Biomedical subjects
Publications and source records attributed to D A Dreiling.
Transhepatic catheterization of the portal system was performed to obtain blood for RIA of insulin. This technique localized insulinomas in two patients after negative celiac, superior mesenteric, and subselective gastroduodenal arteriograms. The tumors were found in the predicted locations at surgery.
Three patients with insulinoma have been presented. Accurate diagnosis, localization and multiplicity are possible employing angiography, sonography, CAT and insulin concentration determinations of specimens obtained by percutaneous, transhepatic simultaneous sampling of the portal, splenic and superior mesenteric veins. Meticulous exploration of the gland will permit enucleation rather than major resection to be a feasible solution and the operation of choice.
Studies in animals demonstrate a gastric hormonal phase of pancreatic exocrine secretion. Endogenous or exogenous gastrin causes a marked elevation in the pancreatic enzymes and a lesser increase in the pancreatic volume and bicarbonate. It is possible that these "gastrin" effects may be the basis of a "cephalic" phase of pancreatic secretion. These observations have been only partially confirmed in human subjects with and without the Zollinger-Ellison syndrome. The physiologic importance of these ecbolic actions as well as a possible trophic effect remains to be elucidated.
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The physiology and pathophysiology of the sphincter of Oddi are poorly understood. The relationships of functional disorders of the sphincter to biliary and pancreatic disease and of organic lesions of the papilla to pancreatic inflammatory disease are subjudice to say the least. The efficacy of sphincter section in the treatment of chronic pancreatitis is unproved. Section of the sphincter may be necessary to treat biliary tract pathology but its use should not be routine or indiscriminative since, there is morbidity as well as mortality. Finally, the price of sphincterotomy is: 1. hemorrhage; 2. duodenal perforation; 3. pancreatic duct damage--a. acute pancreatitis; b. chronic pancreatitis; 4. sphincter incompetence--a. common duct regurgitation--cholangitis; b. pancreatic duct regurgitation--pancreatitis; 5. sphincter stenosis--obstructive jaundice; 6. stasis cholecystitis; 7. diarrhea; 8. morbidity 10%; 9. mortality 1.9%.
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Effects of a synthetic prostaglandin analog--16,16-dimethyl prostaglandin E2 methyl ester (16-diMe-PGE2)--on parotid secretion were evaluated in eight dogs under anesthesia. Graded doses of 16-diMe-PGE2 (0.3, 0.5, 1.0 and 2.5 microgram./kg.) were administered intravenously with the parotid in the resting state or in response to urecholine (intravenous infusion or subcutaneous injections). Profound and prolonged inhibition of volume occurred. Amylase concentration was increased but output was unchanged. Bicarbonate concentration was increased but output was decreased. Nonsteroid inhibitors of endogenous prostaglandin synthesis did not alter these effects. Although these studies do not establish a physiologic role for prostaglandins in the regulation of salivary secretion, they do demonstrate a wide-ranging effect of prostaglandins on the gastrointestinal tract.
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Immunoglobulins A, M and G in the pancreato-duodenal fluid (PDF) of 35 pancreatic disease-free individuals and 48 patients with chronic pancreatitis (25), hypersecretory disorders (10), renal transplanted (4) and with pancreatic cancer (9), were determined by a single radial immunodiffusion method. Although a trend of immunoglobulin hypersecretion in benign diseases and hyposecretion in malignancies was present, individual levels of Ig-A and Ig-M differed statistically only between cancer and other groups. Calculating the ratios of Ig-A to Ig-M (A/M) and Ig-A to total immunoglobulin contents (A/T) in the PDF of patients with chronic pancreatitis or cancer, however, a significantly higher or lower ratio, respectively, was found compared to control group. Differences in A/M ratios could not be detected between patients with benign diseases, but were constantly present when these patients were compared to pancreatic cancer. The underlying mechanism(s) of the disturbed immunosecretory system in pancreatic diseases remains speculative. Nevertheless, immunoglobulin measurements in the PDF of patients with pancreatic diseases offer a simple diagnostic aid in clinical differentiation of pancreatic pathology.
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Fifty-two patients with or without pancreatic disease were studied with both secretin test and endoscopic retrograde pancreatography. Pancreatic histopathology was obtained by exploratory laparotomy in half of these patients. The following conclusions were reached: 1. Secretory tests are the most sensitive indicators of chronic pancreatitis, although not all cases of chronic pancreatitis will be discovered by this test. 2. When secretory tests show low volume output, pancreatography is crucial in differentiating between malignant ductal obstruction or pancreatic replacement by fibrosis or atrophy. 3. Histologic correlation with ductular structure and/or secretin function is frequently discordant. 4. The secretin test and pancreatogram measure different parameters and the use of both these complementary studies will lead to increased diagnostic accuracy and better understanding of pancreatic pathophysiology.
The evaluation of serum pancreatic enzyme activity on whole and diluted serum permits the estimation of serum enzyme inhibitor activity via a ADS/AWS ratio. This has diagnostic value in chronic pancreatic disease. The serum pancreatic ferment activity appears to be regulated in part by serum steroid levels. It is responsive to high protein diet. A physiologic rationale is presented for the use of steroids and high protein diet in the treatment of acute and chronic pancreatic inflammation.
The acute administration of Imuran and hydrocortisone significantly decrease pancreatic flow and protein output in canines. This observed phenomenon may explain the gastrointestinal side reactions encountered in clinical usage of these potent immunosuppresants.
The administration of various dose schedules of 5-FU did not result in any alteration of pancreatic secretion. The findings would not support the thesis that the gastrointestinal side-effects of this potent cancer chemotherapeutic agent are the result of a toxic pancreatic insufficiency.
Parallel studies in parotid and pancreatic function and histology were carried out in Thomas fistula dogs with irradiation-induced chronic pancreatitis. After completion of base line studies of parotid and pancreatic secretion, four dogs were subjected to 2,400 rads tumor dose over two weeks (with a nominal single dose of 1,175 rets); two additional dogs served as control. Sequential studies were performed on pancreatic secretion in response to secretin and on parotid secretion in response to urecholine. After a short-lived period of hypersecretion. There was a progressive reduction in pancreatic secretory rate, bicarbonate and enzyme outputs (greater than 90% after three months). Parotid secretion increased over this period but subsequently decreased, so that at eight months there was a marked reduction both in pancreatic and parotid function. Whereas pancreatic histology showed diffuse interstitial fibrosis and reduction of acinar tissue, no histologic changes were noted in the parotid glands. Although the mechanisms are unclear, alterations in parotid secretion may be of value in the diagnosis of chronic pancreatitis, in the evaluation of its severity, and may yield information on the duration of the disease.