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Evaluation and management of dyspepia

Bazaldua, Oralia V; Schneider, F David. American Family Physician 60.6 (Oct 15, 1999): 1773-84, 1787-8.

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Abstrak
Dyspepsia, often defined as chronic or recurrent discomfort centered in the upper abdomen, can be caused by a variety of conditions. Common etiologies include peptic ulcers and gastroesophageal reflux. Serious causes, such as gastric and pancreatic cancers, are rare but must also be considered. Symptoms of possible causes often overlap, which can make initial diagnosis difficult. In many patients, a definite cause is never established. The initial evaluation of patients with dyspepsia includes a thorough history and physical examination, with special attention given to elements that suggest the presence of serious disease. Endoscopy should be performed promptly in patients who have "alarm symptoms" such as melena or anorexia. Optimal management remains controversial in young patients who do not have alarm symptoms. Although management should be individualized, a cost-effective initial approach is to test for Helicobacter pylori and treat the infection if the test is positive. If the H. pylori test is negative, empiric therapy with a gastric acid suppressant or prokinetic agent is recommended. If symptoms persist or recur after six to eight weeks of empiric therapy, endoscopy should be performed.

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Teks Lengkap
Headnote Dyspepsia, often defined as chronic or recurrent discomfort centered in the upper abdomen, can be caused by a variety of conditions. Common etiologiesinclude peptic ulcers and gastroesophageal reflux. Serious causes, such as gastric and pancreatic cancers, are rare but must also be considered. Symptoms of possible causes often overlap, which can make initial diagnosis difficult. In many patients, a definite cause is never established. The initial evaluation of patients with dyspepsiaincludes a thorough history and physical examination, with special attention given to elements that suggest the presence of serious disease. Endoscopy should be performed promptly in patients who have "alarm symptoms" such as melena or anorexia. Optimal management remains controversial in young patients who do not have alarm symptoms. Although management should be individualized, a cost-effective initial approach is to test for Helicobacter pylori and treat the infection if the test is positive. If the H. pylori test is negative, empiric therapy with a gastric acid suppressant or prokinetic agent is recommended. If symptoms persist or recur after six to eight weeks of empiric therapy, endoscopy should be performed. (Am Fam Physician 1999;60:1773-88.) Dyspepsiais upper abdominal pain or discomfort that is episodic or persistent and often associated with belching, bloating, heartburn, nausea or vomiting.1 The condition is reported

to occur in approximately 25 percent (range: 13 to 40 percent) of the population each year, but most affected persons do not seek medical care.2,3 Nonetheless, dyspepsiais responsible for substantial health care costs (medications and diagnostic evaluations) and considerable time lost from work Even though dyspepsiais a highly prevalent condition, no definitive studies have as yet established guidelines for the work-up of dyspeptic patients in the primary care setting. It is well accepted that patients with peptic ulcer disease associated with Helicobacter pylori infection should be treated with antibiotics to eradicate the organism.4 However, this implies that a diagnosis of ulcer and H. pylori infection has been confirmed. The approach to previously uninvestigated dyspepsiais more difficult. It includes differentiating the cause of dyspepsia, selecting among the available options for initial management and distinguishing between patients who require endoscopy and those who can safely receive empiric drug therapy. The challenge is further increased by the controversy surrounding the role of H. pylori in nonulcer dyspepsia.5,6 Differential Diagnosis Because the differential diagnosis of dyspepsiais broad, initial efforts should be focused on the most common etiologies(Table 1).7,11 In about 50 to 60 percent of patients, a specific etiologyis not identified (i.e., "functional" or nonulcer dyspepsia).7,9,10 Many of these patients are hypothesized to have an augmented perception of visceral pain.8 Structural conditions commonly associated with dyspepsiainclude peptic ulcers and gastroesophageal reflux disease (GERD). Gastric or esophageal cancers are serious causes but account for fewer than 2 percent of cases.7,11 History A thorough history is important in evaluating the patient with dyspepsia, although symptoms alone may not be very useful in establishing a specific diagnosis. One group of investigators found extensive symptom overlap when they attempted to categorize patients into diagnostic groups, which included ulcer-like, dysmotility-like, reflux-- like and unspecified dyspepsia.12 Reflux-like symptoms may be of greater diagnostic value in that symptoms alone can reasonably identify the presence of GERD.6,13 However, symptom identification is only a small part of the full clinical evaluation of dyspepsia. Questions that may be useful in identifying other causes of dyspepsia-like symptoms are presented in Table 2. PEPTIC ULCER DISEASE Patients who present with dyspepsiashould be asked about risk factors associated with peptic ulcers. If a patient has a history of ulcers, a recurrent lesion is likely.' Risk factors for ulcers include a family history of ulcers,'- a history of nonsteroidal antiinflammatory drug (NSAID) use" and current cigarette smoking. 16-18 GASTROESOPHAGEAL REFLUX DISEASE Reflux-like dyspepsia, or GERD, can be distinguished from other gastrointestinal disorders with reasonable accuracy on the basis of symptoms.6, 13 The two symptoms that define this disorder are heartburn and regurgitation.1 The epigastric burning sometimes radiates to the throat and worsens when a patient eats, bends down or lies flat.19 Esophageal spasm from

