Inflamation and intestinal metaplasia in the squamocolumnar junction: The role of Helicobacter pylori infection

Öz

Background/aim: It is reported that the incidence of adenocarcinoma of the cardia and esophagus has increased in western countries simultaneously with a decrease in Helicobacter pylori (Hp) prevalence. In Turkey, Hp positivity is still above 75% in the adult population. In patients without classic Barrett's esophagus, adenocarcinomas of the gastroesophageal junction appear to arise from foci of intestinal metaplasia (IM) at the squamocolumnar junction (SCJ), which occur in 9-36% of patients undergoing gastroscopy. IM is assumed to be a consequence of chronic inflammation. Like inflammation at the SCJ, IM at the cardia has also been associated either with Hp gastritis or with gastroesophageal reflux disease. The aim of this study was detection of IM and inflammation at SCJ in a population with high Hp positivity, by multiple biopsy specimens, and definition of probable correlations. Materials and methods: In this study, endoscopic biopsy specimens were taken from 38 patients (30 male, 8 female) who presented for esophagogastroduodenoscopy (from gastric fundus, corpus, antrum, second portion of duodenum, SCJ, esophagus). Biopsy specimens were examined by one pathologist for inflammation, activity, and presence of atrophy and gastric-cardiac IM. Results: Chronic Hp gastritis was detected in 29 of 36 patients with gastritis; histologic esophagitis in 28 of 38 patients (73.5%); inflammation at SCJ in 37 of 38 patients (97%); and IM at SCJ in 5 of 38 patients (13%)(4 complete, 1 incomplete). A significant correlation was detected between inflammation and activity in fundus, corpus and antrum (p

Anahtar Kelimeler

• Squamocolumnar junction, intestinal metaplasia

Skuamokolumnar bileşkede inflamasyon ve intestinal metaplazi: Helicobacter pylori infeksiyonunun rolü

Öz

Giriş ve amaç: Batı ülkelerinde Helicobacter pylori (Hp) prevalansının azalması ile birlikte, özofagus ve kardiya adenokarsinomalarının insidansında artış olduğu bildirilmektedir. Türkiye’de yetişkin popülasyonda Hp pozitifliği halen %75’in üzerindedir. Klasik Barrett özofagusu bulunmayan hastalarda, gastroözofageal bileşkedeki adenokarsinomaların, gastroskopiye giren hastaların % 9-36’sında saptanan, skuamokolumnar bileşkedeki intestinal metaplazi (İM) odaklarından köken aldıkları görülmektedir. İM’nin, kronik inflamasyonun bir sonucu olduğu var sayılmaktadır. Skuamokolumnar bileşke (SKB)’deki İM’de, bu bölgedeki inflamasyon gibi, Hp veya gastroözofageal reflü hastalığı ile ilişkilidir. Bu çalışmanın amacı, SKB’deki inflamasyon ve İM’nin, Hp pozitifliği yüksek olan bir popülasyonda araştırılması; sözkonusu bakteri ile multipl endoskopik biyopsi örnekleri alınarak olası korelasyonlarını belirlemektir. Gereç ve yöntem: Bu çalışmada, özofagogastroduodenoskopi için başvuran 38 hastada (30 erkek, 8 kadın) gastrik fundus, korpus, antrum, postbulber bölge, SKB ve özofagustan endoskopik biyopsiler alındı. Biyopsi örnekleri tek bir patolog tarafından inflamasyon, aktivite, atrofi varlığı, gastrik ve kardiyak İM açısından değerlendirildi. Bulgular: Sonuçta çalışma grubunda 36 gastrit hastasının 29’unda kronik Hp gastriti; 38 hastanın 28’inde (% 73.5) histolojik özofajit; 38 hastanın 37’sinde (%97) SKB’de inflamasyon, 5’inde (%13) İM (4’ü komplet, 1’i inkomplet) saptandı. Fundus, korpus ve antrumdaki inflamasyon ve aktivite arasında anlamlı korelasyon saptandı (p

Anahtar Kelimeler

• Skuamokolumnar bileşke, intestinal metaplazi

Kaynakça

1. Devesa SS, Blot WJ, Fraumeni JF Jr. Changing patterns in the inci- dence of esophageal and gastric carcinoma in the United States. Cancer 1998; 83: 2049-53.
2. Cameron AJ, Lomboy CT, Pera M, et al. Adenocarcinoma of the esophagogastric junction and Barrett’s esophagus. Gastroentero- logy 1995; 109: 1541-6.
3. Clark GW, Smyrk TC, Burdiles P, et al. Is Barrett’s metaplasia the source of adenocarcinomas of the cardia? Arch Surg 1994; 129: 609-14.
4. Fenoglio-Preiser CM, Noffsinger AE, Stemmerman GM, et al. Gast- rointestinal pathology. An atlas and text, 2ndedition, Philadelphia: Raven Lippincott, 1999: 133.
5. Chandrasoma PT, Lokuhetty DM, Demeester TR, et al. Definition of histopathologic changes in gastroesophageal reflux disease. Am J Surg Pathol 2000; 24: 344-51.
6. Madri JA. Inflammation and healing. In: Kissane JM, ed. Ander- son’s pathology. Volume 1. 9thed. St. Louis, MO: Mosby, 1990: 67- 110.
7. Riddell RH. The biopsy diagnosis of gastroesophageal reflux dise- ase, "carditis", and Barrett’s esophagus and sequela of therapy. Am J Surg Pathol 1996 (20 suppl 1); S31-50. Review.
8. Clark GWB, Ireland AP, Chandrasoma P, et al. Inflammation and metaplasia in the transitional epithelium of the gastrooesophageal junction-A new marker for gastroesophageal reflux disease. Gastro- enterology 106 (4): A63-A63 Suppl. S Apr 1994.

