体质量指数与克罗恩病的关系
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摘要
目的分析体质量指数(body mass index,BMI)与克罗恩病(Crohn’s disease,CD)的关系,观察患者营养状况对CD诊疗的影响。方法回顾性分析初次确诊的54例CD患者的临床资料进行回顾性分析。记录患者初发病时的体质量(kg)和身高(m),计算BMI;收集患者的发病情况,疾病活动严重程度采用CDAI计算法。同时收集患者确诊为CD时的年龄、确诊CD所用时长、是否发生CD相关手术、CD相关并发症、是否有CD相关再住院、相关药物的服用等信息。分析BMI与CD发病的关系,以及BMI对CD并发症及治疗方法选择等方面的影响。结果 47例(87.04%)CD患者发病时处于营养正常或营养不良状态。不同BMI的CD患者诊断延迟率差异有统计学意义(χ~2=6.038,P=0.049),其中18.5 kg/m~2≤BMI<24 kg/m~2组和BMI≥24 kg/m~2组的CD患者诊断延迟率明显高于BMI<18.5 kg/m~2组。随着疾病的发展,不同BMI的CD患者肠狭窄和梗阻的发生率差异有统计学意义(χ~2=11.923,P=0.003),其中BMI<18.5 kg/m~2组的CD患者的发生率明显高于18.5 kg/m~2≤BMI<24 kg/m~2组和BMI≥24 kg/m~2组。在确诊后CD处于重度活动度的患者选择治疗药物方面,BMI<18.5 kg/m~2组的CD患者将英夫利昔单抗作为初始治疗的概率明显高于18.5 kg/m~2≤BMI<24 kg/m~2组和BMI≥24 kg/m~2组患者,差异有统计学意义(χ~2=6.920,P=0.031)。CD患者的确诊年龄与BMI呈正相关(r=0.422,P=0.001);而CD患者发病时的活动度及并发症与BMI呈负相关(r=-0.302,P=0.026;r=-0.312,P=0.002)。结论确诊年龄、疾病活动度和并发症与BMI有相关性。BMI正常或较高的CD患者存在诊断延迟;而BMI较低的患者易发生肠狭窄和梗阻,且确诊后处于重度活动度的营养不良的CD患者倾向于将英夫利昔单抗作为初始药物治疗。
Objective To explore the association of body mass index(BMI) and Crohn's disease(CD), and analyze the influence of patients' nutritional status on the diagnosis and treatment of CD.Methods The clinical data of 54 patients diagnosed as CD for the first time were analyzed retrospectively. The body mass(kg) and height(m) of the patients at the time of initial onset were recorded, and BMI was calculated. The onset of CD was collected and the severity of disease activity was calculated by CDAI. At the same time, informations of the patients were collected, such as the age which the patient was diagnosed with CD, the length of time it took to diagnose CD, CD-related surgery, CD-related complications, CD-related readmission and the administration of drugs. Analyzed the relationship between BMI and the onset of CD, as well as the influence of BMI on CD complications and treatment options.Results Forty-seven CD patients(87.04%) were in normal nutrition and malnutrition state at the time of onset. There was a statistically significant difference between CD patients with different BMI(χ~2=6.038, P=0.049), the diagnostic delay rates of CD patients with 18.5 kg/m~2≤BMI<24 kg/m~2 and those with BMI≥24 kg/m~2 were significantly higher than those of CD patients with BMI<18.5 kg/m~2. With the development of the disease, the difference of intestinal stenosis and obstruction among CD patients with different BMI was statistically significant(χ~2=11.923, P=0.003), the incidences of CD patients with BMI<18.5 kg/m~2 were significantly higher than those with 18.5 kg/m~2≤BMI<24 kg/m~2 and those with BMI≥24 kg/m~2. Regarding the choice of treatment drugs for patients with CD in severe activity after diagnosis, patients with BMI<18.5 kg/m~2 had significantly higher probability of taking Infliximab as initial treatment than patients with 18.5 kg/m~2≤BMI<24 kg/m~2 and patients with BMI≥24 kg/m~2, and the difference was statistically significant(χ~2=6.920, P=0.031).The age of diagnosis of CD was positively correlated with BMI(r=0.422, P=0.001). The activity and complications of CD patients were negatively correlated with BMI(r=-0.302, P=0.026; r=-0.312,P = 0. 002). Conclusion Age of diagnosis,disease activity and complications are related to BMI. Diagnostic delay exists in CD patients with normal or higher BMI. However,patients with low BMI are prone to intestinal stenosis and obstruction,and patients with malnutrition CD who are in severe activity after diagnosis tend to treat Infliximab as an initial drug.
