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Acid peptic disease /dental courses /certified fixed orthodontic courses by Indian dental academy
- 1. Acid-Peptic Disease PUD/GERD/NSAIDs INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com
- 2. Lifestyle measures • • • • • • Raise the head of the bed, or lie on left side Decrease fat intake Avoid certain foods Avoid lying down for 3 hours after eating Stop smoking Lose weight if appropriate
- 3. Role of lifestyle measures • Role in GERD debatable • Many physicians feel that lifestyle advice is worthwhile • Lifestyle measures are generally insufficient by themselves • Lifestyle measures may have a negative impact on patient lifestyle
- 4. Evolution of pharmacological therapy • Antacids • Prokinetics • H2-receptor antagonists • Proton pump inhibitors
- 5. Pharmacological therapy – antacids, prokinetics and H2RAs • Antacids – Prompt but temporary relief – No objective proof of superiority to placebo • Prokinetics – Improvement of symptoms in mild GERD – Effective for healing only mild erosive esophagitis – Can be useful in a select patient population • H2RAs – Relief of symptoms in ~50% of patients – Effective for healing only mild erosive esophagitis Tytgat and Nio. Baillière’s Clin Gastroenterol 1987; Klinkenberg-Knol et al. Drugs 1995; Furman et al. Gastroenterology 1982; Wolfe and Sachs. Gastroenterology 2000
- 6. H2RAs are effective only in mild erosive esophagitis Isolated erosions 78 Longitudinally confluent erosions 38 p < 0.001 23 Circumferential erosions 0 20 40 60 80 6-week healing rate (%) Koelz et al. Gastroenterology 1986 100
- 7. Doubling the dose is ineffective in patients refractory to H2RAs % patients with mild or no heartburn 50 40 30 Standard dose Double dose 20 10 0 Week 4 Week 8 Kahrilas et al. Am J Gastroenterol 1999
- 8. Pharmacological therapy – PPIs • Significantly more effective than H2RAs for both symptom resolution and healing of erosive esophagitis • Also effective in more severe cases of GERD • Most patients respond well to standard therapy, but some require prolonged and/or high-dose treatment Klinkenberg-Knol et al. Drugs 1995
- 9. % esophagitis cases healed PPIs are the most effective drugs for the initial treatment of GERD 100 PPIs 80 60 H2RAs 40 Placebo 20 0 2 4 6 8 Weeks of treatment 10 Chiba et al. Gastroenterology 1997 12 p < 0.0005
- 10. H. pylori: Clinical Manifestations in Children Compared to Adults Chronic-active/chronic gastritis - different histopathology; neutrophils much less frequent Duodenal ulceration - less frequent than adults Gastric ulceration - occurs but uncommon MALT lymphoma - 6 case reports in literature Gastric cancer - one case reported Controversial: recurrent abdominal pain (RAP), non-ulcer dyspepsia; others?
- 11. Age, HP & Acid secretion • Subjects with a mean age of 57 when compared to subjects with a mean age of 33 – higher mean basal – higher meal-stimulated – higher pepsinogen I & II levels • Age positively effected acid secretion • H. pylori negatively effected acid secretion Goldschmiedt, et al., Gastro, 1991
- 12. Age, HP & Acid secretion • The decline in acid output in the elderly was primarily due to atrophic gastritis and partially to tobacco smoking • After adjusting for histology, H. pylori and other variables, age had no independent effect on acid secretion. • Age is associated with reduced pepsin output. Feldman, et al., Gastro, 1996
- 13. Pathogenesis of Ulcers Therapy is directed at enhancing host defense or eliminating aggressive factors; i.e., H. pylori. Aggressive Factors Acid, pepsin Bile salts Drugs (NSAIDs) H. pylori Defensive Factors Mucus, bicarbonate layer Blood flow, cell renewal Prostaglandins Phospholipid Free radical scavengers