gastroesophageal reflux is characterized by sharp, stabbing substernal pain. Heartburn and esophageal reflux and spasm commonly occur at night or after the consumption of a large meal. If the diagnosis of GERD is uncertain, intraesophageal pH monitoring may help in separating the disease from other causes of dyspepsia.7,13 GASTROPARESIS Dysmotility-like dyspepsia, or gastroparesis, is associated with symptoms of bloating, abdominal distention, flatulence and prominent nausea.1,19 Patients with this condition tend to feel hungry but have premature satiety with resultant epigastric heaviness or fullness even after the consumption of small meals.19 Gastroparesis should be suspected in a symptomatic patient who has diabetes mellitus, especially when peripheral neuropathy is present. IRRITABLE BOWEL SYNDROME The abdominal pain associated with irritable bowel syndrome may frequently be confused with the pain of nonulcer dyspepsia.20 However, the syndrome is generally associated with abnormal bowel habits and can usually be distinguished from nonulcer dyspepsiaby the symptoms listed in Table 3.21 BILIARY TRACT DISEASE Gallstones are common and often asymptomatic. When pain occurs, it is episodic and severe, and may last for hours.9 Unlike the pain associated with peptic ulcers, the pain in gall bladder disease tends to occur after eating, especially after the consumption of a large fatty meal. Patients with dyspepsiashould also be asked about the presence of dark urine, jaundice and acholic stools.9 MALIGNANCY AND OTHER SERIOUS DISEASES Fortunately, malignancies are rare in patients with dyspepsia.11,20,22 The symptoms of gastric cancer are similar to those of other causes of epigastric pain. However, the presence of "alarm symptoms," such as dysphagia, unexplained weight loss (greater than 3 kg [6 lb, 8 oz]), history of gastrointestinal bleeding or clinical signs of anemia, may help to identify patients with more serious disease.22 Patients with gastric cancer also tend to be older and to have a shorter presenting history; they complain of continuous pain exacerbated by food and usually have associated anorexia.9 MEDICATION-INDUCED DYSPEPSIA A complete medication history, including prescription and over-the-counter drugs, should always be obtained as part of the evaluation of patients with dyspepsia. Agents that have been associated with dyspepsiaare listed in Table 4. Because dosage reduction or discontinuation of the offending agent may relieve a patient's symptoms, questions directed at identifying medication-induced dyspepsiamay avoid costly diagnostic studies. The use of herbal products, home remedies and other products (e.g., vitamins, minerals and shark cartilage) sold in health food stores should be specifically addressed. Dietary supplements can be harmful, but patients may not consider their use important enough to mention.23 Herbs are currently considered dietary supplements, but they are not regulated by the U.S. Food and Drug Administration. Thus, purity and quality are difficult to ensure, and

