Helicobacter pylori の Cytotoxin-associatedgene A (CagA)陽性株感染および生活習慣と慢性萎縮性胃炎との関係
目的 Helicobacter pylori (H. pylori)のサイトトキシン関連遺伝子 A (Cytotoxin-associated gene A, CagA)陽性株と CagA 陰性株の慢性萎縮性胃炎に対するリスクの評価を行うとともに，慢性萎縮性胃炎に関連する生活習慣要因についても検討した。 方法 福岡県南部の農村地域の基本健康診査を受診した30歳-64歳の住民738人（男295人，女443人）に研究参加を要請し全員から協力を得，対象とした。基本健康診査受診時に生活習慣の情報を得るとともに，採血を行い，H. pylori 抗体，CagA 抗体，血清ぺプシノーゲンI値（PGI）とぺプ...
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| Published in | 日本公衆衛生雑誌 Vol. 49; no. 11; pp. 1152 - 1158 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
日本公衆衛生学会
2002
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0546-1766 2187-8986 |
| DOI | 10.11236/jph.49.11_1152 |
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| Abstract | 目的 Helicobacter pylori (H. pylori)のサイトトキシン関連遺伝子 A (Cytotoxin-associated gene A, CagA)陽性株と CagA 陰性株の慢性萎縮性胃炎に対するリスクの評価を行うとともに，慢性萎縮性胃炎に関連する生活習慣要因についても検討した。 方法 福岡県南部の農村地域の基本健康診査を受診した30歳-64歳の住民738人（男295人，女443人）に研究参加を要請し全員から協力を得，対象とした。基本健康診査受診時に生活習慣の情報を得るとともに，採血を行い，H. pylori 抗体，CagA 抗体，血清ぺプシノーゲンI値（PGI）とぺプシノーゲンII値（PGII）を測定した。 本研究では慢性萎縮性胃炎の診断を PGIと PGIIの値により血清学的に行った。すなわち，PGI<70 μg/l かつ PGI/PGII比<3.0のものを血清学的慢性萎縮性胃炎とした。 成績 H. pylori 抗体陰性を基準にした時，男では H. pylori 抗体陽性・CagA 抗体陽性群の慢性萎縮性胃炎に対するオッズ比は4.26 (95%CI, 2.22-8.17), H. pylori 抗体陽性・CagA 抗体陰性群では3.87 (95%CI, 1.95-7.68)であった。一方，女では前者のオッズ比は4.92 (95%CI, 3.06-7.92)，後者では3.02 (95%CI, 1.23-6.35)であった。慢性萎縮性胃炎に対するリスクは CagA 陽性株感染の方が CagA 陰性株感染より大きいことが示唆された。 生活習慣では緑茶の飲用が慢性萎縮性胃炎に対する抑制因子として働いていた。特に，その効果は CagA 陽性株感染の場合に顕著であった。 結論 慢性萎縮性胃炎に対するリスクは CagA 陽性株感染の方が CagA 陰性株感染より大きいことが示唆された。 |
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| AbstractList | 目的 Helicobacter pylori (H. pylori)のサイトトキシン関連遺伝子 A (Cytotoxin-associated gene A, CagA)陽性株と CagA 陰性株の慢性萎縮性胃炎に対するリスクの評価を行うとともに，慢性萎縮性胃炎に関連する生活習慣要因についても検討した。 方法 福岡県南部の農村地域の基本健康診査を受診した30歳-64歳の住民738人（男295人，女443人）に研究参加を要請し全員から協力を得，対象とした。基本健康診査受診時に生活習慣の情報を得るとともに，採血を行い，H. pylori 抗体，CagA 抗体，血清ぺプシノーゲンI値（PGI）とぺプシノーゲンII値（PGII）を測定した。 本研究では慢性萎縮性胃炎の診断を PGIと PGIIの値により血清学的に行った。すなわち，PGI<70 μg/l かつ PGI/PGII比<3.0のものを血清学的慢性萎縮性胃炎とした。 成績 H. pylori 抗体陰性を基準にした時，男では H. pylori 抗体陽性・CagA 抗体陽性群の慢性萎縮性胃炎に対するオッズ比は4.26 (95%CI, 2.22-8.17), H. pylori 抗体陽性・CagA 抗体陰性群では3.87 (95%CI, 1.95-7.68)であった。一方，女では前者のオッズ比は4.92 (95%CI, 3.06-7.92)，後者では3.02 (95%CI, 1.23-6.35)であった。慢性萎縮性胃炎に対するリスクは CagA 陽性株感染の方が CagA 陰性株感染より大きいことが示唆された。 生活習慣では緑茶の飲用が慢性萎縮性胃炎に対する抑制因子として働いていた。特に，その効果は CagA 陽性株感染の場合に顕著であった。 結論 慢性萎縮性胃炎に対するリスクは CagA 陽性株感染の方が CagA 陰性株感染より大きいことが示唆された。 |
| Author | 宮崎, 元伸 畝, 博 岩橋, 満愛 柴田, 和典 百瀬, 義人 |
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| References | 9) Miki K, Ichinose M, Ishikawa KB, et al. Clinical application of serum pepsinogen I and II levels for mass screening to detect gastric cancer. Jpn J Cancer Res. 1993; 84: 1086-1090. 8) Miki K, Ichinose M. Chronic atrophic gastritis and serum pepsinogen levels. Jpn J Cancer Clin. 1992; 38: 221-229. 23) Hirayama F, Takagi S, Kusuhara H, et al. Induction of gastric ulcer and intestinal metaplasia in Mongolian gerbils infected with Helicobacter pylori. J Gastroenterol. 1996; 31: 755-757. 6) Fukao A, Hisamichi S, Ohsato N, et al. Correlation between the prevalence of gastritis and gastric cancer in Japan. Cancer Caus Cont. 1993; 4: 17-20. 11) SAS 出版局：SAS/STAT user's guide. Release 6.03 Edition, SAS 出版局，東京，1990. 12) Maeda S, Ogura K, Yoshida H, et al. Major virulence factors, vacA and cagA, are commonly positive in Helicobacter pylori isolates in Japan. Gut. 1998; 42: 338-343. 15) Oksanen A, Sipponen P, Karttunen R, et al. Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy. Gut. 2000; 46: 460-463. 26) Miehlke S, Kirsch C, Amiri KA, et al. The Helicobacter pylori vacA s1, m1 genotype and cagA is associated with gastric carcinoma in Germany. Int J Cancer. 2000; 87: 322-327. 29) Okabe S, Ochiai Y, Aida M, et al. Mechanic aspect of green tea as a cancer preventive: effect of components on human stomach cancer cell lines. Jpn J Cancer Res. 1999; 90: 733-739. 24) Blaser MJ, Perez-Perez GI, Kleanthous H, et al. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res. 1995; 55: 2111-2115. 16) E. J. Kuipers. Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer. Aliment pharmacol Ther. 1997; 11(Suppl. 1): 71-88. 10) Miki K, Ichinose M, Shimizu A, et al. Serum pepsinogens as a screening test of extensive chronic gastritis. Gastroenterologia Japonica. 1987; 22: 134-141. 7) Imai T, Kubo T and Watanabe H. Chronic gastritis in Japanese with reference to high incidence of gastriccarcinoma. J Natl Cancer Inst. 1971; 47: 179-195. 4) Shibata K, Moriyama M, Fukushima T, et al. Green tea consumption and chronic atrophic gastritis: a cross-sectional study in a green tea production village. J Epidemiol. 2000; 10: 310-316. 25) Yamaoka Y, Kodama T, Gutierrez O, et al. Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different Countries. J Clin Microbiol. 1999; 37: 2274-2279. 19) Kurihara N, Kamiya S, Yamaguchi H, et al. Characteristics of Helicobacter pylori strains isolated from patients with different gastric diseases. J Gastroenterol. 1998; 33[Supple X]: 10-13. 3) Asaka M, Kimura T, Kato M, et al. Possible role of Helicobacter pylori infection in early gastric cancer development. Cancer. 1994; 73: 2691-2694. 18) Peek RM, Miller GG, Tham KT, et al. Heightened inflammatory response and cytokine expression to cagA+ Helicobacter pylori strains. Lab Invest. 1995; 73: 760-770. 27) Parsonnet J, Friedman GD, Orentreich N, et al. Risk for gastric cancer in people with cagA positive or cagA negative Helicobacter pylori infection. Gut. 1997; 40: 297-301. 5) Correa P. Helicobacter pylori and gastric carciogenesis. Ame J Surg Pathol. 1995; 19(Suppl. 1): S37-S43. 20) Miehlke S, Go MF, Kim JG, et al. Serologic detection of Helicobacter pylori infection with cagA-positive strains in duodenal ulcer, gastric ulcer, and asymptomatic gastritis. J Gastroenterol. 1998; 33[Supple X]: 18-21. 2) Matsukura N, Onda M, Kato S, et al. A cytotoxin genes of Helicobacter pylori in chronic gastritis, gastroduodenal ulcer and gastric cancer: an age and gender matched case-control study. Jpn J Cancer Res. 1997; 88: 532-536. 13) Perez-Perez GI, Bhat N, Gaensbauer J, et al. Country-specific constancy by age in cagA+ proportion of Helicobacter pylori infections. Int J Cancer. 1997; 72: 453-456. 17) Kuipers EJ, Prez-Prez GI, Meuwissen SGM, et al. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst. 1995; 87: 1777-1780. 21) Go MF and Graham DY. Presence of the cagA gene in the majority of Helicobacter pylori strains is independent of whether the individual has duodenal ulcer or asymptomatic gastritis. Helicobacter. 1996; 1: 107-111. 