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Biomedical subjects

M Rünzi

Publications and source records attributed to M Rünzi.

At least 37 records · Page 2Linked to original sources
PubMed1997

Diagnostic dilemma in pancreatic lymphoma. Case report and review.

Non-Hodgkin's lymphoma predominantly involving the pancreas is a rare tumor of the gastrointestinal tract. Diagnosis can be difficult, since lymphoma may mimic carcinoma or pancreatitis. Lymphoproliferative diseases induced by immunosuppressive therapy frequently occur in the gastrointestinal tract of posttransplant patients. However, pancreatic involvement of posttransplant lymphoma is an exceptional condition. We present the case of a cyclosporin-treated renal transplant recipient with pancreatic lymphoma mimicking carcinomatous or inflammatory tumors. The diagnostic difficulties and treatment options of pancreatic lymphoma as well as lymphoproliferative disorders in immunosuppressed renal recipients are discussed in light of the current literature.

Azathioprine↗
PubMed1997

Duodenal and ileal nutrient deliveries regulate human intestinal motor and pancreatic responses to a meal.

It is assumed that in humans pancreatic and gastrointestinal motor responses to a meal are coordinated and regulated mainly by duodenal nutrient exposure. On the other hand, there is evidence that the distal intestine may participate in the regulation of gastrointestinal functions. The aim of this study was to compare human pancreatic and intestinal motility responses to a meal and to correlate them with nutrient exposure of the proximal and distal intestine. After intubation with an oroileal multilumen tube for marker perfusion, duodenal and ileal aspiration, and intestinal manometry, 14 healthy subjects received a mixed test meal (1,257 kJ). Intraluminal nutrient concentrations, enzyme activities, and small intestinal motility were analyzed for 6 h postprandially. Duration of duodenal nutrient exposure was 3.4 +/- 0.2 h, and duration of pancreatic enzyme response and fed motor pattern was 2.5 +/- 0.2 and 3.5 +/- 0.3 h, respectively. Durations of pancreatic secretory and motor responses were correlated (P < 0.05), but neither duration of digestive secretory nor of motor activity correlated with that of prandial duodenal nutrient concentrations. By contrast, they were associated with the relative increase in ileal nutrient delivery late postprandially (P < 0.05). Physiological late postprandial delivery of nutrients to distal intestinal sites is correlated with the termination of digestive pancreatic and motor responses and may participate in their control.

Adult↗
PubMed1996

[Trimethoprim-sulfamethoxazole-induced cholestatic hepatitis. Clinico-immunological demonstration of its allergic origin].

HISTORY AND CLINICAL FINDINGS: A 22-year-old woman was given trimethoprim plus sulphamethoxazole for a urinary infection (160 and 800 mg, respectively, daily), drugs she had not previously taken. After 2 weeks she noticed a rash of small spots on her trunk. In addition she had nausea and vomiting. The rash faded within 2 days of stopping the drug, but progressive jaundice developed. INVESTIGATIONS: SGPT and SGOT concentrations rose to maximally 328 and 83 U/l, total bilirubin to maximally 5.9 mg/dl. There was no evidence for viral hepatitis (B or C, cytomegalovirus, Epstein-Barr), autoimmune hepatitis or primary biliary hepatitis. Liver biopsy showed central acinar cholestasis, which suggested drug-induced liver damage. COURSE: The patient's symptoms regressed over several weeks without any specific treatment and 8 weeks after onset of the rash the laboratory tests also became normal. The allergic cause of the cholestatic hepatitis was confirmed by a lymphocyte transformation test. CONCLUSION: Clinical suspicion of drug allergy as cause of a cholestatic hepatitis can be confirmed reliably and without any risk to the patient with the lymphocyte transformation test.

Adult↗
PubMed1996

Drug-associated pancreatitis: facts and fiction.

In the past, numerous reports on drugs probably causing acute pancreatitis have been published. However, most of these case reports were anecdotal with a lack of obvious evidence and did not present a comprehensive summary. Although drug-associated pancreatitis is rare, it is gaining increasing importance with the introduction of several potent new agents, i.e., anti-acquired immunodeficiency syndrome drugs. The following comprehensive review scrutinizes the evidence present in the world literature on drugs associated with acute or chronic pancreatitis and, based on this, categorizes in a definite, probable, or possible causality. In addition, explanations for the pathophysiological mechanisms are discussed.

Acute Disease↗
PubMed1995

Endocrine and exocrine pancreatic function after camostate-induced growth of the organ.