a number of products contain contaminants. Although documentation is poor, these products have been reported to cause a number of side effects, including dyspepsia(Table 5).23 Harmful drug-herb interactions are also possible. NSAID-Induced Ulcers. New data regarding treatment options for NSAID-induced ulcers are discussed in detail elsewhere.24-27 In general, a proton pump inhibitor or a histamine HZ receptor blocker is used to treat an NSAIDinduced ulcer; a proton pump inhibitor is the agent of choice when a patient is unable to discontinue use of the NSAID.27 No firm conclusions have been reached on the role of H. pylori infection in patients with NSAID-induced peptic ulcers.28 However, experts agree that H. pylori should be eradicated in patients taking NSAIDs who have an ulcer, as the cause of the ulcer is difficult to determine.27 OTHER DISORDERS Patients with ischemic heart disease may relate their symptoms to the stomach rather than the heart. Therefore, cardiac etiologiesneed to be ruled out. Unfortunately, gastrointestinal and cardiac pain may be clinically indistinguishable, posing a difficult diagnostic and therapeutic challenge. Some historical features may help to distinguish between cardiac and gastrointestinal causes of dyspepsia. Burning pain suggests a gastrointestinal etiology, whereas pressure radiating to the left arm suggests a cardiac origin. Pain lasting for hours tends to be gastrointestinal in origin. Positional pain is also more likely to have a gastrointestinal cause. For example, pain that occurs when a patient is lying down is more typical of GERD than of cardiac disease. Metabolic disorders are a rare cause of dyspepsia. Other disorders to consider include malabsorption syndrome, collagen vascular disorders, Zollinger-Ellison syndrome and Crohn's disease. Physical Examination With the exception of epigastric tenderness, the physical examination is usually normal in patients with uncomplicated dyspepsia. In addition to evaluating the epigastric pain, it is important to assess the patient's hemodynamic status because hypotension or tachycardia may indicate significant blood toss from gastrointestinal bleeding. The stool should also be tested for occult blood. An association between dental erosions and GERD has been found,29 but its incidence remains unclear. Thus, an oral examination may suggest the presence of GERD in a patient with extensive loss of enamel and exposed dentin. Jaundice or a positive Murphy's sign suggests gall bladder disease. Signs of hypothyroidism or hyperthyroidism should also be considered in the evaluation of dyspepsia. Weight loss, a positive fecal occult blood test, a palpable mass, signal nodes (Virchow's nodes) and acanthosis nigricans are signs of possible malignancy. Patients with dyspepsia and any of these signs should undergo endoscopy as soon as possible. Clinical signs of anemia, such as brittle nails, cheilosis and pallor of the palpebral mucosa or nail beds, may also suggest malignancy. Laboratory Evaluation

