths in women and * in men. Maori are at higher ris`! with twice the ris` for Maori men compared with non"Maori men! and Äve times the ris` for Maori women compared with non"Maori women. Of the 411 people diagnosed with stomach cancer in 1..8! +3 1* were aged 1** years! and of these! 1+ '* were Maori. ;amily history is an important factor. A Maori family cohort with a genetic predisposition to cancer has been identified! in which the youngest A family history of early gastric cancer warrants investigation of dyspepsia by OGD at any age of presentation. Bodger et al ma`e the reasonable observation that `nowledge of the characteristics of people consulting with dyspepsia in primary care should be an important A further recommendation is that all people with alarm signals should be referred for OGD! primarily to diagnose organic diseases! including gastric cancer. There are now good data to show that most people with gastric cancer below the age of ** years have alarm signals. ;or emample! the British review by Christie et al found that of 31. individuals with gastric cancer! '* presented under the age of **0 of these '*! '4 had one or more suspicious The value of OGD in the management of dyspepsia was recently emamined by Ofman and who undertoo` a systematic review of the literature in an attempt to Änd out whether OGD results in improved outcomes for people with dyspepsia! a reduction in the use of subsefuent medical resources! and$or improved medical decision"ma`ing. They also investigated whether it was cost effective. Twenty"one studies met the inclusion criteria! although they were limited by several factors! including the use of varying tools to measure people¼s response and the difÄculties of comparing studies that did not include H. pylori status with those that did. One RCT showed higher patient satisfaction and lower costs with initial OGD compared with empiric therapy! but no difference in symptoms or fuality of life at one year. The other studies failed to clearly answer the fuestions posed! by failing Barium meal emaminationThis was previously the main method of investigating dyspepsia. >t may still be superior to OGD in the investigation of upper G> motility disorders! particularly in the act of deglutition and in the oesophagus. Otherwise! it should be regarded as a screening investigation if OGD is not available or in certain selected cases eg! dysphagia with normal OGD! or where OGD has failed or is unacceptable to the person. There is evidence that barium meal emamination prior to referral for OGD increases the cost of investigation with no additional beneÄt.3' People with dyspepsiaEmpiric treatment for the remainder of people with dyspepsia will be with either pro`inetic agents or acid inhibition. As most of these people have functional dyspepsia! pro`inetic agents may have some beneÄt. Cisapride 1% mg ta`en before meals and bedtime has most evidence in its support! but recently! identiÄcation of rare but serious cardiological side effects have dampened enthusiasm for its use. Ris`s and beneÄts have to be weighed up in each individual in the light of individual cardiac history and status. A small number of people worldwide have had cardiac arrest on cisapride. Contraindications include concomitant use of potent CYP3A4 inhibitors eg! aoole antifungals! macrolides! H>K protease inhibitors! FT prolongation or conditions leading to FT prolongation eg! bradycardia! hypo`alaemia! medication prolonging FT interval and family history of congenital long FT syndrome.38 ;urthermore! currently cisapride is not funded and Domperidone in the same dose has also been shown to be helpful. Metoclopramide is less favoured because of its potential emtrapyramidal adverse effects! and because no Among acid inhibitors! H RAs are the obvious Ärst choice owing to their reasonable efÄcacy! low incidence of adverse effects! and low cost. PP>s are not recommended as Ärst"choice agents for people with non"speciÄc dyspepsia where heartburn has been emcluded! as they Most studies on therapy have loo`ed at continuous treatment for four wee`s before determining effectiveness! but there are no good data comparing longer or shorter treatment periods or intermittent therapy which is the de facto choice of many people. However! given the preponderance of the four"wee` trial! it seems reasonable to treat for at least There is no recommended duration of a trial of therapy! but three to sim months is reasonable MANAGEMENT O; RECURR>NG UND>;;ERENT>ATED DYSPEPS>A»Treatment failure¼ is difÄcult to deÄne! and no speciÄc evidence could be found about this. Therefore! for the purposes of this guideline! people are deÄned as treatment failures if 1. no improvement or a worsening of symptoms at the end of a four"wee` trial or'. a rapid return of symptoms within a month of cessation of treatment.>t should be noted that good or complete resolution of symptoms! but recurrence after sim People who report only a small improvement! or a recurrence in less than sim months! will People who do not respond to treatment need further evaluation! most often by OGD. Recurrences after sim months or so are empected! given the natural history of the problem! and empiric treatment may be repeated. Some individuals may need regular treatment! but for others! symptoms may be controlled with intermittent treatment. The physician should Studies fuoted in Talley et al! suggest +* – 8* of people with functional dyspepsia will still have symptoms after 1 to 3 years. A 1%"year follow"up study by Aindell et al showed +4 reporting dyspeptic symptoms in the previous year. Notably! there was no increase in numbers of people with peptic ulcer during this 1%"year period compared with the general population of a similar age! and no cases of stomach or oesophageal cancer in '4% for whom records were available from the original sample of ',1. Over +% had had further One concern is that delay in referral for OGD will lead to a worse outloo` for individuals who are eventually diagnosed with gastric cancer which could occur in a management regime of empiric therapy with further investigation restricted to non"responders. However! Martin et al emamined delays in diagnosis of gastric cancer and found no relationship between duration of symptoms and stage of tumour.4% ;urthermore! most people with THE TEST"AND"TREAT STRATEGY/ H. PYAOR> ERAD>CAT>ON >N ;UNCT>ONAA DYSPEPS>AThe role of H. pylori in peptic ulceration and undifferentiated and functional dyspepsia is discussed fully in Chapter 4/ Helicobacter pylori and Peptic Ulceration. >n summary! one of the options in the management of primary"presenting dyspepsia is to test for H. pylori and treat those who are positive. This enables most people with peptic ulcers to be treated! assuming the possibility of NSA>D"related ulcers being emcluded on the history. H. pylori is also a ris` factor for gastric cancer! while ethnic groups with higher prevalence of H. pylori also have a higher incidence of gastric cancer. Treating H. pylori without investigation in these individuals may delay the diagnosis of a tumour! particularly if they have a family history of gastric cancer. Generally! the test"and"treat approach has been shown to be cost"effective! and to reduce the demand for OGD where the prevalence of H. pylori in the population below the age of *% years is reasonably high at least 3%. >n areas where the prevalence of H. pylori is low in the same population eg! in the Dunedin and Christchurch areas! where prevalence at '1 years is 4.1 and 1,.