14) Menegatti M, Holton J, Figura N, et al. Clinical significance of Helicobacter pylori seropositivity and seronegativity in asymptomatic blood donor. Dig Dis Sci. 1998; 43: 2542-2548. 1) Huang JQ, Sridhar S, Chen Y, et al. Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer. Gastroenterol. 1998; 114: 1169-1179. 30) Yamane T, Takahashi T, Kuwata K, et al. Inhibition of N-methyl-N'-nitro-N-nitroso-guanidine-induced carciogenesis by (−)- epigallocatechin gallate in rat glandular stomach. Cancer Res. 1995; 55: 2081-2084. 28) Kono S, Ikeda M, Tokudome S, et al. A case-control study of gastric cancer and diet in northern Kyusyu, Japan. Jpn J Cancer Res. (Gann), 1988; 79: 1067-1074. 22) Ching CK, Wong BCY, Kwok E, et al. Prevalence of cagA-bearing Helicobacter pylori strains detected by the anti-cagA assay in patients with peptic ulcer disease and in controls. Am J Gastroenterol. 1996; 91: 949-953. |
| References_xml | – reference: 13) Perez-Perez GI, Bhat N, Gaensbauer J, et al. Country-specific constancy by age in cagA+ proportion of Helicobacter pylori infections. Int J Cancer. 1997; 72: 453-456. – reference: 22) Ching CK, Wong BCY, Kwok E, et al. Prevalence of cagA-bearing Helicobacter pylori strains detected by the anti-cagA assay in patients with peptic ulcer disease and in controls. Am J Gastroenterol. 1996; 91: 949-953. – reference: 12) Maeda S, Ogura K, Yoshida H, et al. Major virulence factors, vacA and cagA, are commonly positive in Helicobacter pylori isolates in Japan. Gut. 1998; 42: 338-343. – reference: 5) Correa P. Helicobacter pylori and gastric carciogenesis. Ame J Surg Pathol. 1995; 19(Suppl. 1): S37-S43. – reference: 20) Miehlke S, Go MF, Kim JG, et al. Serologic detection of Helicobacter pylori infection with cagA-positive strains in duodenal ulcer, gastric ulcer, and asymptomatic gastritis. J Gastroenterol. 1998; 33[Supple X]: 18-21. – reference: 25) Yamaoka Y, Kodama T, Gutierrez O, et al. Relationship between Helicobacter pylori iceA, cagA, and vacA status and clinical outcome: studies in four different Countries. J Clin Microbiol. 1999; 37: 2274-2279. – reference: 16) E. J. Kuipers. Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer. Aliment pharmacol Ther. 1997; 11(Suppl. 1): 71-88. – reference: 8) Miki K, Ichinose M. Chronic atrophic gastritis and serum pepsinogen levels. Jpn J Cancer Clin. 1992; 38: 221-229. – reference: 4) Shibata K, Moriyama M, Fukushima T, et al. Green tea consumption and chronic atrophic gastritis: a cross-sectional study in a green tea production village. J Epidemiol. 2000; 10: 310-316. – reference: 9) Miki K, Ichinose M, Ishikawa KB, et al. Clinical application of serum pepsinogen I and II levels for mass screening to detect gastric cancer. Jpn J Cancer Res. 1993; 84: 1086-1090. – reference: 24) Blaser MJ, Perez-Perez GI, Kleanthous H, et al. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res. 1995; 55: 2111-2115. – reference: 7) Imai T, Kubo T and Watanabe H. Chronic gastritis in Japanese with reference to high incidence of gastriccarcinoma. J Natl Cancer Inst. 1971; 47: 179-195. – reference: 2) Matsukura N, Onda M, Kato S, et al. A cytotoxin genes of Helicobacter pylori in chronic gastritis, gastroduodenal ulcer and gastric cancer: an age and gender matched case-control study. Jpn J Cancer Res. 1997; 88: 532-536. – reference: 21) Go MF and Graham DY. Presence of the cagA gene in the majority of Helicobacter pylori strains is independent of whether the individual has duodenal ulcer or asymptomatic gastritis. Helicobacter. 