Objective To explore the association of body mass index(BMI) and Crohn's disease(CD), and analyze the influence of patients' nutritional status on the diagnosis and treatment of CD.Methods The clinical data of 54 patients diagnosed as CD for the first time were analyzed retrospectively. The body mass(kg) and height(m) of the patients at the time of initial onset were recorded, and BMI was calculated. The onset of CD was collected and the severity of disease activity was calculated by CDAI. At the same time, informations of the patients were collected, such as the age which the patient was diagnosed with CD, the length of time it took to diagnose CD, CD-related surgery, CD-related complications, CD-related readmission and the administration of drugs. Analyzed the relationship between BMI and the onset of CD, as well as the influence of BMI on CD complications and treatment options.Results Forty-seven CD patients(87.04%) were in normal nutrition and malnutrition state at the time of onset. There was a statistically significant difference between CD patients with different BMI(χ~2=6.038, P=0.049), the diagnostic delay rates of CD patients with 18.5 kg/m~2≤BMI<24 kg/m~2 and those with BMI≥24 kg/m~2 were significantly higher than those of CD patients with BMI<18.5 kg/m~2. With the development of the disease, the difference of intestinal stenosis and obstruction among CD patients with different BMI was statistically significant(χ~2=11.923, P=0.003), the incidences of CD patients with BMI<18.5 kg/m~2 were significantly higher than those with 18.5 kg/m~2≤BMI<24 kg/m~2 and those with BMI≥24 kg/m~2. Regarding the choice of treatment drugs for patients with CD in severe activity after diagnosis, patients with BMI<18.5 kg/m~2 had significantly higher probability of taking Infliximab as initial treatment than patients with 18.5 kg/m~2≤BMI<24 kg/m~2 and patients with BMI≥24 kg/m~2, and the difference was statistically significant(χ~2=6.920, P=0.031).The age of diagnosis of CD was positively correlated with BMI(r=0.422, P=0.001). The activity and complications of CD patients were negatively correlated with BMI(r=-0.302, P=0.026; r=-0.312,P = 0. 002). Conclusion Age of diagnosis,disease activity and complications are related to BMI. Diagnostic delay exists in CD patients with normal or higher BMI. However,patients with low BMI are prone to intestinal stenosis and obstruction,and patients with malnutrition CD who are in severe activity after diagnosis tend to treat Infliximab as an initial drug.
引文
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[13] VAVRICKA S R, SPIGAGLIA S M, ROGLER G, et al. Systematic evaluation of risk factors for diagnostic delay in inflammatory bowel disease [J]. Inflamm Bowel Dis, 2012, 18(3): 496-505. DOI: 10.1002/ibd.21719.
[14] ISIK H, AYNIOGLU O, TIMUR H, et al. Is Xanthine oxidase activity in polycystic ovary syndrome associated with inflammatory and cardiovascular risk factors? [J]. J Reprod Immunol, 2016, 116: 98-103. DOI: 10.1016/j.jri.2016.06.002.
[15] ZUO L, LI Y, ZHU W, et al. Mesenteric adipocyte dysfunction in Crohn’s disease is associated with hypoxia [J]. Inflamm Bowel Dis, 2015, 22(1): 114-126. DOI: 10.1097/MIB.0000000000000571.
[16] WANG X, CHEN Q, PU H, et al. Adiponectin improves NF-κB-mediated inflammation and abates atherosclerosis progression in apolipoprotein E-deficient mice [J]. Lipids Health Dis, 2016, 15: 33. DOI: 10.1186/s12944-016-0202-y.
[17] KARMIRIS K, KOUTROUBAKIS I E, XIDAKIS C, et al. Circulating levels of leptin, adiponectin, resistin, and ghrelin in inflammatory bowel disease [J]. Inflamm Bowel Dis, 2006, 12(2): 100-105. DOI: 10.1097/01.MIB.0000200345.38837.46
[18] MORAN G W, DUBEAU M F, KAPLAN G G, et al. The increasing weight of Crohn’s disease subjects in clinical trials: a hypothesis-generatings time trend analysis [J]. Inflamm Bowel Dis, 2013, 19(13): 2949-2956. DOI: 10.1097/MIB.0b013e31829936a4.
