Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The administration of the currently available H2-blockers (at a dosage that induces only partial inhibition of the intragastric acidity) is effective in nearly all peptic ulcer patients in the short and long- term treatment. The benefits of more profound gastric acid inhibition (as achieved with omeprazole) in the short-term treatment of acid peptic diseases has been demonstrated in clinical studies. However, gastric acid has an important physiological role and the potential consequences of profound inhibition of gastric acid include intragastric bacterial colonization and hypergastrinaemia. Bacterial overgrowth of the stomach renders the gut more susceptible to enteric infection and another possible sequela of intragastric bacteria is the formation of N-nitroso compounds with carcinogenic potency. Hypergastrinaemia has a trofic effect on the gastric mucosa and gastric endocrine cells and, in animal, ECL cell hyperplasia and carcinoid formation has been observed as a result of high serum gastrin levels. So far, these potential risks have precluded the long-term administration of omeprazole.
 ...
PMID:Inhibition of gastric acid secretion: advantages and risks in short and long-term treatment. 198 19

50 carcinoid tumors of different locations in the gastrointestinal and respiratory tracts were examined histochemically for mucin production. Isolated discrete aggregates of mucosubstances were identified in a large number of cases (46% of all carcinoid tumors, ranging from 53 to 36% in different organ locations). Acidity and composition of mucosubstances (sulfomucin vs. sialomucin contents) in carcinoids were not different from those described in their corresponding locations. These data support numerous other observations that point to a common stem cell precursor for both enterochromaffin and mucus-secreting epithelial cells in gastrointestinal and respiratory tract mucosal membranes. A shared endodermal derivation is favored over a separate neuroectodermal origin for the chromaffin cell system.
 ...
PMID:Carcinoid tumors with focal mucin production. 264 Aug 95

It has been shown that chronic lung diseases which increase the concentration of pulmonary carbon dioxide (CO2) at the expense of oxygen stimulate the secretion of biogenic amines and neuropeptides by pulmonary neuroendocrine cells (PNE cells) in man and laboratory animals. This increase in secretory activity is always accompanied by hyperplasia of PNE cells, and smokers with chronic obstructive lung disease are at high risk for the development of neuroendocrine lung cancer. We have previously shown that nicotine and the structurally related nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), stimulate the proliferation of neuroendocrine cell lines derived from lung carcinoid tumors via interaction with nicotinic acetylcholine receptors (nAChR). In our current experiment, we have addressed the mechanisms of cell proliferation in response to nicotine and NNK in normal PNE cells derived from fetal hamster lungs, and two cell lines derived from human neuroendocrine lung cancers. Our data show that in these systems the mitogenic effects of nicotine and NNK are potentiated in a concentration-dependent manner by elevated levels of CO2, an effect blocked by inhibitors of protein kinase C(PKC) and reduced by antagonists of receptors for 5-hydroxytryptamine (5-HT, serotonin) and mammalian bombesin. The observed effects of CO2 were saturable and independent of changes in the acidity of the tissue culture media. Our data suggest that increases in CO2 concentration at the expense of oxygen may stimulate signal transduction pathways in normal and neoplastic neuroendocrine lung cells thus enhancing their susceptibility to the mitogenic effects of tobacco-specific toxicants.
 ...
PMID:Carbon dioxide potentiates the mitogenic effects of nicotine and its carcinogenic derivative, NNK, in normal and neoplastic neuroendocrine lung cells via stimulation of autocrine and protein kinase C-dependent mitogenic pathways. 771 58

Gastroesophageal reflux is a common disease. Its chronic course, even if mild, is sometimes complicated by erosive oesophagitis. Drug therapy acts against gastric acidity and motility disorders. Treatment of gastroesophageal reflux disease has three aims: improvement of symptoms and quality of life, healing erosive lesions and prevention of symptomatic and endoscopic relapses. Non-drug measures are always useful, even if their efficacy is not well established. Initial therapy of a symptomatic reflux or mild oesophagitis is most of the time effective (antacids, prokinetics, H2 receptor antagonists). Proton-pump inhibitors are also effective in healing and preventing severe oesophagitis. Questions about long-term treatment adverse events with powerful acid inhibitors, such as hypergastrinemia and the risk of gastric carcinoid tumours seem to be resolved. Studies are requested to define the optimal long-term maintenance treatment with cisapride, H2 receptor antagonists or proton-pump inhibitors at low doses in prevention of symptomatic and mild oesophagitis relapses.
 ...
PMID:[Therapeutic principles in gastroesophageal reflux]. 857 Sep 62