The initial evaluation of dyspepsiashould include a complete blood count to rule out anemia. If the history and physical examination suggest the presence of gallstones or another hepatobiliary condition, liver function tests and sonographic evaluation should be ordered. Likewise, if pancreatitis is suspected, serum lipase and amylase levels should be obtained. Patients with nausea, vomiting and epigastric fullness may also have generalized electrolyte imbalances. Therefore, electrolyte measurements should be considered. Historically, upper gastrointestinal radiographs were obtained in patients with dyspepsia. Today, radiographs are considered inferior to upper endoscopic examination for confirming or excluding ulcers, reflux disease and malignancies.4,7 Although endoscopy with biopsy is considered the gold standard for diagnosing H. pylori infection,30,31 the procedure is not always practical and may not be cost-effective.30 H. pylori can also be detected in the serum with antibody titers, in the breath with the urea breath test (UBT) and in the stool with a polymerase chain reaction (PCR) test or an antigen enzyme immunoassay (EIA). With the UBT, if H. pylori is present, the urease produced by the organism breaks down ingested carbon 14-labeled urea into ammonia and labeled carbon dioxide, which can be detected in the patients breath. The UBT is more sensitive and specific than serologic testing, but it also tends to be more expensive.32 Because serology is considered to have acceptable sensitivity and specificity for H. pylori infection, its cost and availability make it more practical than the UBT.31 A positive serology test only indicates previous exposure to H. pylori, not active infection. Thus, the test is not useful for confirming eradication of the organism. The UBT is the best test for this purpose, because once H. pylori is eradicated, urease is no longer produced. Noninvasive detection of H. pylori in the feces is of particular importance in young patients. The reported sensitivities of PCR and EIA for H. pylori are 93.7 percent and 88.9 percent, respectively; the respective specificities are 100 percent and 94.6 percent.33 Management After a thorough clinical evaluation and detailed history, conditions such as GERD, irritable bowel syndrome, biliary pain and medication-induced dyspepsiacan most likely be confirmed or excluded.6,34 The remaining patients probably have ulcer-like, dysmotility-like or functional (nonulcer) dyspepsia.6 On investigation, most patients are found to have functional or nonulcer dyspepsia.6 Before any investigation is performed, the physician must decide whether the patient is at high risk for serious disease and should undergo immediate endoscopy or whether the patient can safely receive drug therapy. In 1996, a consensus statement from the American College of Gastroenterology suggested that three options are available for the management of new-onset dyspepsianot caused by NSAIDs: (1) endoscopy in all patients, (2) a trial of empiric antisecretory drug therapy and (3) noninvasive serologic testing for H. pylori infection followed by antibacterial treatment if the test is positive.4 Other options that have been examined include empiric eradication of H. pylori infection and testing for H. pylori infection with endoscopy reserved for use in patients who have a positive test. Unfortunately, the ranking of management options is controversial, and no definitive recommendations can be made.

A number of decision analyses have been conducted to determine the most reasonable management approach.2,35-37 Factors to consider in selecting a strategy include cost, patient and physician attitudes about having an uncertain diagnosis, ethics, patient satisfaction and prevalence of disease. A model for the evaluation of patients who present with dyspepsiais provided in Figure 1. Strategic options for the initial management of patients with new-onset dyspepsiaare compared in Table 6. 7 OPTION 1: ENDOSCOPY Most physicians agree that definitive diagnostic evaluation with endoscopy is indicated in older patients at higher risk for malignancy and in younger patients with alarm symptoms. The guidelines outlined in the Maastricht European Consensus Report recommend endoscopy for patients older than 45 years of age, whereas the American Digestive Health Foundation recommends endoscopy for dyspeptic patients older than 50 years.38 Although clinical judgment is always best, a list of conditions to consider has been developed to serve as a guide in screening patients who may have risk factors for serious disease (Figure 1). If a patient will not accept a probable diagnosis and has concerns about malignancy, early investigation with endoscopy may be appropriate.20 OPTION 2: EMPIRIC ANTISECRETORY DRUG TRIAL Although empiric drug trials are falling out of favor, acid suppression still remains an option in patients with dyspepsia.4 This approach is usually relatively inexpensive and provides relief of symptoms in many patients. However, the cost advantage can be lost if a patient eventually requires diagnostic evaluation. When empiric therapy is used, a step-wise approach is suggested, with a medication being tried for two to four weeks. Therapy begins with an H^sub 2^-receptor blocker; if necessary, a proton pump inhibitor is tried next. Antacids provide little help,8 but some experts suggest that prokinetic agents should be considered as alternatives to antisecretory drugs in an empiric drug trial.7 Uninvestigated new-onset dyspepsiais likely to be a nonulcer condition, although the possibility of ulcers and other disorders still exists. Regardless of response, all drug trials should be stopped after six to eight weeks. If symptoms persist or recur, endoscopy should be performed.' If patients have little to no response to drug therapy after seven to 10 days, endoscopy should be considered.7 Empiric drug therapy has also been recommended for patients with persistent symptoms but normal endoscopic findings. If drug therapy is not successful in these previously investigated patients, other approaches of limited value (e.g., antidepressant drug therapy, behavioral therapy or psychotherapy) may be pursued,34 and the diagnosis should be reevaluated. OPTION 3: HELICOBACTER PYLORI TESTING AND TREATMENT No consensus exists on how, in whom and when to test for the presence of H. pylori infection.5,6 The treatment of dyspepsiaassociated with H. pylori in the absence of ulcers is also controversial.5,6 Some investigations have shown that antibiotics are not useful for relieving symptoms in patients with nonulcer dyspepsia; however, these findings are questionable because of serious methodologic weaknesses in the studies.39 On the other hand, a recent analysis2 and a prospective study suggest that treating nonulcer dyspepsia