* average in those under beneÄt has not been shown. >n these circumstances! empiric drug treatments are OKERK>EL™ Gastro"oesophageal reÅum disease GORD is a common condition presenting with classic symptoms such as heartburn and acid regurgitation burning feeling rising from the epigastrium into the chest and up towards the nec`! and sometimes with atypical symptoms such as unemplained ™ GORD is present in ,* of those with heartburn.™ Severity of symptoms does not necessarily correlate with endoscopic findings as appromimately *% of people with heartburn have no ™ Symptomatic response and healing are more rapid and complete with ™ PP>s are most effective when ta`en with a glass of water 1* to 3% minutes ™ PP>s and H RAs! given to relieve heartburn! can mas` signs of inÅammation at OGD. Lhen referring for OGD! symptoms can be relieved with ™ The role of OGD is to establish whether any inÅammation is present! determine the degree of inÅammation absent – Grade %! A – D for ™ Grades % – B rarely progress to higher grades.™ Aong"term treatment of grades C and D with PP>s reduces the ris` of ™ >n routine management! pH telemetry is of limited value! but can be used when diagnostic problems arise and in those who fail to respond to ™ Aaparascopic fundoplication is an alternative treatment for people who fail to respond to medical therapy or who refuire long"term treatment for effective control of symptoms. >t is more suitable for younger people ™ heartburn burning sensation radiating from the epigastrium towards the ™ non"cardiac chest pain! asthma! chronic cough! hoarseness of voice and GORD SYMPTOMS >N>T>AA MANAGEMENT L>TH EMP>R>C THERAPY TREATMENT O; GORD D>AGNOSED A;TER OGD >NTRODUCT>ONGORD is a common condition presenting with classic symptoms such as heartburn and acid regurgitation burning feeling rising from the epigastrium into the chest and up towards the nec`! and sometimes with atypical symptoms such as unemplained chest pain! asthma! cough! and hoarseness of the voice. Prevalence and incidence may vary signiÄcantly among different ethnic groups. The effect on fuality of life has been found to be similar ;refuent transient! spontaneous! lower oesophageal sphincter relamation TSAOSR appears to be the primary abnormality in GORD. Contrary to previous assumptions! the mere presence of a hiatus hernia rarely accounts for symptoms! although recent evidence suggests that the perturbed anatomy associated with a hiatus hernia is more li`ely to result in reÅum of acid into the lower oesophagus and this is associated with emacerbation of The prevalence of GORD in New Zealand is similar to that in other OECD countries. At OGD! oesophagitis is demonstrated in about *% of people presenting with typical GORD symptoms. >n people with typical symptoms but no signs of oesophagitis at OGD ™ Treat with a step"down drug regimen see ™ >f symptoms recur at stepped"down dosage! continue on lowest effective ™ Treat with ongoing continuous full"dose PP> treatment. ™ age 1*% years™ age *% years and over and there is no comorbidity™ there is inability or unwillingness to ta`e medications™ there is inadefuate control with medical therapy. A>MS O; MANAGEMENT>n a review Bell et al demonstrated that! although GORD is related to a motor dysfunction allowing gastric content to enter the oesophagus! the severity of disease is correlated with the degree and duration of oesophageal acid emposure. The primary aim of treatment is >n people with more severe grades of GORD! the intra"oesophageal pH was 14 for 3+ of the time as opposed to * of the time in people with mild GORD. ;urthermore! most individuals with mild disease emperience oesophageal acid emposure during the day! mostly in the post"prandial period! related to TSAOSR. >n contrast! individuals with more severe The acid inhibition obtained with conventional doses of H RA cannot overcome the integrated stimuli emperienced during the ingestion of food. The efÄcacy of these drugs is therefore suboptimal in controlling the acid emposure of the oesophagus related to TSAOSR. >n contrast! PP>s offer good acid control over prolonged periods! especially during the day after a pre"brea`fast dose. Using data from people with duodenal ulcer! Bell et al showed that PP>s controlled gastric acid secretion pH 34.% for signiÄcantly longer periods than Bell N?K! Burget D! Howden CL! et al. Appropriate acid suppression for the management of gastro">n the Bell study! there was a correlation coefÄcient of %.8, p1%.%* between the healing rate of erosive oesophagitis at eight wee`s and the duration in hours that the intra"gastric pH was maintained above pH 4.% with any particular class of drug. These correlations! based on indirect observations! have been conÄrmed by a later meta"analysis by Chiba et al '+ These authors analysed results of treatment of endoscopically observed erosive oesophagitis in ,+3* individuals0 oesophagitis was indicated as grade ' in +1.8! grade 3 in 31.,! and grade 4 in +.*. Endoscopically observed healing rates were far superior >N>T>AA MANAGEMENT/ EMP>R>C THERAPYThe presence of alarm symptoms should result in urgent referral for OGD. People with persistent heartburn and no alarm features may be further evaluated with a simple fuestionnaire Appendim A. Although this has been shown to substantially facilitate the Treatment should provide sufÄcient control of symptoms and should also increase health"related fuality of life. This is achieved in the ma_ority of people irrespective of GORD Although the traditional lifestyle measures usually recommended to people with GORD ! such as raising the head of the bed! decreasing fat inta`e to reduce body weight and to prevent delayed gastric emptying! cessation of smo`ing! moderation of alcohol inta`e! and avoiding tight clothing! may have some place in overall management! there are no systematic studies on these treatments! and published data are based on disputable Over"the"counter medication antacids! alginate! H RAs provides effective symptom relief A trial of empiric therapy is _ustiÄed in people aged 1*% years presenting with typical GORD symptoms in the absence of alarm signals.''!33!34 >n ascending order of potency and efÄcacy! the choice of drugs available includes/ antacid $alginate! H RAs single then double dose! both twice daily0 pro`inetics0 PP>s half! standard! double doses and combinations of PP>s and H RAs or pro`inetic agents see Appendim B. Pro`inetics eg! domperidone and cisapride are comparable in efÄcacy with H RAs!3* but cisapride is no longer favoured because of rare but potentially serious adverse effects. >t also refuires specialist >n the Cochrane review! van Pinmteren et al analysed the results of 14 studies involving 4,+4 individuals in short"term ' – 1' wee`s RCTs of individuals treated with PP>s! H or pro`inetic agents. These people did not have any endoscopic information involved in their selection. The endpoints of the studies were often difÄcult to assess! but were deÄned as relief of heartburn to no more than one day of mild heartburn per wee`. The results Kan Pinmteren B! Numans ME! Bonis PA! Aau ?. Short"term treatment with proton pump inhibitors! H'"receptor antagonists and pro`inetics for gastro"oesophageal reÅum disease"li`e symptoms and endoscopy Many studies have demonstrated that PP>s provide more symptom relief and better healing than the other treatments.3%!31!3+"38 Bate et al have even used rapid response to PP> treatment as a diagnostic test for GORD0 good response to PP> empiric therapy has a sensitivity of »STEP"DOLN¼ AND »STEP"UP¼ TREATMENT OPT>ONSThere is a choice between the so"called »step"down¼ and »step"up¼ treatment regimens. The step"down approach! starting with a standard dose of PP> ta`en 1* – 3% minutes before brea`fast with water and then gradually stepping down to less potent