- 14. Helicobacter pylori in GERD • Infection with H. pylori may cause a variety of gastric diseases • In the context of GERD, however, H. pylori may have some beneficial effects
- 15. H. pylori –protection against reflux esophagitis? Patients cured of H. pylori infection (n = 244) 25.8% % patients with erosive esophagitis 30 25 20 Patients remaining infected (n = 216) 12.9% 15 10 5 p < 0.001between groups 0 2 6 12 18 24 30 36 Months Labenz et al. Gastroenterology 1997
- 16. H. pylori – improvement of the efficacy of PPIs? p = 0.002 Median 24-hour intragastric pH with PPI 10 8 6 5.51 5.3 5.07 3.53 4 2 0 Hp Placebo Rx Pre–Hp Rx Hp Placebo Rx Post–Hp Rx Van Herwaarden et al. Aliment Pharmacol Ther 1999
- 17. NSAIDs and H. pylori
- 18. Prevention of ulcers in NSAID Users 50 Ulcer Recurrence (%) Placebo n = 155 40 32 Misoprostol 200 ug bid n = 296 Omeprazole 20 mg qd n = 274 30 20 * 10 * 13 10 ** 10 0 12 3 Gastric Ulcer Duodenal Ulcer P<0.001 omeprazole & misoprostol vs placebo P<0.001 omeprazole vs placebo & misoprostol Hawkey et al, 1998
- 19. Prevention of ulcers in NSAID Users Ulcer Recurrence (%) 30 Ranitidine 150 mg bid n = 215 Omeprazole 20 mg qd n = 210 16.3 20 * 5.2 10 5.7 * 0.5 0 Gastric Ulcer Yeomans et al, 1998 Duodenal Ulcer * p< 0.05
- 20. H. pylori & NSAID Ulcers Ulcers Naproxen Naproxen P value HP+ (n=43) HP- (n=38) Gastric 9 2 Duodenal 2 0 Both 1 0 Total 12 (28%) 2 (5%) Chan et al, 1997 0.04 0.007
- 21. H. pylori and ulcer relapse in patients with healed duodenal ulcer: 6 month double-blind trial Ulcer Relapse (%) 100 80 60 H. pylori-negative H. pylori-positive 40 20 0 Placebo Omeprazole Misoprostol 20mg qd 200mg bid Hawkey et al, Gut 1996
- 22. NSAID Use in the Arthritis Patient with a History of Bleeding Ulcer • Treating H. pylori is likely to be of benefit if there was a duodenal ulcer; test and treat for H. pylori is recommended. • Use COX2 Inhibitor • Add a PPI or Misoprostol
- 23. Tests For Initial Diagnosis of Infection Urea Breath Test and Stool Assay Serology Non-invasive, sensitive and specific O.K. for initial diagnosis Fair sensitivity and specificity Endoscopy Not necessary for diagnosis
- 24. Diagnostic Tests to Evaluate Treatment Success • Urea Breath Test and Stool Assay – Can be done 4 weeks post treatment – PPIs can interfere with the Breath Test, not with Stool Assay • Endoscopy (antral and fundal biopsies) – Also allows for bacterial Culture and Sensitivity • Rapid Urease Assays – Also influenced by PPIs, biopsy from antrum and fundus
- 25. What Diseases Have Evidence-Based Justification For Treating H. pylori • • • • • Peptic ulcer disease: duodenal (67%) and gastric ulcers (59%) recur if no eradication Bleeding duodenal ulcer: rebleeding in 30% if no eradication with 1 year follow up MALT lymphoma: justified based on best-available evidence to treat in low-grade MALT lymphoma Gastric cancer: justified in early gastric cancer; 9% recurrence incidence in untreated controls Non-ulcer dyspepsia: evidence not yet definitive; up to 40% with abdominal pain recurrence with . H. pylori eradication
- 26. H. pylori Infection and Ulcer Recurrence 100 Recurrence (%) 80 Twelve-month rates of duodenal ulcer recurrence in patients whom H. pylori was eradicated and those in whom it was not. 60 40 (Walsh JH. N.E.J.M. 1995;333:984) 20 0 Not Eradicated Eradicated
- 27. Known Factors Which Determine Success of H. pylori Therapy Patient compliance or non-compliance Medicine complications or side effects Antimicrobial resistance of infecting H. pylori strains Duration of Therapy Correct dosing Clearance of H. pylori infection is not equivalent to eradication.
