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Biomedical subjects

L C Watson

Publications and source records attributed to L C Watson.

At least 19 recordsLinked to original sources
PubMed1995

Adult-onset Langerhans cell histiocytosis associated with severe abscesses.

We describe the case of an elderly lady who presented with a severe crusting skin eruption, mainly affecting the flexural areas and trunk. A diagnosis of Langerhans cell histiocytosis was confirmed by electron microscopy, and her condition was eventually controlled with systemic prednisolone and short courses of etoposide. An unusual feature of this case was the development of severe pyogenic abscesses, particularly involving the cervical region. No underlying immunological defect has been found to explain this.

Abscess↗
PubMed1985

Effect of divalent cations on gastrointestinal hormone release and exocrine pancreatic secretion in dogs.

The purpose of this study was to examine the effect of three common divalent cations (Ca2+, Mg2+, and Zn2+) on the release of cholecystokinin (CCK-33), pancreatic polypeptide (PP), and gastrin. Five dogs with pancreatic and gastric fistulas were given 1-h intraduodenal infusions of calcium (5 mmol X kg-1 X h-1), magnesium (4 mmol X kg-1 X h-1), or zinc (1 mmol X kg-1h-1). At another time the same dogs were given an intravenous bolus followed immediately by a 1-h infusion of calcium (0.36 mmol/kg [bolus], 0.36 mmol X kg-1 X h-1), magnesium (0.25 mmol/kg [bolus], 0.25 mmol X kg-1 X h-1), or zinc (0.03 mmol/kg [bolus], 0.03 mmol X kg-1 X h-1). Intraduodenal infusions of calcium, magnesium, and zinc significantly stimulated CCK-33, PP, and gastrin release. Intravenous calcium stimulated CCK-33, PP, and gastrin release to 245, 193, and 155% of basal levels, respectively. Intravenous magnesium increased CCK-33 to 123% of basal levels but did not stimulate PP and gastrin levels. Intravenous zinc stimulated release of CCK-33, PP, and gastrin to 126, 185, and 124%, respectively. This study shows that calcium, magnesium, and zinc can stimulate release of CCK-33, PP, and gastrin in much the same manner. We suggest that these cations may have a nonspecific electrical action that results in an alteration of membrane permeability, which leads to release of gastrointestinal hormones.

Animals↗
PubMed1983

Correlation between gallbladder size and release of cholecystokinin after oral magnesium sulfate in man.

In order to determine the effect of oral magnesium sulfate on gallbladder contraction and release of cholecystokinin (CCK) in man, magnesium sulfate (25 g in 100 ml distilled water) was given by mouth to five fasting adult male volunteers. Plasma samples were collected for measurement of CCK by a specific radioimmunoassay. Gallbladder volumes were determined from sonograms obtained from a phased-array real-time ultrasound scanner. Basal concentrations of CCK (82.2 +/- 10.1 pg/ml) increased significantly at 20 minutes after oral magnesium sulfate (113.8 +/- 7.1 pg/ml), and reached a maximal value at 50 minutes (150.0 +/- 42.0 pg/ml). The mean basal volume of the gallbladder was 30.8 +/- 5.3 cm(3) and maximum reduction of gallbladder volume (to one third of original) was achieved at 50 minutes after ingestion of magnesium sulfate. Linear regression analysis showed a close correlation (r = -0.9337) between plasma concentrations of CCK and gallbladder size in response to magnesium sulfate. Oral magnesium sulfate also caused a significant increase in serum gastrin (from basal of 51.4 +/- 9.9 pg/ml to 69.8 +/- 15.5 pg/ml at 5 min); there was no significant correlation between gastrin release and gallbladder contraction. This study provides direct evidence that the mechanism of magnesium sulfate-stimulated gallbladder contraction occurs through the release of CCK, and shows a close correlation between CCK release and contraction of the gallbladder.

Adult↗
PubMed1982

Perforation of the gallbladder due to blunt abdominal trauma.

Gallbladder perforation due to blunt trauma is an uncommon finding. We report our experience with six patients. The factors predisposing to perforation include a distended gallbladder because of either fasting or alcohol ingestion in normal patients, and obstruction of the cystic in patients with cholelithiasis. The diagnosis of gallbladder perforation after blunt injury may be suspected in patients with signs of an acute abdomen and hypotension that is not explained by blood loss. Peritoneal lavage that contains bile suggests the tentative diagnosis of trauma to the biliary tract or gallbladder, as well as to the liver or upper bowel. A cholecystectomy is the preferred treatment when gallbladder perforation occurs in the traumatized patient.

Abdominal Injuries↗
PubMed1982

Correlation between release of cholecystokinin and contraction of the gallbladder in patients with gallstones.

