Two cases of `pancreatic cholera' with features of peptide-secreting adenomatosis of the pancreas

Sircus, W.; Brunt, P. W.; Walker, R. J.; Small, W.; Falconer, C. W. A.; Thomson, Christine G.

doi:10.1136/gut.11.3.197

Cited by 33 publications

(8 citation statements)

References 21 publications

(20 reference statements)

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“…While tumours of endocrine glands usually perform some task of their parent tissue, this is not always the case, and several examples have been published recently of islet tumours which, besides insulin or glucagon, seem to manufacture hormoned entirely different from those produced by normal islets [65,66,67]. The secretion of gastrin by the uleerogenic tumours of the ZollingerEllison syndiome is beyond doubt [1,2].…”

Section: Discussionmentioning

confidence: 99%

Are gastrin-cells present in mammalian pancreatic islets?

1974

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Summary. The possible existence of gastrin-cells in the pancreas was investigated by a comparative immunehistological and immunoehemical study of antral mucosa and pancreas of man, dog, rabbit, rat and pig. Gastrincells were identified in the antral mucosa of all these species with the indirect immunofluorescence and the immunoperoxidase methods. With the same methods, no gastrin-cells were detected in the pancreas in any of the species studied. With radioimmunoassay, serial dilutions of antral or duodenal extracts yielded curves which were identical to those obtained with synthetic human gastrin, whereas pancreatic or islet extracts did not produce any significant displacement of the 125-Igastrin. Therefore, the presence of gastrin-producing ceils in normal pancreas remains questionable.

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Section: Discussionmentioning

confidence: 99%

Are gastrin-cells present in mammalian pancreatic islets?

1974

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“…The variety of clinical presentations associated with hyperplasia or tumour of the islet cells of the pancreas and with secretion of peptides has been referred to (Sircus, Brunt, Walker, Small, Falconer, and Thomson, 1970) and reviewed in detail (Sircus, 1969). It has recently been suggested (Zollinger, Tompkins, Amerson, Endahl, Kraft, and Moore, 1968) that 'pancreatic cholera' may be caused by a secretin-like hormone elaborated by an islet cell tumour.…”

Section: Hospital Edinburghmentioning

confidence: 99%

“…The first patient was found to have choleretic and secretinlike activity in an extract of her pancreatic islet cell tumour and gastrin-like activity in her plasma. The second patient was found to have both secretin and gastrin-like activity in her plasma, as well as choleretic activity.It is concluded that at least part of the profuse, watery electrolyte diarrhoea of the 'pancreatic cholera' syndrome associated with peptide-secreting adenoma of the pancreas is likely to be a reflection of the excessive production of secretin, as well as of gastrin, and possibly also of a choleretic agent.The variety of clinical presentations associated with hyperplasia or tumour of the islet cells of the pancreas and with secretion of peptides has been referred to (Sircus, Brunt, Walker, Small, Falconer, and Thomson, 1970) and reviewed in detail (Sircus, 1969). It has recently been suggested (Zollinger, Tompkins, Amerson, Endahl, Kraft, and Moore, 1968) that 'pancreatic cholera' may be caused by a secretin-like hormone elaborated by an islet cell tumour.…”

mentioning

confidence: 99%

Bio-assay evidence of abnormal secretin-like and gastrin-like activity in tumour and blood in cases of `choleraic diarrhoea'

Cleator¹,

Thomson²,

Sircus³

et al. 1970

Gut

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Hospital, EdinburghSUMMARY Methods for bio-assay of secretin-like humoral agents in both cat and dog are described. Bio-assay of tumour extracts and of plasma from patients with the pancreatic choleraic syndrome are described. The first patient was found to have choleretic and secretinlike activity in an extract of her pancreatic islet cell tumour and gastrin-like activity in her plasma. The second patient was found to have both secretin and gastrin-like activity in her plasma, as well as choleretic activity.It is concluded that at least part of the profuse, watery electrolyte diarrhoea of the 'pancreatic cholera' syndrome associated with peptide-secreting adenoma of the pancreas is likely to be a reflection of the excessive production of secretin, as well as of gastrin, and possibly also of a choleretic agent.

