Abbas, Z

Abid, S

Hamid, S

Jafri, W

Khan, H

Shah, H

English

eCommons@AKU

eCommons@AKUSection of Gastroenterology Department of MedicineDecember 1992Omeprazole in short term treatment of refluxoesophagitisW JafriAga Khan University, wasim.jafri@aku.eduZ AbbasAga Khan University, zaigham.abbas@aku.eduS HamidAga Khan University, saeed.hamid@aku.eduS AbidAga Khan University, shahab.abid@aku.eduH ShahAga Khan University, hasnain.alishah@aku.eduSee next page for additional authorsFollow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterolPart of the Gastroenterology CommonsRecommended CitationJafri, W., Abbas, Z., Hamid, S., Abid, S., Shah, H., Khan, H. (1992). Omeprazole in short term treatment of reflux oesophagitis. Journalof Pakistan Medical Association, 42(12), 290-292.Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/211AuthorsW Jafri, Z Abbas, S Hamid, S Abid, H Shah, and H KhanThis article is available at eCommons@AKU: https://ecommons.aku.edu/pakistan_fhs_mc_med_gastroenterol/211OMEPRAZOLE IN SHORT TERM TREATMENT OFREFLUX OESOPHAGITISPages with reference to book, From 290 To 292 Wasim Jafri, Zaigham Abbas, Saeed Hamid, Hasnain Shah, Haleem Khan ( Department of Medicine, Aga Khan UniversityHospital, Karachi. ) Omeprazole inhibits the gastric secretion by altering the activity of H + /K+ ATPase1,2. The drug itselfis inactive but is converted to the active form, a sulfonamide in the acid milieu of canaliculi of activelysecreting gastric parietal cells3. Though the plasma half life is 60 minutes, the drug binds covalentlywith H+/K+ATPase and duration of action is thereafter increased to greater than 24 hours4. Distaloesophagitis is a complication of gastro-oesophageal reflux. Number and duration of episodes of refluxare important in the pahogenesis5-7. The aim of this study was to assess the efficacy of omeprazole 20mg once daily in our patients for short term treatment of refiux oesophagitis.PATIENTS, METHODS AND RESULTS This was an open labeled, non-comparative single centre study. Outpatients aged 18-70 withendoscopic findings of reflux oesophagitis (grade I to III) were included in the study. Exclusion criteriawere pregnant and lactating mothers, treatment with anti-ulcer or anti-refiux drugs within a week priorto inclusion, patients with concomitant gastric or duodenal ulcer, pyloric stenosis, or any malignantlesion as evident on gastroscopy, oesophageal varices, stricture or Barrett’s oesophagus, previousgastro-oesophageal surgery, patients with abnormal renal or hepatic functions and patients requiringregular use of NSAIDs. Before entry, the severity of symptoms and personal habits were assessed. Acomplete physical examination was performed. Lab investigations including complete blood count(CBC), ESR, urinalysis, blood urea nitrogen (BUN), creatinine, biirubin, alanine aminotransferase(ALT) and alkaline phosphatase were done. Endoscopy was performed within a week prior to theinclusion. Informed consent was taken from all the patients. Patients’ symptoms like heart burns andpains were graded from 0 (none) to 3 (severe). Occasional episodes not interfering with the normalactivity corresponded to grade 1 (mild), episodes interfering with normal activity as grade 2(moderate), frequent episodes constantly interfering with normal activity as grade 3 (severe).Oesophagitis was graded as follows: Grade I, erythema, hyperemia or mucosal friability; grade II,superficial erosions; grade III, ulcerations and grade W, complications, e.g., strictures. Patients wereseen at two and four weeks to record severity of symptoms and any adverse effects, physicalexamination and check of left over capsules. Concomitant use of anti-refiux or other anti-ulcer drugswas forbidden during the study period. Endoscopy was repeated by the same endoscopist at 29±3 daysand laboratory tests performed. Thirty consecutive patients were entered in the study. The clinicalcharacteristics and results are summarized inTable I and II and Figure 1 and 2.Healing defined as complete disappearance of all the lesions and re-epithelization of oesophagealmucosa on endoscopic examination was seen in 19 of 30 patients (68%). Twenty of 30 patients becameasymptomatic and another 9 patients improved symptomatically. No major clinical or biochemical sideeffects were observed. Only one patient complained of some decrease in appetite but he completed thetrial.COMMENTS The randomized clinical trials have proved the superiority of omeprazole over H2 - receptorantagonists8-13. The healing rate at 4 weeks varied between 67-85% as compared to 27-31% whenusing ranitidine. Much higher healing rate was observed at 8 weeks with omeprazole; 85-96% withomeprazole vs 38-50% with ranitidine11-13. There was significantly better symptomatic improvementwith omeprazole. Our results are in accordance with the previous studies. We used 20 mg ofomeprazole daily and assessed our patients at 4 weeks. The healing rate was 63%. Complete healingwas observed in all the cases of grade I oesophagitis and in majority of the patients of grade 11(10 outof 17). The studies indicate that the acid is the major factor in the development of reflux oesophagitis.Omeprazole 20 mg produces 90% reduction in the intragastric acidity whereas 40-60 mg produces 96-98% reduction14-16. Elevation of gastric pH heals peptic oesophagitis but it does not significantly effectthe frequency of postprandial transient lower oesophageal sphincter relaxations and magnitude of basallower oesophageal sphincter pressure17,18. Also omeprazole has no significant effect on gastricemptying in humans19.REFERENCES 1. Sacbs, G., Carlsson, E., Lindberg., P. and Wallmark, B. Gastric H. K-ATPase as therapeutic target.Annu. Rev. Pharmacol. Toxicol., 1988;28:269-84.2. Lind, T., Ccderberg., C., Ekenved, 0., Haglund, U. and Obte, L Effect of omeprazole. -a gastricproton pump inhibitor, on pentagastrin stimulated acid secretion in man. Gut, 1983;24:270- 76.3. Lindberg,. P., Nordberg, P., Alminger, T., Brandstrom, A. and Wallmark, B. The mechanism of actionof the gastric acid secretion inhibitor omeprazole. J.Med.Chem., 1986;29:1327-9.4. Clissold, S.F. and Campoli-Richards, D.M. Omeprazole: a preliminary review of itspharmacodynamics and pharmakinetic properties and therapeutic potential in peptic ulcer disease andZollinger-Ellison Syndrome. Drugs, 1986;3215-47.5. Hendrix, T.R. and Yardley, J.H. Consequences of gastroesophageal reflux. Clin. Gastroenterol.,1976;5:155-74.6. Johnson, LF. and DeMeester, T.R. Twenty-four hour pH monitoring of distal esophagus. Am.J.Gastroenterol., 1974;62:325.32.7. DcMeester, T.R., Johnson, LF., Joseph, GJ., Toscano, M.S., Hall, A.W. and Skinner, D.B. Pattern ofgastroesophageal reflux n health and disease. Ann.Surg., 1916;184:4598. Dehn, T.C.B., Shepherd, HA, Cohn-Jones, D., Kettlewell, M.G.W. and Carroll, NJ. Double blindcomparison of omeprazole (40mg od versus cimetidine 400 mgqid) in the treatment of symptomaticerosive reflux oesophagitis, assessed endoscopically, histologically and by 24 h pH monitoring. Gut,1990;31:509-13.9. Zeitoun, P., Rampat, P., Barbier, P., Isat, J.P., Eriksson, S. and