[19] CSONTOS á A, MOLNáR A, PIRI Z, et al. Malnutrition risk questionnaire combined with body composition measurement in malnutrition screening in inflammatory bowel disease [J]. Rev Esp Enferm Dig, 2017, 109(1): 26-32. DOI: 10.17235/reed.2016.4557/2016.
[20] HARPER J W, SINANAN M N, ZISMAN T L. Increased body mass index is associated with earlier time to loss of response to infliximab in patients with inflammatory bowel disease [J]. Inflamm Bowel Dis, 2013, 19(10): 2118-2124. DOI: 10.1097/MIB.0b013e31829cf401.
[21] KRANE M K, ALLAIX M E, ZOCCALI M, et al. Does morbid obesity change outcomes after laparoscopic surgery for inflammatory bowel disease Review of 626 consecutive cases [J]. J Am Coll Surg, 2013, 216(5): 986-996. DOI: 10.1016/j.jamcollsurg.2013.01.053.
[22] SEMINERIO J L, KOUTROUBAKIS I E, RAMOSRIVERS C, et al. Impact of obesity on the management and clinical course of patients with inflammatory bowel disease [J]. Inflamm Bowel Dis, 2015, 21(12): 2857-2863. DOI: 10.1097/MIB.0000000000000560.
[23] ZWINTSCHER N P, HORTON J D, STEELE S R. Obesity has minimal impact on clinical outcomes in children with inflammatory bowel disease [J]. J Pediatr Surg, 2014, 49(2): 265-268, discussion 268. DOI: 10.1016/j.jpedsurg.2013.11.033.
[24] PRINGLE P L, STEWART K O, PELOQUIN J M, et al. Body mass index, genetic susceptibility, and risk of complications among individuals with Crohn’s disease [J]. Inflamm Bowel Dis, 2015, 21(10): 2304-2310. DOI: 10.1097/MIB.0000000000000498.
[25] BEAUGERIE L, SOKOL H. Clinical, serological and genetic predictors of inflammatory bowel disease course [J]. World J Gastroenterol, 2012, 18(29): 3806-3813. DOI: 10.3748/wjg.v18.i29.3806.
[26] BUSEMEYER L, RUCKELSHAUSEN A, M?LLER K, et al. Precision phenotyping of biomass accumulation in triticale reveals temporal genetic patterns of regulation [J]. Sci Rep, 2013, 3: 2442. DOI: 10.1038/srep02442.
[27] VAN ASSCHE G, BAERT F, VERMEIRE S, et al. Commentary: BMI and the need for adalimumab dose escalation in Crohn’s disease [J]. Aliment Pharmacol Ther, 2012, 35(7): 848, discussion 849. DOI: 10.1111/j.1365-2036.2012.05023.
[28] BULTMAN E, DE HAAR C, VAN LIERE-BARON A, et al. Predictors of dose escalation of adalimumab in a prospective cohort of Crohn’s disease patients [J]. Aliment Pharmacol Ther, 2012, 35(3): 335-341. DOI: 10.1111/j.1365-2036.2011.04946.x.
[29] MOWAT C, COLE A, WINDSOR A, et al. Guidelines for the management of inflammatory bowel disease in adults [J]. Gut, 2011, 60(5): 571-607. DOI: 10.1136/gut.2010.224154.
[30] HEMPERLY A, VANDE CASTEELE N. Clinical pharmacokinetics and pharmacodynamics of infliximab in the treatment of inflammatory bowel disease [J]. Clin Pharmacokinet, 2018, 57(8): 929-942. DOI: 10.1007/s40262-017-0627-0.
[31] FRYMOYER A, PIESTER T L, PARK K T. Infliximab dosing strategies and predicted trough exposure in children with Crohn’s disease [J]. J Pediatr Gastroenterol Nutr, 2016, 62(5): 723-727. DOI: 10.1097/MPG.0000000000001123.
[32] SUMI R, NAKAJIMA K, IIJIMA H, et al. Influence of nutritional status on the therapeutic effect of infliximab in patients with Crohn’s disease [J]. Surg Today, 2016, 46(8): 922-929. DOI: 10.1007/s00595-015-1257-5.
[2] JIANG L, TIAN W, WANG Y, et al. Body mass index and susceptibility to knee osteoarthritis: a systematic review and meta-analysis [J]. Joint Bone Spine, 2012, 79(3): 291-297. DOI: 10.1016/j.jbspin.2011.05.015.