- 28. Who Should Be Treated For H. pylori Infection? Patients who have documented H. pylori infection and: Definitely had or has a duodenal or stomach ulcer Have had stomach lymphoma or family hx of stomach cancer Consider treatment if: Presence of “severe histologic” gastritis and H. pylori infection Ulcer-like dyspepsia in the absence of an ulcer or prior to endoscopy in a young patient
- 29. H. pylori: Treatment Agents Which Inhibit H. pylori In Vivo Antibiotic Resistance Resistance No Antibiotic - metronidazole subcitrate - tinidazole subsalicylate - erythromycin base - clarithromycin - ciprofloxacin - colloidal bismuth - ofloxacin - bismuth - tetracycline - nitrofurantoin - furazolidone
- 30. Monotherapy for H. pylori Infection Drug Azithromycin Doxycycline Metronidazole Tinidazole Tetracycline Bismuth subsalicylate Quinolones Erythromycin Amoxicillin Nitrofurantoin Furazolidone Colloidal bismuth subcitrate Clarithromycin (Blecker U, Gold B. Pediatr Infect Dis J 1997;16:391) Cure Rate (%) 5 5 5 5 5 5-10 10 15 15 20 20-40 30-40 40-60
- 31. H. pylori Treatment: Resistance in Pediatric Strains State No of Strains Tested Resistance (mean %) Antibiotic Georgia 15 Alabama 4 5 20 25 Clarithromycin Metronidazole Metronidazole Florida 12 South Carolina 3 25 60 1 15 Clarithromycin, Metronidazole Amoxicillin Metronidazole Ohio 10 10 Metronidazole
- 32. FDA-Approved Treatment Regimes for H. pylori Infection Omeprazole 20 mg BID + Clarithromycin 500 mg BID + Amoxicillin 1 g BID for 10 days Lansoprazole 30 mg BID +Clarithromycin 500 mg BID + Amoxicillin 1 g BID for 10 days Bismuth subsalicylate (Pepto Bismol) 525 mg QID + Metronidazole 250 mg QID + Tetracycline 500 mg QID X 14 days + H2 receptor antagonist x 4 wks
- 33. H. pylori: Pediatric Treatment Pediatric Treatment Recommendations 2 wks omeprazole (1 - 3 mg/kg/D bid) + clarithromycin (15 mg/kg/D bid) + metronidazole (15 mg/kg/D tid) followed by 2 wks of omeprazole (2 mg/kg/D qd) 2 wks omeprazole (1 - 3 mg/kg/D bid) + clarithromycin (15 mg/kg/D bid) + amoxicillin (50 mg/kg/D tid) followed by 2 wks of omeprazole (2 mg/kg/D qd) 2 wks amoxicillin (50 mg/kg/D tid) + metronidazole (15 mg/kg/D tid) + bismuth subsalicylate (qid) + H2 receptor antagonist (e.g., ranitidine 5 mg/kg/D bid) possible to substitute lansoprazole for omeprazole
- 34. Thank you For more details please visit www.indiandentalacademy.com
Notas do Editor
- Lifestyle measures Lifestyle measures that are sometimes recommended to GERD patients include avoiding factors that are known to aggravate GERD symptoms, such as certain foods, avoiding lying down after meals, raising the head of the bed to reduce nocturnal reflux, and losing weight.
- Role of lifestyle measures Although many physicians feel that advice about lifestyle measures is worthwhile, the value of this approach in the management of GERD remains controversial. Discussion at the Genval Workshop, for example, suggested that the possibility of patients deriving adequate benefit from lifestyle alterations alone is significantly over-estimated (1). Objective evidence for the efficacy of lifestyle measures is lacking. Avoidance of alcohol and certain foods that provoke reflux symptoms can provide symptomatic relief, but is of no benefit in healing erosive esophagitis (1). Moreover, as described in the following two slides, lifestyle modifications such as weight reduction or smoking cessation may not reduce esophageal acid exposure. It is widely accepted that lifestyle measures alone are insufficient, except possibly in patients with mild, infrequent symptoms. Indeed, many patients presenting with GERD symptoms may have already tried lifestyle alterations and found them to be ineffective (1). Lifestyle measures may themselves have a negative impact on patient lifestyle. For example, some patients may have to give up favorite foods. (1) Dent et al. Gut 1999; 44 (Suppl. 2): S1–S16.
- Evolution of pharmacological therapy Four types of drug are used in the management of GERD: antacids prokinetic agents histamine H2-receptor antagonists (H2RAs) proton pump inhibitors (PPIs).
