NSAID起因性小腸傷害の現状と対策
非ステロイド性抗炎症薬（NSAIDs）は骨関節炎や関節リウマチに対して汎用される薬剤であるが，有害事象として胃・十二指腸潰瘍などの上部消化管傷害の頻度が高い．さらに近年カプセル内視鏡やダブルバルーン内視鏡の出現によって，NSAIDsが胃・十二指腸だけでなく小腸傷害を高頻度に惹起することがわかってきた．NSAID起因性小腸傷害の予防策として選択的COX-2阻害剤の使用が挙げられるが，短期の使用では抑制効果を有するものの長期使用では抑制効果が消失する．また疾患修飾性抗リウマチ薬などの抗リウマチ薬はNSAIDsと併用することによって，小腸傷害の発生頻度が高くなると考えられている．一方で抗TNF-α抗...
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| Published in | 臨床リウマチ Vol. 29; no. 2; pp. 77 - 84 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
一般社団法人 日本臨床リウマチ学会
2017
The Japanese Society for Clinical Rheumatology and Related Research |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0914-8760 2189-0595 |
| DOI | 10.14961/cra.29.77 |
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| Abstract | 非ステロイド性抗炎症薬（NSAIDs）は骨関節炎や関節リウマチに対して汎用される薬剤であるが，有害事象として胃・十二指腸潰瘍などの上部消化管傷害の頻度が高い．さらに近年カプセル内視鏡やダブルバルーン内視鏡の出現によって，NSAIDsが胃・十二指腸だけでなく小腸傷害を高頻度に惹起することがわかってきた．NSAID起因性小腸傷害の予防策として選択的COX-2阻害剤の使用が挙げられるが，短期の使用では抑制効果を有するものの長期使用では抑制効果が消失する．また疾患修飾性抗リウマチ薬などの抗リウマチ薬はNSAIDsと併用することによって，小腸傷害の発生頻度が高くなると考えられている．一方で抗TNF-α抗体療法を施行されている関節リウマチ患者においては，NSAID起因性傷害が軽微であることが判明している．さらに臨床上重要な点として，胃酸非依存的傷害であるNSAID起因性小腸傷害に対してプロトンポンプ阻害剤は無効であるばかりか，傷害を増悪させる可能性が示唆されている．NSAID起因性小腸傷害に対して有効性が期待される薬剤としては粘膜防御因子製剤やプロスタグランジン製剤があるが，さらに我々は抗TNF-α抗体療法，プロバイオティクスやコルヒチンが新たな治療薬の候補となりうると考えている．今後これらの新たな知見を踏まえたNSAID起因性消化管傷害に対する治療戦略の確立が必要である． |
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| AbstractList | 非ステロイド性抗炎症薬（NSAIDs）は骨関節炎や関節リウマチに対して汎用される薬剤であるが，有害事象として胃・十二指腸潰瘍などの上部消化管傷害の頻度が高い．さらに近年カプセル内視鏡やダブルバルーン内視鏡の出現によって，NSAIDsが胃・十二指腸だけでなく小腸傷害を高頻度に惹起することがわかってきた．NSAID起因性小腸傷害の予防策として選択的COX-2阻害剤の使用が挙げられるが，短期の使用では抑制効果を有するものの長期使用では抑制効果が消失する．また疾患修飾性抗リウマチ薬などの抗リウマチ薬はNSAIDsと併用することによって，小腸傷害の発生頻度が高くなると考えられている．一方で抗TNF-α抗体療法を施行されている関節リウマチ患者においては，NSAID起因性傷害が軽微であることが判明している．さらに臨床上重要な点として，胃酸非依存的傷害であるNSAID起因性小腸傷害に対してプロトンポンプ阻害剤は無効であるばかりか，傷害を増悪させる可能性が示唆されている．NSAID起因性小腸傷害に対して有効性が期待される薬剤としては粘膜防御因子製剤やプロスタグランジン製剤があるが，さらに我々は抗TNF-α抗体療法，プロバイオティクスやコルヒチンが新たな治療薬の候補となりうると考えている．今後これらの新たな知見を踏まえたNSAID起因性消化管傷害に対する治療戦略の確立が必要である． Non-steroidal anti-inflammatory drugs (NSAIDs) are currently the drugs most frequently used for osteoarthritis and rheumatoid arthritis (RA). It has become a major problem that NSAIDs damage the mucosa of the upper gastrointestinal tract and eventually cause gastric and duodenal ulcer. Moreover, recent studies using video capsule endoscopy and balloon-assisted enteroscopy have clarified that NSAIDs frequently damage the mucosa of small intestine. Although selective COX-2 inhibitors prevent NSAID-induced small intestinal damage in short-term use, it has been shown that the preventive effect is eliminated in long-term use. The use of disease-modifying anti-rheumatic drugs with NSAIDs is considered to aggravate the small intestinal damage. On the other hand, it has been proven that RA patients who receive anti-TNF-α therapy have less severe NSAID-induced small intestinal damage than those who does not receive the therapy. It is clinically significant that proton pump inhibitors (PPIs) cannot protect the small intestine from NSAIDs as hydrochloric acid is not produced in the small intestine. Moreover, some studies have raised the possibility that PPIs might exacerbate the small intestinal damage. Although mucoprotective drug and prostaglandin analogue are expected to be effective for NSAID-induced small intestinal damage at the present, we consider that anti-TNF-α therapy, probiotics, and colchicine could be new candidates for therapeutic agents for the damage. Thus, therapeutic strategies for NSAID-induced gastrointestinal damage need to be established based on these new findings. 