[3] PENG L, WANG J, LI F. Weight reduction for non-alcoholic fatty liver disease [J]. Cochrane Database Syst Rev, 2011, (16): CD003619. DOI: 10.1002/14651858.CD003619.pub3.
[4] MIJAC D D, JANKOVI, et al. Nutritional status in patients with active inflammatory bowel disease: prevalence of malnutrition and methods for routine nutritional assessment [J]. Eur J Intern Med, 2010, 21(4): 315-319. DOI: 10.1016/j.ejim.2010.04.012.
[5] MALIK T A, KASLOW R A, COFIELD S S, et al. Body mass index is associated with mucosal disease in Crohn’s: results of a case-control study [J]. Gastroenterol Res, 2014, 7(5-6): 111-117. DOI: 10.14740/gr631w.
[6] BROWN P, CLARK T, DOWSON G, et al. Relationship of body mass index to clinical outcomes after infliximab therapy in patients with Crohn’s disease [J]. J Crohns Colitis, 2016, 10(10): 1144-1150. DOI: 10.1093/ecco-jcc/jjw079.
[7] 中华医学会消化病学分会炎症性肠病学组. 炎症性肠病诊断与治疗的共识意见(2012年·广州)[J]. 中华内科杂志, 2012, 51(10): 818-831. DOI: 10.3760/cma.j.issn.0578-1426.2012.10.024.
[8] VALENTINI L, SCHULZKE J D. Mundane, yet challenging: the assessment of malnutrition in inflammatory bowel disease [J]. Eur J Intern Med, 2011, 22(1): 13-15. DOI: 10.1016/j.ejim.2010.07.021.
[9] MASSIRONI S, ROSSI R E, CAVALCOLI F A, et al. Nutritional deficiencies in inflammatory bowel disease: therapeutic approaches [J]. Clin Nutr, 2013, 32(6): 904-910. DOI: 10.1016/j.clnu.2013.03.020.
[10] DONG J, CHEN Y, TANG Y, et al. Body mass index is associated with inflammatory bowel disease: a systematic review and Meta-analysis [J]. PLoS One, 2015, 10(12): e0144872. DOI: 10.1371/journal.pone.0144872.
[11] ZHANG M, GAO X, CHEN Y, et al. Body mass index is a marker of nutrition preparation sufficiency before surgery for Crohn’s disease from the perspective of intra-abdominal septic complications: a retrospective Cohort study [J]. Medicine (Baltimore), 2015, 94(35): e1455. DOI: 10.1097/MD.0000000000001455.
[12] SCHOEPFER A M, DEHLAVI M A, FOURNIER N, et al. Diagnostic delay in Crohn’s disease is associated with a complicated disease course and increased operation rate [J]. Am J Gastroenterol, 2013, 108(11): 1744-1754. DOI: 10.1038/ajg.2013.248.
[13] VAVRICKA S R, SPIGAGLIA S M, ROGLER G, et al. Systematic evaluation of risk factors for diagnostic delay in inflammatory bowel disease [J]. Inflamm Bowel Dis, 2012, 18(3): 496-505. DOI: 10.1002/ibd.21719.
[14] ISIK H, AYNIOGLU O, TIMUR H, et al. Is Xanthine oxidase activity in polycystic ovary syndrome associated with inflammatory and cardiovascular risk factors? [J]. J Reprod Immunol, 2016, 116: 98-103. DOI: 10.1016/j.jri.2016.06.002.
[15] ZUO L, LI Y, ZHU W, et al. Mesenteric adipocyte dysfunction in Crohn’s disease is associated with hypoxia [J]. Inflamm Bowel Dis, 2015, 22(1): 114-126. DOI: 10.1097/MIB.0000000000000571.
[16] WANG X, CHEN Q, PU H, et al. Adiponectin improves NF-κB-mediated inflammation and abates atherosclerosis progression in apolipoprotein E-deficient mice [J]. Lipids Health Dis, 2016, 15: 33. DOI: 10.1186/s12944-016-0202-y.
[17] KARMIRIS K, KOUTROUBAKIS I E, XIDAKIS C, et al. Circulating levels of leptin, adiponectin, resistin, and ghrelin in inflammatory bowel disease [J]. Inflamm Bowel Dis, 2006, 12(2): 100-105. DOI: 10.1097/01.MIB.0000200345.38837.46
[18] MORAN G W, DUBEAU M F, KAPLAN G G, et al. The increasing weight of Crohn’s disease subjects in clinical trials: a hypothesis-generatings time trend analysis [J]. Inflamm Bowel Dis, 2013, 19(13): 2949-2956. DOI: 10.1097/MIB.0b013e31829936a4.