Carlsson, R. Omeprazole (20mg daily)compared to ranitidine (150mg twice daily) in the treatment of esophagits caused by reflux: result of adouble blind randomized multicenter trial in France and Belgium. Gastroenterol. Clin. Biol.,1989;13:457-62.10. Havelund, T., Laursen, LS., Skoubo-Kristensen, E., Anderson, B.N., Pedersen. S.A., Jensen, K.B.,Fenger, C., Hanberg-Sarensen, F. and Lauritsen, K. Omeprazol and ranitidine in treatment ofrefluxesophagitis; double blind comparative triaL Br.Med.J., 1988;296:89-92.11. Klinkenberg-Knol., E.C., Jamsen, J.B., Festers, H.P., Meuwissen, S.G. and Lamers., C.B. Double-blind Multicentre comparison of omeprazole and ranitidine in the treatment of reflux esophagitis.Lancet., 1987;1:349-51.12. Vantrappen, G., Ratgeerts, L., Scburmana, P. and Coenegrachis, J.L Omeprazole (40 mg) is superiorto ranitidine in short-term treatment of ulcerative re0ux esophagitis. Dig.Dis.Sci., 1988;33:529.13. Sandmark., S., Carisson, R., Fausa, 0. and Lundell, L Omeprazole or ranitidine in the treatment ofretlux esophagitis. Results of a double-blind, randomized, Scandinavian multicenter study.Scand.J.Gastroenterol., 1988;23:625-3114. Naesdal, 3., Bodemar, S. and Walan, A. Effect of omeprazole, a substituted benzimidazole, on 24-hintragastric acidity in patients with peptic ulcer disease. Scandi. Gaatroenterol., 1984;19:916-22.15. Sharma, BK., Walt, R.P., Pounder, R.E., Gooses, M.D.. Wood, E.C. and Logan, LH. Optimal doseof oral omeprazole for maximal 24 hour decrease of incragastric acidity. Gut, 1984;25:957.64.16. Walan, A. Clinical perspectives of drugs inhibiting acid secretion -H+ K+- ATPase inhibitors.Scand.J.Gastroenterol. (SuppL), 1986;125:50-54.17. Dowoton, J., Dent, 3., Heddle, R. et al Elevation of gastric pH heals peptic esophagitis. J.Gastroenterol. Hepat.ol., 1987;2317-24.18. Adams, M.H., Ostrosky, J.D. and Kirkwood, C.F. Therapeutic evaluation of omeprazole. Clin.Pharm., 1988;7:725-45.19. Horowitz, M., Hetzel, DJ., Buckle, PJ., Chatterton, B.E. and Sbearman, D.J. The effect ofomeprazole on gastric emptying in patients with duodenal ulcer disease. Br.J. Clin. Pharmacol.,1984;18:791-94.OMEPRAZOLE IN SHORT TERM TREATMENT OFREFLUX OESOPHAGITISPages with reference to book, From 290 To 292 Wasim Jafri, Zaigham Abbas, Saeed Hamid, Hasnain Shah, Haleem Khan ( Department of Medicine, Aga Khan UniversityHospital, Karachi. ) Omeprazole inhibits the gastric secretion by altering the activity of H + /K+ ATPase1,2. The drug itselfis inactive but is converted to the active form, a sulfonamide in the acid milieu of canaliculi of activelysecreting gastric parietal cells3. Though the plasma half life is 60 minutes, the drug binds covalentlywith H+/K+ATPase and duration of action is thereafter increased to greater than 24 hours4. Distaloesophagitis is a complication of gastro-oesophageal reflux. Number and duration of episodes of refluxare important in the pahogenesis5-7. The aim of this study was to assess the efficacy of omeprazole 20mg once daily in our patients for short term treatment of refiux oesophagitis.PATIENTS, METHODS AND RESULTS This was an open labeled, non-comparative single centre study. Outpatients aged 18-70 withendoscopic findings of reflux oesophagitis (grade I to III) were included in the study. Exclusion criteriawere pregnant and lactating mothers, treatment with anti-ulcer or anti-refiux drugs within a week priorto inclusion, patients with concomitant gastric or duodenal ulcer, pyloric stenosis, or any malignantlesion as evident on