初发急性胰腺炎后新发糖尿病的危险因素评估

刘慧; 李贤秋; 罗刚; 唐世孝

doi:10.3969/j.issn.1001-5256.2020.12.026

初发急性胰腺炎后新发糖尿病的危险因素评估

DOI: 10.3969/j.issn.1001-5256.2020.12.026

西南医科大学附属医院消化内科

基金项目:

四川省泸州市人民政府-四川医科大学科技战略合作项目[2015LZCYD-SO1（9/15）]；

详细信息

中图分类号: R576;R587.1
计量
- 文章访问数: 4075
- HTML全文浏览量: 55
- PDF下载量: 76
- 被引次数: 0
出版历程
- 收稿日期: 2020-06-29
- 出版日期: 2020-12-20

Risk factors for new-onset diabetes after incipient acute pancreatitis

Department of Gastroenterology,The Affiliated Hospital of Southwest Medical University

Research funding:

摘要

摘要:
目的探索初发急性胰腺炎（AP）后新发糖尿病的相关危险因素。方法回顾性纳入2013年6月-2020年1月西南医科大学附属医院收治的初发AP后发生急性胰腺炎后糖尿病（PPDM-A）的患者95例,为PPDM-A组,以2∶1比例随机抽取同一时间段的初发AP后未发糖尿病的患者190例作为对照组,即非PPDM-A组,收集患者的基线资料和临床资料。计量资料组间比较采用t检验或U检验,计数资料组间比较采用χ2检验或Fisher精确检验,多因素分析采用logistic回归分析。结果两组BMI、体质量、饮酒史、高尿酸血症、脂肪肝比例差异均有统计学意义（P值均<0.>0. 05）。两组不同病因（胆源性、高脂血症性、酒精性AP）比较差异有统计学意义（P<0.>11. 1 mmol/L比例均高于非PPDM-A组（P值均<0.>0. 05）。PPDM-A...
- 急性胰腺炎 /
- 胰源性糖尿病 /
- 危险因素
Abstract:
Objective To investigate the risk factors for new-onset diabetes after incipient acute pancreatitis( AP). Methods A retrospective analysis was performed for 95 patients with post-acute pancreatitis diabetes mellitus( PPDM-A) after incipient AP who were admitted to The Affiliated Hospital of Southwest Medical University from June 2013 to January 2020( PPDM-A group),and 190 patients without diabetes after incipient AP during the same period of time were selected at a ratio of 2 ∶ 1 and were enrolled as non-PPDM-A group. Baseline data and clinical data were collected. The t-test or the U test was used for comparison of continuous data,and the chi-square test or the Fisher's exact test was used for comparison of categorical data; a logistic regression analysis was used for multivariate analysis. Results There were significant differences between the two groups in body mass index( BMI),body weight,and proportion of patients with a drinking history,hyperuricemia,or fatty liver disease( all P < 0. 05),while there were no significant differences between the two groups in age,male sex,and proportion of patients with a smoking history,a family history of diabetes,or hypertension( all P > 0. 05).There were also significant differences in etiologies( biliary,hyperlipidemic,and alcoholic AP) between the two groups( P < 0. 05). Compared with the non-PPDM-A group,the PPDM-A group had significantly higher triglyceride,blood glucose,white blood cell count( WBC),C-reactive protein,and proportion of patients with blood glucose > 11. 1 mmol/L on admission( all P < 0. 05),while there were no significant differences in Ca2 +,blood amylase,and blood lipase between the two groups( all P >0. 05). Compared with the non-PPDM-A group,the PPDM-A group had significantly higher incidence rates of acute peripancreatic necrotic collections and acute peripancreatic fluid collections,proportion of patients with multiple onset of AP,and proportion of patients with CTSI score > 4( all P < 0. 05),while there were no significant differences in the proportion of patients with systemic inflammatory response syndrome and disease severity between the two groups( both P > 0. 05). The multivariate analysis showed that the outcome of PPDM-A in alcoholic AP patients was 5. 868 times that in biliary AP patients( 95% confidence interval [CI]: 1. 607-21. 418,P = 0. 007),and the outcome of PPDM-A in hyperlipidemic AP patients was 3. 312 time that in biliary AP patients( 95% CI: 1. 593-6. 887,P = 0. 001). The outcome of PPDM-A in overweight patients was 3. 694 times that in patients with normal BMI( 95% CI: 1. 575-8. 667,P = 0. 003),and the outcome of PPDM-A in obese patients was 5. 964 times that in patients with normal BMI( 95% CI: 2. 516-14. 139,P < 0. 001). Multiple onset of AP( OR = 4. 522,95%CI: 2. 298-8. 900,P < 0. 001),blood glucose on admission > 11. 1 mmol/L( OR = 6. 749,95% CI: 3. 381-13. 469,P < 0. 001),CTSI score > 4( OR = 1. 176,95% CI: 1. 008-1. 371,P = 0. 039),and WBC( OR = 1. 082,95% CI: 1. 009-1. 160,P = 0. 026) were independent risk factors for PPDM-A. Conclusion Multiple onset of AP,alcoholic AP,hyperlipidemic AP,blood glucose on admission > 11. 1 mmol/L,overweight or obesity,CTSI score > 4,and WBC are independent risk factors for PPDM-A,which can provide a reference for formulating strategies to prevent or reduce the onset of PPDM-A.
- acute pancreatitis /
- pancreatic diabetes mellitus /
- risk factors

HTML全文

参考文献(42)

[1] Pancreas Study Group,Chinese Society of Gastroenterology,Chinese Medical Association; Editorial Board of Chinese Journal of Pancreatology; Editorial Board of Chinese Journal of Digestion. Chinese guidelines for the management of acute pancreatitis(Shenyang,2019)[J]. J Clin Hepatol,2019,35(12):2706-2711.(in Chinese)中华医学会消化病学分会胰腺疾病学组，《中华胰腺病杂志》编委会，《中华消化杂志》编委会．中国急性胰腺炎诊治指南(2019年，沈阳)[J]．临床肝胆病杂志，2019,35(12):2706-2711.

[2] Italian Association for the Study of the Pancreas(AISP),PEZZILLI R,ZERBI A,et al. Consensus guidelines on severe acute pancreatitis[J]. Dig Liver Dis,2015,47(7):532-543.

[3] JIN D,NIU CY. The effect of nonalcoholic fatty liver disease on the severity of acute pancreatitis[J]. J Pract Med,2017,33(21):3563-3565.(in Chinese)金豆，牛春燕．非酒精性脂肪性肝病对急性胰腺炎严重程度的影响[J]．实用医学杂志，2017,33(21):3563-3565.

[4] KISS CM,BYHAM-GRAY L,DENMARK R,et al. The impact of implementation of a nutrition support algorithm on nutrition care outcomes in an intensive care unit[J]. Nutr Clin Pract,2012,27(6):793-801.

[5] TAKEDA K,TAKADA T,KAWARADA Y,et al. JPN Guidelines for the management of acute pancreatitis:Medical management of acute pancreatitis[J]. J Hepatobiliary Pancreat Surg,2006,13(1):42-47.

[6] OLH A,ROMICS L Jr. Enteral nutrition in acute pancreatitis:A review of the current evidence[J]. World J Gastroenterol,2014,20(43):16123-16131.

[7] AL-OMRAN M,ALBALAWI ZH,TASHKANDI MF,et al. Enteral versus parenteral nutrition for acute pancreatitis[J]. Cochrane Database Syst Rev,2010,1:CD002837.

[8] QIN HL,ZHENG JJ,TONG DN,et al. Effect of Lactobacillus plantarum enteral feeding on the gut permeability and septic complications in the patients with acute pancreatitis[J]. Eur J Clin Nutr,2008,62(7):923-930.

[9] EWALD N,KAUFMANN C,RASPE A,et al. Prevalence of diabetes mellitus secondary to pancreatic diseases(type 3c)[J]. Diabetes Metab Res Rev,2012,28(4):338-342.

[10] FLSCH UR,NITSCHE R,LDTKE R,et al. Early ERCP and papillotomy compared with conservative treatment for acute biliary pancreatitis. The German Study Group on Acute Biliary Pancreatitis[J]. N Engl J Med,1997,336(4):237-242.

[11] American Diabetes Association(2019). 2. Classification and diagnosis of diabetes:Standards of medical care in diabetes-2019[J]. Diabetes Care,2019,42(Suppl 1):s13-s28.

[12] NODA Y,GOSHIMA S,FUJIMOTO K,et al. Utility of the portal venous phase for diagnosing pancreatic necrosis in acute pancreatitis using the CT severity index[J]. Abdom Radiol(NY),2018,43(11):3035-3042.

[13] CHO NH,SHAW JE,KARURANGA S,et al. IDF diabetes atlas:Global estimates of diabetes prevalence for 2017 and projections for 2045[J]. Diabetes Res Clin Pract,2018,138:271-281.

[14] ABDI H,HOSSEINPANAH F,AZIZI F,et al. Screening for dysglycemia:A comment on classification and diagnosis of diabetes in american diabetes association standards of medical care in diabetes-2016[J]. Arch Iran Med,2017,20(6):389.

[15] Authors/Task Force Members,RYDN L,GRANT PJ,et al.ESC Guidelines on diabetes,pre-diabetes,and cardiovascular diseases developed in collaboration with the EASD:The Task Force on diabetes,pre-diabetes,and cardiovascular diseases of the European Society of Cardiology(ESC)and developed in collaboration with the European Association for the Study of Diabetes(EASD)[J]. Eur Heart J,2013,34(39):3035-3087.

[16] XIAO AY,TAN ML,WU LM,et al. Global incidence and mortality of pancreatic diseases:A systematic review,meta-analysis,and meta-regression of population-based cohort studies[J].Lancet Gastroenterol Hepatol,2016,1(1):45-55.

[17] PENDHARKAR SA,MATHEW J,PETROV MS. Age-and sex-specific prevalence of diabetes associated with diseases of the exocrine pancreas:A population-based study[J]. Dig Liver Dis,2017,49(5):540-544.

[18] PENDHARKAR SA,ASRANI VM,XIAO AY,et al. Relationship between pancreatic hormones and glucose metabolism:A cross-sectional study in patients after acute pancreatitis[J].Am J Physiol Gastrointest Liver Physiol,2016,311(1):g50-g58.

[19] DAS SL,SINGH PP,PHILLIPS AR,et al. Newly diagnosed diabetes mellitus after acute pancreatitis:A systematic review and meta-analysis[J]. Gut,2014,63(5):818-831.

[20] WOODMANSEY C,MCGOVERN AP,MCCULLOUGH KA,et al. Incidence,emographics,and clinical characteristics of diabetes of the exocrine pancreas(type 3c):A retrospective cohort study[J]. Diabetes Care,2017,40(11):1486-1493.

[21] SHEN HN,YANG CC,CHANG YH,et al. Risk of diabetes mellitus after first-attack acute pancreatitis:A national population-based study[J]. Am J Gastroenterol,2015,110(12):1698-1706.

[22] DAS SL,SINGH PP,PHILLIPS AR,et al. Newly diagnosed diabetes mellitus after acute pancreatitis:A systematic review and meta-analysis[J]. Gut,2014,63(5):818-831.

[23] HO TW,WU JM,KUO TC,et al. Change of both endocrine and exocrine insufficiencies after acute pancreatitis in non-diabetic patients:A nationwide population-based study[J].Medicine(Baltimore),2015,94(27):e1123.

[24] LEE YK,HUANG MY,HSU CY,et al. Bidirectional relationship between diabetes and acute pancreatitis:A populationbased cohort study in Taiwan[J]. Medicine(Baltimore),2016,95(2):e2448.

[25] SOO D,PENDHARKAR SA,JIVANJI CJ,et al. Derivation and validation of the prediabetes self-assessment screening score after acute pancreatitis(PERSEUS)[J]. Dig Liver Dis,2017,49(10):1146-1154.

[26] SAIKALA M,TALUKDAR R,PAVAN KUMAR P,et al．β-Cell dysfunction in chronic pancreatitis[J]. Dig Dis Sci,2012,57(7):1764-1772.

[27] JETHWA P,SODERGREN M,LALA A,et al. Diabetic control after total pancreatectomy[J]. Dig Liver Dis,2006,38(6):415-419.

[28] BRUNICARDI FC,CHAIKEN RL,RYAN AS,et al. Pancreatic polypeptide administration improves abnormal glucose metabolism in patients with chronic pancreatitis[J]. J Clin Endocrinol Metab,1996,81(10):3566-3572.

[29] GILLIES N,PENDHARKAR SA,ASRANI VM,et al. Interleukin-6 is associated with chronic hyperglycemia and insulin resistance in patients after acute pancreatitis[J]. Pancreatology,2016,16(5):748-755.

[30] GILLIES NA,PENDHARKAR SA,SINGH RG,et al. Fasting levels of insulin and amylin after acute pancreatitis are associated with pro-inflammatory cytokines[J]. Arch Physiol Biochem,2017,123(4):238-248.

[31] PENDHARKAR SA,SINGH RG,CHAND SK,et al. Pro-inflammatory cytokines after an episode of acute pancreatitis:Associations with fasting gut hormone profile[J]. Inflamm Res,2018,67(4):339-350.

[32] PENDHARKAR SA,ASRANI VM,MURPHY R,et al. The role of gut-brain axis in regulating glucose metabolism after acute pancreatitis[J]. Clin Transl Gastroenterol,2017,8(1):e210.

[33] PENDHARKAR SA,SINGH RG,PETROV MS. Cross-talk between innate cytokines and the pancreatic polypeptide family in acute pancreatitis[J]. Cytokine,2017,90:161-168.

[34] PENDHARKAR SA,WALIA M,DRURY M,et al. Calcitonin gene-related peptide:Neuroendocrine communication between the pancreas,gut,and brain in regulation of blood glucose[J]. Ann Transl Med,2017,5(21):419.

[35] GILLIES NA,PENDARKAR SA,SINGH RG,et al. Lipid metabolism in patients with chronic hyperglycemia after an episode of acute pancreatitis[J]. Diabetes Metab Syndr,2017,11(Suppl 1):s233-s241.

[36] PENDHARKAR SA,SINGH RG,PETROV MS,et al. Pro-inflammatory cytokine-induced lipolysis after an episode of acute pancreatitis[J]. Arch Physiol Biochem,2018,124(5):401-409.

[37] SINGH RG,PENDHARKAR SA,PLANK LD,et al. Role of human lipocalin proteins in abdominal obesity after acute pancreatitis[J]. Peptides,2017,91:1-7.

[38] BHARMAL SH,PENDHARKAR SA,SINGH RG,et al. Relationship between circulating levels of pancreatic proteolytic enzymes and pancreatic hormones[J]. Pancreatology,2017,17(6):876-883.

[39] PENDHARKAR SA,ASRANI VM,XIAO AY,et al. Relationship between pancreatic hormones and glucose metabolism:A cross-sectional study in patients after acute pancreatitis[J].Am J Physiol Gastrointest Liver Physiol,2016,311(1):g50-g58.

[40] DESOUZA SV,SINGH RG,YOON HD,et al. Pancreas volume in health and disease:A systematic review and meta-analysis[J]. Expert Rev Gastroenterol Hepatol,2018,12(8):757-766.

[41] MACHICADO JD,CHARI ST,TIMMONS L,et al. A population-based evaluation of the natural history of chronic pancreatitis[J]. Pancreatology,2018,18(1):39-45.

[42] SINGH RG,PENDHARKAR SA,CERVANTES A,et al. Abdominal obesity and insulin resistance after an episode of acute pancreatitis[J]. Dig Liver Dis,2018,50(10):1081-1087.

施引文献

资源附件(0)

访问统计