- Pharmacological therapy – antacids, prokinetics and H2RAs Antacids are widely used as first-line treatment for GERD, and many patients will use such remedies before consulting their doctors. These agents can provide prompt symptom relief, but their effect is only temporary due to rapid gastric emptying (1). There is little objective evidence that they are superior in efficacy to placebo (1–4). Prokinetic agents act by increasing LES pressure and stimulating esophageal peristalsis and gastric emptying. These agents are as effective as antacids and H2RAs in relieving symptoms in patients with mild GERD, but are only effective in healing mild degrees of erosive esophagitis (2). Furthermore, their usefulness is limited by adverse effects (2). H2RAs act by inhibiting histamine-stimulated gastric acid secretion. Placebo-controlled studies have shown that these agents relieve reflux symptoms in approximately 50% of patients, but are less effective in healing erosive esophagitis (2). (1) Tytgat, Nio. Baillière’s Clin Gastroenterol 1987; 1: 791–807. (2) Klinkenberg-Knol et al. Drugs 1995; 49: 695–710. (3) Furman et al. Gastroenterology 1982; 82: 1062. (4) Wolfe, Sachs. Gastroenterology 2000; 118: S9–S31.
- Antacids may be no more effective than placebo This slide and the one that follows provide data supporting statements made on the previous slide. Although antacids have been the traditional therapy for GERD for many years and are still widely used, there is little evidence concerning their efficacy. Indeed, the results of some studies suggest that antacids may be no more effective than placebo in alleviating symptoms and influencing the natural history of the disease. For example, in one study, an antacid was compared with placebo in 32 patients with symptomatic gastroesophageal reflux (1). The two test treatments, each taken 7 times daily, both produced significant increases in the time needed to reproduce heartburn with a timed acid perfusion (Bernstein) test. However, the mean increase was somewhat greater with placebo (169 +/- 66 versus 41 +/- 20 seconds, or 4.1-fold) than with the antacid (120 +/- 57 versus 42 +/- 16 seconds, or 2.9-fold). (1) Graham, Patterson. Dig Dis Sci 1983; 28: 559–63.
- H2RAs are effective only in mild erosive esophagitis A number of studies have shown that treatment with H2RAs promotes healing of erosive esophagitis. However, the evidence also suggests that these benefits are largely confined to individuals with only mild degrees of erosive esophagitis. In a study of 108 patients with erosive esophagitis, the effects of treatment with an H2RA on the healing of esophageal lesions were compared with those of placebo. After 6 weeks, those patients with the mildest degree of esophagitis (isolated erosions), as assessed endoscopically, showed a healing rate of 78 %. The frequency of healing was considerably lower in individuals with more extensive lesions: 38 % in those with longitudinally confluent lesions and 23 % in those with circumferential erosions of the distal esophagus (1). (1) Koelz et al. Gastroenterology 1986; 91: 1198–205.
- Doubling the dose is ineffective in patients refractory to H2RAs One approach that has been used in an attempt to improve treatment outcomes in patients refractory to H2RAs is doubling of the dose. The data shown here demonstrate that this approach is ineffective. Kahrilas et al. gave 481 GERD patients with moderate or severe heartburn a standard dose of an H2RA for 6 weeks (1). They then randomized patients who were still symptomatic (n = 271) to receive standard- or double-dose treatment with the same H2RA for a further 8 weeks. As shown on the slide, the proportion of these patients with mild or no heartburn after 4 or 8 weeks was no greater with the double dose than with the standard dose. This proportion was less than 40% in both treatment groups after 4 weeks and less than 50% in both groups after 8 weeks. (1) Kahrilas et al. Am J Gastroenterol 1999; 94: 92–7. Reproduced with permission from the American College of Gastroenterology.
- Pharmacological therapy – PPIs PPIs provide prolonged inhibition of acid secretion, irrespective of the stimulus, and are significantly more effective than H2RAs in controlling gastric acid (1). Comparative trials have consistently shown that these agents are more effective than H2RAs in relieving GERD symptoms and healing erosive esophagitis (1). Furthermore, PPIs are effective in patients with severe erosive esophagitis or Barrett’s esophagus (1). Although most patients can be treated effectively with PPI therapy, there is some variability in response. As a result, some patients, particularly those with nocturnal reflux, may require prolonged therapy, higher doses, or both (1). (1) Klinkenberg-Knol et al. Drugs 1995; 49: 695–710.