with an H. pylori regimen is reasonable and cost-effective. Investigators in one study suggested that the role of H. pylori infection in nonulcer dyspepsia is uncertain for two reasons.2 First, treatment has not consistently alleviated symptoms. Second, epidemiologic evidence of an association between H. pylori gastritis and nonulcer dyspepsiais equivocal. These investigators concluded that initial anti-H. pylori therapy is the most cost-effective management strategy in H. pylori-seropositive patients with dyspepsia.2 Other investigators have disagreed, stating that, like endoscopy, anti-H. pylori treatment has cost and feasibility issues." Most importantly, several investigators have stressed the need to consider potential adverse outcomes associated with the widespread use of antimicrobials, including problems with altering the normal flora and increasing antimicrobial resistance.41 Two recent studies reached opposite conclusions regarding the efficacy of eradicating H. pylori infection in patients with nonulcer dyspepsia.42 Thus, more investigation is needed before an evidence-based conclusion can be drawn. Based on a review of the literature and available decision analyses, the American Gastroenterological Association suggested that the most reasonable strategy for the management of patients who present with dyspepsiais noninvasive testing for H. pylori infection followed by eradication of the organism if the test is positive.7 A cost-utility study in a primary care setting reached the same conclusions.37 Supporting data included the comparative cost-effectiveness of this approach and its lower potential for antibiotic resistance. OPTION 4: EMPIRIC HELICOBACTER PYLORI ERADICATION One cost-utility study found that empiric H. pylori eradication was similarly cost-effective to initial H. pylori testing followed by eradication when the test is positive.37 However, most evidence does not favor this strategy because it is more likely to lead to antibiotic resistance, as well as the unnecessary use of antibiotics.7 OPTION 5: NONINVASIVE HELICOBACTER PYLORI TESTING AND ENDOSCOPY Noninvasive testing for H. pylori followed by endoscopy is another option. However, this strategy is unlikely to be as cost-effective as testing for and treating H. pylori infection.7 NONPHARMACOLOGIC MANAGEMENT All patients with dyspepsiashould be advised to stop smoking and, if their medical condition permits, to discontinue ulcerogenic medications. They should also avoid foods and other factors that precipitate their symptoms. Because dyspepsiamay be aggravated by stress, anxiety or depression, it may be useful to explore these issues. Reassurance is a key step in managing dyspepsia, but advice regarding stress-reducing activities such as exercise and relaxation is also important. Final Comment Questions about the evaluation and management of dyspepsiaremain unanswered. Unfortunately, little consensus data are available to guide physicians in the diagnosis and management of patients presenting with dyspepsiain the primary care setting. The situation is complicated by the need to have a costeffective, yet rational approach to dyspepsia.

