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Esomeprazole response

MedGen UID:
450454
Concept ID:
CN077982
Sign or Symptom
Synonym: Nexium response
Drug:
Esomeprazole
MedGen UID:
215246
Concept ID:
C0937846
Pharmacologic Substance
The S-isomer of omeprazole, with gastric proton pump inhibitor activity. In the acidic compartment of parietal cells, esomeprazole is protonated and converted into the active achiral sulfenamide; the active sulfenamide forms one or more covalent disulfide bonds with the proton pump hydrogen-potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting its activity and the parietal cell secretion of H+ ions into the gastric lumen, the final step in gastric acid production. H+/K+ ATPase is an integral membrane protein of the gastric parietal cell. [from NCI]
 
Genes (locations): CYP2C19 (10q23.33); CYP3A4 (7q22.1)

Definition

Esomeprazole (brand name Nexium) is a proton pump inhibitor (PPI) used to treat gastroesophageal reflux disease (GERD) and to reduce the risk of gastric ulcers associated with nonsteroidal anti-inflammatory drug NSAID use. Esomeprazole is also used in the treatment of hypersecretory conditions, such as Zollinger-Ellison syndrome, and in combination with antibiotics to eradicate Helicobacter pylori (H. pylori) infection. Esomeprazole reduces the acidity (raises the pH) in the stomach by inhibiting the secretion of gastric acid. The level of esomeprazole an individual is exposed to is influenced by several factors, such as the dose used and how quickly the drug is metabolized and inactivated. Esomeprazole is primarily metabolized by the CYP2C19 enzyme. Individuals with increased CYP2C19 enzyme activity (“CYP2C19 ultrarapid metabolizers”) may have an insufficient response to standard doses of esomeprazole, because the drug is inactivated at a faster rate. In contrast, individuals who have reduced or absent CYP2C19 enzyme activity (i.e., CYP2C19 intermediate and poor metabolizers) have a greater exposure to esomeprazole. The 2018 FDA-approved drug label for esomeprazole states that 3% of Caucasians, and 15–20% of Asians are CYP2C19 poor metabolizers, and that poor metabolizers have approximately twice the level of exposure to esomeprazole, compared with CYP2C19 normal metabolizers. However, the drug label does not include dosing recommendations for CYP2C19 poor metabolizers. Esomeprazole recommendations have been published by the Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy (KNMP), which indicates that no change in dosing is recommended for CYP2C19 poor, intermediate, or ultrarapid metabolizers. The DPWG states that although genetic variation in CYP2C19 influences the plasma concentration of esomeprazole, there is insufficient evidence to support an effect on treatment outcomes or side effects. [from Medical Genetics Summaries]

Additional description

From NCBI curation
Esomeprazole blocks the secretion of gastric acid and belongs to the drug class of proton pump inhibitors. It is used to treat gastroesophageal reflux disease (GERD) and to reduce the risk of gastric ulcers associated with the use of non-steroidal anti-inflammatory drugs (NSAIDs). Esomeprazole is also used in the treatment of hypersecretory conditions, such as Zollinger-Ellison syndrome, and is used in combination with antibiotics to eradicate Helicobacter pylori (H. pylori) infection. Esomeprazole is metabolized primarily by the CYP2C19 enzyme. Approximately 3% of Caucasians and 15 to 20% of Asians have reduced or absent CYP2C19 enzyme activity ("poor metabolizers"). In these individuals, standard doses of esomeprazole leads to higher exposure of the drug. In contrast, individuals with increased CYP2C19 activity ("ultrarapid metabolizers") may be exposed to lower levels of esomeprazole and have an insufficient response to treatment. The FDA-approved drug label for esomeprazole states that poor metabolizers are exposed to approximately twice the level of drug compared to the rest of the population ("extensive metabolizers"), but the label does not require dose changes for poor metabolizers. However, the Pharmacogenetics Working Group of the Royal Dutch Association for the Advancement of Pharmacy (KNMP) has published dose alterations based on CYP2C19 genotype. For CYP2C19 poor metabolizers, they do not recommend altering the dose; however for ultrarapid metabolizers, they recommend being extra alert to an insufficient response to treatment. For the eradication of H. pylori in ultrarapid metabolizers, KNMP recommends increasing the dose of omeprazole by 50–100%, and to consider the same dose increase for other conditions.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  

Professional guidelines

PubMed

Tighe MP, Andrews E, Liddicoat I, Afzal NA, Hayen A, Beattie RM
Cochrane Database Syst Rev 2023 Aug 22;8(8):CD008550. doi: 10.1002/14651858.CD008550.pub3. PMID: 37635269Free PMC Article
Gibson P, Wang G, McGarvey L, Vertigan AE, Altman KW, Birring SS; CHEST Expert Cough Panel
Chest 2016 Jan;149(1):27-44. Epub 2016 Jan 6 doi: 10.1378/chest.15-1496. PMID: 26426314Free PMC Article
Ford C
Laryngoscope 2006 Sep;116(9):1717-8; author reply 1718. doi: 10.1097/01.mlg.0000225956.60488.6c. PMID: 16955013

Curated

Royal Dutch Pharmacists Association (KNMP). Dutch Pharmacogenetics Working Group (DPWG). Pharmacogenetic Recommendation.