非ステロイド性抗炎症薬（NSAIDs）は骨関節炎や関節リウマチに対して汎用される薬剤であるが，有害事象として胃・十二指腸潰瘍などの上部消化管傷害の頻度が高い．さらに近年カプセル内視鏡やダブルバルーン内視鏡の出現によって，NSAIDsが胃・十二指腸だけでなく小腸傷害を高頻度に惹起することがわかってきた．NSAID起因性小腸傷害の予防策として選択的COX-2阻害剤の使用が挙げられるが，短期の使用では抑制効果を有するものの長期使用では抑制効果が消失する．また疾患修飾性抗リウマチ薬などの抗リウマチ薬はNSAIDsと併用することによって，小腸傷害の発生頻度が高くなると考えられている．一方で抗TNF-α抗体療法を施行されている関節リウマチ患者においては，NSAID起因性傷害が軽微であることが判明している．さらに臨床上重要な点として，胃酸非依存的傷害であるNSAID起因性小腸傷害に対してプロトンポンプ阻害剤は無効であるばかりか，傷害を増悪させる可能性が示唆されている．NSAID起因性小腸傷害に対して有効性が期待される薬剤としては粘膜防御因子製剤やプロスタグランジン製剤があるが，さらに我々は抗TNF-α抗体療法，プロバイオティクスやコルヒチンが新たな治療薬の候補となりうると考えている．今後これらの新たな知見を踏まえたNSAID起因性消化管傷害に対する治療戦略の確立が必要である． |
| Author | 渡辺, 俊雄 大谷, 恒史 藤原, 靖弘 |
| Author_FL | Watanabe Toshio Fujiwara Yasuhiro Otani Koji |
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| References | 22) Nadatani Y, Watanabe T, Tanigawa T, et al: High mobility group box 1 promotes small intestinal damage induced by nonsteroidal anti-inflammatory drugs through Toll-like receptor 4. Am J Pathol, 181:98-110, 2012. 10) Furst DE: Clinical pharmacology of very low dose methotrexate for use in rheumatoid arthritis. J Rheumatol, Suppl 12, 11-14, 1985. 19) Watanabe T, Tanigawa T, Nadatani Y, et al: Mitochondrial disorders in NSAIDs-induced small bowel injury. J Clin Biochem Nutr, 48:117-121, 2011. 4) Graham DY, Opekun AR, Willingham FF, et al: Visible small-intestinal mucosal injury in chronic NSAID users. Clin Gastroenterol Hepatol, 3:55-59, 2005. 9) Maiden L, Thjodleifsson B, Seigal A, et al: Long-term effects of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 selective agents on the small bowel: a cross-sectional capsule enteroscopy study. Clin Gastroenterol Hepatol, 5:1040-1045, 2007. 2) Goldstein JL, Eisen GM, Lewis B, et al: Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole, and placebo. Clin Gastroenterol Hepatol, 3:133-141, 2005. 5) Sugimori S, WatanabeT, Tabuchi M, et al: Evaluation of small bowel injury in patients with rheumatoid arthritis by capsule endoscopy: effects of anti-rheumatoid arthritis drugs. Digestion, 78:208-213, 2008. 17) Watanabe T, Tanigawa T, Nadatani Y, et al: Risk factors for severe nonsteroidal anti-inflammatory drug-induced small intestinal damage. Dig Liver Dis, 45:390-395, 2013. 12) Watanabe T, Higuchi K, Hamaguchi M, et al: Monocyte chemotactic protein-1 regulates leukocyte recruitment during gastric ulcer recurrence induced by tumor necrosis factor-alpha. Am J Physiol Gastrointest Liver Physiol, 287:G919-928, 2004. 1) Maiden L, Thjodleifsson B, Theodors A, et al: A quantitative analysis of NSAID-induced small bowel pathology by capsule enteroscopy. Gastroenterology, 128:1172-1178, 2005. 11) Watanabe T, Higuchi K, Kobata A, et al: Non-steroidal anti-inflammatory drug-induced small intestinal damage is Toll-like receptor 4 dependent. Gut, 57:181-187, 2007. 18) Takeuchi K, Sato H: NSAID-induced small intestinal damage--roles of various pathogenic factors. Digestion, 91:218-232, 2015. 20) Lamkanfi M, Dixit VM: Mechanisms and functions of inflammasomes. Cell, 157: 1013-1022, 2014. 28) Watanabe T, Nishio H, Tanigawa T, et al: Probiotic Lactobacillus casei strain Shirota prevents indomethacin-induced small intestinal injury: involvement of lactic acid. Am J Physiol Gastrointes Liver Physiol, 297:G506-513, 2009. 