Dyspepsiahas a large number of possible etiologies. Most commonly, it is caused by gastric ulcers or GERD, although malignancies and other serious conditions also need to be considered. In many patients, a definitive investigation reveals no specific etiology. Because symptoms alone are not useful in distinguishing between causes, all aspects of the patient's evaluation, including the medical history, physical examination and laboratory review, are essential in the diagnosis. Primary care physicians must determine when to treat empirically and when to arrange endoscopy for patients. Patients at high risk for malignancy should have early endoscopy. In young patients without signs or symptoms of a serious underlying disorder, the most evidence-based initial management strategy appears to be H. pylori testing followed by eradication of the organism when the test is positive.8,40 If symptoms resolve, no further treatment is necessary. A gastric acid suppressant or prokinetic agent can be used in patients with nonulcer dyspepsiawho do not have H. pylori infection and in patients with H. pylori infection who do not respond to anti-H. pylori agents (probably a large number of such patients, if not the majority43). If symptoms still do not improve, endoscopy and more specialized testing are indicated.8 If, after endoscopy and all other specialized testing, the diagnosis is functional or nonulcer dyspepsiaand the symptoms do not respond to all previous treatments, dietary, environmental and emotional triggers should be evaluated and addressed.43 Additional treatments can include antidepressant drug therapy, stress management, relaxation therapy, hypnotherapy or psychotherapy.44 Future breakthroughs in dyspepsiamanagement are likely to come from the evaluation of visceral sensitivity and brain-gut interactions.43 The authors thank Glenn W W Gross, M.D., associate professor of medicine and surgery in the gastroenterology division at the University of Texas Health Science Center in San Antonio, for his review of the manuscript. Footnote Each year members of a different family practice department develop articles for "ProblemOriented Diagnosis." This series is coordinated by the Department of Family Practice at the University of Texas Health Science Center at San Antonio. Guest editors of the series are David A. Katerndahl, M.D., and Clinton Colmenares. Footnote A patient information handout on dyspepsia, written by the authors of this article, is provided on page 1787. Footnote See editorial on page 1649. References REFERENCES References

1. Heading RC. Definitions of dyspepsia. Scand J Gastroenterol (Suppl) 1991;182:1-6. 2. Ofman JJ, Etchason J, Fullerton S, Kahn KL, Scand J Soll AH. Management strategies for Helicobacter pylori-seropositive patients with dyspepsia: clinical and economic consequences. Ann Intern Med 1997;126:280-91. 3. Drossman DA, Li Z, Andruzzi E, Temple RD, Talley NJ, Thompson WG, et al. U.S. householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact. Dig Dis Sci 1993;38:1569-80. Soil AH. Medical treatment of peptic ulcer disease. Practice guidelines. JAMA 1996;275:6229 [Published erratum in JAMA 1996;275:1314]. Lambert JR. The role of Helicobacter pylori in non References ulcer dyspepsia. A debate-for. Gastroenterol Clin North Am 1993;22:141-51. 6. Talley NJ. The role of Helicobacter pylori in nonulcer dyspepsia. A debate-against. Gastroenterol Clin North Am 1993;22:153-67. 7. Talley NJ, Silverstein MD, Agreus L, Nyren 0, Sonnenberg A, Holtmann G. AGA technical review: evaluation of dyspepsia. Gastroenterology 1998; 114:582-95. 8. Fisher RS, Parkman HP. Management of nonulcer dyspepsia. N Engl J Med 1998;339:1376-81. 9. Richter JE. Dyspepsia: organic causes and differential characteristics from functional dyspepsia. Scand J Gastroenterol (Supply 1991;182:11-6. 10. Thompson WG. Nonulcer dyspepsia. Can Med Assoc J 1984; 130:565-9. 11. Endoscopy in the evaluation of dyspepsia. Ann Intern Med 1985;102:266-9. 12. Talley NJ, Zinsmeister AR, Schleck CD, Melton U 3d. Dyspepsiaand dyspepsia subgroups: a population-based study. Gastroenterology 1992; 102(4 pt 1):1259-68. 13. Colin-Jones DG. Dyspepsiaupdate. Scand J Gastroenterol (Supply 1995;210:32-5. 14. Adang RP, Vismans JF, Talmon JL, Hasman A, Ambergen AW, Stockbrugger RW. Appropriateness of indications for diagnostic upper gastrointestinal endoscopy: association with relevant endoscopic disease. Gastrointest Endosc 1995;42:390-7. 15. Brenner H, Rothenbacher D, Bode G, Adler G. The individual and joint contributions of Helicobacter pylori infection and family history to the risk for peptic ulcer disease. J Infect Dis 1998; 177:1124-7. 16. Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking. J Clin Gastroenterol 1997;24:2-17. 17. Eastwood GL. Is smoking still important in the pathogenesis of peptic ulcer disease? J Clin Gastroenterol 1997;25(suppl 1):S1-7. 18. Zell SC, Budhraja M. An approach to dyspepsiain the ambulatory care setting: evaluation based on risk stratification. J Gen Intern Med 1989;4:14450. References 19. Management of dyspepsia: report of a working party. Lancet 1988;1(8585):576-9. 20. Talley NJ. Nonulcer dyspepsia: current approaches to diagnosis and management. Am Fam Physician 1993;47:1407-16.