1996; 1: 107-111. – reference: 19) Kurihara N, Kamiya S, Yamaguchi H, et al. Characteristics of Helicobacter pylori strains isolated from patients with different gastric diseases. J Gastroenterol. 1998; 33[Supple X]: 10-13. – reference: 15) Oksanen A, Sipponen P, Karttunen R, et al. Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy. Gut. 2000; 46: 460-463. – reference: 27) Parsonnet J, Friedman GD, Orentreich N, et al. Risk for gastric cancer in people with cagA positive or cagA negative Helicobacter pylori infection. Gut. 1997; 40: 297-301. – reference: 23) Hirayama F, Takagi S, Kusuhara H, et al. Induction of gastric ulcer and intestinal metaplasia in Mongolian gerbils infected with Helicobacter pylori. J Gastroenterol. 1996; 31: 755-757. – reference: 3) Asaka M, Kimura T, Kato M, et al. Possible role of Helicobacter pylori infection in early gastric cancer development. Cancer. 1994; 73: 2691-2694. – reference: 17) Kuipers EJ, Prez-Prez GI, Meuwissen SGM, et al. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst. 1995; 87: 1777-1780. – reference: 29) Okabe S, Ochiai Y, Aida M, et al. Mechanic aspect of green tea as a cancer preventive: effect of components on human stomach cancer cell lines. Jpn J Cancer Res. 1999; 90: 733-739. – reference: 1) Huang JQ, Sridhar S, Chen Y, et al. Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer. Gastroenterol. 1998; 114: 1169-1179. – reference: 28) Kono S, Ikeda M, Tokudome S, et al. A case-control study of gastric cancer and diet in northern Kyusyu, Japan. Jpn J Cancer Res. (Gann), 1988; 79: 1067-1074. – reference: 14) Menegatti M, Holton J, Figura N, et al. Clinical significance of Helicobacter pylori seropositivity and seronegativity in asymptomatic blood donor. Dig Dis Sci. 1998; 43: 2542-2548. – reference: 18) Peek RM, Miller GG, Tham KT, et al. Heightened inflammatory response and cytokine expression to cagA+ Helicobacter pylori strains. Lab Invest. 1995; 73: 760-770. – reference: 26) Miehlke S, Kirsch C, Amiri KA, et al. The Helicobacter pylori vacA s1, m1 genotype and cagA is associated with gastric carcinoma in Germany. Int J Cancer. 2000; 87: 322-327. – reference: 11) SAS 出版局：SAS/STAT user's guide. Release 6.03 Edition, SAS 出版局，東京，1990. – reference: 30) Yamane T, Takahashi T, Kuwata K, et al. Inhibition of N-methyl-N'-nitro-N-nitroso-guanidine-induced carciogenesis by (−)- epigallocatechin gallate in rat glandular stomach. Cancer Res. 1995; 55: 2081-2084. – reference: 6) Fukao A, Hisamichi S, Ohsato N, et al. Correlation between the prevalence of gastritis and gastric cancer in Japan. Cancer Caus Cont. 1993; 4: 17-20. – reference: 10) Miki K, Ichinose M, Shimizu A, et al. Serum pepsinogens as a screening test of extensive chronic gastritis. Gastroenterologia Japonica. 1987; 22: 134-141. |
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| Snippet | 目的 Helicobacter pylori (H. pylori)のサイトトキシン関連遺伝子 A (Cytotoxin-associated gene A, CagA)陽性株と CagA 陰性株の慢性萎縮性胃炎に対するリスクの評価を... |
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| Title | Helicobacter pylori の Cytotoxin-associatedgene A (CagA)陽性株感染および生活習慣と慢性萎縮性胃炎との関係 |
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