drugs! is recommended. Advantages of such an approach include rapid pain relief! ease and efÄciency of prescribing! and avoidance of over"investigation and its costs.3. Disadvantages are that initial drug cost is higher and there is the possibility of some individuals being The main advantage of a step"up regimen is that it avoids initial over"treatment and costs. However! disadvantages include unnecessary ongoing symptoms in about half of those being treated! wasting of doctors¼ and individuals¼ time for repeat visits over a prolonged period! over"investigation for persistent symptoms! and _udgment of the endpoint of PP>s are usually started in conventional doses of omepraoole '% mg! lansopraoole 3% mg and pantopraoole 4% mg daily 1* – 3% minutes before brea`fast with a glass of water. An evening dose before a meal can also be considered in some cases. H RAs are usually prescribed in standard doses twice daily ranitidine 1*%–3%% mg! and famotidine '% 4% mg. The initial treatment trial should cover at least ' – 4 wee`s! but the dosage may be continued for + – 8 wee`s in total before step"down is attempted! according to symptom control. Savary M! Miller G. Der oesophagus! Kerlag Gassman! Soloturn! Switoerland. 1.,8! p13*"4'! as fuoted by Cotton PB! Tytgat GN?! Lilliams CB Eds Annual of Gastrointestinal Endoscopy! Gower Academic Histological emamination of a normal"loo`ing oesophageal mucosa rarely provides further information about the diagnosis and is therefore not currently recommended in routine H. pylori plays no role in GORD and eradication is not recommended for this indication.11!'%!43!44 As noted earlier! treatment is aimed at acid control and not H. PYAOR> AND GORD H. pylori has no `nown role in the cause or direct treatment of GORD! and eradication is A number of studies have indicated that eradication of H. pylori infection may increase the incidence of GORD in people with duodenal ulcers! although this Änding has not been found consistently.+'!+3 Some have observed that oesophagitis in H. pylori"positive patients! heals more rapidly with a PP> than in those who are H. pylori and that H. pylori infection may increase the efÄcacy of PP>s in reducing acid secretion. However! Moayyedi et al ++ have shown in a randomised control trial that H. pylori eradication does not Another consideration involving H. pylori eradication in GORD is whether this results in signiÄcant gastric atrophy! with a potential to develop intestinal metaplasia and possibly gastric cancer after prolonged therapy. There is some evidence to support this progression! +, although this remains controversial owing to other studies not supporting the Ändings. >n a prospective study! Sung et al showed that gastric inÅammation and atrophy could be reduced one year after H. pylori eradication compared to those with continuing infection. This conÄrms the Ändings of a previous study. Aonger study periods are clearly refuired. Chiba N! Hunt R. Gastroesophageal reÅum disease. >n McDonald ?! Burroughs A! ;eagan. Evidence Grades %! A and B rarely progress to higher grades. >n a retrospective analysis of nearly 4%%% individuals! Re_eb et al found that peptic strictures were very rare in the minor grades of oesophagitis! and they suggested that symptomatic treatment is all that is necessary in >n grades % to B! a step"down regimen should be tried! going down to the lowest dose of acid inhibition if any refuired to control symptoms! as on"demand treatment has GRADES C AND DMany studies of individuals with various grades of oesophagitis have been underta`en. The meta"analysis by Chiba et al has already been fuoted see Table 3.3. Although most of the individuals +1.8 were the efuivalent of grade B! 31 were grade C and only +.* were grade D. Some correlation emists between higher grades of GORD C and D and more severe symptoms. Those with these grades of oesophagitis demonstrated at OGD refuire long"term treatment with PP>s. >ndeed! some individuals with grades C and D * – 1% may need full"dose repeated twice"daily maintenance treatment. >n a New Zealand study of +. individuals with oesophageal strictures! Barbeoat et al showed that long"term PP> use reduced the ris` of stricture recurrence. Aong"term treatment with PP>s has been demonstrated to be safe for over 1% years. There is no need for re"OGD in most individuals with well"controlled symptoms. Lhere there is suboptimal! or no response to treatment! alternative PP>s can be tried as differences in metabolic pathways ;or those people who are on high"dose treatment and who do not become asymptomatic! '4"hour pH telemetry should be considered. Repeat OGD may also be an option. The success of pooled 1"year GORD relapses in people with proven erosive oesophagitis grades Chiba N! Hunt R. Gastroesophageal reÅum disease. >n McDonald ?! Burroughs A! ;eagan. Evidence BARRETT¼S OESOPHAGUS This is deÄned as the presence of specialised intestinal epithelium in the lower oesophagus. Barrett¼s oesophagus should be investigated in specialist centres some with surveillance OGD. The biological age of the person and comorbidity will determine frefuency of surveillance! generally at 3 to *"year intervals if the histology does not show any dysplasia! while surveillance is usually stopped at about age ,% years. Protocols for managing epithelial dysplasia in people with Barrett¼s oesophagus are beyond the scope of this guideline. Aong"term treatment with PP>s appears reasonable in people with Barrett¼s oesophagus as this condition represents a complication of severe GORD Grade D.4. OGD surveillance of coincidental normal macroscopic appearance short"segment Barrett¼s RSaRSKOUca and intestinal metaplasia in the area of the gastric cardia is not recommended currently.14!1,!4. New treatment modalities! such as photodynamic eradication or argon plasma coagulation of intestinal metaplasia of the oesophagus! are currently being ;URTHER >NKEST>GAT>ON'4"HOUR PH TEAEMETRY This measures intra"oesophageal pH at two sites using a Äne tube introduced via the nose into the distal oesophagus. The pH is recorded electronically and can be reproduced on a graph using an appropriate computer programme. The '4"hour pH proÄle in the distal oesophagus can be related to pain events mar`ed by the person! who continues normal >nterpretation of '4"hour pH telemetry is difÄcult without a deÄnitive test for the diagnosis of GORD. >t is most reliable in individuals with typical symptoms where it is least needed! but may be of considerable beneÄt when it is clearly positive in individuals with atypical symptoms. A negative test does not necessarily emclude GORD. Previously! measurement of '4"hour oesophageal acidity was considered the gold standard for differentiating individuals with grade"% GORD from individuals with other problems. However! in their technical review of clinical oesophageal pH recordings! @ahrilas and Fuigley found that only about *% of grade % GORD individuals had abnormal acid reÅum! and that some individuals appear to be much more sensitive to normal acid emposure of the lower Thus! measurement of oesophageal acidity reaches a high sensitivity in a selected group those with typical GORD symptoms! but does not reach the sensitivity in Currently! '4"hour pH telemetry should be used to investigate high"dosage treatment failures or to assess individuals with grade"% GORD prior to considering surgery usually People with GORD all grades not responding to high"dosage twice"daily PP>s and with signs of »acid brea`"through¼ particularly at night demonstrated on pH telemetry while on medication! need the mamimum twice"daily dose of PP>s! as well as nocturnal H >n a controlled trial! Peghini et al showed that a bedtime H RA was more effective than a bedtime PP> on residual nocturnal acid secretion in individuals receiving twice"daily PP>s. Additional pro`inetic agents can be recommended for those with symptoms suggesting ReÅum heartburn and regurgitation are relieved in more than .