- 同
- cytochrome C450 2C19
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/04/09 06:21:57」(JST)
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Cytochrome P450, family 2, subfamily C, polypeptide 19 |
PDB rendering based on 1r9o. |
Available structures |
PDB |
Ortholog search: PDBe, RCSB |
List of PDB id codes |
4GQS
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Identifiers |
Symbols |
CYP2C19 ; CPCJ; CYP2C; P450C2C; P450IIC19 |
External IDs |
OMIM: 124020 MGI: 1306818 HomoloGene: 133565 IUPHAR: CYP2C19 ChEMBL: 3622 GeneCards: CYP2C19 Gene |
EC number |
1.14.13.48, 1.14.13.49, 1.14.13.80 |
Gene ontology |
Molecular function |
• monooxygenase activity
• iron ion binding
• steroid hydroxylase activity
• oxidoreductase activity
• (S)-limonene 6-monooxygenase activity
• (S)-limonene 7-monooxygenase activity
• oxygen binding
• enzyme binding
• heme binding
• (R)-limonene 6-monooxygenase activity
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Cellular component |
• endoplasmic reticulum membrane
• intracellular membrane-bounded organelle
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Biological process |
• xenobiotic metabolic process
• steroid metabolic process
• monoterpenoid metabolic process
• drug metabolic process
• arachidonic acid metabolic process
• epoxygenase P450 pathway
• exogenous drug catabolic process
• small molecule metabolic process
• heterocycle metabolic process
• oxidation-reduction process
• omega-hydroxylase P450 pathway
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Sources: Amigo / QuickGO |
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RNA expression pattern |
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More reference expression data |
Orthologs |
Species |
Human |
Mouse |
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Entrez |
1557 |
69888 |
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Ensembl |
ENSG00000165841 |
ENSMUSG00000067229 |
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UniProt |
P33261 |
n/a |
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RefSeq (mRNA) |
NM_000769 |
NM_001011707 |
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RefSeq (protein) |
NP_000760 |
NP_001011707 |
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Location (UCSC) |
Chr 10:
96.45 – 96.61 Mb |
Chr 19:
39.11 – 39.19 Mb |
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PubMed search |
[1] |
[2] |
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Cytochrome P450 2C19 (abbreviated CYP2C19) is an enzyme. This protein, a member of the cytochrome P450 mixed-function oxidase system, is involved in the metabolism of xenobiotics, including many proton pump inhibitors and antiepileptics. In humans, the CYP2C19 protein is encoded by the CYP2C19 gene.[1][2] CYP2C19 is a liver enzyme that acts on 5-10% of drugs in current clinical use,[3] including the anticoagulant clopidogrel (Plavix), antiulcer drugs such as omeprazole, antiseizure drugs such as mephenytoin, the antimalarial proguanil, and the anxiolytic diazepam.[4]
CYP2C19 has been annotated as (R)-limonene 6-monooxygenase and (S)-limonene 6-monooxygenase in UniProt.
Contents
- 1 Function
- 2 Genetic polymorphism and pharmacogenomics
- 3 Ligands
- 4 See also
- 5 References
- 6 External links
- 7 Further reading
Function
The gene encodes a member of the cytochrome P450 superfamily of enzymes. These proteins are monooxygenases that catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and is known to metabolize many drugs. Polymorphism within this gene is associated with variable ability to metabolize mephenytoin, known as the poor metabolizer and extensive metabolizer phenotypes. The gene is located within a cluster of cytochrome P450 genes on chromosome no.10 arm q24.[5]
Genetic polymorphism and pharmacogenomics
Genetic polymorphism (mainly CYP2C19*2, CYP2C19*3 and CYP2C19*17) exists for CYP2C19 expression, with approximately 3–5% of Caucasian and 15–20% of Asian populations being poor metabolizers with no CYP2C19 function.[6][7] This may reduce the efficacy of clopidogrel (Plavix). In patients with an abnormal CYP2C19 variant certain benzodiazepines should be avoided, such as diazepam (Valium), lorazepam (Ativan), oxazepam (Serax), and temazepam (Restoril).[8] On the basis of their ability to metabolize (S)-mephenytoin or other CYP2C19 substrates, individuals can be classified as extensive metabolizers (EM) or poor metabolizers (PM).[7] Eight variant alleles (CYP2C19*2 to CYP2C19*8) that predict PMs have been identified.[7]
Ligands
The following is a table of selected substrates, inducers and inhibitors of CYP2C19. Where classes of agents are listed, there may be exceptions within the class.
Inhibitors of CYP2C19 can be classified by their potency, such as:
- Strong being one that causes at least a 5-fold increase in the plasma AUC values, or more than 80% decrease in clearance.[9]
- Moderate being one that causes at least a 2-fold increase in the plasma AUC values, or 50-80% decrease in clearance.[9]
- Weak being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values, or 20-50% decrease in clearance.[9]
Selected inducers, inhibitors and substrates of CYP2C19
Substrates |
Inhibitors |
Inducers |
- antidepressants
- TCAs
- amitriptyline[10][9]
- clomipramine[10][9]
- imipramine[10][9]
- SSRIs
- moclobemide[10][9]
- Bupropion[11]
- antiepileptics
- diazepam[10][9]
- mephenytoin[10][9]
- nordazepam[10]
- phenytoin[10]
- phenobarbital[9]
- primidone[9]
- hexobarbital[9]
- methylphenobarbital[9]
- proton pump inhibitors
- lansoprazole[10][9]
- omeprazole[10][9]
- pantoprazole[10][9]
- rabeprazole[9]
- esomeprazole[10]
- clopidogrel[10][9] (antiplatelet drug)
- proguanil[10][9] (prophylactic antimalarial)
- propranolol[10][9] (beta blocker)
- gliclazide (sulfonylurea)[12][13]
- carisoprodol[9] (muscle relaxant)
- chloramphenicol[9] (bacteriostatic antimicrobial)
- cyclophosphamide[9] (alkylating antineoplastic agent)
- indomethacin[9] (NSAID)
- nelfinavir[9] (antiretroviral)
- nilutamide[9] (antiandrogen)
- progesterone[9] (sex hormone)
- teniposide[9] (chemotherapeutic)
- warfarin[9] (anticoagulant)
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Strong:
- moclobemide[10] (antidepressant)
- fluvoxamine[10] (SSRI)
- chloramphenicol[14] (bacteriostatic antimicrobial)
Weak:
- Several anticonvulsants
- felbamate[15]
- topiramate[15]
Unspecified potency:
- proton pump inhibitors
- lansoprazole[9]
- omeprazole[9]
- pantoprazole[9]
- rabeprazole[9]
- cimetidine[9] (H2-receptor antagonist)
- fluoxetine[9] (SSRI)
- indomethacin[9] (NSAID)
- ketoconazole[9] (antifungal)
- modafinil[9] (eugeroic)
- probenecid[9] (uricosuric)
- ticlopidine[9] (antiplatelet)
- JWH-018[citation needed]
- isoniazid[16]
|
- rifampicin[10][9] (bactericidal)
- artemisinin[10] (in malaria)
- carbamazepine[9] (anticonvulsant, mood stabilizing)
- norethisterone[9] (contraceptive)
- prednisone[9] (corticosteroid)
- Aspirin - Low doses (89mg)[17]
|
See also
References
- ^ Romkes M, Faletto MB, Blaisdell JA, Raucy JL, Goldstein JA (April 1991). "Cloning and expression of complementary DNAs for multiple members of the human cytochrome P450IIC subfamily". Biochemistry 30 (13): 3247–55. doi:10.1021/bi00227a012. PMID 2009263.
- ^ Gray IC, Nobile C, Muresu R, Ford S, Spurr NK (July 1995). "A 2.4-megabase physical map spanning the CYP2C gene cluster on chromosome 10q24". Genomics 28 (2): 328–32. doi:10.1006/geno.1995.1149. PMID 8530044.
- ^ "Cytochrome P450 2C19 Genotyping". Genele X. Retrieved October 2014.
- ^ "Cytochrome P450 2C19 (CYP2C19) Genotype". Mayo Medical Laboratories. Retrieved October 2014.
- ^ "Entrez Gene: CYP2C19 cytochrome P450, family 2, subfamily C, polypeptide 19".
- ^ Bertilsson L (September 1995). "Geographical/interracial differences in polymorphic drug oxidation. Current state of knowledge of cytochromes P450 (CYP) 2D6 and 2C19". Clin Pharmacokinet 29 (3): 192–209. doi:10.2165/00003088-199529030-00005. PMID 8521680.
- ^ a b c Desta, Z., et al. (2002). Clinical significance of the cytochrome P450 2C19 genetic polymorphism. Clin Pharmacokinet 41(12) 913-58. PMID 12222994
- ^ Forest, M.D., P.H., Tennant. "American Association of Clinical Chemistry Annual Meeting 2014". AutoGenomics. Retrieved October 2014.
- ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as Flockhart DA (2007). "Drug Interactions: Cytochrome P450 Drug Interaction Table". Indiana University School of Medicine. Retrieved on July 2011
- ^ a b c d e f g h i j k l m n o p q r s t FASS (drug formulary): Swedish environmental classification of pharmaceuticals Facts for prescribers (Fakta för förskrivare). Retrieved July 2011
- ^ Zhu, A. Z. X.; Zhou, Q.; Cox, L. S.; Ahluwalia, J. S.; Benowitz, N. L.; Tyndale, R. F. (3 September 2014). "Gene Variants in CYP2C19 Are Associated with Altered In Vivo Bupropion Pharmacokinetics but Not Bupropion-Assisted Smoking Cessation Outcomes". Drug Metabolism and Disposition 42 (11): 1971–1977. doi:10.1124/dmd.114.060285. PMID 25187485.
- ^ Zhang Y, Si D, Chen X, Lin N, Guo Y, Zhou H, Zhong D (July 2007). "Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects". Br J Clin Pharmacol 64 (1): 67–74. doi:10.1111/j.1365-2125.2007.02846.x. PMC 2000619. PMID 17298483.
- ^ Xu H, Williams KM, Liauw WS, Murray M, Day RO, McLachlan AJ (April 2008). "Effects of St John's wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide". Br. J. Pharmacol. 153 (7): 1579–86. doi:10.1038/sj.bjp.0707685. PMC 2437900. PMID 18204476.
- ^ Park JY, Kim KA, Kim SL (November 2003). "Chloramphenicol Is a Potent Inhibitor of Cytochrome P450 Isoforms CYP2C19 and CYP3A4 in Human Liver Microsomes". Antimicrob. Agents Chemother. 47 (11): 3464–9. doi:10.1128/AAC.47.11.3464-3469.2003. PMC 253795. PMID 14576103.
- ^ a b Page 100 in: Rene H., PhD. Levy; Rene H. Levy; Levy, René H.; Mattson, Richard H; Meldrum, Brian S. (2002). Antiepileptic drugs. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-2321-3.
- ^ Wen X, Wang JS, Neuvonen PJ, Backman JT. "Isoniazid is a mechanism-based inhibitor of cytochrome P450 1A2, 2A6, 2C19 and 3A4 isoforms in human liver microsomes.". PMID 11868802.
- ^ Clin Pharmacol Ther. 2003 Mar;73(3):264-71. Isozyme-specific induction of low-dose aspirin on cytochrome P450 in healthy subjects. Chen XP1, Tan ZR, Huang SL, Huang Z, Ou-Yang DS, Zhou HH.
External links
- PharmGKB: Annotated PGx Gene Information for CYP2C19
Further reading
- Goldstein JA, de Morais SM (1995). "Biochemistry and molecular biology of the human CYP2C subfamily". Pharmacogenetics 4 (6): 285–99. doi:10.1097/00008571-199412000-00001. PMID 7704034.
- Smith G, Stubbins MJ, Harries LW, Wolf CR (1999). "Molecular genetics of the human cytochrome P450 monooxygenase superfamily". Xenobiotica 28 (12): 1129–65. doi:10.1080/004982598238868. PMID 9890157.
- Ding X, Kaminsky LS (2003). "Human extrahepatic cytochromes P450: function in xenobiotic metabolism and tissue-selective chemical toxicity in the respiratory and gastrointestinal tracts". Annu. Rev. Pharmacol. Toxicol. 43: 149–73. doi:10.1146/annurev.pharmtox.43.100901.140251. PMID 12171978.
- Romkes M, Faletto MB, Blaisdell JA et al. (1991). "Cloning and expression of complementary DNAs for multiple members of the human cytochrome P450IIC subfamily". Biochemistry 30 (13): 3247–55. doi:10.1021/bi00227a012. PMID 2009263.