[19] CSONTOS á A, MOLNáR A, PIRI Z, et al. Malnutrition risk questionnaire combined with body composition measurement in malnutrition screening in inflammatory bowel disease [J]. Rev Esp Enferm Dig, 2017, 109(1): 26-32. DOI: 10.17235/reed.2016.4557/2016.
[20] HARPER J W, SINANAN M N, ZISMAN T L. Increased body mass index is associated with earlier time to loss of response to infliximab in patients with inflammatory bowel disease [J]. Inflamm Bowel Dis, 2013, 19(10): 2118-2124. DOI: 10.1097/MIB.0b013e31829cf401.
[21] KRANE M K, ALLAIX M E, ZOCCALI M, et al. Does morbid obesity change outcomes after laparoscopic surgery for inflammatory bowel disease Review of 626 consecutive cases [J]. J Am Coll Surg, 2013, 216(5): 986-996. DOI: 10.1016/j.jamcollsurg.2013.01.053.
[22] SEMINERIO J L, KOUTROUBAKIS I E, RAMOSRIVERS C, et al. Impact of obesity on the management and clinical course of patients with inflammatory bowel disease [J]. Inflamm Bowel Dis, 2015, 21(12): 2857-2863. DOI: 10.1097/MIB.0000000000000560.
[23] ZWINTSCHER N P, HORTON J D, STEELE S R. Obesity has minimal impact on clinical outcomes in children with inflammatory bowel disease [J]. J Pediatr Surg, 2014, 49(2): 265-268, discussion 268. DOI: 10.1016/j.jpedsurg.2013.11.033.
[24] PRINGLE P L, STEWART K O, PELOQUIN J M, et al. Body mass index, genetic susceptibility, and risk of complications among individuals with Crohn’s disease [J]. Inflamm Bowel Dis, 2015, 21(10): 2304-2310. DOI: 10.1097/MIB.0000000000000498.
[25] BEAUGERIE L, SOKOL H. Clinical, serological and genetic predictors of inflammatory bowel disease course [J]. World J Gastroenterol, 2012, 18(29): 3806-3813. DOI: 10.3748/wjg.v18.i29.3806.
[26] BUSEMEYER L, RUCKELSHAUSEN A, M?LLER K, et al. Precision phenotyping of biomass accumulation in triticale reveals temporal genetic patterns of regulation [J]. Sci Rep, 2013, 3: 2442. DOI: 10.1038/srep02442.
[27] VAN ASSCHE G, BAERT F, VERMEIRE S, et al. Commentary: BMI and the need for adalimumab dose escalation in Crohn’s disease [J]. Aliment Pharmacol Ther, 2012, 35(7): 848, discussion 849. DOI: 10.1111/j.1365-2036.2012.05023.
[28] BULTMAN E, DE HAAR C, VAN LIERE-BARON A, et al. Predictors of dose escalation of adalimumab in a prospective cohort of Crohn’s disease patients [J]. Aliment Pharmacol Ther, 2012, 35(3): 335-341. DOI: 10.1111/j.1365-2036.2011.04946.x.
[29] MOWAT C, COLE A, WINDSOR A, et al. Guidelines for the management of inflammatory bowel disease in adults [J]. Gut, 2011, 60(5): 571-607. DOI: 10.1136/gut.2010.224154.
[30] HEMPERLY A, VANDE CASTEELE N. Clinical pharmacokinetics and pharmacodynamics of infliximab in the treatment of inflammatory bowel disease [J]. Clin Pharmacokinet, 2018, 57(8): 929-942. DOI: 10.1007/s40262-017-0627-0.
[31] FRYMOYER A, PIESTER T L, PARK K T. Infliximab dosing strategies and predicted trough exposure in children with Crohn’s disease [J]. J Pediatr Gastroenterol Nutr, 2016, 62(5): 723-727. DOI: 10.1097/MPG.0000000000001123.
[32] SUMI R, NAKAJIMA K, IIJIMA H, et al. Influence of nutritional status on the therapeutic effect of infliximab in patients with Crohn’s disease [J]. Surg Today, 2016, 46(8): 922-929. DOI: 10.1007/s00595-015-1257-5.