Comparison of the patients with diffuse antral and multifocal atrophic gastritis for gastric juice ascorbic acid levels and epithelial cell proliferations

Öz

Background/aim: Diffuse antral gastritis (DAG) is a duodenal ulcer phenotype of chronic Helicobacter pylori gastritis, while multifocal atrophic gastritis (MAG) is a gastric cancer phenotype. The aim of this study was to investigate ascorbic acid (vitamin C) levels in the gastric juice in patients with DAG and MAG, to compare the gastric epithelial cell proliferation rates between the groups and also to examine any correlation between ascorbic acid levels in gastric juice and the cell proliferation rates. Materials and methods: Thirty-seven patients with chronic H. pylori gastritis (27 MAG, 10 DAG) were included in the study (male/female: 15/22, range: 19-74, mean age: 43.6 yrs). Ascorbic acid concentrations in fasting plasma and gastric juice samples of the patients were measured. Loss of maturation in foveolar epithelium due to cell proliferation was shown immunohistochemically using cytokeratin-20 antibody in antral and corporal regions of both patient groups. Results: There was no significant difference in plasma ascorbic acid levels between the two groups. No statistically significant difference could be demonstrated in gastric juice ascorbic acid concentrations between patients with DAG and MAG (0.93±0.97 mg/dl and 0.96±1.12 mg/dl, respectively; p>0.05). Immunohistochemical examination revealed that staining for cytokeratin- 20 was significantly less in MAG patients than in those with DAG (74.7% vs 90.9%, respectively; p

Anahtar Kelimeler

• Ascorbic acid, H. pylori, chronic gastritis, cell proliferation

Diffüz antral gastrit ve multifokal atrofik gastritli hastalarda mide sıvısı askorbik asit düzeyleri ve epitel hücre proliferasyonlarının karşılaştırılması

Öz

Giriş ve amaç: Diffüz antral gastrit (DAG), kronik Helicobacter pylori gastritinin duodenal ülser fenotipini, multifokal atrofik gastrit (MAG) ise gastrik kanser fenotipini oluşturmaktadır. Bu çalışmada DAG ve MAG’lı olgularda gastrik sıvı askorbik asit düzeylerinin incelenmesi, grupların mide epitel hücre proliferasyon oranları açısından karşılaştırılması ve mide sıvısı askorbik asit (C vitamini) düzeyleriyle hücre proliferasyon oranları arasındaki olası korelasyonların araştırılması amaçlanmıştır. Gereç ve yöntem: H. pylori’ye bağlı 27 MAG, 10 DAG saptanan 37 hasta çalışmaya alındı (22 kadın, 15 erkek, 19-74, yaş ort: 43,6). Hastaların plazma ve gastrik sıvı örneklerinde askorbik asit düzeyleri ölçüldü. Olguların antrum ve korpuslarında hücre proliferasyonundan dolayı foveolar epiteldeki maturasyon kaybının varlığı, sitokeratin-20 (CK-20) antikoru kullanılarak immunohistokimyasal yöntemle gösterildi. Bulgular: Her iki grubun plazma askorbik asit düzeyleri arasında anlamlı farklılık yoktu. Gruplar, mide sıvısı askorbik asit düzeyleri açısından karşılaştırıldığında istatistiksel anlamlı bir farklılık gözlenmedi (DAG ve MAG için sırasıyla; 0.93±0.97, 0.96±1.12mg/dl, p > 0.05) MAG grubunda CK-20 için boyanma yüzdesi DAG grubundakilere göre anlamlı derecede düşüktü (%74.7 ve %90.9, p < 0.01). Boyanma yüzdeleriyle mide sıvısı askorbik asit değerleri arasında bir korelasyon saptanmadı. Sonuç: Bu çalışmada diffüz antral gastrit ve multifokal atrofik gastritli hastalar arasında mide sıvısı askorbik asit düzeyleri açısından anlamlı farklılık bulunmamıştır. Ancak, multifokal atrofik gastritin intestinal tip gastrik karsinogenez sürecinin proksimal aşamalarında yer aldığını destekleyecek şekilde, bu gastrit formunda epitel hücre proliferasyonunun artmış olduğu gösterilmiştir.

