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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 林君榮 | |
dc.contributor.author | Yu-Fan Yang | en |
dc.contributor.author | 楊喻帆 | zh_TW |
dc.date.accessioned | 2021-06-08T07:31:28Z | - |
dc.date.copyright | 2008-08-13 | |
dc.date.issued | 2008 | |
dc.date.submitted | 2008-06-24 | |
dc.identifier.citation | Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med 2002;347:1175-86.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/26902 | - |
dc.description.abstract | 簡介
質子幫浦為主的三合一療法為目前幽門螺旋桿菌的標準療法之一,一般建議的療程為7~14天;縮短的三合一療法雖可以降低醫療支出、減少副作用、增進病人服藥順服性,但因為到目前為止的研究結果分歧,故仍未被建議使用於治療中。Rabeprazole是質子幫浦抑制劑中效果較強,也較不受到代謝酵素CYP2C19基因型影響的一個藥物,然而,現今已證實,rabeprazole藥動、藥效特性仍受到CYP2C19基因型的影響,因此,CYP2C19緩慢代謝者是否可因此得到較好的治療成效,與此治療優勢是否可進一步將療程縮短為7天以下值得研究。 方法 本研究收納台大醫院內證實受到幽門螺旋桿菌感染的胃炎及消化道潰瘍病人,依照受試者CYP2C19基因型隨機分為4組,其中A~C組在研究第1~7天皆服用rabeprazole 20 mg bid PO,D組則服用esomeprazole 40 mg bid,而抗生素部分,皆服用amoxicillin 1 g bid PO與clarithromycin 500 mg bid PO,A組於研究第1~4天使用,B組於第4~7天使用,C與D組於第1~7天使用,為分析藥動藥效特性,受試者於用藥第1、4、7天抽血測質子幫浦抑制劑與胃泌素濃度,所得資料使用NONMEM進行分析;而為進一步分析治療結果,受試者在治療前及治療後分別執行13碳尿素呼氣試驗。 結果 在rabeprazole藥動學部分,受試者CYP2C19基因型與體表面積兩個因子被發現可改善藥動學模型,故被納入完整藥動模型中,依照完整模型預估結果,CYP2C19緩慢代謝者在清除率與排除速率常數部分皆顯著小於快速代謝者,而單劑量與多劑量下rabeprazole藥動特性並沒有顯著差異;藥效部分,直接及間接模型皆被納入分析中,兩模型結果一致,皆由於緩慢代謝者血中rabeprazole濃度較高,故預估CYP2C19緩慢代謝者在使用rabeprazole上有較佳的酸分泌抑制效果,然而,在使用質子幫浦抑制劑的第4及7天胃泌素濃度比較上,不同CYP2C19基因型受試者並無顯著差異,可能原因應來自CYP2C19緩慢代謝者第1天起始的胃泌素濃度低於快速代謝者所造成。在esomeprazole部分,藥動學特性在單劑量及多劑量上有顯著差異,包括擬似分布體積與清除率皆在多劑量給藥下有降低現象,藥效學上,esomeprazole經模型預估後,發現使用esomeprazole受試者之藥效反應較使用rabeprazole的受試者差。臨床幽門螺旋桿菌治療成果上,不同CYP2C19基因型與不同治療方式間,治療成功率皆無顯著差異,但在CYP2C19緩慢代謝者中可觀察到較好的治療成功率。 結論 CYP2C19緩慢代謝者在使用rabeprazole為主的三合一療法時,有較好治療成效的趨勢,且在縮短療程中,CYP2C19緩慢代謝者也可達到很好的治療結果,因此,可能具有將療程縮短為4天的潛力,但因本研究樣本數較小,故無法達到統計上顯著差異,可能需進一步試驗來驗證本研究所觀察到的現象。 | zh_TW |
dc.description.provenance | Made available in DSpace on 2021-06-08T07:31:28Z (GMT). No. of bitstreams: 1 ntu-97-R95451002-1.pdf: 2574621 bytes, checksum: 985d5d81d4dc19c3eed4fc2e664fa671 (MD5) Previous issue date: 2008 | en |