21. Drossman DA, Whitehead WE, Camelleri M. Irritable bowel syndrome: a technical review for practice guideline development. Gastroenterology 1997; 112:2120-37. 22. Nyren 0. Therapeutic trial in dyspepsia: its role in the primary care setting. Scand J Gastroenterol (Supply 1991;182:61-9. 23. Pharmacist's letter continuing education booklet: therapeutic use of herbs #422-000-98079-Hot. Stockton, Calif.: Therapeutic Research Center, 1988. 24. Yeomans ND, Tulassay Z, Juhasz L, Racz I, Howard JM, van Rensburg CJ, et al. A comparison of omep References razole with ranitidine for ulcers associated with nonsteroidal antiinflammatory drugs. N Engl J Med 1998;338:719-26. 25. Hawkey CJ, Karrasch JA, Szczepanski L, Walker DG, Barkun A, Swannell AJ, et al. Omeprazole compared with misoprostol for ulcers associated with nonsteroidal antiinflammatory drugs. N Engl J Med 1998;338:727-34. 26. Yeomans ND. New data on healing of nonsteroidal anti-inflammatory drug-associated ulcers and erosions. Am J Med 1998;104(3A):565-61 S. 27. Lanza FL. A guideline for the treatment and prevention of NSAID-induced ulcers. Am J Gastroenterol 1998;93:2037-46. 28. Malfertheiner P, Labenz J. Does Helicobacter pylori status affect nonsteroidal antiinflammatory drug-associated gastroduodenal pathology? Am J Med 1998;102(3A):355-405. 29. Schroeder PL, Filler SJ, Ramirex B, Lazarchik DA, Vaezi MF, Richter JE. Dental erosion and acid reflux disease. Ann Intern Med 1995;122:809-15. 30. Agreus L, Talley NJ. Dyspepsia: current understanding and management. Ann Rev Med 1998;49:47593. References 31. Megraud F How should Helicobacter pylori infection be diagnosed? Gastroenterology 1997; 113(6 suppl 1):593-8. 32. The report of the Digestive Health Initiative's International Update Conference on Helicobacter pylori. Gastroenterology 1997;113(6 suppl):S4-8. 33. Makristathis A, Pasching E, Schutze K, Wimmer M, Rotter ML, Hirschl AM. Detection of Helicobacter pylori in stool specimens by PCR and antigen enzyme immunoassay. J Clin Microbiol 1998;36: 2772-4. 34. American Gastroenterological Association medical position statement: evaluation of dyspepsia. Gastroenterology 1998;114:579-81. 35. Silverstein MD, Petterson T, Talley NJ. Initial References endoscopy or empirical therapy with or without testing for Helicobacter pylori for dyspepsia: a decision analysis. Gastroenterology 1996; 110:72-83. 36. Briggs AH, Sculpher MJ, Logan RP, Aldous J, Ramsay ME, Baron JH. Cost effectiveness of screening for and eradication of Helicobacter pylori in management of dyspeptic patients under 45 years of age. BMJ 1996;312:1321-5 [Published erratum in BMJ 1996;312:1647].