16) Endo H, Sakai E, Taniguchi L, et al: Risk factors for small-bowel mucosal breaks in chronic low-dose aspirin users: data from a prospective multicenter capsule endoscopy registry. Gastrointest Endosc, 80: 826-834, 2014. 29) Endo H, Higurashi T, Hosono K, et al: Efficacy of Lactobacillus casei treatment on small bowel injury in chronic low-dose aspirin users: a pilot randomized controlled study. J Gastroenterol, 46:894-905, 2011. 13) Watanabe T, Tanigawa T, Shiba M, et al: Anti-tumour necrosis factor agents reduce non-steroidal anti-inflammatory drug-induced small bowel injury in rheumatoid arthritis patients. Gut, 63:409-414, 2013. 15) Washio E, Esaki M, Maehata Y, et al: Proton pump inhibitors increase incidence of nonsteroidal anti-inflammatory drug-induced small bowel injury: A randomized, placebo-controlled trial. Clin Gastroenterol Hepatol, 14:809-815, 2016. 21) Wen H, Miao EA, Ting JP: Mechanisms of NOD-like receptor-associated inflammasome activation. Immunity, 39:432-441, 2013. 3) Fujimori S, Seo T, Ehara A, et al: Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy. Gastrointest Endosc, 69:1339-1346, 2009. 27) Kuramoto T, Umegaki E, Nouda S, et al: Preventive effect of irsogladine or omeprazole on non-steroidal anti-inflammatory drug-induced esophagitis, peptic ulcers, and small intestinal kesions in humans, a prospective randomized controlled study. BMC Gastroenterol, 13:85, 2013. 25) Fujimori S, Takahashi Y, Gudis K, et al: Rebamipide has the potential to reduce the intensity of NSAID-induced small intestinal injury: a double-blind, randomized, controlled trial evaluated by capsule endoscopy. J Gastroenterol, 46:57-64, 2011. 26) Fujimori S, Seo T, Gudis K, et al: Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy. Gastrointest Endosc, 69:1339-1346, 2009. 31) Misawa T, Takahama M, Kozaki T, et al: Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome. Nat Immunol, 14:454-460, 2013. 14) Wallace JL, Syer S, Denou E, et al: Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Gastroenterology, 141:1314-1322, 2011. 24) Niwa Y, Nakamura M, Ohmiya N, et al: Efficacy of rebamipide for diclofenac-induced small intestinal mucosal injuries in healthy subjects: a prospective, randomized, double-blinded, placebo-controlled, cross-over study. J Gastroenterol, 43:270-276, 2008. 7) Hawkey CJ, Ell C, Simon B, et al: Less small-bowel injury with lumiracoxib compared with naproxen plus omeprazole. Clin Gastroenterol Hepatol, 6: 536-544, 2008. 23) Higashimori A, Watanabe T, Nadatani Y, et al: Mechanisms of NLRP3 inflammasome activation and its role in NSAID-induced enteropathy. Mucosal Immunology, 9:659-668, 2016. 6) Simon LS, Weaver AL, Graham DY, et al: Anti-inflammatory and upper gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomized controlled trial. JAMA, 282:1921-1928, 1999. 8) Goldstein JL, Eisen GM, Lewis B, et al: Small bowel mucosal injury is reduced in healthy subjects treated with celecoxib compared with ibuprofen plus omeprazole, as assessed by video capsule endoscopy. Aliment Pharmacol Ther, 25:1211-1222, 2007. 30) Otani K, Watanabe T, Shimada S, et al: Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome. Scientific Reports, 6:32587, 2016. |
