RESUMO
We report a case of developing multiple adenocarcinoma foci in multiple hyperplastic polyps in a patient with Helicobacter pylori infection and hypergastrinemia during long-term proton pump inhibitor (PPI) therapy. A 57-year-old man, who was undergoing hemodialysis for chronic renal failure, underwent an upper gastrointestinal endoscopy to elucidate the cause of anemia. Atrophic gastritis with H. pylori infection and multiple adenocarcinoma foci in multiple hyperplastic polyps were found in the endoscopic and histological examinations. Enterochromaffin-like micronests and parietal cell protrusion in the background of the polyps suggested the existence of hypergastrinemia. The serum gastrin level was markedly high-10,206 pg/ml (normal range 37-172 pg/ml). The cause of this marked hypergastrinemia was not autoimmune gastritis and gastrinoma. After discontinuing PPI therapy and successful eradication of H. pylori, the serum gastrin level decreased to normal range. These findings indicate that hypergastrinemia may be caused by long-term PPI therapy in patients with H. pylori infection. This case suggests that hypergastrinemia may mediate gastric carcinogenesis in patients with H. pylori infection.
Assuntos
Adenocarcinoma/etiologia , Infecções por Helicobacter/complicações , Helicobacter pylori , Inibidores da Bomba de Prótons/efeitos adversos , Neoplasias Gástricas/etiologia , Cocarcinogênese , Esquema de Medicação , Gastrinas/sangue , Gastrite Atrófica/complicações , Gastroscopia , Humanos , Hiperplasia , Masculino , Pessoa de Meia-Idade , Pólipos/diagnóstico , Pólipos/etiologia , Inibidores da Bomba de Prótons/administração & dosagem , Neoplasias Gástricas/diagnósticoRESUMO
A 51-old-female patient was admitted because of dyspnea. This case was diagnosed inoperable advanced gastric cancer and pulmonary carcinomatous lymphangiosis. She was treated by combination of docetaxel (TXT) and TS-1. TXT (40 mg/m2) was administered on day 1, and TS-1 (80 mg/body/day) was then administered for 14 days followed by a 7-day interval as one course. After two courses of chemotherapy, carcinomatous lymphangiosis declined, tumor markers decreased, and dyspnea improved. Administration of oxygen was thus discontinued. No side effects appeared (hematological or non-hematological).
Assuntos
Adenocarcinoma/tratamento farmacológico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Gástricas/tratamento farmacológico , Adenocarcinoma/patologia , Docetaxel , Esquema de Medicação , Combinação de Medicamentos , Feminino , Humanos , Neoplasias Pulmonares/patologia , Metástase Linfática , Pessoa de Meia-Idade , Invasividade Neoplásica , Ácido Oxônico/administração & dosagem , Piridinas/administração & dosagem , Neoplasias Gástricas/patologia , Taxoides/administração & dosagem , Tegafur/administração & dosagemRESUMO
Bile acids, especially those with hydrophobic properties, are known to possess cytotoxicity. However, the mechanisms responsible for the cytotoxicity of bile acids are still under investigation. On the other hand, the hydrophilic bile acid, ursodeoxycholic acid has been reported to exhibit therapeutic effects against cytotoxic hydrophobic bile acids. The aim of the present study was to investigate the cytotoxicity of individual bile acids and combinations of bile acids using the intestinal cell lines IEC-6 and Caco-2 cells. The cytotoxicities of individual bile acids and the effects of various bile acid combinations were evaluated using the MTS [3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxy-phenyl)-2-(4-sulfophenyl)-2H-tetrazolium] assay. The bile acids induced cytotoxic effects depending on their hydrophobicity except for hyodeoxycholic acid. In the study for the effects of combined bile acids, not only ursodeoxycholic acid but other hydrophilic bile salts such as cholic acid and hyocholic acid exhibited cytoprotection against deoxycholic acid-induced cytotoxicity. Moreover, even some hydrophobic bile acids, such as chenodeoxycholic acid also exhibited cytoprotection. It is possible that the cytotoxicity of hydrophobic bile acids is ameliorated by more hydrophilic bile acids under certain conditions. The understanding of the precise mechanism of this phenomenon remains to be determined.
Assuntos
Ácidos e Sais Biliares/metabolismo , Intestinos/citologia , Ácidos e Sais Biliares/química , Ácidos e Sais Biliares/farmacologia , Células CACO-2 , Linhagem Celular , Sobrevivência Celular , Colagogos e Coleréticos/farmacologia , Cromatografia Líquida de Alta Pressão , Relação Dose-Resposta a Droga , Humanos , Intestinos/efeitos dos fármacos , Sais de Tetrazólio/farmacologia , Tiazóis/farmacologia , Fatores de Tempo , Ácido Ursodesoxicólico/farmacologiaRESUMO
INTRODUCTION: Ws/Ws rats have a small deletion of the c-kit gene and are deficient in both mucosal-type mast cells and connective tissue-type mast cells. AIM: To investigate the role of pancreatic mast cells in the development of experimental closed duodenal loop (CDL)-induced pancreatitis using Ws/Ws rats. METHODOLOGY: Pancreatitis was induced by the CDL technique for 5 and 12 hours, and the subsequent ascites volume, wet pancreatic weight, pancreatic myeloperoxidase activities, and serum amylase levels were evaluated. The pancreatic tissue damage was also evaluated histologically. RESULTS: The CDL technique induced equally severe ascites, pancreatic edema and hyperemia, and hyperamylasemia in the Ws/Ws versus the control (+/+) rats. The microscopic mucosal damage score was also equivalent in the Ws/Ws and control (+/+) rats, and there were no significant differences in mucosal myeloperoxidase activity between the Ws/Ws and control (+/+) rats. CONCLUSION: These results indicate that mast cells may not be crucial for the development of CDL-induced pancreatitis.