% assessed in follow up over three years. Notably! atypical symptoms cough! asthma! laryngitis are only relieved in two"thirds of people. As with medical therapy! surgery is more successful in the typical! well"deÄned erosive oesophagitis. Surgery does not avoid the cancer ris` or the need for 1. The disease severity! in terms of symptoms and OGD Ändings! is predictive of the long"term prognosis on medical therapy0 GORD grades %! A and B have a good complication"free long"term prognosis! whereas complications may occur in grades '. The recognised complications of uncontrolled reÅum are stricturing! ulceration and intestinal metaplasia. Good drug treatment compliance is essential if these are to be 3. Surgery is more cost effective! and safer! in people of young biological age.4. Comorbidity! such as cardio"pulmonary disease! increases the ris` of surgery. *. Post"operatively! dietary restrictions may be necessary and Åatulence and inability to vomit may be problems. Although dysphagia is usually self"limiting within a few +. Previous abdominal surgery can ma`e laparoscopic surgery difÄcult. ,. The morbidity of surgery must be compared with the `nown side effects of medical therapy. Although long"term PP> is considered safe! most long"term studies only 8. The emperience of the surgeon with this particular operation is a critical factor in the >N>T>AA D>AGNOST>C >NKEST>GAT>ON ;OR H. PYAOR>>N>T>AA TREATMENT O; H. PYAOR> ™ who originate from areas of high 33% ™ with present or past history of peptic ulcer™ with Mucosa"associated lymphoid tissue lymphoma™ with a family history of gastric cancer. ™ Urea breath test UBT is the recommended non"invasive test. Stop ™ Although UBT and faecal antigen tests are also valid options! serology ™ ;aecal antigen test is also recommended! although it is not yet universally ™ >f OGD is being performed for investigation of dyspepsia! consider testing H. PYAOR> TREATMENT ;A>AURECON;>RMAT>ON O; H. PYAOR> ERAD>CAT>ON ™ an alternative triple therapy regimen PP> plus two of the following/ ™ fuadruple therapy standard triple therapy plus bismuth. ™ review compliance factors and consider testing for bacterial resistance™ consider retreatment for ' wee`s. ™ UBT is the recommended non"invasive test serology should not be used ™ ;or people having OGD to chec` for healing of gastric ulcer! conÃrm ™ Perform at least one month after completion of eradication regimen™ ;or people ta`ing PP>s! perform at least one wee` after cessation of PP>. PREKAAENCE O; H. PYAOR> >N;ECT>ONThe mode of transmission of H. pylori infection of the gastric mucosa is uncertain! but there is evidence for spread person"to"person via oral"oral or faecal"oral routes. Aiving conditions are more important than genetic factors in transmission of infection/ the incidence of infection is inversely proportional to socio"economic status and lower household income! and particularly with consefuent overcrowding. Childhood is the period of ma_or ris` for acfuisition of H. pylori infection. The prevalence of infection increases with increasing The infection incidence rates vary around the world! and within New Zealand. >t is more prevalent in poorer regions. Decreasing incidence in OECD countries is believed to be due to improved hygiene! improved childhood nutrition! smaller family sioes! larger time intervals Detailed data relating to prevalence around New Zealand are limited! but Dunedin and Christchurch population"based studies suggest that prevalence in the central and southern Auc`land A study by ;raser et al showed that rates of sero"positivity vary according to age and ethnicity! and that the incidence of infection was not signiÄcantly associated with gender! ;raser AG! Scragg R! Metcalf P! et al. Prevalence of Helicobacter pylori infection in different ethnic Lellington >n an unpublished study! '' of all people presenting for OGD in the Lellington$Hutt Dunedin ;awcett et al! in a longitudinal study! reported that spontaneous reversion of H. pylori sero"prevalence may occur in childhood and adolescence! and that sero"conversion was rare after age 11. The sero"prevalence of this cohort was signiÄcantly lower than that of most Re"bleed withno therapy  There have been three trials comparing eradication of H. pylori and ranitidine maintenance therapy in recurrence of bleeding from a peptic ulcer. They show that eradication therapy  Gastric cancerH. pylori is now recognised as a class > carcinogen by the Lorld Health Organioation. Progression from H. pylori infection to gastric adenocarcinoma appears to be dependent on the interaction between environmental and genetic factors both of the host and the strain of H. pylori! and is currently the topic of intense research. However! not all gastric cancers are associated with H. pylori infection. Lhen ad_usting for the prevalence of H. pylori infection in a population! as well as for the sensitivity and speciÄcity of particular tests! it appears that between 3* OECD countries and +8 non"OECD countries of Overall! New Zealand has a low"to"moderate incidence of gastric cancer! although some areas! such as South Auc`land and the east coast of the North >sland! do have high rates. Males have a greater incidence of gastric cancer than females! and Maori and PaciÄc The prognosis for survival is generally poor. >t is currently recommended that H. pylori infection be treated following resection of early gastric cancer where the prognosis is a little more favourable. Uemera found that % %$+* of individuals developed recurrence of gastric cancer following endoscopic resection and H. pylori eradication compared with . +$+, recurrence rate following endoscopic resection and no H. pylori eradication. However! different forms of early gastric cancer may emist in ?apan! ma`ing interpretation of their research studies difÄcult. There is no evidence that eradication of H. pylori infection reverses atrophic gastritis and prevents the development of gastric adenocarcinoma. >t is not `nown at what point the progression to gastric cancer might be reversed with eradication of H. pylori! and currently there are no established predictors for the development of gastric However! in a further ?apanese study! Uemera et al showed that people with H. pylori and gastric ulcer! severe gastric atrophy! corpus predominant gastritis or intestinal metaplasia were at increased ris` of developing gastric cancer. Those with H. pylori! NUD and hyperplastic polyps were also found to be at increased ris`! but those with duodenal about .% – .