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Special Consideration of Drug Disposition
Published in Gary M. Matoren, The Clinical Research Process in the Pharmaceutical Industry, 2020
Achlorhydria in a patient can lead to decreased absorption of weakly acidic drugs. Conversely, the decreased level of acid in the stomach favors the faster absorption of all basic drugs, especially those which are relatively weak bases. On the basis of this information, it should not be surprising, therefore, that achlorhydria, which is certainly not a rare phenomenon in the senior population, might distort absorption and blood level studies in older age groups and affect clinical response.
The Stomach
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
Patients that are found to have any sort of chronic gastritis are at high risk. Autoimmune gastritis (with pernicious anemia) and atrophic gastritis carry a major risk of being precancerous, and close follow-up by gastroscopy and biopsies is highly recommended. These two types of chronic gastritis can also be associated with achlorhydria, depending on the extent of the mucosal involvement.
Endoscopic screening for upper gastrointestinal malignancy
Published in David Westaby, Martin Lombard, Therapeutic Gastrointestinal Endoscopy A problem-oriented approach, 2019
Patients with hypogammaglobulinaemia and pernicious anaemia have chronic atrophic gastritis. Certainly, achlorhydria results from the chronic atrophic gastritis and 75% of patients with gastric carcinoma are achlorhydric. Strickland has divided chronic atrophic gastritis into two subgroups:Type A, which is associated with pernicious anaemia, predominantly affects the fundus and body and is autoimmune in origin.Type B gastritis affects the antrum and is related to environmental factors. It is also found in the stomach some years after gastrectomy for benign peptic ulcer disease. It may be regarded as a failure of the gastric mucosa to respond to repeated injury.
Potential risk factors related to the development of gastric polyps
Published in Immunopharmacology and Immunotoxicology, 2018
Wenjun Cao, Guoqiang Hou, Xin Zhang, Hongxia San, Jianzhong Zheng
The etiology of hyperplastic polyp is unclear. Excessive regeneration of foveolar epithelium following mucosal lesion may cause hyperplastic polyp. Inflammatory fibroid polyp, detecting throughout the gastrointestinal tract, often occurs in antropyloric site (about 80%). In some cases, it is often associated with achlorhydria or hypochlorhydria. FGPs especially multiple FGPs are often observed in familial adenomatous polyposis. Sporadic FGPs discovered in middle-aged male or females by upper endoscopy are the most common type of GPs. The malignant rate of hyperplastic polyps, usually occurring in polyps with a diameter larger than 1 cm, is less than 1% [3], Sporadic FGPs have characteristically been considered as benign polyps without malignant potential; however, but some of the other GPs had malignant risk. Carmack has described sporadic FGPs containing low-grade dysplasia [4]. Molecular alterations within GPs may lead to unknown risks of neoplastic development [5].
The role of gastric microbiota in gastric cancer
Published in Gut Microbes, 2020
Oliver A. Stewart, Fen Wu, Yu Chen
Other studies have also utilized the INS-GAS mouse model to explore the association between the gastric microbiota and gastric cancer39,41,42 (Table 3). Particularly, studies have attempted to demonstrate how the complexity of the microbiota affects gastric cancer development in the INS-GAS mouse model. Through manipulating the microbiota of the transgenic mouse model, Lofgren et al. demonstrated that germ-free INS-GAS mice developed a reduced number of gastric lesions compared to INS-GAS with a more complex microbiota at 11 month postinfection with H. pylori.39 Lertpiriyapong et al. further expanded upon this knowledge by assessing if the presence of a diverse microbiota is a necessary requirement for the development of gastric lesions.41 In order to do this, investigators compared the postinfection gastric cancer risk in INS-GAS mice with three different microbiota compositions: complex, germ-free, and restricted (containing only Lactobacillus, Clostridium, and Bacteroides genera). In their study, they found that a restricted gastric microbiota was associated with a similar rate of gastric cancer development as a complex microbiota in the mice.41 However, compared to the germ-free mice, the INS-GAS mice with the restricted microbiota had significantly increased gastric corpus inflammation, epithelial defects, oxyntic gland atrophy, epithelial hyperplasia, and dysplasia.41 Taken together, the data indicate that H. pylori can act synergistically with a community of bacteria to promote gastric neoplasia. These results suggest that the microbiota may play a role in the development of gastric cancer following H. pylori infection, but a diverse microbiota may not necessarily be a requirement for the development of gastric cancer. Previous researchers have hypothesized that the achlorhydria associated with gastric atrophy following H. pylori infection may allow overgrowth of commensal bacteria in addition to colonization from bacteria of the lower bowel.13 It is possible that this overgrowth of bacteria may play a role in gastric cancer development. However, in the INS-GAS mouse model, it appears that the presence of only a limited range of microbes was sufficient to produce gastric cancer at similar rates as the more complex microbiota.