The role of endogenously released cholecystokinin (CCK) in mediating gallblader (GB) contraction was evaluated in 12 normal volunteers and 24 patients with gallstones (11 additional gallstone patients were excluded because of failure of adequate ultrasonographic visualization). CCK concentrations before and after oral administration of fat (Lipomul((R))) were measured by a specific radioimmunoassay. CCK release was correlated with changes in GB volume determined simultaneously by ultrasonography. On the basis of gallbladder contraction and operative findings, gallstone patients were divided into "contractors" (14), "noncontractors" (6), and "hydrops" (4). Lipomul caused prompt release of CCK in normal volunteers and all groups of gallstone patients. The changes (basal to peak) in plasma CCK (pg/ml) for the different groups were as follows: normal volunteers (108 +/- 9 to 200 +/- 16), contractors (77 +/- 10 to 128 +/- 13), noncontractors (59 +/- 7 to 159 +/- 38), and hydrops (43 +/- 5 to 113 +/- 47). The total integrated output of CCK (0-60 min) was greater in normal volunteers (3975 +/- 762 pg-min/ml) than in contractors (1530 +/- 567 pg-min/ml). Lipomul caused similar GB contraction in normal volunteers and contractors (from basal volumes to maximal contraction); these changes were from 19.5 +/- 2.3 ml to 5.6 +/- 1.0 ml in normal volunteers, and from 19.6 +/- 3.2 to 5.2 +/- 1.0 in contractors. Plasma concentrations of CCK and GB volume were highly correlated in the 12 normal volunteers (r = -0.89, p < 0.01) and in the 14 contractors (r= -0.99, p < 0.01)), but the GB was significantly (p < 0.01) more sensitive to changes in plasma CCK in the gallstone contractors than in the normal volunteers. The authors suggest that there may be two groups of gallstone patients, noncontractors and contractors. Stasis may be important in the pathogenesis of gallstones in the noncontractors, whereas in contractors, the authors speculate that an abnormality in the CCK-gallbladder relationship (characterized by diminished CCK release and increased GB sensitivity to CCK) may be involved in the evolution of the disease.

Adult↗
PubMed1982

Effect of colectomy on cholecystokinin and gastrin release.

Studies were conducted to determine the effect of resection of the colon on the release of cholecystokinin (CCK) and gastrin. A standard food stimulation test was performed in five dogs. Peripheral blood samples were collected for future measurement of CCK and gastrin by specific radioimmunoassay. Each dog underwent subtotal colectomy with side-to-end ileoproctostomy. The food stimulation test was repeated at approximately weekly intervals for eight weeks after colectomy. Basal plasma CCK levels of 139 +/- 21 pg/ml before colectomy did not change after colectomy. Total amount CCK released after food was increased significantly at both four (5.94 +/- 0.78 ng min/ml) and eight (13.00 +/- 2.72 ng min/ml) weeks after colectomy in comparison with that observed prior to colectomy (2.94 +/- 0.54 ng min/ml). Basal serum gastrin levels of 28 +/- 9 pg/ml did not change significantly after colectomy. Total amount of gastrin released after food was increased significantly at both two (8651 +/- 2294 pg min/ml) and three (6940 +/- 1426 pg min/ml) weeks after operation, but at none of the later weeks. The precolectomy output, used for comparison, was 5608 +/- 1346 pg min/ml. It was concluded that resection of the colon leads to an increase in release of CCK and gastrin after food stimulation. This finding provides further evidence that the colon contains a factor that inhibits the release of CCK and gastrin, and that the colon functions as an endocrine organ.

Animals↗
PubMed1982

Removal of circulating gastrin and cholecystokinin into the lumen of the small intestine.

This study was undertaken to investigate the mechanism by which the small intestine removes circulating gastrin and cholecystokinin (CCK). A 100-cm (acute study, 10 dogs) or a 50-cm (chronic study, 5 dogs) segment of midjejunum was excluded in all 15 dogs. The excluded loop was perfused with 0.1 M phosphate buffer (pH 7.4), which was constantly recirculated by a peristaltic pump. It the acute control study (5 dogs), gastrin concentrations in the intestinal perfusate were increased gradually to a level of 320 +/- 49 pg/ml at 90 min (i.e., 7.6 +/- 0.9 times higher than serum gastrin levels). In the antrectomy group (5 dogs), perfusate gastrin concentrations were greatly decreased after antrectomy, in consonance with the decrease in serum gastrin concentrations. In the chronic study (5 dogs), perfusate gastrin concentrations were significantly increased after food stimulation, in consonance with the increase in serum gastrin concentrations. CCK was also released into the bowel lumen in considerable amounts basally and after endogenous release. Although one cannot exclude the possibility that a considerable amount of gastrin or CCK in the lumen may originate from the bowel segment, this study shows that the small bowel removes gastrin and CCK from the circulation by their secretion into the bowel lumen. Loss of this mechanism might partially explain the rise in gastrin levels that is observed in some patients after extensive small bowel resections.