*. The yield is improved if multiple biopsies are ta`en from the body and the antrum! although ingestion of PP>s! antimicrobials and bismuth compounds may reduce sensitivity. Histology has similar success! and this can be increased by using special stains. Culture of the organism is not performed routinely! but may be useful where bacterial resistance presents a therapeutic challenge. The bacterium refuires prolonged incubation Tygat GN. AGA Spring Postgraduate Course! San Diego! May '%%%! syllabus! p3%! fuoting Go! Clin >N>T>AA TREATMENT O; H. PYAOR>This relies on triple therapy. Combinations of two antibiotics plus another drug are usually refuired! the choice depending on a number of factors! including penicillin allergy and drug resistance. >n a comprehensive meta"analysis! Aahei_ et al found that regimens containing a PP> and clarithromycin have been shown to be the most effective. Although bismuth is still an effective compound! its popularity has declined because of the greater reliability and shorter course of treatment refuired with other drugs. Ranitidine bismuth citrate is a drug combining ranitidine and bismuth in a novel molecule! but this was not resistance in the place where the study is performed has a signiÄcant impact on eradication rates! as does compliance with triple therapy regimens. Thus! there are problems in applying / P 2 proton pump inhibitor! A 2 amomycillin! C 2 clarithromycin! M 2 metronidaoole! The most effective therapy! which refuires a combination of drugs! is PP>"based triple therapy! in which a PP> omepraoole or pantopraoole or lansopraoole is used in combination An audit of ++* individuals treated in Auc`land over Äve years found that metronidaoole resistance signiÄcantly affected H. pylori eradication for regimens containing metronidaoole without clarithromycin.88 Eradication with metronidaoole without clarithromycin was achieved in .% of metronidaoole"sensitive strains and ** of resistant strains. >n contrast! eradication with metronidaoole combined with clarithromycin was achieved in 8+ of metronidaoole"sensitive strains and ,8 of resistant strains. The authors commented that the clinical implication of the rising rate of metronidaoole resistance in New Zealand is that treatments An audit in Dunedin showed that '% of strains 1%$*% were found to be metronidaoole" RAN>T>D>NE B>SMUTH C>TRATERanitidine bismuth citrate is a new chemical entity! which incorporates bismuth into the ranitidine molecule! but is not available in New Zealand. >t appears to act synergistically in combination with other antimicrobials against metronidaoole" and clarithromycin"resistant >; >N>T>AA TREATMENT ;A>ASAn alternative triple therapy regimen can be used in the Ärst instance. >f triple therapy should fail to achieve eradication! fuadruple therapy is recommended for seven days. ™ PP> omepraoole '% mg or lansopraoole 3% mg or pantopraoole 4% mg twice daily™ Tetracycline HCl *%% mg fid™ Metronidaoole 4%% mg twice daily or tds or fid ™ Colloidal bismuth subcitrate 1'% mg fid An alternative is standard triple therapy with PP>! clarithromycin! amomycillin or metronidaoole Testing for antibiotic sensitivities is recommended with failure of two or more regimens if CON;>RMAT>ON O; ERAD>CAT>ONThere are no randomised controlled trials comparing outcomes with and without et al and Graham et al recommend conÄrmation of cure of H. pylori infection with However! a decision analysis performed by Gene et al concluded that in healthy people with uncomplicated duodenal ulcer! post"treatment UBT after H. pylori eradication therapy mar`edly increased costs! with no signiÄcant improvement in outcomes..4 The authors suggested that post"therapy urea breath testing should be reserved for those with symptom recurrence! complicated duodenal ulcers! comorbidity and gastric ulcers. Those living in places where treatment facilities are difÄcult to access might also be considered MANAGEMENT O; H. PYAOR>"NEGAT>KE PEPT>C UACERS H. pylori"negative peptic ulcers that are associated with NSA>D use! see Chapter */ H. pylori"negative peptic ulcers not associated with NSA>D use! acid suppression is Burget et al reported the Ändings of a wor`shop investigating duodenal ulcers healing relative to gastric acid suppression. >n their meta"analysis! 1. drug regimens used in '' studies provided data on duodenal ulcers healing at various endoscopic endpoints and compared these with data on acid suppression. There was a highly signiÄcant correlation >NTRODUCT>ONNSA>Ds! which can be purchased without prescription! are pharmacological agents very commonly used for the relief of pain! and as anti"inÅammatory compounds to reduce inÅammation in arthritis. Another property of NSA>Ds especially aspirin is to reduce platelet stic`iness and the ris` of thrombosis! particularly in the coronary and cerebral vasculature! Unfortunately! prostaglandins are an important component of systems responsible for maintaining normal G> mucosal function. NSA>Ds inhibit cycloomygenase COM enoymes! which are refuired to convert arachidonic acid to prostaglandins. There are two COM isoforms/ COM"1 maintains normal G> mucosal function! and COM"' is induced and related to inÅammation. Analgesic and anti"inÅammatory activity is related to COM"' inhibition. The action of COM enoymes on platelets is mediated via COM"1. Most NSA>Ds including aspirin inhibit both COM"1 and COM"' isoforms. Since the mid"1..%s! drugs have become available the comib group that are COM"' selective! and therefore have less adverse effects in the G> tract. However! ta`ing COM"' selective NSA>Ds with aspirin negates the selective NSA>Ds act primarily by the systemic route! although local concentrations can be increased even further when the drugs are ta`en orally. People are at ris` of adverse effects whether the drugs are ta`en orally! parenterally or as suppositories. Gastric mucosal prostaglandins THE R>S@S O; NSA>DSThere are generally three levels of adverse effects with NSA>Ds. The Ärst includes dyspepsia symptoms! the second! the development of intestinal mucosal abnormalities including peptic ulceration! and the third! ulcer complications predominantly bleeding and perforation. Unfortunately! ulcers and$or their complications are not necessarily preceded by dyspepsia >n '%%%! PHARMAC paid subsidies of ,3'!'3' on NSA>Ds prescriptions in New Zealand! RECOMMENDAT>ONS ontinued.. The choice of which NSA>D to use is important. Henry et al conducted a collaborative meta"analysis of variability of ris`s of G> complications for a range of NSA>Ds using ibuprofen as a reference. They found that ibuprofen is associated with the lowest relative ris` of severe G> tomicity! but that there is a positive dose"tomicity relationship with all NSA>Ds! The authors suggest that it cannot be assumed that the apparent advantage of ibuprofen emists when the dosage is increased beyond 1+%% mg daily. Unfortunately! NSA>Ds with a / Henry D! Aim AAY! Rodrigueo AAG! et al. Kariability in ris` of G> complications with individual NSA>Ds/ The incidence of untoward events and the degree of anti"inÅammatory activity for aspirin and non"aspirin NSA>Ds are both dose"related.'' Many studies have reported that decreasing the daily dose of aspirin also decreases the ris` of G> complications. Nevertheless! any dose of aspirin has the potential to induce gastric lesions and G> complications! even COM"' SEAECT>KE NSA>DSThe prediction that COM"' selective agents would have fewer adverse effects on the G> tract than non"selective NSA>Ds has generally been supported in the literature. >n the Bombardier review a meta"analysis by Aangman et al was conducted of perforations! ulcers and bleeds PUBs of all rofecomib RCTs/ *43* individuals mean age +3! range 38 – .4 years were included. PUBs over 4 months were identical for rofecomib and placebo groups but the cumulative incidence of PUBs over 1' months for rofecomib was half that The gastro"duodenal adverse effects of NSA>Ds can be minimised by the simultaneous ingestion of a PP> at least for the prevention of the development of peptic ulcers. >n an RCT! Chan et al investigated the efÄcacy of diclofenac and omepraoole compared to celecomib in preventing re"bleeding of peptic ulcers in patients with arthritis. >nterestingly! the probability of recurrent bleeding over + months for those on celecomib was 4.. .* C> 3.1 – +., and +.4 .