Recent clinical studies

Etiology

Yang E, Yu KS, Lee S
CPT Pharmacometrics Syst Pharmacol 2023 Jun;12(6):865-877. Epub 2023 Mar 26 doi: 10.1002/psp4.12959. PMID: 36967484Free PMC Article
Lee JW, Kim N, Nam RH, Lee SM, Soo In C, Kim JM, Lee DH
J Gastroenterol Hepatol 2019 Apr;34(4):666-672. Epub 2019 Feb 25 doi: 10.1111/jgh.14625. PMID: 30726563
Scheiman JM, Lanas A, Veldhuyzen van Zanten S, Baldycheva I, Svedberg LE, Nagy P
Int J Cardiol 2015 Mar 1;182:500-2. Epub 2014 Dec 30 doi: 10.1016/j.ijcard.2014.12.140. PMID: 25618787
Liberopoulos EN, Elisaf MS, Tselepis AD, Archimandritis A, Kiskinis D, Cokkinos D, Mikhailidis DP
Platelets 2006 Feb;17(1):1-6. doi: 10.1080/09537100500237004. PMID: 16308180
Dickson EJ, Stuart RC
Am J Pharmacogenomics 2003;3(5):303-15. doi: 10.2165/00129785-200303050-00002. PMID: 14575519

Diagnosis

Yang E, Yu KS, Lee S
CPT Pharmacometrics Syst Pharmacol 2023 Jun;12(6):865-877. Epub 2023 Mar 26 doi: 10.1002/psp4.12959. PMID: 36967484Free PMC Article
Escobar-Serna DP, Peralta-Palmezano FJ, Peralta-Palmezano JJ
Arch Argent Pediatr 2022 Apr;120(2):e98-e101. Epub 2022 Feb 4 doi: 10.5546/aap.2022.eng.e98. PMID: 35338825
Sakurai K, Suda H, Fujie S, Takeichi T, Okuda A, Murao T, Hasuda K, Hirano M, Ito K, Tsuruta K, Hattori M
Dig Dis Sci 2019 Mar;64(3):815-822. Epub 2018 Nov 10 doi: 10.1007/s10620-018-5365-0. PMID: 30415407Free PMC Article
Philpott H, Nandurkar S, Royce SG, Thien F, Gibson PR
Aliment Pharmacol Ther 2016 May;43(9):985-93. Epub 2016 Mar 4 doi: 10.1111/apt.13576. PMID: 26939578
Wilcox GM, Mattia AR
J Clin Gastroenterol 2009 Jul;43(6):551-3. doi: 10.1097/MCG.0b013e31817d3fa1. PMID: 19142168

Therapy

Ierardi E, Losurdo G, Fortezza RF, Principi M, Barone M, Leo AD
World J Gastroenterol 2019 Sep 14;25(34):5097-5104. doi: 10.3748/wjg.v25.i34.5097. PMID: 31558859Free PMC Article
Med Lett Drugs Ther 2010 Sep 20;52(1347):74-5. PMID: 20847717
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Calvet X, Gomollón F
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McColl KE, Kennerley P
Dig Liver Dis 2002 Jul;34(7):461-7. doi: 10.1016/s1590-8658(02)80102-5. PMID: 12236477

Prognosis

Yang E, Yu KS, Lee S
CPT Pharmacometrics Syst Pharmacol 2023 Jun;12(6):865-877. Epub 2023 Mar 26 doi: 10.1002/psp4.12959. PMID: 36967484Free PMC Article
Mod AT, Katz R
Am J Health Syst Pharm 2023 Mar 7;80(6):343-347. doi: 10.1093/ajhp/zxac370. PMID: 36480341
Lau J, Lind T, Persson T, Eklund S
J Dig Dis 2017 Feb;18(2):99-106. doi: 10.1111/1751-2980.12447. PMID: 28070941
Scheiman JM, Lanas A, Veldhuyzen van Zanten S, Baldycheva I, Svedberg LE, Nagy P
Int J Cardiol 2015 Mar 1;182:500-2. Epub 2014 Dec 30 doi: 10.1016/j.ijcard.2014.12.140. PMID: 25618787
Scheiman JM, Herlitz J, Veldhuyzen van Zanten SJ, Lanas A, Agewall S, Nauclér EC, Svedberg LE, Nagy P
J Cardiovasc Pharmacol 2013 Mar;61(3):250-7. doi: 10.1097/FJC.0b013e31827cb626. PMID: 23188121

