Endoscopic and histologic findings in patients referred for endoscopy by general practitioners in 2008-2013
Endoskopowe i histopatologiczne wyniki badania endoskopowego przełyku pacjentów skierowanych przez lekarzy rodzinnych w latach 2008-2013
Gastroesophageal reflux disease (GERD) is caused by retrograde flow of stomach contents (1). GERD can present as non-erosive reflux disease (NERD) or as erosive esophagitis (EE) (2). The former is recognized when typical symptoms of GERD occur without visible mucosal injury during endoscopy the latter present with histopathological changes in esophageal mucosa (2-7). Long-standing gastroesophageal reflux disease is a risk factor for Barret’s esophagus and esophageal cancer (8-11). Symptoms of esophageal cancer could resemble these of GERD (12-17).
The aim of the study was to present endoscopic and histopathologic findings in the esophagus in patients referred by general practitioners to the Department of Gastrointestinal and General Surgery, Wroclaw Medical University in years 2008-2013 with initial diagnosis of GERD, in which the family doctor did not achieve the expected results of the implemented conservative treatment with proton pump inhibitors.
The study group consisted of patients who were undergoing endoscopy for gastroesophageal reflux in year 2008-2013. The retrospective analysis of documentation was performed. The inclusion criteria was the referral letter from his General Practitioner that the patient did not have improvement after empirical therapy for reflux oesophagitis.
The clinical material included 122 patients. They represented 1.9% of all patients diagnosed and treated with diseases of the gastrointestinal tract in the department.
Continuous variable was presented as means and standard deviation, and compared with Student’s t-test. Discrete variables were presented as numbers and percentages and compared with chi2 test with Yates correction when necessary.
Multivariate analysis was performed with Classification and Regression trees (CART) analysis.
The independent variable were chosen on the basis of the prevalence of the results. Moreover, esophageal cancer was chosen as an independent variable taken because of its importance as a cause of death.
P less than 0.05 was considered as significant.
On endoscopy it was found a wide range of macroscopic changes starting from hiatal hernia and ending with Barrett’s esophagus. Two types of complications of gastroesophageal reflux disease was distinguished – benign and malignant.
The most prevalent diagnosis was hernia hiatus oesophagi (n = 41; 33.6%) and the least Barrett’s esophagus (n = 6; 4.9%).
In men the most prevalent diagnosis was adenocarcinoma (n = 22; 31.0%) and in women hiatal hernia (n = 24; 47.1%).
Hiatal hernia is related with female gender.
Near 60% patients were found to have histopathologic abnormalities. The most common finding was oesophageal cancer (n = 22; 18.0%) and the least dysplasia (n = 7; 5.7%). In men the most prevalent diagnosis was adenocarcinoma (n = 21; 29.6%) and in women esophagitis (n = 8; 11.3%) and Barrett’s esophagus (n = 8; 11.3%).
The study group consisted of 122 patients aged 55.8 ± 14.1 (range 19-89). There were 71 men aged 55.7 ± 14.7 and 51 women aged 56.0 ± 14.0. Men constituted a higher percentage of studied group than women (58.2 vs 41.8%; p = 0.01).
1. Vakil N, van Zanten SV, Kahrilas P et al.; Global Consensus Group: The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol 2006; 101(8): 1900-1920.
2. Sifrim D, Holloway R: Transient lower esophageal sphincter relaxations: how many or how harmful? Am J Gastroenterol 2001; 96: 2529-2532.
3. Liakakos T, Karamanolis G, Patapis P et al.: Gastroesophageal reflux disease: medical or surgical treatment. Gastroenterol Res Pract 2009; 2009: 371580.
4. Tarnowski W, Bielecki K: Refluks żołądkowo-przełykowy – patofizjologia, diagnostyka, leczenie. Medical Adviser 2001; 3.
5. Wallner G, Solecki M, Tarnowski W et al.: Choroba refluksowa przełyku – zalecenia dla praktyki klinicznej. Wideochir Tech Małoinwaz 2009; 4 (suppl. 1): S53-S61.
6. Parasa S, Sharma P: Complications of gastro-oesophageal reflux disease. Best Pract Res Clin Gastroenterol 2013; 27(3): 433-442.
7. Armstrong D: Endoscopic evaluation of gastro-esophageal reflux disease. Yale J Biol Med 1999; 72(2-3): 93-100.
8. Belhocine K, Galmiche JP: Epidemiology of the complications of gastroesophageal reflux disease. Dig Dis 2009; 27(1): 7-13.
9. Pisegna J, Holtmann G, Howden CW et al.: Review article: oesophageal complications and consequences of persistent gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2004; 20 (suppl. 9): 47-56.
10. Theisen J, Nigro JJ, DeMeester TR et al.: Chronology of the Barrett’s metaplasia-dysplasia-carcinoma sequence. Dis Esophagus 2004; 17(1): 67-70.
11. Spechler SJ, Fitzgerald RC, Prasad GA et al.: History, molecular mechanisms, and endoscopic treatment of Barrett’s esophagus. Gastroenterology 2010; 138(3): 854-869.
12. Czarzasty W, Chybicki J: Współczesne metody rozpoznawania i leczenia przełyku Barretta. Cancer Surgery 2011; 1: 19-22.