- Meier UT, Meyer UA (1988). "Genetic polymorphism of human cytochrome P-450 (S)-mephenytoin 4-hydroxylase. Studies with human autoantibodies suggest a functionally altered cytochrome P-450 isozyme as cause of the genetic deficiency". Biochemistry 26 (25): 8466–74. doi:10.1021/bi00399a065. PMID 3442670.
- De Morais SM, Wilkinson GR, Blaisdell J et al. (1994). "Identification of a new genetic defect responsible for the polymorphism of (S)-mephenytoin metabolism in Japanese". Mol. Pharmacol. 46 (4): 594–8. PMID 7969038.
- Romkes M, Faletto MB, Blaisdell JA et al. (1993). "Cloning and expression of complementary DNAs for multiple members of the human cytochrome PH50IIC subfamily". Biochemistry 32 (5): 1390. doi:10.1021/bi00056a025. PMID 8095407.
- Goldstein JA, Faletto MB, Romkes-Sparks M et al. (1994). "Evidence that CYP2C19 is the major (S)-mephenytoin 4'-hydroxylase in humans". Biochemistry 33 (7): 1743–52. doi:10.1021/bi00173a017. PMID 8110777.
- de Morais SM, Wilkinson GR, Blaisdell J et al. (1994). "The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans". J. Biol. Chem. 269 (22): 15419–22. PMID 8195181.
- Gray IC, Nobile C, Muresu R et al. (1996). "A 2.4-megabase physical map spanning the CYP2C gene cluster on chromosome 10q24". Genomics 28 (2): 328–32. doi:10.1006/geno.1995.1149. PMID 8530044.
- Karam WG, Goldstein JA, Lasker JM, Ghanayem BI (1997). "Human CYP2C19 is a major omeprazole 5-hydroxylase, as demonstrated with recombinant cytochrome P450 enzymes". Drug Metab. Dispos. 24 (10): 1081–7. PMID 8894508.
- Xiao ZS, Goldstein JA, Xie HG et al. (1997). "Differences in the incidence of the CYP2C19 polymorphism affecting the S-mephenytoin phenotype in Chinese Han and Bai populations and identification of a new rare CYP2C19 mutant allele". J. Pharmacol. Exp. Ther. 281 (1): 604–9. PMID 9103550.
- Guengerich FP, Johnson WW (1998). "Kinetics of ferric cytochrome P450 reduction by NADPH-cytochrome P450 reductase: rapid reduction in the absence of substrate and variations among cytochrome P450 systems". Biochemistry 36 (48): 14741–50. doi:10.1021/bi9719399. PMID 9398194.
- Ferguson RJ, De Morais SM, Benhamou S et al. (1998). "A new genetic defect in human CYP2C19: mutation of the initiation codon is responsible for poor metabolism of S-mephenytoin". J. Pharmacol. Exp. Ther. 284 (1): 356–61. PMID 9435198.
- Ibeanu GC, Goldstein JA, Meyer U et al. (1998). "Identification of new human CYP2C19 alleles (CYP2C19*6 and CYP2C19*2B) in a Caucasian poor metabolizer of mephenytoin". J. Pharmacol. Exp. Ther. 286 (3): 1490–5. PMID 9732415.
- Ibeanu GC, Blaisdell J, Ghanayem BI et al. (1999). "An additional defective allele, CYP2C19*5, contributes to the S-mephenytoin poor metabolizer phenotype in Caucasians". Pharmacogenetics 8 (2): 129–35. doi:10.1097/00008571-199804000-00006. PMID 10022751.
- Foster DJ, Somogyi AA, Bochner F (1999). "Methadone N-demethylation in human liver microsomes: lack of stereoselectivity and involvement of CYP3A4". British Journal of Clinical Pharmacology 47 (4): 403–12. doi:10.1046/j.1365-2125.1999.00921.x. PMC 2014231. PMID 10233205.
- Ibeanu GC, Blaisdell J, Ferguson RJ et al. (1999). "A novel transversion in the intron 5 donor splice junction of CYP2C19 and a sequence polymorphism in exon 3 contribute to the poor metabolizer phenotype for the anticonvulsant drug S-mephenytoin". J. Pharmacol. Exp. Ther. 290 (2): 635–40. PMID 10411572.