| References_xml | – reference: 31) Misawa T, Takahama M, Kozaki T, et al: Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome. Nat Immunol, 14:454-460, 2013. – reference: 8) Goldstein JL, Eisen GM, Lewis B, et al: Small bowel mucosal injury is reduced in healthy subjects treated with celecoxib compared with ibuprofen plus omeprazole, as assessed by video capsule endoscopy. Aliment Pharmacol Ther, 25:1211-1222, 2007. – reference: 28) Watanabe T, Nishio H, Tanigawa T, et al: Probiotic Lactobacillus casei strain Shirota prevents indomethacin-induced small intestinal injury: involvement of lactic acid. Am J Physiol Gastrointes Liver Physiol, 297:G506-513, 2009. – reference: 6) Simon LS, Weaver AL, Graham DY, et al: Anti-inflammatory and upper gastrointestinal effects of celecoxib in rheumatoid arthritis: a randomized controlled trial. JAMA, 282:1921-1928, 1999. – reference: 20) Lamkanfi M, Dixit VM: Mechanisms and functions of inflammasomes. Cell, 157: 1013-1022, 2014. – reference: 16) Endo H, Sakai E, Taniguchi L, et al: Risk factors for small-bowel mucosal breaks in chronic low-dose aspirin users: data from a prospective multicenter capsule endoscopy registry. Gastrointest Endosc, 80: 826-834, 2014. – reference: 25) Fujimori S, Takahashi Y, Gudis K, et al: Rebamipide has the potential to reduce the intensity of NSAID-induced small intestinal injury: a double-blind, randomized, controlled trial evaluated by capsule endoscopy. J Gastroenterol, 46:57-64, 2011. – reference: 27) Kuramoto T, Umegaki E, Nouda S, et al: Preventive effect of irsogladine or omeprazole on non-steroidal anti-inflammatory drug-induced esophagitis, peptic ulcers, and small intestinal kesions in humans, a prospective randomized controlled study. BMC Gastroenterol, 13:85, 2013. – reference: 5) Sugimori S, WatanabeT, Tabuchi M, et al: Evaluation of small bowel injury in patients with rheumatoid arthritis by capsule endoscopy: effects of anti-rheumatoid arthritis drugs. Digestion, 78:208-213, 2008. – reference: 15) Washio E, Esaki M, Maehata Y, et al: Proton pump inhibitors increase incidence of nonsteroidal anti-inflammatory drug-induced small bowel injury: A randomized, placebo-controlled trial. Clin Gastroenterol Hepatol, 14:809-815, 2016. – reference: 7) Hawkey CJ, Ell C, Simon B, et al: Less small-bowel injury with lumiracoxib compared with naproxen plus omeprazole. Clin Gastroenterol Hepatol, 6: 536-544, 2008. – reference: 11) Watanabe T, Higuchi K, Kobata A, et al: Non-steroidal anti-inflammatory drug-induced small intestinal damage is Toll-like receptor 4 dependent. Gut, 57:181-187, 2007. – reference: 14) Wallace JL, Syer S, Denou E, et al: Proton pump inhibitors exacerbate NSAID-induced small intestinal injury by inducing dysbiosis. Gastroenterology, 141:1314-1322, 2011. – reference: 24) Niwa Y, Nakamura M, Ohmiya N, et al: Efficacy of rebamipide for diclofenac-induced small intestinal mucosal injuries in healthy subjects: a prospective, randomized, double-blinded, placebo-controlled, cross-over study. J Gastroenterol, 43:270-276, 2008. – reference: 18) Takeuchi K, Sato H: NSAID-induced small intestinal damage--roles of various pathogenic factors. Digestion, 91:218-232, 2015. – reference: 3) Fujimori S, Seo T, Ehara A, et al: Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy. Gastrointest Endosc, 69:1339-1346, 2009. – reference: 2) Goldstein JL, Eisen GM, Lewis B, et al: Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole, and placebo. Clin Gastroenterol Hepatol, 3:133-141, 2005. – reference: 29) Endo H, Higurashi T, Hosono K, et al: Efficacy of Lactobacillus casei treatment on small bowel injury in chronic low-dose aspirin users: a pilot randomized controlled study. J Gastroenterol, 46:894-905, 2011. – reference: 9) Maiden L, Thjodleifsson B, Seigal A, et al: Long-term effects of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 selective agents on the small bowel: a cross-sectional capsule enteroscopy study. Clin Gastroenterol Hepatol, 5:1040-1045, 2007. – reference: 17) Watanabe T, Tanigawa T, Nadatani Y, et al: Risk factors for severe nonsteroidal anti-inflammatory drug-induced small intestinal damage. Dig Liver Dis, 45:390-395, 2013. – reference: 22) Nadatani Y, Watanabe T, Tanigawa T, et al: High mobility group box 1 promotes small intestinal damage induced by nonsteroidal anti-inflammatory drugs through Toll-like receptor 4. Am J Pathol, 181:98-110, 2012. – reference: 4) Graham DY, Opekun AR, Willingham FF, et al: Visible small-intestinal mucosal injury in chronic NSAID users. Clin Gastroenterol Hepatol, 3:55-59, 2005. – reference: 13) Watanabe T, Tanigawa T, Shiba M, et al: Anti-tumour necrosis factor agents reduce non-steroidal anti-inflammatory drug-induced small bowel injury in rheumatoid arthritis patients. Gut, 63:409-414, 2013. – reference: 10) Furst DE: Clinical pharmacology of very low dose methotrexate for use in rheumatoid arthritis. J Rheumatol, Suppl 12, 11-14, 1985. – reference: 26) Fujimori S, Seo T, Gudis K, et al: Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy. Gastrointest Endosc, 69:1339-1346, 2009. – reference: 23) Higashimori A, Watanabe T, Nadatani Y, et al: Mechanisms of NLRP3 inflammasome activation and its role in NSAID-induced enteropathy. Mucosal Immunology, 9:659-668, 2016. – reference: 1) Maiden L, Thjodleifsson B, Theodors A, et al: A quantitative analysis of NSAID-induced small bowel pathology by capsule enteroscopy. Gastroenterology, 128:1172-1178, 2005. – reference: 21) Wen H, Miao EA, Ting JP: Mechanisms of NOD-like receptor-associated inflammasome activation. Immunity, 39:432-441, 2013. – reference: 12) Watanabe T, Higuchi K, Hamaguchi M, et al: Monocyte chemotactic protein-1 regulates leukocyte recruitment during gastric ulcer recurrence induced by tumor necrosis factor-alpha. Am J Physiol Gastrointest Liver Physiol, 287:G919-928, 2004. – reference: 19) Watanabe T, Tanigawa T, Nadatani Y, et al: Mitochondrial disorders in NSAIDs-induced small bowel injury. J Clin Biochem Nutr, 48:117-121, 2011. – reference: 30) Otani K, Watanabe T, Shimada S, et al: Colchicine prevents NSAID-induced small intestinal injury by inhibiting activation of the NLRP3 inflammasome. Scientific Reports, 6:32587, 2016. |
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| Snippet | 非ステロイド性抗炎症薬（NSAIDs）は骨関節炎や関節リウマチに対して汎用される薬剤であるが，有害事象として胃・十二指腸潰瘍などの上部消化管傷害の頻度が高い．さらに... Non-steroidal anti-inflammatory drugs (NSAIDs) are currently the drugs most frequently used for osteoarthritis and rheumatoid arthritis (RA). It has become... |
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| SubjectTerms | colchicine NSAIDs PPI small intestine TNF-α |
| Title | NSAID起因性小腸傷害の現状と対策 |
| URI | https://www.jstage.jst.go.jp/article/cra/29/2/29_77/_article/-char/ja https://cir.nii.ac.jp/crid/1390282679318110208 |
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| ispartofPNX | 臨床リウマチ, 2017/06/30, Vol.29(2), pp.77-84 |
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