gastroscopy, oesophageal varices, stricture or Barrett’s oesophagus, previousgastro-oesophageal surgery, patients with abnormal renal or hepatic functions and patients requiringregular use of NSAIDs. Before entry, the severity of symptoms and personal habits were assessed. Acomplete physical examination was performed. Lab investigations including complete blood count(CBC), ESR, urinalysis, blood urea nitrogen (BUN), creatinine, biirubin, alanine aminotransferase(ALT) and alkaline phosphatase were done. Endoscopy was performed within a week prior to theinclusion. Informed consent was taken from all the patients. Patients’ symptoms like heart burns andpains were graded from 0 (none) to 3 (severe). Occasional episodes not interfering with the normalactivity corresponded to grade 1 (mild), episodes interfering with normal activity as grade 2(moderate), frequent episodes constantly interfering with normal activity as grade 3 (severe).Oesophagitis was graded as follows: Grade I, erythema, hyperemia or mucosal friability; grade II,superficial erosions; grade III, ulcerations and grade W, complications, e.g., strictures. Patients wereseen at two and four weeks to record severity of symptoms and any adverse effects, physicalexamination and check of left over capsules. Concomitant use of anti-refiux or other anti-ulcer drugswas forbidden during the study period. Endoscopy was repeated by the same endoscopist at 29±3 daysand laboratory tests performed. Thirty consecutive patients were entered in the study. The clinicalcharacteristics and results are summarized inTable I and II and Figure 1 and 2.Healing defined as complete disappearance of all the lesions and re-epithelization of oesophagealmucosa on endoscopic examination was seen in 19 of 30 patients (68%). Twenty of 30 patients becameasymptomatic and another 9 patients improved symptomatically. No major clinical or biochemical sideeffects were observed. Only one patient complained of some decrease in appetite but he completed thetrial.COMMENTS The randomized clinical trials have proved the superiority of omeprazole over H2 - receptorantagonists8-13. The healing rate at 4 weeks varied between 67-85% as compared to 27-31% whenusing ranitidine. Much higher healing rate was observed at 8 weeks with omeprazole; 85-96% withomeprazole vs 38-50% with ranitidine11-13. There was significantly better symptomatic improvementwith omeprazole. Our results are in accordance with the previous studies. We used 20 mg ofomeprazole daily and assessed our patients at 4 weeks. The healing rate was 63%. Complete healingwas observed in all the cases of grade I oesophagitis and in majority of the patients of grade 11(10 outof 17). The studies indicate that the acid is the major factor in the development of reflux oesophagitis.Omeprazole 20 mg produces 90% reduction in the intragastric acidity whereas 40-60 mg produces 96-98% reduction14-16. Elevation of gastric pH heals peptic oesophagitis but it does not significantly effectthe frequency of postprandial transient lower oesophageal sphincter relaxations and magnitude of basallower oesophageal sphincter pressure17,18. Also omeprazole has no significant effect on gastricemptying in humans19.REFERENCES 1. Sacbs, G., Carlsson, E., Lindberg., P. and Wallmark, B. Gastric H. K-ATPase as therapeutic target.Annu. Rev. Pharmacol. Toxicol., 1988;28:269-84.2. Lind, T., Ccderberg., C., Ekenved, 0., Haglund, U. and Obte, L Effect of omeprazole. -a gastricproton pump inhibitor, on pentagastrin stimulated acid secretion in man. Gut, 1983;24:270- 