* C> 4.3 – 8.4 for those on the PP>"NSA>D combination! which was not statistically signiÄcant. Real adverse events were recorded in '4.3 of patients on celecomib and 3%.8 of those on combination therapy. These complications are therefore common in this particular group of patients. This prompted an editorial suggesting that Pandora¼s bom had been opened and that a false sense of security engendered by the ADKERSE E;;ECTS O; COM"' AGENTSAdverse events of COM"' selective agents include epigastric discomfort *.+! heartburn *! nausea '"8 and diarrhoea 4"1'. These rates do not differ from ordinary NSA>Ds. Renal function may also be affected adversely including Åuid retention. Rash! bronchospasm and rarely angio"oedema have been recorded.3!',!38 >nteraction between rofecomib and warfarin has been reported! and although this was originally thought not to be of clinical reports have been received of very signiÄcant interactions of both rofecomib and also been recorded following ingestion of celecomib and rofecomib. >n a post"mar`eting survey! celecomib was associated with oedema in '.1 of patients! hypertension in %.8 and emacerbation of pre"emisting hypertension in %.+! a proÄle similar to that seen with non" The fuestion of predisposition to myocardial infarction in patients on the COM"' agents was raised in the K>GOR study %.4 with rofecomib vs %.1 with napromen over . months.33 This could be a result of loss of anti"platelet activity with COM"' selective drugs but other mechanisms have been postulated. The CAASS study did not show any such effect but '1 of patients were ta`ing aspirin while the beneÄts of the COM"' agents over 1' months is still in some dispute. Subsefuent studies recorded no increase in thromboembolic events with either celecomib43 or rofecomib.44 The debate about the safety of COM"' agents is LHEN SHOUAD LE USE COM"' AGENTS4The answer to this fuestion is still being developed! but a number of important factors ™ COM"' agents are most beneÄcial in high"ris` patients see Table *.3! and of ™ Overall adverse effect proÄle in non"G> areas are at least similar to other NSA>Ds.™ Selective COM"' effect is largely negated by simultaneous use of aspirin! and care ™ COM"' agents do not offer signiÄcant protection against upper G> haemorrhage in ™ COM"' agents are not yet funded in New Zealand and cost up to ten times more ™ Alternative protection against NSA>D"adverse effects is available in the form of co" To date there is no evidence to support the co"prescription of gastro"protective agents PP> Celecomib Upper G> ulcer complications0 annualioed incidence rate  Upper G> ulcer complications symptomatic ulcers0 annualioed incidence rate  Upper G> ulcer complications0 annualioed incidence rate  Upper G> ulcer complications symptomatic ulcers0 annualioed incidence rate  Lithdrawals due to adverse effects  Study properties Multicentre US! double"blind! RCT0 n 2 8%*.! with either OA or RA! '% on aspirin! ;or a critifue of these data! see ?uni P! Rut_es ALS! Dieppe PA. Are selective COM ' inhibitors superior to traditional nonsteroidal anti"inÅammatory drugs4 Adefuate analysis of the CAASS trial indicates this may Source Silverstein ;E! et al. Gastrointestinal tomicity with celecomib vs nonsteroidal anti"inÅammatory drugs for osteoarthritis and rheumatoid arthritis/ the CAASS study/ a randomioed controlled trial. ?AMA PP>s signiÄcantly reduced the ris` of both duodenal and gastric ulcers! with results being similar for both primary and secondary prophylamis trials.1% Although NSA>D"induced ulcers are effectively prevented by co"prescription of PP>s! evidence is only available to demonstrate / Meta"analysis of 33 RCTs0 adults refuiring 33 w` duration NSA>D drugs0 primary and secondary / Rostom A! Lells G! Tugwell P! et al. Prevention of NSA>D induced gastro"duodenal ulcers Cochrane Overall! it has been found that H RAs and PP>s are better tolerated than misoprostol! and reduce NSA>D"related dyspeptic symptoms.1% However! PP>s are recommended over H RAs No economic or therapeutic advantages have been shown in using double doses of H RAs! rather than standard doses of PP>s which provide more potent and reliable acid inhibition see Table 3.1.'. ;urthermore! although the meta"analysis by @och demonstrates that RAs in standard doses afford some protection against NSA>D"related duodenal ulcers! they are not effective in preventing gastric ulcers. As these are more commonly related to NSA>D use than duodenal ulcers! standard doses of H RAs cannot be recommended for Misoprostol is the only prophylactic agent to date that has been evaluated in a true clinical outcome trial with NSA>Ds in standard dose The PP> lansopraoole has been shown to Misoprostol 8%% mcg$day is more effective at reducing gastric ulcers than 4%% mcg$day. Although it is associated with statistically signiÄcant adverse effects! which are more common at higher doses! the evidence for the effectiveness of low doses 4%% mcg$day in the reduction of clinical ulcer complications is controversial.'. Diarrhoea in . – 13 of individuals and abdominal cramps may limit compliance with misoprostol but these are often transient and may be reduced by starting with a low dose.*!, Additionally! misoprostol  RCT! double"blind! in two phases0 .3 centres in 14 countries Europe! Scandinavia! North America0 n2.3*!  RCT! double"blind! in two phases0 ,3 centres in 1* countries Europe! Scandinavia! Canada0 n2*41! aged Although omepraoole has been shown to heal both gastric and duodenal ulcers irrespective of continued NSA>D use! caution should be emercised in emtrapolating these results to people presenting with NSA>D"induced upper G> haemorrhage because safety and efÄcacy have ;ewer people remaining on NSA>Ds relapse on misoprostol than on omepraoole or placebo! The appropriate choice of therapy for secondary prophylamis against NSA>D"related ulcer recurrence among chronic NSA>D users is problematic. Currently! the only agent with proven efÄcacy for the primary prevention of NSA>D ulcers is misoprostol! which is also the only agent that has been of proven beneÄt in the primary prevention of NSA>D"induced clinical events. However! although there is an absence of evidence for the effectiveness of PP>s protecting against clinically important primary G> events bleeding! perforation! pyloric stenosis! omepraoole has been found to be successful in healing NSA>D"induced gastric and duodenal ulcers and lesions. >t is reasonable to empect that peptic ulcer The cost"effectiveness of PP>s for the primary or secondary prophylamis against NSA>D induced upper G> tomicity has not been clearly established.'. Adverse effects with misoprostol have distracted signiÄcantly from routine use of this drug! and its use is also restricted to Care ;acilities Provider Organisations and Professional Bodies™ Primary Health Organisations™ >ndependent Practitioners Associations >PAs™ Academic lecturers! curriculum planners involved in medical training™ Medical colleges™ Professional bodies™ PHARMACOther Agencies Commercial Organisations ™ Providers of medications discussed or recommended in the guidelineDevelopment of Performance >ndicators™ Primary Health Organisations are to be encouraged to identify appropriate clinical EKENTS! PRESENTAT>ON AND TRA>N>NGThe guideline should be presented to health care practitioners to familiarise them with the recommendations. They should be presented at ma_or meetings or small education groups included in postgraduate medical education. This process has already been initiated during the development phase of the guideline. >t is anticipated that members of the Lor`ing Party National Aevel™ ;ormal endorsement and presentation at general practitioner and specialty and sub" ™ Educational seminars and wor`shops for practitioners and >PAs™ SpeciÄc educational initiatives for particular interest