PDB gallery
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1r9o: Crystal Structure of P4502C9 with Flurbiprofen bound
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Cytochromes, oxygenases: cytochrome P450 (EC 1.14)
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CYP1 |
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CYP2 |
- A6
- A7
- A13
- B6
- C8
- C9
- C18
- C19
- D6
- E1
- F1
- J2
- R1
- S1
- U1
- W1
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CYP3 (CYP3A) |
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CYP4 |
- A11
- A22
- B1
- F2
- F3
- F8
- F11
- F12
- F22
- V2
- X1
- Z1
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CYP5-20 |
- CYP5 (A1)
- CYP7 (A1, B1)
- CYP8 (A1, B1)
- CYP11 (A1, B1, B2)
- CYP17 (A1)
- CYP19 (A1)
- CYP20 (A1)
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CYP21-51 |
- CYP21 (A2)
- CYP24 (A1)
- CYP26 (A1, B1, C1)
- CYP27 (A1, B1, C1)
- CYP39 (A1)
- CYP46 (A1)
- CYP51 (A1)
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UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
English Journal
- Correlation Between the CYP2C19 Phenotype Status and the Results of Three Different Platelet Function Tests in Cardiovascular Disease Patients Receiving Antiplatelet Therapy: An Emphasis on Newly Introduced Platelet Function Analyzer-200 P2Y Test.
- Li S1, Choi JL1, Guo LZ2, Goh RY1, Kim BR1, Woo KS1, Kim MH2, Han JY3.
- Annals of laboratory medicine.Ann Lab Med.2016 Jan;36(1):42-8. doi: 10.3343/alm.2016.36.1.42.
- BACKGROUND: An association has been reported between CYP2C19 polymorphism and the altered antiplatelet activity of clopidogrel. We investigated this association using the newly introduced platelet function analyzer (PFA)-200 (INNOVANCE PFA-200 System; Siemens Healthcare, Germany) P2Y test.METHODS: P
- PMID 26522758
- Elucidating the Mechanisms of Formation for Two Unusual Cytochrome P450-Mediated Fused Ring Metabolites of GDC-0623, a MAPK/ERK Kinase Inhibitor.
- Takahashi RH1, Ma S2, Robinson SJ2, Yue Q2, Choo EF2, Khojasteh SC2.
- Drug metabolism and disposition: the biological fate of chemicals.Drug Metab Dispos.2015 Dec;43(12):1929-33. doi: 10.1124/dmd.115.067181. Epub 2015 Oct 5.
- Two isomeric metabolites of GDC-0623 [5-((2-fluoro-4-iodophenyl)amino)-N-(2-hydroxyethoxy)imidazo[1,5-a]pyridine-6-carboxamide], a mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) kinase inhibitor, were identified in radiolabeled mass balance studies in rats and dogs
- PMID 26438627
- Time-Dependent Inhibition of CYP2C19 by Isoquinoline Alkaloids: In Vitro and In Silico Analysis.
- Salminen KA1, Rahnasto-Rilla M2, Väänänen R2, Imming P2, Meyer A2, Horling A2, Poso A2, Laitinen T2, Raunio H2, Lahtela-Kakkonen M2.
- Drug metabolism and disposition: the biological fate of chemicals.Drug Metab Dispos.2015 Dec;43(12):1891-904. doi: 10.1124/dmd.115.065755. Epub 2015 Sep 23.
- The cytochrome P450 2C19 (CYP2C19) enzyme plays an important role in the metabolism of many commonly used drugs. Relatively little is known about CYP2C19 inhibitors, including compounds of natural origin, which could inhibit CYP2C19, potentially causing clinically relevant metabolism-based drug inte
- PMID 26400396
Japanese Journal
- 日本感染症医薬品協会奨励賞受賞講演会記録 2014年度受賞講演 ボリコナゾールのCYP2C19遺伝子多型解析に基づく至適投与量設計法の確立
- 2 コンパートメント−肝薬物貯槽−融合型 tube モデルを用いたフルボキサミン併用による薬物間相互作用のシミュレーションと in-vivo 酵素阻害定数の見積もり
- 総合文化研究所紀要 = Bulletin of Institute for Interdisciplinary Studies of Culture Doshisha Women's College of Liberal Arts 32, 34-53, 2015-07-16
- NAID 120005651679
- In vivo radioactive metabolite analysis for individualized medicine: A basic study of a new method of CYP activity assay using 123I-IMP
Related Links
- このサイトは医療関係者向けです。 ... 2)CYP2C19の遺伝子多型とPPIの胃酸分泌抑制効果 PPIのCYP2C19の違いによる血中濃度の違いは胃酸分泌抑制効果の違いとして現れ 7) 、反復投与後でも認められる 5)
- CYP2C19 遺伝子多型受託解析 薬物に対する生体応答には大きな個体差が存在し、その要因として肝臓における薬物代謝酵素活性は重要なもののひとつです。この薬物代謝酵素の中心を担っているCYPは遺伝的な多型が存在し、この多型に ...
