scholarly journals Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study

2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Jianfeng Tu ◽  
Jingzhu Zhang ◽  
Lu Ke ◽  
Yue Yang ◽  
Qi Yang ◽  
...  
2018 ◽  
Vol 41 (3) ◽  
pp. 20-30
Author(s):  
J. Tu ◽  
J. Zhang ◽  
L. Ke ◽  
Y. Yang ◽  
Q. Yang ◽  
...  

Introduction. 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 (χ2 = 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.


2020 ◽  
Vol 105 (12) ◽  
pp. e4351-e4359
Author(s):  
Huseyin Demirbilek ◽  
Atilla Cayir ◽  
Sarah E Flanagan ◽  
Ruken Yıldırım ◽  
Yılmaz Kor ◽  
...  

Abstract Context Biallelic mutations in the PTF1A enhancer are the commonest cause of isolated pancreatic agenesis. These patients do not have severe neurological features associated with loss-of-function PTF1A mutations. Their clinical phenotype and disease progression have not been well characterized. Objective To evaluate phenotype and genotype characteristics and long-term follow-up of patients with PTF1A enhancer mutations. Setting Twelve tertiary pediatric endocrine referral centers. Patients Thirty patients with diabetes caused by PTF1A enhancer mutations. Median follow-up duration was 4 years. Main Outcome Measures Presenting and follow-up clinical (birthweight, gestational age, symptoms, auxology) and biochemical (pancreatic endocrine and exocrine functions, liver function, glycated hemoglobin) characteristics, pancreas imaging, and genetic analysis. Results Five different homozygous mutations affecting conserved nucleotides in the PTF1A distal enhancer were identified. The commonest was the Chr10:g.23508437A&gt;G mutation (n = 18). Two patients were homozygous for the novel Chr10:g.23508336A&gt;G mutation. Birthweight was often low (median SDS = –3.4). The majority of patients presented with diabetes soon after birth (median age of diagnosis: 5 days). Only 2/30 presented after 6 months of age. All patients had exocrine pancreatic insufficiency. Five had developmental delay (4 mild) on long-term follow-up. Previously undescribed common features in our cohort were transiently elevated ferritin level (n = 12/12 tested), anemia (19/25), and cholestasis (14/24). Postnatal growth was impaired (median height SDS: –2.35, median BMI SDS: –0.52 SDS) with 20/29 (69%) cases having growth retardation. Conclusion We report the largest series of patients with diabetes caused by PTF1A enhancer mutations. Our results expand the disease phenotype, identifying recurrent extrapancreatic features which likely reflect long-term intestinal malabsorption.


2008 ◽  
Vol 21 (6) ◽  
pp. 523-532
Author(s):  
Birgit Rami ◽  
Saadet Mercimek-Mahmutoglu ◽  
Martha Feucht ◽  
Marion Herle ◽  
Olaf Rittinger ◽  
...  

Abstract Aim: To assess the neurological and clinical long-term outcome of patients diagnosed with congenital hyperinsulinism (CHI) in Austria. Patients and Methods: Fourteen patients diagnosed with CHI (1978-2000) were investigated retrospectively by reviewing hospital records. Thirteen of them were evaluated with either a questionnaire or clinical, neurological and biochemical investigations (age at evaluation 4.2- 25.5 years) in a follow-up study in the year 2004. Results: Fifty percent of the patients needed a pancreatectomy. The prevalence of mental retardation was 31%, of epilepsy 15% and of pancreatic insufficiency 14%. None of our patients had developed diabetes mellitus. Additionally the prevalence of obesity was 43% in patients after pancreatectomy. Sixty-nine percent of the patients had no further treatment at the time of follow-up. Conclusion: Despite early diagnosis and intensive treatment, 31% of the patients presented with mental retardation.


2004 ◽  
Vol 171 (4S) ◽  
pp. 194-195
Author(s):  
Kyoichi Tomita ◽  
Haruki Kume ◽  
Keishi Kashibuchi ◽  
Satoru Muto ◽  
Shigeo Horie ◽  
...  

2020 ◽  
Author(s):  
Satoshi Kiyofuji ◽  
Hirofumi Nakatomi ◽  
Hideaki Ono ◽  
Minoru Tanaka ◽  
Kazuo Tsutsumi ◽  
...  

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