Postprandial gastric function in pancreatic insufficiency.

Regan, P T; Malagelada, Juan–R.; DiMagno, Eugene P.; Go, Vay Liang W.

doi:10.1136/gut.20.3.249

Cited by 51 publications

(19 citation statements)

References 16 publications

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“…On the other hand, ulcer has been re ported to be common after pancreatectomy [7] which impairs the exocrine pancreatic function. Moreover, an increased pentagastrin acid output has been observed in chronic pancreatitis with steatorrhea [20] even if Re gan et al [17] found a slight reduction in the postprandial acid output. The acidic duode num could be considered a producing or en hancing factor of DU formation in patients with pancreatic insufficiency.…”

Section: Discussionmentioning

confidence: 99%

Duodenal Ulcer in Chronic Relapsing Pancreatitis

Vantini¹,

Piubello²,

Scuro³

et al. 1982

Digestion

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Frequency of duodenal ulcer in patients with chronic pancreatitis is still controversial. This study aims to prospectively investigate the frequency of duodenal ulcer in a group of 190 patients (162 males and 28 females) affected by chronic relapsing pancreatitis admitted to our department between 1970 and 1979. 41 cases (21.5%) were endoscopically observed (22% of the males and 17.9% of the females; male:female ratio 1.2:1). Drinking habits, cigarette consumption, presence of pancreatic calcifications and surgery did not affect the frequency of duodenal ulcer. Exocrine pancreatic insufficiency, as fecal fat excretion higher than 7 g/day, seems to be linked with an increased frequency of duodenal ulcer (exact Fisher’s test: p = 0.0586). Moreover, duodenal ulcer was present in about one third of the patients who afterwards died, but it was the cause of death in only 1 case. Even if a prospective control population is lacking, the male:female ratio of duodenal ulcer in chronic pancreatitis seems to be different from that observed in a comparable hospitalized group (1.2:1 vs. 2.4:1) and from that reported in literature in the general adult population.

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Section: Discussionmentioning

confidence: 99%

Duodenal Ulcer in Chronic Relapsing Pancreatitis

Vantini¹,

Piubello²,

Scuro³

et al. 1982

Digestion

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“…T here were two pscudocysts in the body and ( 14, I 5). This hypcrgastrincmia may be secondary to chronirnll y reduced gastric acid secretion ( 14). On the other hand, a more recent study indicated that patients with severe pancrcmic insufficiency frequently have had gawic acid hypcrsccretion ( 15).…”

Section: Case Presentationmentioning

confidence: 99%

Antral Gastrin Cell Hyperfunction Associated with Chronic Pancreatitis

Ertan

Litwin

Hammer

et al. 1988

Canadian Journal of Gastroenterology

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ABSTRAC T: T h is report describes a patient with antral gastrin cell hyperfunction who also had pancreatic pseudocy:m and partial common bile duct obstruction secondary ro ch ron ic pancreatitis. A 60-year-old female had a th ree-month h istory of wor~ening epigastric discomfort with episodes of nausea, vomiting and weigh t loss. The patient had no history of peptic ulcer d isease and no ulcers were demonstrated during diagnostic work-up. Baseline fasti ng serum gastrins were 715 and 1000 pg/ml [normal 50 to 170 pg/m l). These decreased to 515 pg/ml du ring an in travenous secreti n test and increased up to 2 155 pg/ml after a protein meal test. The patient also had chronic pancreatitis. multiple pancreatic pseudocysts and a partial common bile duct obstruction. Tru ncal vagotomy and antrectomy fo r antral gastrin cell hyperfunction. Roux-en-Y cyscjejunostomy for pancreatic pseudocysts and choledochojejunostomy for common bile duct stricture were performed. Th ree mon ths after the operation. the patient was symptom-free and fasting serum gastrin levels at one week, two months and three mon ths after the su rgery were ll, 40 and 50 pg/ml, respectively. Ca n J Gasti:oe nte rol 1988;2(3):123-1 26.Key W o rds: A nrral gasrrm cell hyperJ1me11on. Chronic pancreaii11s

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“…In chronic pan creatitis. it normally takes several years for severe exocrine pancreatic insufficiency to de velop, but lipase secretion is more rapidly impaired than the secretion of proteolytic en zymes [17], because lipase in the intestinal lumen is more fragile than the other enzymes. Lipase is easily inactivated by acidic pH and digested by proteolytic enzymes.…”

Section: Association Of Altered Gastrointestinal Functions With Distumentioning

confidence: 99%

Relevant Aspects of Physiology in Chronic Pancreatitis

Beglinger

1992

Dig Dis

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Specific points of physiology which are relevant for the understanding and management of chronic pancreatitis are focussed on. First, the regulatory factors of exocrine pancreatic secretion are described, discussing the role of the cholinergic system and of the classical gut hormones cholecystokinin and secretin. The association of upper gastrointestinal dysfunctions with a disturbed exocrine pancreatic response is also dealt with. Lastly, these changes are related to clinical consequences such as maldigestion or malabsorption.

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Postprandial gastric function in pancreatic insufficiency.

Cited by 51 publications

References 16 publications

Duodenal Ulcer in Chronic Relapsing Pancreatitis

Duodenal Ulcer in Chronic Relapsing Pancreatitis

Antral Gastrin Cell Hyperfunction Associated with Chronic Pancreatitis

Relevant Aspects of Physiology in Chronic Pancreatitis

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