scholarly journals EXOCRINE PANCREAS DYSFUNCTION IN TYPE 1 DIABETES

2020 ◽  
Vol 26 (12) ◽  
pp. 1505-1513
Author(s):  
Timothy P. Foster ◽  
Brittany Bruggeman ◽  
Martha Campbell-Thompson ◽  
Mark A. Atkinson ◽  
Michael J. Haller ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Exocrine Pancreas ◽  
Pancreatic Enzyme ◽  
Β Cell ◽  
Exocrine Insufficiency ◽  
Enzyme Replacement ◽  
Fecal Elastase ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Pancreatic Exocrine

Objective: Type 1 diabetes (T1D) is characterized by autoimmune β-cell destruction, but exocrine pancreas abnormalities may also play a role in the disease pathophysiology. Herein, we review the current evidence of exocrine damage in T1D and discuss its underlying pathophysiology, clinical evaluation, and treatment. Method: Extensive literature search was performed for “type 1 diabetes” and “exocrine dysfunction” on PubMed and Google Scholar databases. Results: T1D pancreata are significantly smaller than controls, both in weight and volume. T cells, dendritic cells, neutrophils, and products of complement activation are seen in T1D exocrine tissues. Exocrine pancreas fibrosis, arteriosclerosis, fatty infiltration, and acinar atrophy are also observed on histology. Pancreatic exocrine insufficiency (PEI) can be assessed through direct exocrine testing, fecal elastase concentration, and measurement of serum exocrine enzymes. The prevalence of PEI in T1D varies by modality and study but is consistently greater than controls. The clinical relevance of PEI in T1D is debatable, as many patients with laboratory evidence of PEI are asymptomatic. However, in PEI-symptomatic patients reported benefits of pancreatic enzyme replacement therapy (PERT) include relief of gastrointestinal symptoms, improved quality of life, better glycemic control, and optimal nutrition. Conclusion: Exocrine pancreas abnormalities often occur in T1D. Whether exocrine dysfunction occurs simultaneously with β-cell destruction, as a result of β-cell loss, or as a combination of both remains to be definitively answered. In T1D with gastrointestinal complaints, PEI should be evaluated, usually via fecal elastase measurements. PERT is recommended for T1D patients with symptoms and laboratory evidence of PEI. Abbreviations: AAb+ = autoantibody positive; AAb− = autoantibody negative; FEC = fecal elastase concentration; PEI = pancreatic exocrine insufficiency; PERT = pancreatic enzyme replacement therapy; PP = pancreatic polypep-tide; T1D = type 1 diabetes

Pancreatic enzyme replacement therapy in patients with pancreatic exocrine insufficiency

Pancreatology ◽  
2017 ◽  
Vol 17 (4) ◽  
pp. S39 ◽  
Author(s):  
Mila Kovacheva-Slavova ◽  
Sylvie Siminkovitch ◽  
Jordan Genov ◽  
Branimir Golemanov ◽  
Rumyana Mitova ◽  
...  
Keyword(s):  
Enzyme Replacement Therapy ◽  
Replacement Therapy ◽  
Pancreatic Enzyme ◽  
Pancreatic Exocrine Insufficiency ◽  
Exocrine Insufficiency ◽  
Enzyme Replacement ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Pancreatic Exocrine

scholarly journals Chronic pancreatitis: review and update of etiology, risk factors, and management

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 607 ◽  
Author(s):  
Angela Pham ◽  
Christopher Forsmark
Keyword(s):  
Chronic Pancreatitis ◽  
Islet Cells ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Exocrine Insufficiency ◽  
Disease Etiology ◽  
Enzyme Replacement ◽  
Endocrine Insufficiency ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Pancreatic Exocrine

Chronic pancreatitis is a syndrome involving inflammation, fibrosis, and loss of acinar and islet cells which can manifest in unrelenting abdominal pain, malnutrition, and exocrine and endocrine insufficiency. The Toxic-Metabolic, Idiopathic, Genetic, Autoimmune, Recurrent and Severe Acute Pancreatitis, Obstructive (TIGAR-O) classification system categorizes known causes and factors that contribute to chronic pancreatitis. Although determining disease etiology provides a framework for focused and specific treatments, chronic pancreatitis remains a challenging condition to treat owing to the often refractory, centrally mediated pain and the lack of consensus regarding when endoscopic therapy and surgery are indicated. Further complications incurred include both exocrine and endocrine pancreatic insufficiency, pseudocyst formation, bile duct obstruction, and pancreatic cancer. Medical treatment of chronic pancreatitis involves controlling pain, addressing malnutrition via the treatment of vitamin and mineral deficiencies and recognizing the risk of osteoporosis, and administering appropriate pancreatic enzyme supplementation and diabetic agents. Cornerstones in treatment include the recognition of pancreatic exocrine insufficiency and administration of pancreatic enzyme replacement therapy, support to cease smoking and alcohol consumption, consultation with a dietitian, and a systematic follow-up to assure optimal treatment effect.

Should we Investigate Gastroenterology Patients for Pancreatic Exocrine Insufficiency? A Dual Centre UK Study

2016 ◽  
Vol 25 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Jennifer A. Campbell ◽  
David S. Sanders ◽  
Katherine A. Francis ◽  
Matthew Kurien ◽  
Sai Lee ◽  
...  
Keyword(s):  
Secondary Care ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Pancreatic Exocrine Insufficiency ◽  
Exocrine Insufficiency ◽  
Enzyme Replacement ◽  
Co Morbidity ◽  
Immunodeficiency Virus ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Pancreatic Exocrine

Background & Aims: Pancreatic exocrine insufficiency may be under recognised in gastroenterological practice. We aimed to identify the prevalence of pancreatic insufficiency in secondary care gastroenterology clinics and determine if co-morbidity or presenting symptoms could predict diagnosis. A secondary aim was to assess response to treatment. Methods: A dual centre retrospective analysis was conducted in secondary care gastroenterology clinics. Patients tested for pancreatic exocrine insufficiency with faecal elastase-1 (FEL-1) between 2009 and 2013 were identified in two centres. Demographics, indication and co-morbidities were recorded in addition to dose and response to pancreatic enzyme replacement therapy. Binary logistic regression was used to assess if symptoms or co-morbidities could predict pancreatic insufficiency. Results: 1821 patients were tested, 13.1% had low FEL-1 (<200μg/g). This prevalence was sub-analysed with 5.4% having FEL-1 100-200μg/g (mild insufficiency) and 7.6% having faecal elastase readings <100μg/g. Low FEL-1 was most significantly associated with weight loss or steatorrhoea. Co-morbidity analysis showed that low levels were significantly associated with excess alcohol intake, diabetes mellitus or human immunodeficiency virus; 80.0% treated with enzyme supplements reported symptomatic benefit with no difference in response between high and low dose supplementation (p=0.761). Conclusion: Targeting the use of FEL-1 in individuals with specific symptoms and associated conditions can lead to improved recognition of pancreatic exocrine insufficiency in a significant proportion of secondary care patients. Intervening with lifestyle advice such as smoking cessation and minimising alcohol intake could improve outcomes. In addition, up to 80% of patients with low faecal elastase respond to supplementation. Abbreviations: CFA: coefficient of fat absorption; CP: chronic pancreatitis; ELISA: enzyme-linked immune-absorbent assay; PEI: pancreatic exocrine insufficiency; FEL-1: faecal elastase-1; HIV: human immunodeficiency virus; IBD: inflammatory bowel disease; IBS: irritable bowel syndrome; PERT: pancreatic enzyme replacement therapy.

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