Related Pictures
★リンクテーブル★
[★]
- 英
- reflux esophagitis
- 同
- peptic esophagitis
- 関
- 胸骨下痛、食道炎、バレット食道、胃食道逆流症 GERD
概念
- 胃食道の逆流防止機構が十分に作動せず、胃・小腸内容液の逆流から粘膜傷害をきたした状態(IMD)。
- 上位の疾患概念に胃食道逆流症 GERDがある。
分類
- ロサンゼルス分類:(内視鏡的な分類)
- Savary-Miller分類
- 食道疾患研究会による分類:色調変化型、びらん型、潰瘍型、隆起肥厚型
リスク
- 肥満、妊娠(腹腔内圧上昇、エストロゲン・プロゲステロンによるLES圧低下)、過食、高カロリー食(チョコレート、和菓子、高脂肪食、餅)・刺激物、食後臥位(3時間以内)、喫煙、アルコール、薬剤(Ca拮抗薬、硝酸薬、テオフィリン)
- 滑脱型食道裂孔ヘルニア、LES機能不全、胃切除後
症状
- 食道症状:胸焼け、呑酸、嚥下困難
- 食道外症状:咳嗽、前胸部痛(胸骨後部痛)、嚥下困難、嚥下痛、つまり感
検査
- 確定診断のために、食道内24時間pHモニター、食道内圧測定、内視鏡検査が重要。特に食道内24時間pHモニターでpHの低下が証明できなければ、胃食道逆流症は否定的。(QB.A-53)
- X線造影
- 胃カメラ
- 食道内24時間pHモニター
24-hour pH monitoring
治療
- (胃酸分泌抑制)H2受容体阻害薬、プロトンポンプ阻害薬
- (胃の逆流阻害)消化管運動促進薬 ← 本当?
- 粘膜保護薬 (QB.A-53)
- 術後胃で十二指腸液の逆流があるばあいには酸分泌抑制薬は無効であり、メシル酸カモスタットが用いられる。
プロトンポンプ阻害薬
- hospitalist vol.2 no.3 2014.9 P.741
- 血液濃度が低い:腸溶コーティングされたPPIが長時間胃に留まると胃の中で溶解してしまい成分が失活して、血液中濃度が十分に上昇しない場合がある。腸管運動の運動改善薬が有効なことがある。
- rapid metabolizer:PPIはCYP2C19の代謝を受けるが、遺伝子多形により代謝の速度が異なる(homozygous extensive metabolizer, heterozygous extenstive metabolizer, poor metabolizer)。ランソプラゾールでは多型の影響をうける。エソメプラゾールやラベプラゾールは影響が少ない。
- 胃内環境が酸性でない:PPIの活性化には酸性環境が必要であるが、食後など胃内に大量の食物がある場合には胃酸が希釈されて酸性環境が得られない場合がある。これに対して腸管の運動改善薬や食前内服が等の対策が必要。
胃酸以外の逆流の可能性
国試
[★]
- 英
- fluconazole
- 同
- FLCZ
- 商
- ジフルカン、ニコアゾリン、ビスカルツ、フラノス、フルカード、フルカジール、フルコナゾン、フルタンゾール、ミコシスト
- 関
- 抗真菌薬
-
ADME
阻害
排泄
添付文書
- ジフルカンカプセル50mg/ジフルカンカプセル100mg
http://www.info.pmda.go.jp/go/pack/6290002M1020_2_01/6290002M1020_2_01?view=body
- ジフルカン静注液50mg/ジフルカン静注液100mg/ジフルカン...
http://www.info.pmda.go.jp/go/pack/6290401A1099_2_01/6290401A1099_2_01?view=body