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“…The term 'pseudo-Verner-Morrison syndrome' was first used by these authors to describe such a condition (Bloom and Polak, 1976). Two cases of 'pancreatic cholera', one of which was attributed to islet cell hyperplasia, were described by Sircus et al (1970). In other instances pancreatic islet cell hyperplasia has been associated with antropyloric gastrinoma (Larsson et al, 1973) and with familial endocrine adenomatosis (Vance et al, 1969).…”

Section: Discussionmentioning

confidence: 99%

Chronic laxative abuse associated with pancreatic islet cell hyperplasia.

Lesna¹,

Hamlyn²,

Venables³

et al. 1977

Gut

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SUMMARY Marked pancreatic islet cell hyperplasia was found in a patient with laxative-induced diarrhoea. It is suggested that laxative abuse might be an important aetiological factor in patients with pancreatic islet cell hyperplasia and the watery diarrhoea syndrome but in whom no hormonal excess can be demonstrated.The abuse of laxatives is a well-recognised cause of watery diarrhoea and is most frequently seen in middle-aged women (Cummings et al., 1974). The diagnosis of this condition can frequently be difficult because such patients ingest laxatives only intermittently and vegetable laxatives cannot easily be detected in stool and urine. The watery diarrhoea syndrome is an important differential diagnosis and, in the absence of a tumour mass, this is frequently associated with pancreatic islet cell hyperplasia (Verner and Morrison, 1974). In this paper we describe a patient with watery diarrhoea caused by chronic laxative abuse in whom marked pancreatic islet cell hyperplasia was also found. Case historyA thirty-nine year old Caucasian male first presented in 1971 when he required five admissions to hospital for pilonidal sinus surgery. In 1972 he developed a discharging sinus in the right groin and after excision first developed diarrhoea with the passage of bloodstained mucus. Investigations, including barium meal, barium enema, and sigmoidoscopy, were normal. The diarrhoea continued and after losing 19 kg (3 stones) in weight he was admitted for investigation but no abnormality was found apart from a low serum folate. About this time he first complained of cramping lower abdominal pain. In 1973 he was admitted on three occasions for vasectomy, re-excision of a pilonidal sinus, and appendicectomy (appendix histology normal) but during this time the diarrhoea had subsided. In early 1974 he was admitted with chest pain and later that year he developed heartburn, vomiting, and weight loss of 16 kg (2j stones). Investigations were normal Received for publication 30 May 1977 but a laparotomy and cholecystectomy were performed. Neurological and psychiatric assessments at this time were normal.In August 1974 he had a lymph node biopsy and soon after this presented to Medical Outpatients with intractable diarrhoea with a stool volume of 3 1 per day, some lower abdominal pain, and weight loss. At this time laxative abuse was considered but this he denied and tests for phenolphthalein and magnesium in the stool were negative. The watery diarrhoea syndrome was also considered but serum gastrin, enteroglucagon, secretin, vasoactive intestinal polypeptide, and urinary 5 hydroxyindolactic acid concentrations were normal. He never became hypokalaemic. In May 1975 he was admitted for a further laparotomy because of continuing disabling symptoms but the intra-abdominal organs were completely normal. A distal pancreatectomy was performed and a 10 cm segment of the ileum was reversed in an attempt to slow down intestinal transit. Postoperatively there was an immediate cessation of symptoms and his weight returned to nor...

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Two cases of `pancreatic cholera' with features of peptide-secreting adenomatosis of the pancreas

Cited by 33 publications

References 21 publications

Are gastrin-cells present in mammalian pancreatic islets?

Are gastrin-cells present in mammalian pancreatic islets?

Bio-assay evidence of abnormal secretin-like and gastrin-like activity in tumour and blood in cases of `choleraic diarrhoea'

Chronic laxative abuse associated with pancreatic islet cell hyperplasia.

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