76.3. Lindberg,. P., Nordberg, P., Alminger, T., Brandstrom, A. and Wallmark, B. The mechanism of actionof the gastric acid secretion inhibitor omeprazole. J.Med.Chem., 1986;29:1327-9.4. Clissold, S.F. and Campoli-Richards, D.M. Omeprazole: a preliminary review of itspharmacodynamics and pharmakinetic properties and therapeutic potential in peptic ulcer disease andZollinger-Ellison Syndrome. Drugs, 1986;3215-47.5. Hendrix, T.R. and Yardley, J.H. Consequences of gastroesophageal reflux. Clin. Gastroenterol.,1976;5:155-74.6. Johnson, LF. and DeMeester, T.R. Twenty-four hour pH monitoring of distal esophagus. Am.J.Gastroenterol., 1974;62:325.32.7. DcMeester, T.R., Johnson, LF., Joseph, GJ., Toscano, M.S., Hall, A.W. and Skinner, D.B. Pattern ofgastroesophageal reflux n health and disease. Ann.Surg., 1916;184:4598. Dehn, T.C.B., Shepherd, HA, Cohn-Jones, D., Kettlewell, M.G.W. and Carroll, NJ. Double blindcomparison of omeprazole (40mg od versus cimetidine 400 mgqid) in the treatment of symptomaticerosive reflux oesophagitis, assessed endoscopically, histologically and by 24 h pH monitoring. Gut,1990;31:509-13.9. Zeitoun, P., Rampat, P., Barbier, P., Isat, J.P., Eriksson, S. and Carlsson, R. Omeprazole (20mg daily)compared to ranitidine (150mg twice daily) in the treatment of esophagits caused by reflux: result of adouble blind randomized multicenter trial in France and Belgium. Gastroenterol. Clin. Biol.,1989;13:457-62.10. Havelund, T., Laursen, LS., Skoubo-Kristensen, E., Anderson, B.N., Pedersen. S.A., Jensen, K.B.,Fenger, C., Hanberg-Sarensen, F. and Lauritsen, K. Omeprazol and ranitidine in treatment ofrefluxesophagitis; double blind comparative triaL Br.Med.J., 1988;296:89-92.11. Klinkenberg-Knol., E.C., Jamsen, J.B., Festers, H.P., Meuwissen, S.G. and Lamers., C.B. Double-blind Multicentre comparison of omeprazole and ranitidine in the treatment of reflux esophagitis.Lancet., 1987;1:349-51.12. Vantrappen, G., Ratgeerts, L., Scburmana, P. and Coenegrachis, J.L Omeprazole (40 mg) is superiorto ranitidine in short-term treatment of ulcerative re0ux esophagitis. Dig.Dis.Sci., 1988;33:529.13. Sandmark., S., Carisson, R., Fausa, 0. and Lundell, L Omeprazole or ranitidine in the treatment ofretlux esophagitis. Results of a double-blind, randomized, Scandinavian multicenter study.Scand.J.Gastroenterol., 1988;23:625-3114. Naesdal, 3., Bodemar, S. and Walan, A. Effect of omeprazole, a substituted benzimidazole, on 24-hintragastric acidity in patients with peptic ulcer disease. Scandi. Gaatroenterol., 1984;19:916-22.15. Sharma, BK., Walt, R.P., Pounder, R.E., Gooses, M.D.. Wood, E.C. and Logan, LH. Optimal doseof oral omeprazole for maximal 24 hour decrease of incragastric acidity. Gut, 1984;25:957.64.16. Walan, A. Clinical perspectives of drugs inhibiting acid secretion -H+ K+- ATPase inhibitors.Scand.J.Gastroenterol. (SuppL), 1986;125:50-54.17. Dowoton, J., Dent, 3., Heddle, R. et al Elevation of gastric pH heals peptic esophagitis. J.Gastroenterol. Hepat.ol., 1987;2317-24.18. Adams, M.H., Ostrosky, J.D. and Kirkwood, C.F. Therapeutic evaluation of omeprazole. Clin.Pharm., 1988;7:725-45.19. Horowitz, M., Hetzel, DJ., Buckle, PJ., Chatterton, B.E. and Sbearman, D.J. The effect ofomeprazole on gastric emptying in patients with duodenal ulcer disease. Br.J. Clin. Pharmacol.,1984;18:791-94.

Omeprazole in short term treatment of reflux oesophagitis

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Omeprazole in short term treatment of reflux oesophagitis

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