dc.description.tableofcontents | 中文摘要 i
Abstract iii 目錄 v 圖目錄 viii 表目錄 ix 附圖目錄 x 附表目錄 xi 第1章 前言 1 第2章 文獻探討 2 2.1 Helicobacter pylori (H.pylori)與消化道潰瘍 2 2.1.1 消化道潰瘍 2 2.1.2 Helicobacter pylori 2 2.1.3 Helicobacter pylori治療 3 2.2 質子幫浦抑制劑- rabeprazole (Pariet®) 6 2.2.1 質子幫浦 6 2.2.2 質子幫浦抑制劑 6 2.3 胃泌素 11 2.3.1 介紹 11 2.3.2 胃泌素與質子幫浦抑制劑 11 2.3.3 胃泌素與Helicobacter pylori 12 2.4 CYP2C19基因多型性 13 2.4.1 CYP2C19基因多型性對rabeprazole之影響 13 2.5 族群藥物動力學與NONMEM 15 2.5.1 與傳統藥物動力學比較 15 2.5.2 分析方式 15 2.5.3 NONMEM 16 第3章 研究目的 29 第4章 研究方法 30 4.1 受試者收納 30 4.1.1 給藥方式 30 4.1.2 抽血時間 30 4.2 實驗室分析 31 4.2.1 CYP2C19基因型分析 31 4.2.2 內視鏡、組織學、微生物學檢驗 31 4.2.3 13C尿素呼氣試驗 31 4.2.4 Rabeprazole與esomeprazole血中濃度 31 4.2.5 胃泌素濃度 32 4.3 藥動/藥效分析 33 4.3.1 藥動分析 33 4.3.2 藥效分析 33 4.4 統計方法 35 第5章 結果 36 5.1 受試者特性 36 5.2 Rabeprazole藥物動力學資料與模型建立 37 5.2.1 血中濃度 37 5.2.2 Rabeprazole藥物動力學模型建構 37 5.3 胃泌素血中濃度與模型建立 38 5.3.1 血中濃度 38 5.3.2 藥動/藥效關係 38 5.4 Esomeprazole 40 5.4.1 Esomeprazole血中濃度與藥動模型 40 5.4.2 胃泌素血中濃度與藥效模型 40 5.5 臨床治療結果 41 第6章 討論 66 6.1 CYP2C19基因型與質子幫浦抑制劑之PK/PD 66 6.2 質子幫浦抑制劑之PK/PD關聯性 67 6.3 質子幫浦抑制劑族群藥動學與其他研究比較 68 6.4 胃酸抑制、胃泌素與H.pylori 69 6.5 臨床結果 70 6.6 限制與未來展望 72 第7章 結論 73 第8章 參考資料 74 附錄 84 | |
dc.language.iso | zh-TW | |
dc.title | CYP2C19基因多型性對短療程rabeprazole三合一療法之藥動/藥效關係及療效影響之評估 | zh_TW |
dc.title | Role of CYP2C19 polymorphisms in short-term rabeprazole-based triple therapy- Implication of PK/PD correlation | en |
dc.type | Thesis | |
dc.date.schoolyear | 96-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 李勇進,楊智欽,林淑文 | |
dc.subject.keyword | CYP2C19,rabeprazole,三合一療法,幽門螺旋桿菌,族群藥動學,NONMEM, | zh_TW |
dc.subject.keyword | CYP2C19,rabeprazole,triple therapy,H.pylori,population pharmacokinetics, | en |
dc.relation.page | 104 | |
dc.rights.note | 未授權 | |
dc.date.accepted | 2008-06-24 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 臨床藥學研究所 | zh_TW |
顯示於系所單位: | 臨床藥學研究所 |
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