37. Ebell MH, Warbasse L, Brenner C. Evaluation of the dyspeptic patient: a cost-utility study. J Fam Pract 1997;44:545-55 [Published erratum in J Fam Pract 1997;45:169[. 38. Malfertheiner P Commentary: how, in whom, and when to diagnose Helicobacter pylori. Gastroenterology 1997;113(6 suppl 1):51 18-9. 39. Talley NJ. A critique of therapeutic trials in Helicobacter pylori-positive functional dyspepsia. Gastroenterology 1994;106:1174-83. 40. McColl K, Murray L, EI-Omar E, Dickson A, ElNujumi A, Wirz A, et al. Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med 1998; 339:1869-74. 41. Rabeneck L, Graham DY. Helicobacter pylori: when to test, when to treat [Editorial]. Ann Intern Med 1997;126:315-6. 42. Blum AL, Talley NJ, O'Morain C, van Zanten SV, Labenz J, Stolte M, et al. Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl I Med 1998;339:1875-81. 43. Freiedman LS. Helicobacter pylori and nonulcer dyspepsia[Editorial]. N Engl J Med 1998;339:192830. 44. McQuaid K. Dypepsia. In: Feldman M, Sleisenger MH, Scharschmidt BF, eds. Sleisenger &Fordtran's Gastrointestinal and liver disease: pathology, diagnosis, management. 6th ed. Vol 1. Philadelphia: Saunders, 1998:108-17. AuthorAffiliation ORALIA V. BAZALDUA, PHARM.D., and F. DAVID SCHNEIDER, M.D., M.S.P.H. University of Texas Health Science Center at San Antonio, San Antonio, Texas AuthorAffiliation The Authors ORALIA V. BAZALDUA, PHARM.D., is assistant professor of family practice at the University of Texas Health Science Center at San Antonio and clinical assistant professor at the University of Texas School of Pharmacy. She received her doctorate in pharmacy from the University of Oklahoma, Oklahoma City, and completed a primary care/managed care residency at the University of Colorado and Kaiser Permanente, both in Denver. Dr. Bazaldua is a board-certified pharmacotherapy specialist. F DAVID SCHNEIDER, M.D., M.S.P.H., is associate professor of family practice and director of medical student education at the University of Texas Health Science Center at San Antonio. Address correspondence to Oralia V Bazaldua, Pharm. D., Department of Family Practice, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78284-7795. Reprints are not available from the authors.

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Pengindeksan (detail)
Subjek Medical disorders;

Health care; Ulcers; Digestive system MeSH Colonic Diseases, Functional -- diagnosis, Decision Trees, Diagnosis, Differential, Digestive System Diseases -- complications, Digestive System Neoplasms -- diagnosis, Gastroesophageal Reflux -- diagnosis, Gastroparesis -- diagnosis, Helicobacter Infections -diagnosis, Helicobacter pylori, Humans, Patient Education as Topic, Peptic Ulcer -- diagnosis, Teaching Materials, DigestiveSystem Diseases -- diagnosis (utama), Dyspepsia -- etiology (utama), Dyspepsia -- therapy (utama) Evaluation and management of dyspepia Bazaldua, Oralia V; Schneider, F David American Family Physician 60 6 1773-84, 1787-8 1999 Oct 15, 1999 1999 Leawood American Academy of Family Physicians Leawood United States Medical Sciences 0002838X AFPYBF Scholarly Journals English Journal Article Medical disorders, Ulcers, Digestive system, Health care 10537391, 04520678 234299134 http://search.proquest.com/docview/234299134?accountid=50268 Copyright American Academy of Family Physicians Oct 15, 1999 2010-06-11 ProQuest Medical Library << Link ke dokumen di ProQuest

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