Clinical prediction guides

Lee JW, Kim N, Nam RH, Lee SM, Soo In C, Kim JM, Lee DH
J Gastroenterol Hepatol 2019 Apr;34(4):666-672. Epub 2019 Feb 25 doi: 10.1111/jgh.14625. PMID: 30726563
Lee HA, Lee KR, Jang SB, Chung SY, Yu KS, Lee H
Eur J Pharm Sci 2019 Mar 15;130:1-10. Epub 2019 Jan 11 doi: 10.1016/j.ejps.2019.01.009. PMID: 30641142
Sakurai K, Suda H, Fujie S, Takeichi T, Okuda A, Murao T, Hasuda K, Hirano M, Ito K, Tsuruta K, Hattori M
Dig Dis Sci 2019 Mar;64(3):815-822. Epub 2018 Nov 10 doi: 10.1007/s10620-018-5365-0. PMID: 30415407Free PMC Article
Lau J, Lind T, Persson T, Eklund S
J Dig Dis 2017 Feb;18(2):99-106. doi: 10.1111/1751-2980.12447. PMID: 28070941
Scheiman JM, Herlitz J, Veldhuyzen van Zanten SJ, Lanas A, Agewall S, Nauclér EC, Svedberg LE, Nagy P
J Cardiovasc Pharmacol 2013 Mar;61(3):250-7. doi: 10.1097/FJC.0b013e31827cb626. PMID: 23188121

Recent systematic reviews

Tomizawa Y, Melek J, Komaki Y, Kavitt RT, Sakuraba A
J Clin Gastroenterol 2018 Aug;52(7):596-606. doi: 10.1097/MCG.0000000000000878. PMID: 28787360
Shamliyan TA, Middleton M, Borst C
Clin Ther 2017 Feb;39(2):404-427.e36. Epub 2017 Feb 9 doi: 10.1016/j.clinthera.2017.01.011. PMID: 28189362
Lucendo AJ, Arias Á, Molina-Infante J
Clin Gastroenterol Hepatol 2016 Jan;14(1):13-22.e1. Epub 2015 Aug 3 doi: 10.1016/j.cgh.2015.07.041. PMID: 26247167
Edwards SJ, Lind T, Lundell L, DAS R
Aliment Pharmacol Ther 2009 Sep 15;30(6):547-56. Epub 2009 Jun 25 doi: 10.1111/j.1365-2036.2009.04077.x. PMID: 19558609
Edwards SJ, Lind T, Lundell L
Aliment Pharmacol Ther 2001 Nov;15(11):1729-36. doi: 10.1046/j.1365-2036.2001.01128.x. PMID: 11683686

Therapeutic recommendations

From Medical Genetics Summaries

This section contains excerpted 1 information on gene-based dosing recommendations. Neither this section nor other parts of this review contain the complete recommendations from the sources.

2018 Statement from the US Food and Drug Administration (FDA)

Metabolism

Esomeprazole is extensively metabolized in the liver by the cytochrome P450 (CYP) enzyme system. The metabolites of esomeprazole lack antisecretory activity. The major part of esomeprazole’s metabolism is dependent upon the CYP2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites. The remaining amount is dependent on CYP3A4, which forms the sulphone metabolite. CYP2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15 to 20% of Asians lack CYP2C19 and are termed Poor Metabolizers. At steady state, the ratio of AUC in Poor Metabolizers to AUC in the rest of the population (Normal Metabolizers) is approximately 2.

[...]

Interaction with Clopidogrel

Avoid concomitant use of esomeprazole magnesium with clopidogrel. Clopidogrel is a prodrug. Inhibition of platelet aggregation by clopidogrel is entirely due to an active metabolite. The metabolism of clopidogrel to its active metabolite can be impaired by use with concomitant medications, such as esomeprazole, that inhibit CYP2C19 activity. Concomitant use of clopidogrel with 40 mg esomeprazole reduces the pharmacological activity of clopidogrel. When using esomeprazole magnesium consider alternative anti-platelet therapy.

Please review the complete therapeutic recommendations located here: (1).

2018 Summary of recommendations from the Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Association for the Advancement of Pharmacy (KNMP)

CYP2C19 Poor Metabolizer (PM)

No action is needed for this gene-drug interaction.

Although the genetic variation leads to a higher plasma concentration of esomeprazole, there is insufficient evidence to support an effect on the therapeutic effectiveness and side effects.

CYP2C19 Intermediate Metabolizer (IM)

No action is needed for this gene-drug interaction.

Although the genetic variation leads to a higher plasma concentration of esomeprazole, there is insufficient evidence to support an effect on the therapeutic effectiveness and side effects.

CYP2C19 Ultrarapid Metabolizer (UM)

No action is required for this gene-drug interaction.

Although the genetic variation may lead to faster inactivation of esomeprazole, there is insufficient evidence to support an effect on the therapeutic effectiveness and side effects.

Background information

For more information about the PM, IM, and UM phenotypes: see the general background information about CYP2C19 on the KNMP Knowledge Bank or on www.knmp.nl (search for CYP2C19). Access requires KNMP membership.

Please review the complete therapeutic recommendations that are located here: (2).

1 The FDA labels specific drug formulations. We have substituted the generic names for any drug labels in this excerpt. The FDA may not have labeled all formulations containing the generic drug. Certain terms, genes and genetic variants may be corrected in accordance with nomenclature standards, where necessary. We have given the full name of abbreviations, shown in square brackets, where necessary.

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      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

    • DPWG, 2023
      Royal Dutch Pharmacists Association (KNMP). Dutch Pharmacogenetics Working Group (DPWG). Pharmacogenetic Recommendation.

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