M1368 Prescription and Response to Pancreatic Enzyme Therapy in Exocrine Insufficiency Due to Chronic Pancreatitis; a Dutch National Survey

2010 ◽  
Vol 138 (5) ◽  
pp. S-390
Author(s):  
Edmée C. Sikkens ◽  
Djuna L. Cahen ◽  
Casper H. van Eijck ◽  
Ernst J. Kuipers ◽  
Marco J. Bruno
Keyword(s):  
Chronic Pancreatitis ◽  
National Survey ◽  
Pancreatic Enzyme ◽  
Enzyme Therapy ◽  
Exocrine Insufficiency

Chronic pancreatitis

2020 ◽  
pp. 3218-3227
Author(s):  
Marco J. Bruno ◽  
Djuna L. Cahen
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Pancreatitis ◽  
Pancreatic Enzyme ◽  
Exocrine Insufficiency ◽  
Endocrine Insufficiency ◽  
Diabetes Mellitus Diagnosis ◽  
Permanent Loss ◽  
Stimulation Tests ◽  
Enteric Coated ◽  
Pancreatic Duct Stricture

Chronic pancreatitis is a major source of morbidity, loss in quality of life, and healthcare expenditure. It is most commonly caused by chronic alcoholism in adults and cystic fibrosis in children, but there are many other causes. Patients typically present with severe abdominal pain, but this may vary and even be absent. Exo- and endocrine insufficiency usually occur late in the disease course and reflect permanent loss of pancreatic parenchyma due to ongoing inflammation and fibrosis, exocrine insufficiency manifesting as steatorrhea and weight loss due to fat maldigestion and endocrine insufficiency as diabetes mellitus. Diagnosis is confirmed by imaging investigations such as CT, MRI, and endoscopic ultrasonography. Endoscopic retrograde cholangiopancreatography to diagnose chronic pancreatitis is obsolete. Hormone stimulation tests (e.g. secretin–cholecystokinin stimulation test) to diagnose exocrine insufficiency are largely abandoned because of their complexity and burden to patients. They are replaced by faecal elastase testing, even though this test is less sensitive. Management focuses on the treatment of pain using a stepwise approach. Initially, nonopioid analgesics are prescribed. Next, when feasible, endoscopic therapy is initiated, including pancreatic stone fragmentation by extracorporeal shock-wave lithotripsy, endotherapy to remove stone fragments, and placement of plastic stents to dilate any concomitant pancreatic duct stricture. If that fails or when, for example, the pancreatic head is enlarged, surgical intervention is indicated. Medical management includes enteric-coated pancreatic enzyme preparations and treatment of diabetes mellitus, usually by means of insulin. Abstinence from alcohol and smoking cessation are important predictors of disease and treatment outcome.

Patients with exocrine insufficiency due to chronic pancreatitis are undertreated: A Dutch national survey

Pancreatology ◽  
2012 ◽  
Vol 12 (1) ◽  
pp. 71-73 ◽  
Author(s):  
Edmée C.M. Sikkens ◽  
Djuna L. Cahen ◽  
Casper van Eijck ◽  
Ernst J. Kuipers ◽  
Marco J. Bruno
Keyword(s):  
Chronic Pancreatitis ◽  
National Survey ◽  
Exocrine Insufficiency

Increased postprandial responses of GLP-1 and GIP in patients with chronic pancreatitis and steatorrhea following pancreatic enzyme substitution

2007 ◽  
Vol 292 (1) ◽  
pp. E324-E330 ◽  
Author(s):  
Filip K. Knop ◽  
Tina Vilsbøll ◽  
Steen Larsen ◽  
Patricia V. Højberg ◽  
Aage Vølund ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Chronic Pancreatitis ◽  
Pancreatic Enzyme ◽  
Control Group ◽  
Β Cell ◽  
Exocrine Insufficiency ◽  
Liquid Meal ◽  
Postprandial Plasma Glucose ◽  
Glucagon Like Peptide 1 ◽  
Pancreatic Enzyme Substitution

We aimed to investigate how assimilation of nutrients affects the postprandial responses of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and to evaluate the effect of pancreatic enzyme substitution (PES) on insulin secretion in patients with chronic pancreatitis (CP) and pancreatic exocrine insufficiency (PEI). Eight male patients with CP and PEI were studied. Blood was sampled frequently on two separate days after ingestion of a liquid meal with and without PES, respectively. Eight healthy male subjects served as a control group. β-Cell responsiveness was estimated as changes in insulin secretion rates in response to changes in postprandial plasma glucose (PG). There was no difference in the PG incremental area under curve (AUC) for patients with and without PES [406 ± 100 vs. 425 ± 80 mM·4 h (mean ± SE), P = 0.8]. The response of total GLP-1 was higher after PES (AUC: 7.8 ± 1.2 vs. 5.3 ± 0.6 nM·4 h, P = 0.01), as was the response of total GIP (AUC: 32.7 ± 7.5 vs. 21.1 ± 8.3 nM·4 h, P = 0.01). Concurrently, both plasma insulin, plasma C-peptide, and total insulin secretion increased after PES (AUC: 17.7 ± 4.2 vs. 13.6 ± 2.9 nM·4 h, P = 0.02; 237 ± 31.4 vs. 200 ± 27.4 nM·4 h, P = 0.005; and 595 ± 82 vs. 497 ± 80 pmol·kg−1·4 h, P = 0.01, respectively). β-Cell responsiveness to glucose was not significantly different on the two study days for patients with CP. These results suggest that the secretion of GLP-1 and GIP is under influence of the digestion and absorption of nutrients in the small intestine and that PES increases insulin secretion.

Antroduodenal motility in chronic pancreatitis: are abnormalities related to exocrine insufficiency?

2000 ◽  
Vol 278 (3) ◽  
pp. G458-G466 ◽  
Author(s):  
M. K. Vu ◽  
J. Vecht ◽  
E. H. Eddes ◽  
I. Biemond ◽  
C. B. H. W. Lamers ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Pancreatic Insufficiency ◽  
Motor Pattern ◽  
Pancreatic Enzyme ◽  
Gastrointestinal Hormone ◽  
Hormone Release ◽  
Exocrine Insufficiency ◽  
Liquid Meal ◽  
Gut Hormone ◽  
Antroduodenal Motility

In patients with chronic pancreatitis (CP) the relation among exocrine pancreatic secretion, gastrointestinal hormone release, and motility is disturbed. We studied digestive and interdigestive antroduodenal motility and postprandial gut hormone release in 26 patients with CP. Fifteen of these patients had pancreatic insufficiency (PI) established by urinary para-aminobenzoic acid test and fecal fat excretion. Antroduodenal motility was recorded after ingestion of a mixed liquid meal. The effect of pancreatic enzyme supplementation was studied in 8 of the 15 CP patients with PI. The duration of the postprandial antroduodenal motor pattern was significantly ( P < 0.01) prolonged in CP patients (324 ± 20 min) compared with controls (215 ± 19 min). Antral motility indexes in the first hour after meal ingestion were significantly reduced in CP patients. The interdigestive migrating motor complex cycle length was significantly ( P < 0.01) shorter in CP patients (90 ± 8 min) compared with controls (129 ± 8 min). These abnormalities were more pronounced in CP patients with exocrine PI. After supplementation of pancreatic enzymes, these alterations in motility reverted toward normal. Digestive and interdigestive antroduodenal motility are abnormal in patients with CP but significantly different from controls only in those with exocrine PI. These abnormalities in antroduodenal motility in CP are related to maldigestion.

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.

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