Article

Review article: The long-term use of proton-pump inhibitors

Durham University, Durham, England, United Kingdom
Alimentary Pharmacology & Therapeutics (Impact Factor: 5.73). 09/2005; 22 Suppl 1(s1):55-63. DOI: 10.1111/j.1365-2036.2005.02611.x
Source: PubMed

ABSTRACT

More than 15 years after the launch of omeprazole in 1988, proton-pump inhibitors remain central to the management of acid-suppression disorders and are unchallenged with regard to their efficacy and popularity among doctors and patients. They are considered safe despite early concerns about the possibility of an association with cancer and gastric atrophy; current concerns about long-term proton-pump inhibitor therapy are centred mainly on a possible association with fundic gland polyps and between Helicobacter pylori and gastric atrophic changes. Long-term proton-pump inhibitor usage accounts for the majority of the total proton-pump inhibitor usage. Long-term usage is difficult to define and most patients take proton-pump inhibitors non-continuously. Data indicate that a substantial proportion of long-term users do not have a clear indication for their therapy and there is thus room for reduction or rationalization of treatment. Overall, on-demand therapy is more cost-effective than continuous therapy and should be considered wherever possible.

Download full-text

Full-text

Available from: C. A. O’Morain, Oct 01, 2014
  • Source
    • "Equally interestingly, it is a first-in-class proton pump inhibitor and one of the most commonly prescribed drugs internationally. In a number of countries OME is available as an over the counter drug and is used by millions of people with more than 720 million prescriptions issued within 15 years from the year of approval (Kaunitz, 2014; Raghunath et al., 2005; Shaheen et al., 2006). Given the roles of P450s in the synthesis of epoxy-fatty acids, their induction by OME could have functional consequences. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Epoxyeicosatrienoic acids (EETs) are potent endogenous analgesic metabolites produced from arachidonic acid by cytochrome P450s (P450s). Metabolism of EETs by soluble epoxide hydrolase (sEH) reduces their activity, while their stabilization by sEH inhibition decreases both inflammatory and neuropathic pain. Here, we tested the complementary hypothesis that increasing the level of EETs through induction of P450s by omeprazole (OME), can influence pain related signaling by itself, and potentiate the anti-hyperalgesic effect of sEH inhibitor. Rats were treated with OME (100mg/kg/day, p.o., 7days), sEH inhibitor TPPU (3mg/kg/day, p.o.) and OME (100mg/kg/day, p.o., 7days)+TPPU (3mg/kg/day, p.o., last 3days of OME dose) dissolved in vehicle PEG400, and their effect on hyperalgesia (increased sensitivity to pain) induced by PGE2 was monitored. While OME treatment by itself exhibited variable effects on PGE2 induced hyperalgesia, it strongly potentiated the effect of TPPU in the same assay. The significant decrease in pain with OME+TPPU treatment correlated with the increased levels of EETs in plasma and increased activities of P450 1A1 and P450 1A2 in liver microsomes. The results show that reducing catabolism of EETs with a sEH inhibitor yielded a stronger analgesic effect than increasing generation of EETs by OME, and combination of both yielded the strongest pain reducing effect under the condition of this study.
    Full-text · Article · Nov 2015 · Toxicology and Applied Pharmacology
  • Source
    • "Older studies described gastric hyperplastic polyps as the most common type of gastric polyps, a more recent US study found fundic gland polyps to be the most common type of benign gastric polyp [12]. Fundic gland polyps are particularly common in patients with GERD and appear related to long-term suppression of gastric acid secretion with proton pump inhibitors [25] [26]. Their presence is inversely associated with the presence of gastric H. pylori infection, as demonstrated by the present analysis, as well as previously published data [27]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of the study was to utilize a large national histopathology database for the analysis of the clinical epidemiology of gastric polyps. In a case-control study, 71,575 case subjects with gastric polyps were compared to 741,351 control subjects without gastric polyps. Of all patients, 7.72% harboured fundic gland polyps, 1.79% gastric hyperplastic polyps, 0.09% gastric adenomas, and 0.06% type I neuroendocrine tumours. All types showed a clear-cut age-dependent rise. Reflux disease was significantly more common in patients with fundic gland polyps and significantly less common in patients with gastric adenomas or neuroendocrine tumours. Anaemia was more common in patients with gastric hyperplastic polyps, gastric adenomas, or neuroendocrine tumours. Helicobacter pylori was found significantly less frequently in all subjects with gastric polyps than in controls. Intestinal metaplasia and gastric atrophy were both more common in gastric adenoma and neuroendocrine tumours and less common in fundic gland polyps than in controls. Different polyp types tended to coincide in the same patients. Gastric hyperplastic polyps appeared to mark the beginning of a progression from chronic gastritis to intestinal metaplasia and gastric atrophy, which leads to diminished gastric acid output and increased gastrin secretion. Gastric adenoma and neuroendocrine tumours reflect later stages of this process. Copyright © 2014. Published by Elsevier Ltd.
    Full-text · Article · Nov 2014 · Digestive and Liver Disease
  • Source
    • "As a result, a large proportion of patients currently prescribed PPI do not have acid-related symptoms and thus, have no true indication for such therapy. Some studies also showed that up to 33% of patients who initiate PPI treatment redeem repeated prescriptions without any obvious indication for maintenance therapy [212] [226]. This empirical behavior may complicate PPI discontinuation, due to the development of rebound acid hypersecretion, leading to the relapse of the symptoms of the underlying acid-related disease (heartburn, acid regurgitation and dyspepsia) that might result in resumption of therapy [204] [205]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The homeopathic model applies the secondary action or vital reaction of the organism as a therapeutic method and thus prescribes treatment by similitude, which consists in administering to ill individuals substances that cause similar symptoms in healthy individuals. The vital, homeostatic or paradoxical reaction of the organism might be explained scientifically by means of the rebound effect of modern drugs, which might cause fatal iatrogenic events after discontinuation of antipathic (a term used in alternative medicine for palliative treatment, also known as enantiopathic) treatment. Although the rebound effect is studied by modern pharmacology, it is poorly communicated to and discussed among healthcare professionals, who are thus deprived of information needed for the safe management of modern drugs. This article presents an up-to-date review on the rebound effect of modern drugs that grounds the homeopathic principle of healing and calls the attention of doctors to this type of adverse effect that is usually unnoticed. The rebound effect of modern palliative drugs, which was pointed out by Hahnemann more than two centuries ago, might cause fatal adverse events and is illustrated by the examples of acetylsalicylic acid, anti-inflammatory agents, bronchodilators, antidepressants, statins, proton-pump inhibitors, etc. Although the rebound effect is expressed by a small fraction of (susceptible) individuals and might be avoided by gradual tapering of antipathic drugs, it exhibits epidemiologic importance as a function of the massive use of such palliative drugs and the lack of knowledge in its regard.
    Full-text · Article · Jul 2012
Show more