groups! including general practitioners and pharmacists eg! develop a tool`it for pharmacy facilitators and ™ Aiaison with bodies controlling funding and resources to ensure that district health ™ Corrective measures need to be ta`en to ensure that rural areas have access to appropriate investigation and treatment. Representatives of rural communities ™ @ey recommendations may be promoted by groups such as Best Practice Advocacy NZ ™ Conferences/ – The Combined NZ Rural General Practice Networ`  Rural Nurse National Networ` Conference! April – College of General Practitioners¼ Conference! ?uly! Lellington – General practitioner CME Meeting! ?uly – National Gastroenterology Conference! NovemberAocal Aevel™ Aocal CME activities can include this guideline as part of their programmes™ Aocal general practitioners and specialists should meet to discuss speciÄcally referral ™ >PA pharmacists can play a very important role in prescriber education and in PublicityThe guideline needs to be publicised in the media! including the local medical press. This has already been initiated via certain professional group meetings eg! general practitioners! ™ _ournals and health professional publications! including the New Zealand Medical ™ a well"publicised formal launch of the guideline and a planned seminar programme. This should inform health care practitioners! not only of the contents of the guideline ™ public education to ensure that there is widespread and realistic understanding of radio and television interviews! which can be conducted by members of the Lor`ing Party. Care needs to be ta`en to ensure that public empectation and reality are well balanced.ACCESS TO OESOPHAGO"GASTRO"DUODENOSCOPYThe guideline aims to ensure that people are referred appropriately and that those referred for OGD are those most li`ely to beneÄt from it. >t is not envisaged that the guideline should greatly increase the demand for this procedure. However! current access to OGD is poor in certain parts of the country and this will need to be addressed by the Ministry of Health. People emperiencing dyspepsia and heartburn have an interest in the fuality of care and management of dyspepsia and heartburn. This places a responsibility on service providers to collect information relevant to the Numbers of referrals! fuality of referrals Access to the guideline! use and practicality of the guideline! efÄcacy Monitoring or auditing of/ – use of PP>s and other treatments recommended in this guideline – use of medications! especially the step"down process with acid lowering agents – use of maintenance therapy – – numbers of patients referred for investigation especially OGD. Recommendations for treatment could be audited in OGD reports Primary Care Organisations >PAs! PHOs! M~ori  PaciÃc Health Care Measurement of practice patterns! referral patterns! national Prescribing by general practitioners " may be able to lin` with General Prescribing patterns at the national level – Drugs for G> ulcer and other gastric conditions should be monitored – >nformation on access to OGD services should be recorded – Recommendations for treatment in patient discharge letters and in procedure OGD reports could be monitored or audited – The appropriatementss of stepdown or maintenance regimens should be emplicit – Numbers of patients referred for OGD should be monitored.>deally! a formal evaluation of the implementation of the Guideline recommendations could ™ practical usefulness™ acceptability of recommendations to/ – patients – medical practitioners – pharmacists – other health care professionals.™ areas where empansion is refuired™ areas needing updating of information™ difÄculties or improvements with access to procedures or treatments™ cost savings or changes in costs of treatments.During this year! a Group should be nominated to ta`e up the recommendations of the FUEST>ONNA>RE ;OR PEOPAE L>TH GASTRO"OESOPHAGEAA RE;AUM D>SEASEThis standardised fuestionnaire for people with gastro"oesophageal reÅum disease GORD 1. Lhich one of these four statements BEST DESCR>BES the main discomfort you get in '. Having chosen one of the above! please now chose which one of the nemt three 3. How do the following affect your main discomfort4 Lorsens >mproves No effect$unsure Aarger than usual meal ;ood rich in fat Strongly Åavoured or spicy food 4. Lhich one of the following BEST DESCR>BES the effect of indigestion medicines on *. Lhich one of the following BEST DESCR>BES the effect of lying Åat! stooping or +. Lhich one of the following BEST DESCR>BES the effect of lifting or straining or any ,. >f food or acid tasting lifuid returns to your throat or mouth what effect does it have RECOMMENDED MED>CAT>ON ;OR HEARTBURN AND$OR DYSPEPS>AProton pump inhibitors "receptor antagonists 3%% mg nocte Pro`inetic agents H. pylori eradication therapy ™ unemplained weight loss™ food bloc`ing when swallowing™ vomiting of blood or coffee ground"li`e material™ passage of blac` bowel motions ™ when symptoms are associated with ta`ing NSA>DS.All symptoms should be regarded as more serious in people who are aged greater than *% years when presenting for the Ärst time! and those with a family history of stomach LHAT CAN MY DOCTOR DO4He$she will assess your symptoms in the light of your medical history and decide an 1. Giving lifestyle advice/ attention to diet! eating habits! weight! smo`ing! alcohol inta`e! and psychosocial stresses. Some people ta`ing medications which can cause '. Prescribing simple antacids or acid lowering medications for a short course of 3. Test for the bacteria Helicobactor pylori. This germ may be lin`ed to peptic ulceration and can be detected by simple tests. Testing for H. pylori and treating people who have a positive test can be useful in areas and groups where the germ is common! eg! South and Lest Auc`land! Maori! Polynesian and Asian populations. Blood tests are inempensive! but have variable reliability. ;aeces tests are very good! and the H. pylori needs to be treated with an acid lowering agent and two antibiotics for one wee` if the test is positive. >nstructions for treatment must be followed closely to avoid 4. Motility modifying agents include domperidone Motilium or metoclopramide *. Prescribing acid lowering agents. These include ranitidine eg! Zantac and famotidine eg! Pepsidine which are mild in their effect and omepraoole Aosec or pantopraoole Somac which are very potent. These will be prescribed initially for a deÄned period eg! one month. These are the drugs of choice in heartburn but may also be effective Pharmaceutical Management Agency The government¼s drug"purchasing agency. Per protocol Proton Pump >nhibitors Perforation! Ulceration! Bleeding Rheumatoid arthritis Randomised controlled trial Relative ris` The ratio of the ris` of disease or death among those emposed to the ris` among the unemposed also called the »ris` ratio¼. >f the RR 3 1.% this suggests the emposure is harmful the ris` of disease or death is higher in the emposed group. >f the RR 1 1.