Effect of the proton-pump Inhibitor pantoprazole on MycoPhenolic ACid exposure in kidney and liver transplant recipienTs (IMPACT study): a randomized trial.


Journal

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402

Informations de publication

Date de publication:
01 06 2020
Historique:
received: 30 01 2020
accepted: 31 03 2020
entrez: 10 6 2020
pubmed: 10 6 2020
medline: 24 11 2020
Statut: ppublish

Résumé

Mycophenolic acid (MPA) is widely utilized as an immunosuppressant in kidney and liver transplantation, with reports suggesting an independent relationship between MPA concentrations and adverse allograft outcome. Proton-pump inhibitors (PPIs) may have variable effects on the absorption of different MPA formulations leading to differences in MPA exposure. A multicentre, randomized, prospective, double-blind placebo-controlled cross-over study was conducted to determine the effect of the PPI pantoprazole on the MPA and its metabolite MPA-glucuronide (MPA-G) area under the curve (AUC) >12 h (MPA-AUC12 h) in recipients maintained on mycophenolate mofetil (MMF) or enteric-coated mycophenolate sodium (EC-MPS). We planned a priori to examine separately recipients maintained on MMF and EC-MPS for each pharmacokinetic parameter. The trial (and protocol) was registered with the Australian New Zealand Clinical Trials Registry on 24 March 2011, with the registration number of ACTRN12611000316909 ('IMPACT' study). Of the 45 recipients screened, 40 (19 MMF and 21 EC-MPS) were randomized. The mean (standard deviation) recipient age was 58 (11) years with a median (interquartile range) time post-transplant of 43 (20-132) months. For recipients on MMF, there was a significant reduction in the MPA-AUC12 h [geometric mean (95% confidence interval) placebo: 53.9 (44.0-65.9) mg*h/L versus pantoprazole: 43.8 (35.6-53.4) mg*h/L; P = 0.004] when pantoprazole was co-administered compared with placebo. In contrast, co-administration with pantoprazole significantly increased MPA-AUC12 h [placebo: 36.1 (26.5-49.2) mg*h/L versus pantoprazole: 45.9 (35.5-59.3) mg*h/L; P = 0.023] in those receiving EC-MPS. Pantoprazole had no effect on the pharmacokinetic profiles of MPA-G for either group. The co-administration of pantoprazole substantially reduced the bioavailability of MPA in patients maintained on MMF and had the opposite effect in patients maintained on EC-MPS, and therefore, clinicians should be cognizant of this drug interaction when prescribing the different MPA formulations.

Sections du résumé

BACKGROUND
Mycophenolic acid (MPA) is widely utilized as an immunosuppressant in kidney and liver transplantation, with reports suggesting an independent relationship between MPA concentrations and adverse allograft outcome. Proton-pump inhibitors (PPIs) may have variable effects on the absorption of different MPA formulations leading to differences in MPA exposure.
METHODS
A multicentre, randomized, prospective, double-blind placebo-controlled cross-over study was conducted to determine the effect of the PPI pantoprazole on the MPA and its metabolite MPA-glucuronide (MPA-G) area under the curve (AUC) >12 h (MPA-AUC12 h) in recipients maintained on mycophenolate mofetil (MMF) or enteric-coated mycophenolate sodium (EC-MPS). We planned a priori to examine separately recipients maintained on MMF and EC-MPS for each pharmacokinetic parameter. The trial (and protocol) was registered with the Australian New Zealand Clinical Trials Registry on 24 March 2011, with the registration number of ACTRN12611000316909 ('IMPACT' study).
RESULTS
Of the 45 recipients screened, 40 (19 MMF and 21 EC-MPS) were randomized. The mean (standard deviation) recipient age was 58 (11) years with a median (interquartile range) time post-transplant of 43 (20-132) months. For recipients on MMF, there was a significant reduction in the MPA-AUC12 h [geometric mean (95% confidence interval) placebo: 53.9 (44.0-65.9) mg*h/L versus pantoprazole: 43.8 (35.6-53.4) mg*h/L; P = 0.004] when pantoprazole was co-administered compared with placebo. In contrast, co-administration with pantoprazole significantly increased MPA-AUC12 h [placebo: 36.1 (26.5-49.2) mg*h/L versus pantoprazole: 45.9 (35.5-59.3) mg*h/L; P = 0.023] in those receiving EC-MPS. Pantoprazole had no effect on the pharmacokinetic profiles of MPA-G for either group.
CONCLUSIONS
The co-administration of pantoprazole substantially reduced the bioavailability of MPA in patients maintained on MMF and had the opposite effect in patients maintained on EC-MPS, and therefore, clinicians should be cognizant of this drug interaction when prescribing the different MPA formulations.

Identifiants

pubmed: 32516810
pii: 5855235
doi: 10.1093/ndt/gfaa111
doi:

Substances chimiques

Enzyme Inhibitors 0
Proton Pump Inhibitors 0
Pantoprazole D8TST4O562
Mycophenolic Acid HU9DX48N0T

Banques de données

ANZCTR
['ACTRN12611000316909']

Types de publication

Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1060-1070

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Auteurs

Andrew Sunderland (A)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.

Graeme Russ (G)

Department of Nephrology & Transplantation Services, Royal Adelaide Hospital, and University of Adelaide, Adelaide, Australia.

Benedetta Sallustio (B)

Discipline of Pharmacology, Adelaide Medical School, The University of Adelaide, Adelaide, Australia.
Department of Clinical Pharmacology, The Queen Elizabeth Hospital, Adelaide, Australia.

Matthew Cervelli (M)

Department of Pharmacy, Royal Adelaide Hospital, Adelaide, Australia.

David Joyce (D)

School of Biomedical Sciences, University of Western Australia, Perth, Australia.
Biochemistry and Toxicology, PathWest, Perth, Australia.
Faculty of Health and Medical Sciences, Medical School, University of Western Australia, Perth, Australia.

Esther Ooi (E)

School of Biomedical Sciences, University of Western Australia, Perth, Australia.
Faculty of Health and Medical Sciences, Medical School, University of Western Australia, Perth, Australia.

Gary Jeffrey (G)

Faculty of Health and Medical Sciences, Medical School, University of Western Australia, Perth, Australia.
Department of Hepatology Unit, Sir Charles Gairdner Hospital, Perth, Australia.

Neil Boudville (N)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.
Faculty of Health and Medical Sciences, Medical School, University of Western Australia, Perth, Australia.

Aron Chakera (A)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.

Gursharan Dogra (G)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.

Doris Chan (D)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.

Germaine Wong (G)

Sydney School of Public Health, University of Sydney, Sydney, Australia.
Centre for Transplant and Renal Research, Westmead Hospital, Sydney, Australia.
Centre for Kidney Research, The Children's Hospital at Westmead, Sydney, Australia.

Wai H Lim (WH)

Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Australia.
Faculty of Health and Medical Sciences, Medical School, University of Western Australia, Perth, Australia.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH