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Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study
BACKGROUND: Patients could develop endocrine and exocrine pancreatic insufficiency after acute pancreatitis (AP), but the morbidity, risk factors and outcome remain unclear. The aim of the present study was to evaluate the incidence of endocrine and exocrine pancreatic insufficiency after AP and the...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658961/ https://www.ncbi.nlm.nih.gov/pubmed/29078749 http://dx.doi.org/10.1186/s12876-017-0663-0 |
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author | Tu, Jianfeng Zhang, Jingzhu Ke, Lu Yang, Yue Yang, Qi Lu, Guotao Li, Baiqiang Tong, Zhihui Li, Weiqin Li, Jieshou |
author_facet | Tu, Jianfeng Zhang, Jingzhu Ke, Lu Yang, Yue Yang, Qi Lu, Guotao Li, Baiqiang Tong, Zhihui Li, Weiqin Li, Jieshou |
author_sort | Tu, Jianfeng |
collection | PubMed |
description | BACKGROUND: Patients could develop endocrine and exocrine pancreatic insufficiency after acute pancreatitis (AP), but the morbidity, risk factors and outcome remain unclear. The aim of the present study was to evaluate the incidence of endocrine and exocrine pancreatic insufficiency after AP and the risk factors of endocrine pancreatic insufficiency through a long-term follow-up investigation. METHODS: Follow-up assessment of the endocrine and exocrine function was conducted for the discharged patients with AP episodes. Oral Glucose Tolerance Test (OGTT) and faecal elastase-1(FE-1) test were used as primary parameters. Fasting blood-glucose (FBG), fasting insulin (FINS), glycosylated hemoglobin HBA1c, 2-h postprandial blood glucose (2hPG), Homa beta cell function index (HOMA-β), homeostasis model assessment of insulin resistance (HOMA-IR) and FE-1 were collected. Abdominal contrast-enhanced computed tomography (CECT) was performed to investigate the pancreatic morphology and the other related data during hospitalization was also collected. RESULTS: One hundred thirteen patients were included in this study and 34 of whom (30.1%) developed diabetes mellitus (DM), 33 (29.2%) suffered impaired glucose tolerance (IGT). Moreover, 33 patients (29.2%) developed mild to moderate exocrine pancreatic insufficiency with 100μg/g<FE-1<200μg/g and 7 patients (6.2%) were diagnosed with severe exocrine pancreatic insufficiency with FE-1<100μg/g. The morbidity of DM and IGT in patients with pancreatic necrosis was significant higher than that in the non-pancreatic necrosis group (X (2) = 13.442,P = 0.001). The multiple logistic regression analysis showed that extent of pancreatic necrosis<30% (P = 0.012, OR = 0.061) were the protective factors of endocrine pancreatic insufficiency. HOMA-IR (P = 0.002, OR = 6.626), Wall-off necrosis (WON) (P = 0.013, OR = 184.772) were the risk factors. CONCLUSION: The integrated morbidity of DM and IGT after AP was 59.25%, which was higher than exocrine pancreatic insufficiency. 6.2% and 29.2% of patients developed severe and mild to moderate exocrine pancreatic insufficiency, respectively. The extent of pancreatic necrosis>50%, WON and insulin resistance were the independent risk factors of new onset diabetes after AP. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12876-017-0663-0) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5658961 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56589612017-10-31 Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study Tu, Jianfeng Zhang, Jingzhu Ke, Lu Yang, Yue Yang, Qi Lu, Guotao Li, Baiqiang Tong, Zhihui Li, Weiqin Li, Jieshou BMC Gastroenterol Research Article BACKGROUND: Patients could develop endocrine and exocrine pancreatic insufficiency after acute pancreatitis (AP), but the morbidity, risk factors and outcome remain unclear. The aim of the present study was to evaluate the incidence of endocrine and exocrine pancreatic insufficiency after AP and the risk factors of endocrine pancreatic insufficiency through a long-term follow-up investigation. METHODS: Follow-up assessment of the endocrine and exocrine function was conducted for the discharged patients with AP episodes. Oral Glucose Tolerance Test (OGTT) and faecal elastase-1(FE-1) test were used as primary parameters. Fasting blood-glucose (FBG), fasting insulin (FINS), glycosylated hemoglobin HBA1c, 2-h postprandial blood glucose (2hPG), Homa beta cell function index (HOMA-β), homeostasis model assessment of insulin resistance (HOMA-IR) and FE-1 were collected. Abdominal contrast-enhanced computed tomography (CECT) was performed to investigate the pancreatic morphology and the other related data during hospitalization was also collected. RESULTS: One hundred thirteen patients were included in this study and 34 of whom (30.1%) developed diabetes mellitus (DM), 33 (29.2%) suffered impaired glucose tolerance (IGT). Moreover, 33 patients (29.2%) developed mild to moderate exocrine pancreatic insufficiency with 100μg/g<FE-1<200μg/g and 7 patients (6.2%) were diagnosed with severe exocrine pancreatic insufficiency with FE-1<100μg/g. The morbidity of DM and IGT in patients with pancreatic necrosis was significant higher than that in the non-pancreatic necrosis group (X (2) = 13.442,P = 0.001). The multiple logistic regression analysis showed that extent of pancreatic necrosis<30% (P = 0.012, OR = 0.061) were the protective factors of endocrine pancreatic insufficiency. HOMA-IR (P = 0.002, OR = 6.626), Wall-off necrosis (WON) (P = 0.013, OR = 184.772) were the risk factors. CONCLUSION: The integrated morbidity of DM and IGT after AP was 59.25%, which was higher than exocrine pancreatic insufficiency. 6.2% and 29.2% of patients developed severe and mild to moderate exocrine pancreatic insufficiency, respectively. The extent of pancreatic necrosis>50%, WON and insulin resistance were the independent risk factors of new onset diabetes after AP. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12876-017-0663-0) contains supplementary material, which is available to authorized users. BioMed Central 2017-10-27 /pmc/articles/PMC5658961/ /pubmed/29078749 http://dx.doi.org/10.1186/s12876-017-0663-0 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Tu, Jianfeng Zhang, Jingzhu Ke, Lu Yang, Yue Yang, Qi Lu, Guotao Li, Baiqiang Tong, Zhihui Li, Weiqin Li, Jieshou Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title | Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title_full | Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title_fullStr | Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title_full_unstemmed | Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title_short | Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
title_sort | endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658961/ https://www.ncbi.nlm.nih.gov/pubmed/29078749 http://dx.doi.org/10.1186/s12876-017-0663-0 |
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