1,721,353 research outputs found
Antisecretory drugs, Helicobacter pylori infection and symptom relief in GORD: still an unexplored triangle
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Poor effectiveness of proton pump inhibitors in non-erosive reflux disease: the truth in the end!
No full textDespite acid secretion being normal in the majority of patients with gastro-esophageal reflux disease (GERD) or Barrett's esophagus, acid inhibition represents the mainstay of treatment for both these conditions, with the aim of reducing the aggressive nature of the refluxate toward the esophageal mucosa. Proton pump inhibitors (PPIs) represent, therefore, the first choice medical treatment for GERD, in that they are able to provide an 80-85% healing rate for esophageal lesions, a 56-76% symptom relief and also reduce the incidence of complications, such as strictures as well as dysplasia and adenocarcinoma in Barrett's esophagus. According to a widely quoted systematic review, compared to patients with erosive esophagitis, patients with non-erosive reflux disease (i.e., NERD) display a reduced symptom relief with PPIs, with about 20% reduction of therapeutic gain. In this issue of NeuroGastroenterology & Motility, Weijenborg et al. address for the first time the PPI efficacy in subpopulations of patients with NERD. The study shows clearly that, when the diagnosis is accurately made by including a functional test, NERD patients respond to PPI therapy in a similar way to those with erosive disease. Although not as frequent as previously suggested, however, PPI-refractory heartburn does exist. Some 20% (range: 15-27%) of correctly diagnosed and appropriately treated patients do not respond to PPI treatment at standard doses. Although the pathophysiology underlying PPI failure in GERD is complex and likely multifactorial, acid (be it the sole component of refluxate or not) still remains a major causative factor. A better and more predictable form of acid suppression should therefore be pursued
Pharmacological stimulation of gastrointestinal motility: where we are and where are we going?
No full textDrugs affecting gastrointestinal motility have become valuable in the management of a number of diseases. Medications that enhance the transit of material through the gastrointestinal tract are called prokinetics. Although symptom improvement can be seen in a variety of motility disorders, these medications have not shown a selective benefit for a particular motility disturbance or symptom complex. This class of drugs includes several subclasses, each with a distinct mechanism of action. Amongst the existing prokinetic compounds, dopamine antagonists, on the one hand, and cholinomimetic drugs, on the other hand, should be distinguished. Since compounds endowed with dopamine antagonism have the disadvantage of causing neuroendocrine side effects and/or extrapyramidal dyskinetic reactions (seen especially after metoclopramide), the recently developed non-cholinergic non-antidopaminergic compound, cisapride, seems to be the most effective one. Its main mechanism of action is considered to be the stimulation of myenteric cholinergic nerves with consequent increase of acetylcholine release. Recent evidence suggests that blockade of CCK receptors and stimulation of motilin receptors are also promising avenues to increase gastrointestinal motility. Since drugs acting on 5-HT receptors are presently the best available motor-stimulating compounds, new derivatives are being developed as gastrokinetic drugs. Although the long-acting somatostatin analog, octreotide, and the GnRH agonist, leuprolide, have shown prokinetic properties in particular clinical conditions, their widespread use cannot be recommended at present. Further work is needed to determine the predictive value of objective abnormalities for the efficacy of a drug in the individual patient. This is the crucial point to define a rational strategy in clinical practice, especially to establish if functional investigation is needed before a prokinetic drug be given
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