% this suggests the emposure is protective. Relative Ris` Reduction The adverse event rate in the placebo group P minus the adverse event rate in the active treatment group A! divided by the adverse event rate in the placebo group. RRR 2 P"A $ P. The RRR gives the proportion of adverse events occurring without treatment! which could be avoided by active treatment. Transient! spontaneous! lower oesophageal sphincter relamation Urea breath test CHAPTER 1/ BAC@GROUND1. ?ones R! Aydeard S. Prevalence of symptoms of dyspepsia in the community. '. Colin"?ames DG! Bloom B! Bodemar G 3. Dent ?! Brun ?! ;endric` 4. Cohen S! Par`man HP. Heartburn¸a serious symptom. N Engl ? Med *. Hession PT! Malagelada ?"R. Review article/ The initial management of +. Heading RC! Lager E! Tooley P?. Reliability of symptom assessment in ,. Hafue M! Lyeth ?L! Stace NH! 8. @nill"?ones RP. Geographical differences in the prevalence of dyspepsia. .. Rabenec` A! Lray NP! Graham DY. Managing Dyspepsia/ Lhat Do Le @now 1%. Aoc`e GR. Prevalence! incidence and natural history of dyspepsia and functional 11. ;raser AG! Scragg R! Metcalf P! 1'. Aydeard S! ?ones R. ;actors affecting the decision to consult with dyspepsia/ 13. Masterman A! ;arrington M. National Sentinel Clinical Audit Pro_ect 14. McAvoy B! Davis P! Raymont A! Gribben B. The Lai`ato Medical Care 1*. Richter ?E. Stress and psychologic and environmental factors in functional 1+. Talley N?! Leaver AA! Zinsmeister AR. >mpact of functional dyspepsia on fuality 1,. Dimenas E! Glise H! Hallerbac` B! 18. Haug TT! Sveba` S! Lilhelmsen >! 1.. Meineche"Schmidt K! Talley N?! Pap A! '%. Goves ?! Oldring ?@! @err D! '1. Enc` P! Dubois D! Marfuis P! ''. @aplan"Machlis B! Speigler GE! Revichi DA. Health"related fuality of life in '3. Dent ?! Brun ?! ;endric` A! '4. Galmiche ?P! Bruley DK. Symptoms and disease severity in gastro"oesophageal '*. ?ones RH! Hungin APS! Phillips ?! primary care in Europe/ clinical presentation and endoscopic Ändings. Eur ? '+. Ollyo ?B! Monnier P! ;ontolliet C. The natural history! prevalence and incidence ',. Ben Re_eb M! Bouch‚ O! Zeitoun P. Study of 4, consecutive patients with peptic '8. @urata ?H! Nogawa AN. Meta"analysis of ris` factors for peptic ulcer. ? Clin '.. Haw`ey C?. Nonsteroidal anti"inÅammatory drug gastropathy. Gastroenterology 3%. Hansson A"E! Nyren O! Hsing AL! 31. Pinn G. *%. Talley N?! Zinsmeister AR! Schlec` CD! Melton A?. Dyspepsia and dyspepsia *1. Martin >G! Young S! Sue"Aing H! ?ohnston D. Delays in the diagnosis of *'. Nyren O! Adami H"O! Gustavsson S! *3. Nyren O! Adami H"O! Gustavsson S! *4. Bytoer P! Hansen ?M! Schaffalits`y de Muc`adell OB. Empirical H **. PHARMAC. Annual Review. PHARMAC! Lellington! '%%'! p1*.CHAPTER '/ UND>;;ERENT>ATED DYSPEPS>A 1. Delaney BC! >nnes MA! Dee`s ?! '. American Gastroenterological Association. American Gastroenterological 3. Talley N?! Silverstein MD! Agreus A! 4. Talley N?! Amon A! Bytoer P! *. Soo S! Moayyedi P! Dee`s ?! +. Moayyedi P! Soo S! Dee`s ?! ,. Aaine A! Schoenfeld P! ;ennerty MB. Therapy for 8. ;inney ?S! @innersley N! Hughes M! .. Keldhuyoen van Zanten S! ?ones ?O! Kerlinden M! Talley N?. EfÄcacy of ',. New Zealand Health >nformation Service. '8. Guilford P! Hop`ins ?! Harraway ?! '.. Bodger @! Daly M?! Heatley RK. Prescribing patterns for dyspepsia in primary 3%. Christie ?! Shepherd NA! Codling BL! Kalori RM. Gastric cancer below the age 31. Ofman ??! Rabenec` A. The effectiveness of endoscopy in the management of 3'. Aongstreth G;! Aongterm costs of the gastroenterology consultation with endoscopy versus radiography in dyspepsia! Gastrointest Endosc 1..'038/'3–+.33. Pappa @A! Gooch LM! Buaron @! 34. Pappa @A! Lilliams BO! Payne ?E! 3*. Pappa @A! Buaron @! Payne ?E! 3+. Mearin ;! Balboa A! Zarate N! 3,. >senberg ?>! Peterson LA! Elashoff ?D 38. New Ethical Catalog. Nov '%%'–May '%%3! Adis >nternational! Auc`land! 3.. Aindell GH! Celebioglu ;! Graffner HO. Non"ulcer dyspepsia in the long"term 4%. Martin >G! Young S! Sue"Aing H! ?ohnston D. Delays in the diagnosis of 41. Sung ??Y! Aao! LC! Aai MS! 4'. ;awcett ?P! Shaw ?P! Coc`burn M! 43 ;awcett ?P! Shaw ?P! Broo`e M! 44 Talley N?. Dyspepsia management in the millenium/ The death of test and treat4 4* Richter ?E. Dyspepsia/ organic causes and differential characteristics from CHAPTER 3/ GORD1. Ahu_a K! Yencha ML! Aassen A;. Head and nec` manifestations of '. @ato PO. Chest pain of esophageal origin. Current Opinion in Gastroenterology 3. >rwin RS! Zawachi ?@. Accurately diagnosing and successfully treating chronic 4. Theodoropoulos D! Aoc`ey R;! Boyce HL ?r! Bu`anto SC. Gastroesophageal *. Ho @Y! @ang ?Y! Seow A. Prevalence of gastrointestinal symptoms in a multiracial Asian population with particular reference to reÅum"li`e symptoms. +. Aoc`e GR! Talley N?! ;ett S! ,. Enc` P! Dubois D! Marfuis P! 8. @aplan"Machlis B! Speigler GE! Revichi DA. Health"related fuality of life in .. Galmiche?"P! Bruley DK. Symptoms and disease severity in gastro"oesophageal 1%. @ahrilas P?! Shi G! Man`a M! ?oehl R?. >ncreased frefuency of transient lower 11. Dent ?! Brun ?! ;endric` A! 1'. DeKault @R! Castell DO! et al. Updated guidelines for the diagnosis and treatment of gastroesophageal reÅum disease. Am ? Gastroenterol 1...0.4/1434–4'. '8. Aoc`e GR! Talley N?! Leaver AA! Zinsmeister AR. A new fuestionnaire for '.. Bardhan @D! Cherian P! Kaishnavi A! 3%. @romer L! Horbach S! Auhmann R. Relative efÄcacies of gastric proton pump 31. Sandmar` S! Carlsson R! ;ausa O! 3'. De Meester TR! Lang C>! Lernly ?A! 33. ;ass R! Ofman ??! Gralne` >M 34. Sonnenberg A! Delco ;! El"Serag HB. Empirical therapy versus diagnostic tests in 3*. Arvanita`is C! Ni`opoulos A! Theoharidis A! 3+. Bate CM! Riley SA! Chapman RL! 3,. Crawley ?A. Cost effectiveness of treatment for gastro"oesophageal reÅum 38. Heudebert GR! Mar`s R! Lilcom CM! Centor RM. Choice of long"term strategy 3.. >nadomi ?M! ?amal ?! Murata GH! 4%. Carlsson R! Galmiche ?P! Dent ?! 41. @usano M! >no @! Yamada T! *8. Laring ?P! Hunter ?G! Oddsdottir M! *.. Bowrey D?! Peters ?H. Aaparoscopic esophageal surgery. Surg Clin North Am +%. Aabeno ?! Blum AA! Beyerdorffer +'. Ka`il N! Hahn B! McSorley D. Recurrent symptoms and gastro"oesophageal +3. McColl @E! Dic`son A! El"Nu_umi A! El"Omar E! @elman A. Symptomatic beneÄt +4. Holtmann G! Cain C! Malfertheiner P. Gastric +*. Aabeno ?! Tillenburg B! Peito U ++. Moayyedi P! Bardhan C! Young A +,. @uipers E?! Aundell A! @lin`enberg"@nol EC +8. Aundell A! Dalenbac` ?! Hattleba`` ? ,%. van der Hulst RLM! van der Ende A! De``er ;L ,1. Ka`il NB Aliment Review article/ gastro"oesophageal reÅum disease and CHAPTER 4/ H. PYAOR> AND PEPT>C UACERAT>ON1. Borody T?! George AA! Brandl S! '. @uipers E?! Thi_s ?C! ;esten HP. The prevalence of 3. Marshall B?! Larren ?R. UnidentiÄed curved bacilli in the stomach of patients 4. Nomura A! Stemmermann GN! Chyou P"H! *. Larren ?R! Marshall B?. UnidentiÄed curved bacilli on gastric epithelium in +. Tytgat GN?! Aee A! Graham DY! ,. Ciociola AA! McSorley D?! Turner @! 8. Henry A! Batey RG. Aow prevalence of .. Moayyedi P! Soo S! Dee`s ?! 1%. Aaine A! Schoenfeld P! ;ennerty MB. Therapy for 11. Howden CL. ;or what conditions is there evidence"based _ustiÄcation for 1'. ;iedore` SC! Malaty HM! Evans DA! 13. Graham DY! Malaty HM! Evans D? ?r! 14. Malaty HM! Graham DY. >mportance of childhood socioeconomic status on the 1*. Malaty HM! Graham DY! >sa`sson >! 1+. Malaty HM! Graham DY! Lattigney LA! 34. Parsonnet ?! Hansen S! Rodrigueo A! 3*. Parsonnet ?. 3+. ?yotheeswaran S! Shah A! ?in H! patients in greater Rochester! NY/ is empirical therapy _ustiÄed4 Am ? 3,. @atelaris PH! Adamthwaite D! Midolo P! 38. Hop`ins R?! Girardi AS! Turney EA. Relationship between 3.. Aam S@! Talley N?. Report on the 1.., Asia PaciÄc conference on the 4%. Thi_s ?C! @uipers E?! Kan Zwet AA! 41. Bayerdorffer E! Miehl`e S! Aehn N! 4'. Aabeno ?! Borsch G. Evidence for the essential role of 43. Borody T?! Brandl S! Andrews P! 44. Graham DY! Hepps @S! Ramireo ;C! et al. Treatment of H. pylori reduces the rate of rebleeding in peptic ulcer disease. Scand ? Gastroenterol 1..30'8/.3.–4'.4*. ?aspersen D! @oerner T! Schorr L! 4+. ?aspersen D! @oerner T! Schorr L! 4,. Macri G! Milani S! Surrenti E! 48. Ro``as T! @arameris A! Maurogeorgis A! 4.. 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