OBJECTIVES: To evaluate the degree of gastritis and the prevalence of Helicobacter pylori in Japanese patients with pernicious anemia (PA). METHODS: Histological assessment for mucosal atrophy and inflammation was performed in gastric biopsy specimens taken from 24 Japanese patients with PA and from 24 age- and sex-matched controls. The prevalence of H. pylori was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin and pepsinogens were determined by radioimmunoassay. RESULTS: All patients with PA had severe fundic atrophic gastritis, and 17 (71%) also had antral atrophic gastritis. Thirteen (54%) of 24 age- and sex-matched controls had fundic atrophic gastritis, and 15 (62%) also had antral atrophic gastritis. Mucosal inflammation was identified in the fundus of all 24 patients and in 15 (62%) controls and in the antrum of 22 (92%) patients and 16 (67%) controls. H. pylori was not detected by Giemsa staining or serum IgG antibodies to H. pylori in any patient with PA but was present in 16 (67%) controls. Serum gastrin levels were significantly higher, and serum pepsinogen I, II, and the I/II ratio were significantly lower in patients than in controls (p < 0.001). CONCLUSIONS: Our results confirm that H. pylori infection is infrequent in PA and is unlikely to be a factor in producing type A gastritis in PA.
OBJECTIVES: To evaluate the degree of gastritis and the prevalence of Helicobacter pylori in Japanese patients with pernicious anemia (PA). METHODS: Histological assessment for mucosal atrophy and inflammation was performed in gastric biopsy specimens taken from 24 Japanese patients with PA and from 24 age- and sex-matched controls. The prevalence of H. pylori was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin and pepsinogens were determined by radioimmunoassay. RESULTS: All patients with PA had severe fundic atrophic gastritis, and 17 (71%) also had antral atrophic gastritis. Thirteen (54%) of 24 age- and sex-matched controls had fundic atrophic gastritis, and 15 (62%) also had antral atrophic gastritis. Mucosal inflammation was identified in the fundus of all 24 patients and in 15 (62%) controls and in the antrum of 22 (92%) patients and 16 (67%) controls. H. pylori was not detected by Giemsa staining or serum IgG antibodies to H. pylori in any patient with PA but was present in 16 (67%) controls. Serum gastrin levels were significantly higher, and serum pepsinogen I, II, and the I/II ratio were significantly lower in patients than in controls (p < 0.001). CONCLUSIONS: Our results confirm that H. pyloriinfection is infrequent in PA and is unlikely to be a factor in producing type A gastritis in PA.
Authors: K Iijima; T Koike; Y Abe; H Yamagishi; N Ara; K Asanuma; K Uno; A Imatani; N Nakaya; S Ohara; T Shimosegawa Journal: Dig Dis Sci Date: 2009-06-10 Impact factor: 3.199
Authors: M Ohana; K Okazaki; C Oshima; K Kawasaki; T Fukui; H Tamaki; M Matsuura; M Asada; T Nishi; K Uchida; S Uose; H Nakase; M Iwano; Y Matsushima; H Hiai; T Chiba Journal: Gut Date: 2003-08 Impact factor: 23.059
Authors: William L Neumann; Elizabeth Coss; Massimo Rugge; Robert M Genta Journal: Nat Rev Gastroenterol Hepatol Date: 2013-06-18 Impact factor: 46.802