- PPIs are the most effective drugs for the initial treatment of GERD The ACG guidelines state that acid suppression is the mainstay of therapy for GERD, and that “proton pump inhibitors provide rapid symptomatic relief and healing in the highest percentage of patients” (1). This conclusion is based on the evidence from 33 randomized trials involving more than 3000 patients. In these trials, symptom control was achieved in 83% of patients treated with PPIs, compared with 60% of patients receiving H2RAs and 27% of placebo-treated patients. Healing of erosive esophagitis was achieved in 78%, 50% and 24% of patients respectively. (1) DeVault et al. Am J Gastroenterol 1999; 94: 1434–42.
- PPIs are the most effective drugs for the initial treatment of GERD This figure is taken from a meta- analysis of randomized, single- or double-blind clinical trials conducted in GERD patients with endoscopically proven erosive or ulcerative esophagitis (1). The meta-analysis incorporated a total of 43 studies involving 7635 patients treated for 2–12 weeks. The figure shows that, for all time points between 2 and 12 weeks, the mean percentage of patients in whom esophagitis was healed was considerably higher with PPIs than with H2RAs. Notably, the mean proportion healed after 2 weeks with PPIs (63.4%) was similar to the mean proportion healed after 12 weeks with H2RAs (60.2%). The overall proportion of cases healed, regardless of the duration of treatment, was 83.6% with PPIs, 51.9% with H2RAs and 28.2% with placebo (p < 0.0005 between groups). (1) Chiba et al. Gastroenterology 1997; 112: 1798–810. Reproduced with permission from the American Gastroenterological Association.
- Helicobacter pylori in GERD In general, infection with the bacterium H. pylori is detrimental to health. This bacterium has been implicated in a variety of gastric diseases, including chronic active gastritis, peptic ulcer disease, ulcer bleeding, mucosa-associated lymphoid tissue (MALT) lymphoma and distal gastric cancer. In the context of GERD, H. pylori may have certain beneficial effects: protection against reflux esophagitis, protection against serious complications of GERD and improvement of the efficacy of PPI therapy. These effects are described in more detail on the slides that follow. It is important to note that the relationship between H. pylori and GERD is complex and not yet fully understood. This is why the titles of the following slides end with a question mark.
- H. pylori – protection against reflux esophagitis? The data shown here indicate that H. pylori may be protective against reflux esophagitis. They are taken from a study in which patients with duodenal ulcer but no erosive esophagitis were followed up prospectively after cure of H. pylori infection (n = 244) or after diagnosis of persisting infection (n = 216) (1). Over 3 years, the incidence of erosive esophagitis was 25.8% in H. pylori-negative patients but only 12.9% in H. pylori-positive patients (p < 0.001). These data are contradicted by others showing that eradication of H. pylori has little effect on the incidence of GERD. In a study involving 242 patients with endoscopically documented duodenal ulcers, for example, only one patient showed evidence of erosive esophagitis 6 months after treatment to eradicate H. pylori (2). Moreover, the proportion of patients experiencing new heartburn 1 month and 6 months after treatment was not significantly higher in patients in whom H. pylori was eradicated than in those in whom infection persisted. (1) Labenz et al. Gastroenterology 1997; 112: 1442–7. Reproduced with permission from the American Gastroenterological Association. (2) Vakil et al. Aliment Pharmacol Ther 2000; 14: 45–51.
- H. pylori – improvement of the efficacy of PPIs? These data suggest an explanation for the findings shown on the previous slide. They indicate that the efficacy of PPIs in healing esophagitis may be improved in the presence of H. pylori because infection with this bacterium enhances the ability of PPIs to control acid secretion. The data come from a study carried out in 19 healthy volunteers infected with H. pylori (1). These volunteers were randomized to receive either placebo or H. pylori eradication therapy. Before treatment, median 24-hour intragastric pH during the administration of a PPI was approximately 5.5 in both groups. After treatment, this variable was not significantly changed in the placebo group but was reduced to 3.53 in the eradication group (p = 0.002). Therefore, it appears that eradication of H. pylori reduced the ability of the PPI to elevate intragastric pH. These results are supported by findings from a study conducted in healthy volunteers by Katsube et al, which show that the absence of H. pylori is associated with nocturnal acid breakthrough (2). At night, median intragastric pH was significantly lower in H. pylori-negative subjects than in H. pylori-positive subjects, and the proportion of the time for which intragastric pH was below 4 was significantly higher – regardless of whether subjects were given a PPI or not. (1) Van Herwaarden et al. Aliment Pharmacol Ther 1999; 13: 731–40. (2) Katsube et al. Aliment Pharmacol Ther 2000; 14: 1049–56.