Anahtar Kelimeler

• Askorbik asit, H. pylori, kronik gastrit, hücre proliferasyonu

Kaynakça

1. Kuipers EJ, Uyterlinde AM, Peña AS, et al. Long-term sequelae of Helicobacter pylori gastritis. Lancet 1995; 345: 1525-28.
2. Houghton J, Fox JG, Wang TC. Gastric cancer: laboratory bench to clinic. J Gastroenterol Hepatol 2002; 17: 495-502.
3. Hansson L, Nyren O, Hsing A, et al. The risk of stomach cancer in patients with gastric or duodenal ulcer disease. N Engl J Med 1996; 335: 242-49.
4. Faraji EI, Frank BB. Multifocal atrophic gastritis and gastric car- cinoma. Gastroenterol Clin North Am 2002; 31: 499-516.
5. Ruiz B, Rood JC, Fontham ETH, et al. Vitamin C concentrations in gastric juice before and after anti Helicobacter pylori treatment. Am J Gastroenterol 1994; 89: 533-39.
6. Banerjee S, Hawksby C, Miller S, et al. Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid. Gut 1994; 35: 317-22.
7. Rokkas T, Papatheodorou G, Karameris A, et al. Helicobacter pylo- ri infection and gastric juice vitamin C levels. Impact of eradicati- on. Dig Dis Sci 1995; 40: 615-21.
8. Cahill RJ, Kilgallen C, Beattie S, et al. Gastric epithelial cell kine- tics in the progression from normal mucosa to gastric carcinoma. Gut 1996; 38: 177-81.

9. Houghton J, Macera-Bloch LS, Harrison L, et al. Tumor necrosis factor alpha and interleukin 1beta up-regulate gastric mucosal fas antigen expression in Helicobacter pylori infection. Infect Immun 2000; 68: 1189-95.
10. de Freitas D, Urbano M, Goulao MH, et al. The effect of Helicobac- ter pylori infection on apoptosis and cell proliferation in gastric epithelium. Hepatogastroenterology 2004; 51: 876-82.
11. De Luca A, De Falco M, Iaquinto S, et al. Effects of Helicobacter pylori infection on cell cycle progression and the expression of cell cycle regulatory proteins. J Cell Physiol 2004; 200: 334-42.
12. Sobola G, Schorah C, Sanderson M, et al. Ascorbic acid in the hu- man stomach. Gastroenterology 1989; 97: 357-63.
13. Correa P. Chronic gastritis: a clinico-pathological classification. Am J Gastroenterol 1988; 83: 504-9.
14. Sipponen P, Stolte M. Clinical impact of routine biopsies of the gast- ric antrum and body. Endoscopy 1997; 29: 671-8.
15. Schwerer MJ, Kraft K, Baczako K. Structural changes in the gastric foveolar epithelium in Helicobacter pylori-positive gastritis revealed by keratin immunohistochemistry. Hum Pathol 1997; 28: 1260-7.
16. Lauwers GY, Furman J, Michael LE, et al. Cytoskeletal and kinetic epithelial differences between NSAID gastropathy and Helicobacter pylori gastritis: an immunohistochemical determination. Histopat- hology. 2001; 39: 133-40.
17. Correa P, Fontham ET, Ruiz B, et al. Gastric juice ascorbic acid af- ter intravenous injection: effect of ethnicity, pH, and Helicobacter pylori infection. J Natl Cancer Inst 1995; 87: 52-3.
18. Yönetçi N, Akarca US, Özütemiz AÖ, ve ark. Gastroduodenal bozuk- luklarda askorbik asit. T Klin Gastroenterohepatoloji 1995; 6: 238- 44.
19. Rathbone BJ, Johnson AW, Wyatt JI, et al. Ascorbic acid: a factor concentrated in human gastric juice. Clin Sci 1989; 76: 237-41.
20. Correa P. Helicobacter pylori and gastric carcinogenesis. Am J Surg Pathol 1995; 19 (Suppl. 1): S37-S43.
21. Cahill RJ, Sant S, Beattie S, et al. Helicobacter pylori and increased epithelial cell proliferation: a risk factor for cancer. Eur J Gastro- enterol Hepatol 1994; 6: 1123-7.
22. Brenes F, Ruis B, Correa P, et al. Helicobacter pylori causes hyperproliferation of the gastric epithelium: pre and post eradicati- on indices of proliferating cell nuclear antigen. Am J Gastroenterol 1993; 88: 1870-5.
23. Correa P. The biological model of gastric carcinogenesis. IARC Sci Publ 2004; 157: 301-10.
24. Fong LY, Lee JS, Chan WC, et al. Zinc deficiency and the develop- ment of esophageal and forestomach tumors in Sprague-Dawley rats fed precursors of N-nitroso-N-benzylmethylamine. J Natl Can- cer Inst 1984; 72: 419-25.
25. Bartsch J, Ohshima H, Shuker D, et al. Human exposure to endoge- nous N-nitroso compounds: Quantitative estimates in subjects at high risk for cancer of the oral cavity, esophagus, stomach, and uri- nary bladder. Cancer Surv 1989; 8: 335-62.
26. Knekt P, Jarvinen R, Dich J, et al. Risk of colorectal and other gast- ro-intestinal cancers after exposure to nitrate, nitrite and N-nitroso compounds: A follow-up study. Int J Cancer 1999; 80: 852-56.
27. van Loon A, Botterweck A, Goldbohm R, et al. Intake of nitrate and nitrite and the risk of gastric cancer: A prospective cohort study. Br J Cancer 1998; 78: 129-35.