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.

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.

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.

scholarly journals Clinical and pharmacological approaches to the management of exocrine pancreatic insufficiency in chronic pancreatitis

2021 ◽  
pp. 58-67
Author(s):  
V. N. Drozdov ◽  
E. V. Shikh ◽  
A. A. Astapovskiy ◽  
Yu. V. Kotlyachkova ◽  
L. E. Dobrovolskaya ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Enzyme Replacement Therapy ◽  
Replacement Therapy ◽  
Pancreatic Insufficiency ◽  
Fibrous Tissue ◽  
Pancreatic Enzyme ◽  
The United States ◽  
Exocrine Insufficiency ◽  
Enzyme Replacement ◽  
Endocrine Insufficiency

Chronic pancreatitis is a multifactorial disease in which repeated episodes of inflammation of the pancreas contribute to the development of fibrous tissue, leading to chronic pain, as well as exocrine and endocrine insufficiency. The incidence and prevalence of chronic pancreatitis in the world are growing, as evidenced by current statistics. In addition, the annual costs associated with the treatment of exocrine and endocrine insufficiency are also increasing. In the United States alone, the annual cost of treating these complications is $ 75.1 million. Exocrine insufficiency is one of the most frequent complications, which is characterized by a deficiency of pancreatic enzymes, leading to the development of malabsorption syndrome (impaired absorption of nutrients, vitamins and minerals). Due to the increased incidence and deterioration of the quality of life associated with this condition, the goal of treatment is to compensate for the deficiency of exocrine enzymes with oral pancreatic enzyme replacement therapy. The core of this therapy is to deliver activated, unbroken enzymes directly to the small intestine during a meal. Many studies have shown that prescribing enzyme replacement therapy improves symptoms associated with exocrine insufficiency, reduces the progression of osteopenia, and improves survival in such patients. The use of pancreatin contributes to the correction of exocrine insufficiency in patients with chronic pancreatitis. The data presented in the article indicate that the drug is a safe and effective agent, meets all modern standards and requirements, and can be used to correct enzymatic pancreatic 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.

scholarly journals A Case of Chronic Pancreatic Insufficiency Due to Valproic Acid in a Child

2001 ◽  
Vol 15 (2) ◽  
pp. 127-130 ◽  
Author(s):  
Mary Anne Cooper ◽  
Aubrey Groll
Keyword(s):  
Valproic Acid ◽  
Weight Loss ◽  
Acute Pancreatitis ◽  
Abdominal Pain ◽  
Chronic Pancreatitis ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Exocrine Pancreatic Insufficiency ◽  
Radiological Evaluation ◽  
Enzyme Replacement

A 14-year-old child treated with valproic acid over several years for a seizure disorder developed abdominal pain with radiological evidence of acute pancreatitis. The association with valproic acid was not recognized, and the child continued to take the drug. The patient eventually developed steatorrhea and weight loss that improved with pancreatic enzyme replacement. Radiological evaluation showed an atrophic pancreas. Without evidence of other etiological factors, valproic acid by itself appeared to be the cause of chronic pancreatitis with exocrine pancreatic insufficiency in this patient.

scholarly journals COMPARING THE ENZYME REPLACEMENT THERAPY COST IN POST PANCREATECTOMY PATIENTS DUE TO PANCREATIC TUMOR AND CHRONIC PANCREATITIS

2016 ◽  
Vol 53 (2) ◽  
pp. 94-97 ◽  
Author(s):  
Anna Victoria FRAGOSO ◽  
Martha Regina PEDROSO ◽  
Paulo HERMAN ◽  
André Luis MONTAGNINI
Keyword(s):  
Chronic Pancreatitis ◽  
Enzyme Replacement Therapy ◽  
Replacement Therapy ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Gastrointestinal Surgery ◽  
Exocrine Pancreatic Insufficiency ◽  
Intractable Pain ◽  
Enzyme Replacement ◽  
Significant Difference

ABSTRACT Background - Among late postoperative complications of pancreatectomy are the exocrine and endocrine pancreatic insufficiencies. The presence of exocrine pancreatic insufficiency imposes, as standard treatment, pancreatic enzyme replacement. Patients with chronic pancreatitis, with intractable pain or any complications with surgical treatment, are likely to present exocrine pancreatic insufficiency or have this condition worsened requiring adequate dose of pancreatic enzymes. Objective - The aim of this study is to compare the required dose of pancreatic enzyme and the enzyme replacement cost in post pancreatectomy patients with and without chronic pancreatitis. Methods - Observational cross-sectional study. In the first half of 2015 patients treated at the clinic of the Department of Gastrointestinal Surgery at Hospital das Clínicas, Universidade de São Paulo, Brazil, who underwent pancreatectomy for at least 6 months and in use of enzyme replacement therapy were included in this series. The study was approved by the Research Ethics Committee. The patients were divided into two groups according to the presence or absence of chronic pancreatitis prior to pancreatic surgery. For this study, P<0.05 was considered statistically significant. Results - The annual cost of the treatment was R$ 2150.5 ± 729.39; R$ 2118.18 ± 731.02 in patients without pancreatitis and R$ 2217.74 ± 736.30 in patients with pancreatitis. Conclusion - There was no statistically significant difference in the cost of treatment of enzyme replacement post pancreatectomy in patients with or without chronic pancreatitis prior to surgical indication.

Gut hormone secretion, gastric emptying, and glycemic responses to erythritol and xylitol in lean and obese subjects

2016 ◽  
Vol 310 (11) ◽  
pp. E1053-E1061 ◽  
Author(s):  
Bettina K. Wölnerhanssen ◽  
Lucian Cajacob ◽  
Nino Keller ◽  
Alison Doody ◽  
Jens F. Rehfeld ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Plasma Glucose ◽  
Hormone Secretion ◽  
Sweet Taste ◽  
Diabetic Patients ◽  
Gastrointestinal Hormone ◽  
Hormone Release ◽  
Potential Health ◽  
Gut Hormone ◽  
Glucose Ingestion

With the increasing prevalence of obesity and a possible association with increasing sucrose consumption, nonnutritive sweeteners are gaining popularity. Given that some studies indicate that artificial sweeteners might have adverse effects, alternative solutions are sought. Xylitol and erythritol have been known for a long time and their beneficial effects on caries prevention and potential health benefits in diabetic patients have been demonstrated in several studies. Glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) are released from the gut in response to food intake, promote satiation, reduce gastric emptying (GE), and modulate glucose homeostasis. Although glucose ingestion stimulates sweet taste receptors in the gut and leads to incretin and gastrointestinal hormone release, the effects of xylitol and erythritol have not been well studied. Ten lean and 10 obese volunteers were given 75 g of glucose, 50 g of xylitol, or 75 g of erythritol in 300 ml of water or placebo (water) by a nasogastric tube. We examined plasma glucose, insulin, active GLP-1, CCK, and GE with a [13C]sodium acetate breath test and assessed subjective feelings of satiation. Xylitol and erythritol led to a marked increase in CCK and GLP-1, whereas insulin and plasma glucose were not (erythritol) or only slightly (xylitol) affected. Both xylitol and erythritol induced a significant retardation in GE. Subjective feelings of appetite were not significantly different after carbohydrate intake compared with placebo. In conclusion, acute ingestion of erythritol and xylitol stimulates gut hormone release and slows down gastric emptying, whereas there is no or only little effect on insulin release.

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