Animals↗
PubMed1982

Reduction of postprandial release of pancreatic polypeptide after development of pancreatic fibrosis.

We have measured the plasma pancreatic polypeptide response to a meal before and after the development of pancreatic fibrosis in dogs. Peripheral blood samples were collected in five dogs before and after a standard meal for measurement of pancreatic polypeptide by a specific radioimmunoassay. The next day, all of the pancreatic ducts were ligated in each dog, and one month after pancreatic ductal ligation, the food study was repeated. The dogs were sacrificed on the following day, and the pancreas of each dog was studied morphologically. Before pancreatic ductal ligation, plasma pancreatic polypeptide concentrations showed a biphasic response to a meal; a primary, rapid increase lasted 30 to 45 minutes, and a secondary, prolonged increase lasted for more than 180 minutes. One month after pancreatic ductal ligation, plasma concentrations of pancreatic polypeptide, at each time period during the initial 60 minutes after food, were significantly less than the corresponding sample before pancreatic ductal ligation. The total amount of pancreatic polypeptide released after a meal during the initial 60 minutes was diminished significantly by pancreatic ductal ligation. Neither plasma concentrations of pancreatic polypeptide nor the total amount of pancreatic polypeptide release after a meal showed a significant change during the last 180 minutes after food. Results of histologic observations showed destruction and fibrotic replacement of the acini of the pancreas after ligation of the pancreatic ducts. The islets were well preserved. Since the cells of origin of pancreatic polypeptide are distributed in both the acini and islets of the pancreas in dogs, we suggest that the primary, rapid phase of pancreatic polypeptide after a meal may be derived chiefly from cells in the acini, whereas the secondary phase of response may be derived chiefly from cells in the islets.

Animals↗
PubMed1981

Pancreatic polypeptide. A review.

Pancreatic polypeptide (PP), 36-amino acid peptide, may function as an important feedback inhibitor of pancreatic secretion after a meal. It arises from both islet and acinar cells of the pancreas. Release of PP by a meal, primarily protein, occurs in a biphasic manner. The first rapid release occurs as a result of vagal stimulation; the second, more prolonged rise (the so-called intestinal phase) occurs in response to hormonal stimulation, predominantly cholecystokinin. Plasma PP levels increase with age; PP levels are elevated above those of age-controlled normal subjects in diabetic patients and in some patients with pancreatic amine precursor uptake decarboxylase tumors. The value of plasma PP as a possible marker for pancreatic tumors is as yet unsettled but may be a valuable tool.

Animals↗
PubMed1981

Release of cholecystokinin in man: correlation of blood levels with gallbladder contraction.

Although it is generally assumed that release of cholecystokinin (CCK) is the chief mechanism by which a fatty meal causes contraction of the gallbladder, measured release of CCK and gallbladder contraction have never been correlated. We have achieved this correlation in eight adult male volunteers, by means of a specific radioimmunoassay for CCK and by ultrasonographic imaging of the gallbladder. This study validates our CCK radioimmunoassay and correlates measured concentrations of CCK with changes in gallbladder size measured by ultrasonographic examination. Basal concentrations of CCK (82.6 +/- 10.4 pg/ml) rose significantly to a maximum of 411.1 +/- 79.9 pg/ml at 16 minutes after intraduodenal instillation of medium-chain triglyceride (Lipomul). Mean basal volume of the gallbladder was 34.6 cm3; maximum reduction of gallbladder volume (to one-third of original) was achieved at 18 minutes. Elevated CCK concentrations began to fall toward basal, and the gallbladder began to refill at 25 minutes. Results obtained after oral ingestion of Lipomul provide similar results. Linear regression analysis demonstrated excellent correlation between concentrations of CCK and gallbladder size during both contraction and relaxation phases. Future study of this correlation may be useful in patients with manifest dysfunction of the gallbladder, as well as in individuals known to be at risk of gallbladder disease.

Adult↗
PubMed1980

Ectopic parathyroid adenomas.

Two cases of parathyroid tumours occurring in unusual situations are described. Such cases may cause difficulty in both the diagnosis and the surgical treatment of hyperparathyroidism. The cases described illustrate the importance of a definitive aetiological diagnosis in hypercalcaemia, if appropriate surgery is to be performed. The value of discriminant function analysis and hydrocortisone suppression tests are discussed.

Adenoma↗