Dementia, cognitive impairment and proton pump inhibitor therapy: A systematic review

Batchelor, R.; Gilmartin, Julia Fiona-Maree; Kemp, William; Hopper, Ingrid; Liew, Danny

doi:10.1111/jgh.13750

Cited by 51 publications

(49 citation statements)

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“…An alternative mechanism for the observed association between PPI use and cardiovascular risk is esomeprazole accelerating endothelial senescence, via inhibition of proteostasis and accumulation of protein aggregates linked to endothelial dysfunction . This mechanism would also explain an association between PPI use and risk of chronic kidney disease and vascular dementia …”

Section: Discussionmentioning

confidence: 99%

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Batchelor

Kumar

Gilmartin‐Thomas

et al. 2018

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Batchelor

Kumar

Gilmartin‐Thomas

et al. 2018

Aliment Pharmacol Ther

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“…A meta‐analysis conducted by Wijarnpreecha, Thongprayoon, Panjawatanan, and Ungprasert () failed to find a significant association between PPI use and an increased risk of dementia with a between‐study heterogeneity of 99%. In conclusion, the evidence supporting an association between an increased risk of dementia and PPI use is actually quite limited (Batchelor et al, ) and might have been initially overestimated. These data are reassuring because PPIs are among the most widely used drug classes.…”

Section: Resultsmentioning

confidence: 93%

“…Although most epidemiological studies suggest that PPI use does not increase the dementia risk, in vivo and in vitro studies have shown that PPIs could interact with the pathophysiological pathway of AD. Indeed, lansoprazole increased amyloid β production (Aß40 and Aß42 oligomers) by enhancing ß‐secretase activity and modulating γ‐secretase (Batchelor et al, ). By inhibiting the vacuolar proton pump in microglial lysosomes, PPIs could basify lysosomes and thus hamper the degradation of fibrillar β‐amyloid (Haenisch et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…By inhibiting the vacuolar proton pump in microglial lysosomes, PPIs could basify lysosomes and thus hamper the degradation of fibrillar β‐amyloid (Haenisch et al, ). Furthermore, chronic exposure to PPIs impairs endothelial function and accelerates human endothelial senescence by reducing telomere lengths (Batchelor et al, ). Finally, by decreasing the gastric pH, PPIs reduce the absorption of weak acids, such as cyanocobalamin, which might be a risk factor for dementia.…”

Section: Resultsmentioning

confidence: 99%

“…These drugs can generally be divided into drugs targeting CNS disorders such as benzodiazepines (BZDs) (Billioti de Gage, Pariente, & Bégaud, 2015) and opiates (Dublin et al, 2015) and drugs not targeting the CNS such as proton pump inhibitors (PPIs) (Tai et al, 2017). These drugs could act directly on cognitive function (CF) by modulating neurotransmission, ion channels, or receptor activity or indirectly via pathophysiological pathways related to vascular or neurodegenerative dementia by interacting with amyloid β production (Batchelor, Gilmartin, Kemp, Hopper, & Liew, 2017), τ hyperphosphorylation (Ramage et al, 2005), neuroinflammation, oxidative stress, endothelial function, or even cerebrovascular reactivity (Mendoza-Oliva, Zepeda, & Arias, 2014).…”

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confidence: 99%

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Drug interactions with dementia‐related pathophysiological pathways worsen or prevent dementia

Barus

Béné

Deguil

et al. 2019

British J Pharmacology

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Many risk factors are known to induce or precipitate dementia. Drugs acting via different mechanisms can modulate cognitive performance and exert either beneficial or deleterious effects on cognition through functional or neuropathological mechanisms. This review discusses the association between several classes of drugs and cognitive impairment and dementia risk. These drugs can be divided into drugs targeting CNS disorders (e.g., anticholinergic drugs, antiepileptics, antipsychotics, benzodiazepines, and opioids) and drugs targeting non‐CNS disorders (e.g., antidiabetics, antihypertensives, proton pump inhibitors, and statins). Furthermore, we sought to highlight the pharmacological mechanisms underlying their possible detrimental or beneficial effects on cognition. Anticholinergic and antiepileptic drugs were excluded from this review because their effects on cognition are well known. Studies investigating benzodiazepines have revealed an increased risk of dementia. Conclusions on dementia risk or cognitive impairment regarding opioids and antipsychotic drugs are difficult to draw. These different classes appear to impair cognition not by a single clear mechanism of action specific to each class but by several relatively interdependent and interconnected mechanisms (e.g., impaired neurotransmission, neuroinflammation, neuronal death, oxidative stress, or interactions with dementia‐related pathways). The dementia risk initially associated with the use of proton pump inhibitors might have been overestimated. In contrast, statins, antihypertensive medications, and antidiabetics could potentially decrease the risk of dementia and cognitive impairment by acting in ways opposite to the mechanisms cited above. Linked Articles This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc

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The association between proton pump inhibitor use and the risk of tuberculosis: A case‐control study

Song

Park

et al. 2019

Pharmacoepidemiology and Drug

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Purpose: Few studies have reported an association between proton pump inhibitor (PPI) use and tuberculosis. Tuberculosis incidence is relatively high in Asian people, and an increase in PPI prescriptions has been reported in South Korea. Thus, we investigated the association between PPI use and tuberculosis development. Methods:We conducted a case-control study on 25 672 newly diagnosed tuberculosis patients using the National Health Insurance Service-National Sample Cohort (NHIS-NSC) database (2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013). We selected a control group without tuberculosis using 1:1 exact matching based on age, sex, index year, insurance type, and income level. We investigated PPI exposure 2 years prior to the index date and classified the subjects into nonuser, continuous user, recent user, and former user groups. Odds ratios (ORs) and 95% confidence intervals (CIs) for tuberculosis development were calculated using conditional logistic regression.Results: A total of 51 344 cases and controls were analyzed. Recent PPI use (adjusted odds ratio [aOR], 1.28; 95% CI, 1.18-1.39) and continuous PPI use (aOR, 1.13; 95% CI 1.10-1.28) were significantly associated with tuberculosis development, compared with nonuse of PPIs. An increased tuberculosis incidence was not observed in the former use group compared with the nonuse group (aOR 1.05, 95% CI 0.95-1.17). Conclusions:In this case-control study, we found that recent PPI use and continuous PPI use were associated with increased tuberculosis development. Although further investigation is needed, the tuberculosis risk accompanying PPI treatment should be considered.

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Dementia, cognitive impairment and proton pump inhibitor therapy: A systematic review

Cited by 51 publications

References 52 publications

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Drug interactions with dementia‐related pathophysiological pathways worsen or prevent dementia

The association between proton pump inhibitor use and the risk of tuberculosis: A case‐control study

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