13. Choroby przełyku. [W:] Da?browski A (red.): Gastroenterologia. Wielka Interna. Medical Tribiune Polska. Warszawa 2010: 10-28.
14. Yamada T: Podre?cznik gastroenterologii. PZWL, Warszawa 2005: 255-258.
15. Hvid-Jansen F, Pedrsen L, Drewes A et al.: Incidens of adenocarcinoma among patients with Barrett’s esophagus. Engl J Med 2011; 365(15): 1375-1383.
16. Roman S, Kahrilas PJ: Mechanisms of Barrett’s esophagus (clinical): LES dysfunction, hiatal hernia, peristaltic defects. Best Pract Res Clin Gastroenterol 2015; 29(1): 17-28.
17. Runge TM, Abrams JA, Shaheen NJ: Epidemiology of Barrett’s Esophagus and Esophageal Adenocarcinoma. Gastroenterol Clin North Am 2015; 44(2): 203-231.
18. Fass R, Shapiro M, Dekel R et al.: Systematic review: proton-pump inhibitor failure in gastro-oesophageal reflux disease – where next? Aliment Pharmacol Ther 2005; 22: 79-94.
19. Lowe RC, Wolfe MM: The pharmacological management of gastroesophageal reflux disease. Minerva Gastroenterol Diabetol 2004; 50(3): 227-237.
20. Zerbib F, Duriez A, Roman S et al.: Determinants of gastro-oesophageal reflux perception in patients with persistent symptoms despite proton pump inhibitors. Gut 2008; 57(2): 157-160.
21. Ferguson DD: Evaluation and management of benign esophageal strictures. Dis Esophagus 2005; 18(6): 359-364.
22. Hoang CD, Koh PS, Maddaus MA: Short esophagus and esophageal stricture. Surg Clin North AM 2005; 85(3): 433-451.
23. Pregun I, Hritz I, Tulassay Z et al.: Peptic esophageal stricture: medical treatment. Dig Dis 2009; 27(1): 31-37.
24. Triadafilopoulos G: Endotherapy and surgery for GERD. J Clin Gastroenterol 2007; 41 (suppl. 2): S87-96.
25. Falk GW: Risk factors for esophageal cancer development. Surg Oncol Clin N Am 2009; 18(3): 469-485.
26. Cossentino MJ, Wong RK: Barrett’s esophagus and risk of esophageal adenocarcinoma. Semin Gastrointest Dis 2003; 14(3): 128-135.
27. Spechler SJ, Goyal RK: Barrett’s esophagus. N Engl J Med 1986; 315: 362-371.
28. Lagergren J, Bergstrom R, Lindgren A et al.: Symptomatic gastroesophageal re?ux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999; 340: 825-831.
29. Cook MB, Chow WH, Devesa SS: Oesophageal cancer incidence in the United States by race, sex, and histologic type, 1977-2005. Br J Cancer 2009; 101: 855-859.
30. Kahrilas PJ: Clinical practice. Gastroesophageal re?ux disease. N Engl J Med 2008; 359: 1700-1707.
31. Whiteman DC, Sadeghi S, Pandeya N et al.: Combined effects of obesity, acid re?ux and smoking on the risk of adenocarcinomas of the oesophagus. Gut 2008; 57: 173-180.
32. Abnet CC, Freedman ND, Hollenbeck AR et al.: A prospective study of BMI and risk of oesophageal and gastric adenocarcinoma. Eur J Cancer 2008; 44: 465-471.
33. Vaughan TL, Davis S, Kristal A et al.: Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev 1995; 4: 85-92.
34. Ranka S, Gee JM, Johnson IT et al.: Non-steroidal anti-in?ammatory drugs, lower oesophageal sphincter-relaxing drugs and oesophageal cancer. A case-control study. Digestion 2006; 74: 109-115.
35. Lagergren J, Bergstrom R, Adami HO et al.: Association between medications that relax the lower esophageal sphincter and risk for esophageal adenocarcinoma. Ann Intern Med 2000; 133: 165-175.
36. Vaughan TL, Farrow DC, Hansten PD et al.: Risk of esophageal and gastric adenocarcinomas in relation to use of calcium channel blockers, asthma drugs, and other medications that promote gastroesophageal re?ux. Cancer Epidemiol Biomarkers Prev 1998; 7: 749-756.
37. Fortuny J, Johnson CC, Bohlke K et al.: Use of anti-in ?ammatory drugs and lower esophageal sphincter-relaxing drugs and risk of esophageal and gastric cancers. Clin Gastroenterol Hepatol 2007; 5: 1154-1159.e3.
38. Alexandre L, Broughton T, Loke Y et al.: Meta-analysis: risk of esophageal adenocarcinoma with medications which relax the lower esophageal sphincter. Dis Esophagus 2011; 25(6): 535-544.
39. Galindo G, Vassalle J, Marcus SN et al.: Multimodality evaluation of patients with gastroesophageal reflux disease symptoms who have failed empiric proton pump inhibitor therapy. Dis Esophagus 2013; 26(5): 443-450.
40. Kim YS, Kim N, Kim GH: Sex and Gender Differences in Gastroesophageal Reflux Disease. J Neurogastroenterol Motil 2016; 22(4): 575-588.