9. Genta RM, Huberman RM, Graham DY. The gastric cardia in Heli- cobacter pylori infection. Hum Pathol 1994; 25: 915-9.
10. Goldblum JR, Vicari JJ, Falk GW, et al. Inflammation and intesti- nal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology 1998; 114: 633-9.
11. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and speci- alized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997; 226: 522-30; dis- cussion 530-32.
12. Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophago- gastric junction: prevalence and clinical data. Gastroenterology 1999; 116: 277-85.
13. Macdonald CE, Wicks AC, Playford RJ. Ten years’ experience of screening patients with Barrett’s oesophagus in a university teac- hing hospital. Gut 1997; 41: 303-7.
14. Spechler SJ, Zeroogian JM, Antonioli DA, et al. Prevalence of me- taplasia at the gastro-oesophageal junction. Lancet 1994; 344: 1533-6.
15. Bytzer P, Christensen PB, Damkier P, et al. Adenocarcinoma of the esophagus and Barrett’s esophagus: a population-based study. Am J Gastroenterol 1999; 94: 86-91.
16. Conio M, Cameron AJ, Romero Y, et al. Secular trends in the epide- miology and outcome of Barrett’s oesophagus in Olmsted County, Minnesota. Gut 2001; 48: 304-9.
17. Johnston MH, Hammond AS, Laskin W, et al. The prevalance and clinical characteristics of short segments of specialized intestinal metaplasia in the distal esophagus on routine endoscopy. Am J Gastroenterol 1996; 91: 1507-11.
18. Nandurkar S, Talley NJ, Martin CJ, et al. Short segment Barrett’s oesophagus: prevalence, diagnosis and associations. Gut 1997; 40: 710-5.
19. Spechler SJ. The role of gastric carditis in metaplasia and neopla- sia at the gastroesophageal junction. Gastroenterology 1999; 117: 218-28. Review.
20. Trudgill NJ, Suvarna SK, Kapur KC, et al. Intestinal metaplasia at the squamocolumnar junction in patients attending for diagnostic gastroscopy. Gut 1997; 41: 585-9.
21. Ormsby AH, Kilgore SP, Goldblum JR, et al. The location and fre- quency of intestinal metaplasia at the esophagogastric junction in 223 consecutive autopsies: Implications for patient treatment and preventive strategies in Barrett’s esophagus. Mod Pathol 2000; 13: 614-20.
22. Blaser MJ. Hypothesis: The changing relationships of Helicobacter pylori and humans: implications for health and disease. J Infect Dis 1999; 179: 1523-30.
23. Özden A ve ark. Helicobacter pylori infeksiyonunun ülkemizdeki se- roepidemiyolojisi. Turk J Gastroenterol 1992; 3(4): 664-68.
24. Özden A ve ark. Dispeptik yakınmalarla başvuran hastalarda H. pylori infeksiyonu ile dispepsi subgrupları ve dispeptik semptomlar arasındaki ilişki. Turk J Gastroenterol 2000; 11, Supplement 1.
25. Oksanen A, Sipponen P, Karttunen R, et al. Inflammation and intes- tinal metaplasia at the squamocolumnar junction in young patients with or without Helicobacter pylori infection. Gut 2003; 52: 194-8.
26. Chandrasoma PT, Der R, Ma Y, et al. Histology of the gastroesop- hageal junction: an autopsy study. Am J Surg Pathol 2000; 24: 402- 9.
27. Kilgore SP, Ormsby AH, Gramlich TL, et al. The gastric cardia: fact or fistion? Am J Gastroenterol 2000; 95: 921-4.
28. Bowrey DJ, Clark GW, Williams GT. Patterns of gastritis in patients with gastro-oesophageal reflux disease. Gut 1999; 45: 798-803.
29. Genta RM, Graham DY. Comparison of biopsy sites for the histopat- hologic diagnosis of Helicobacter pylori: a topographic study of H. pylori density and distribution. Gastrointest Endosc 1994; 40: 342- 5.
30. Filipe MI, Potet F, Bogomoletz WV, et al. Incomplete sulphomucin- secreting intestinal metaplasia for gastric cancer. Preliminary data from a prospective study from three centers. Gut 1985; 26: 1319-26.
31. Voutilainen M, Farkkila M, Juhola M, et al. Complete and incomp- lete intestinal metaplasia at the oesophagogastric junction: preva- lences and associations with endoscopic erosive oesophagitis and gastritis. Gut 1999; 45: 644-8.
32. Aste H, Bonelli L, Ferraris R, et al. Gastroesophageal reflux dise- ase: relationship between clinical and histological features. GOS- PE. Gruppo Operativo per lo Studio delle Precancerosi dell'Esofa- go. Dig Dis Sci 1999; 44: 2412-8.
33. Eloubeidi MA, Provenzale D. Does this patient have Barrett’s esop- hagus? The utility of predicting Barrett’s esophagus at the index en- doscopy. Am J Gastroenterol 1999; 94: 937-43.
34. Hackelsberger A, Gunther T, Schultze V, et al. Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease? Gut 1998; 43: 17-21.