Gastrite auto-imune e gastrite associada à infecção pelo helicobacter pylori: estudo histológico e imuno-histoquímico da mucosa gástrica oxintica e correlação com a densidade mineral óssea
| Ano de defesa: | 2008 |
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| Autor(a) principal: | |
| Orientador(a): | |
| Banca de defesa: | |
| Tipo de documento: | Tese |
| Tipo de acesso: | Acesso aberto |
| Idioma: | por |
| Instituição de defesa: |
Universidade Federal de Minas Gerais
UFMG |
| Programa de Pós-Graduação: |
Não Informado pela instituição
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| Departamento: |
Não Informado pela instituição
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| País: |
Não Informado pela instituição
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| Palavras-chave em Português: | |
| Link de acesso: | http://hdl.handle.net/1843/ECJS-7K2H8C |
Resumo: | Background and aims: Helicobacter pylori infection and autoimmune gastritis are important causes of gastric mucosa atrophy and both have been related to decreased bone mineral density and to an increased risk for gastric cancer. We studied the histopathological aspects of two forms of chronic gastritis, associated to Helicobacter pylori and autoimmune gastritis, and a possible relationship with bone mineral density. Methods: A hundred-thirteen patients divided in two groups were studied: (1) 81 dyspeptic or asymptomatic patients (76 women), mean age 62.1 ± 8.4 years and, (2) 32 patients with autoimmune gastritis (27 women), meanage 54 ± 14.7 years submitted to gastroduodenal endoscopy and bone densitometry by dual energy X-ray absorciometry. Tissue samples were submitted to hematoxilin-eosin staining for histopathological study and to immunohistochemistry with antiparietal cell monoclonal antibodies. Body gastric atrophy was evaluated in four degrees according to the updatedSydney system: absent, mild, moderate and severe. Helicobacter pylori infection was evaluated by histology, urease test and 13C-urea breath test. Results: In the 113 patients, forty-nine patients presented gastric mucosa without atrophy, nine had mild atrophy, 14 had moderate atrophy, and in 41 the atrophy was severe In group 1 patients, parietal cell density(CP/mm2) was 927 ± 185 for patients without atrophy, 870 ± 180 for those with mild atrophy, 683 ± 151 for moderate atrophy, and 379 ± 345 for patients with severe atrophy (p<0.001). In the autoimmune gastritis group gastric mucosa atrophy was moderate in four cases and severein 28 cases, and by immunohistochemistry, parietal cells showed to be absent in 22 cases (68.7%). Mean lumbar spine mineral density (g/cm2) was 1.011±0.198 in group 1 and 1.065±0.209 for autoimmune gastritis patients (p>0.05). Mean hip mineral density in group 1 and in autoimmune gastritis group was 0.908±0.153 and 0.930±0.139, respectively (p>0.05). Helicobacter pylori prevalence was 51.8% (42/81) and 9.3% (3/32), in groups 1 and 2, respectively, p<0.0001, but bone mineral densities were not different in patients with or without Helicobacter pylori infection (p>0.05). Conclusions: Gastric mucosa atrophy and the presence of H. pylori could not be considered risk factors for decreased bone mineral density. Immunohistochemistry with antiparietal cell monoclonal antibody allowed an objective study of the presence of gastric mucosa atrophy and identification of its different degrees. |