It is well known that oral administration of camostate induces hyperplasia and hypertrophy of the rat pancreas. It is not clear, however, whether pancreatic hormone and enzyme secretion are affected by camostate treatment. In rats, daily administration of 200 mg camostate/kg b. wt for 14 days significantly increased pancreatic weight and pancreatic content of DNA, protein, amylase, lipase, trypsin and chymotrypsin, as well as the amount of insulin, glucagon and somatostatin. In the intact animal, blood glucose levels and serum concentrations of insulin and glucagon in response to an oral glucose load were not impaired after camostate treatment. In the isolated perfused pancreas, however, insulin and glucagon secretions were reduced, whereas somatostatin release was not affected. The volume of pancreatic juice produced by the unstimulated isolated perfused organ, as well as protein and enzyme secretion, were increased after camostate treatment. Likewise, the isolated perfused pancreas from camostate-treated rats secreted a larger volume of pancreatic juice and more protein in response to cholecystokinin (CCK), while enzyme secretion was affected in a non-parallel manner: amylase release was markedly reduced, lipase release was unchanged, and release of trypsin and chymotrypsin was increased.

Animals↗
PubMed1995

Biochemical and morphological changes that characterise recovery from necrotising biliary pancreatitis in the opossum.

The events that characterise recovery from severe biliary pancreatitis have not been defined. This study used a reversible model of necrotising pancreatitis, induced by obstructing the opossum common bile pancreatic duct (CBPD), to evaluate this phenomenon. The CBPD of opossums was obstructed with a balloon tipped catheter for five days and then decompressed by removal of the catheter. Recovery was evaluated 0-90 days after relief of obstruction. Serum bilirubin and amylase values rapidly declined, reaching control values 7-14 days after removal of the obstructing catheter. Pancreatic protein and amylase values were transiently increased shortly after relief of obstruction but returned to control values 21 days after decompression. Pancreatic ornithine decarboxylase activity and incorporation of [3H]-thymidine into DNA were transiently increased 14 days after duct decompression suggesting that regeneration occurs at approximately that time. Foci of pancreatic necrosis involved roughly 40% of the gland at time of decompression but these foci gradually disappeared and the gland resembled that of control animals 60 days after decompression. Evidence of fibrosis or collagen deposition in the pancreas was not noted at any time. These studies show that recovery after necrotising biliary pancreatitis occurs comparatively rapidly and the restitution ad integrum occurs. Recovery from necrotising acute pancreatitis in this model is not associated with the development of chronic pancreatitis.

Acute Disease↗
PubMed1995

Luminal endocytosis and intracellular targeting by acinar cells during early biliary pancreatitis in the opossum.

Cell necrosis in acute experimental pancreatitis is preceded by a redistribution of digestive enzymes into a lysosomal subcellular compartment. We have investigated whether endocytosis from the acinar cell lumen might contribute to this disturbance of intracellular compartmentation. In an animal model of pancreatitis involving pancreatic bile duct ligation in opossums, we have studied in vivo endocytosis of dextran 40 and [14C]dextran 70, cationized ferritin, and horseradish peroxidase from the apical surface of acinar cells before the onset of necrosis. Marker solutions were instilled into the pancreatic duct of anesthetized animals at physiological pressure. Tissue samples obtained at intervals of up to 60 min after instillation of markers were studied by electron microscopy and electron microscope autoradiography. All markers were taken up by acinar cells in control animals and in animals with obstructed pancreatic bile ducts. Markers for membrane-mediated endocytosis (cationated ferritin and horseradish peroxidase) were transported to lysosomes in both groups. In contrast, the fluid-phase tracer dextran was transported to the secretory pathway in controls but to lysosomes after duct ligation. Since dextran and luminally present secretory proteins can be expected to follow the same route after endocytosis, our findings suggest that altered intracellular targeting of endocytosed proteases might be one mechanism by which digestive zymogens reach an intracellular compartment in which premature activation can occur. This phenomenon may be a critical and early event in the pathogenesis of biliary pancreatitis.

Acute Disease↗
PubMed1995

Evaluation of necrotizing pancreatitis in the opossum by dynamic contrast-enhanced computed tomography: correlation between radiographic and morphologic changes.

BACKGROUND: The ability to quantitate the extent of acinar cell necrosis with contrast-enhanced computed tomography (CT) during acute pancreatitis is uncertain. STUDY DESIGN: Acute hemorrhagic necrotizing pancreatitis was induced in opossums by obstructing their biliopancreatic duct for up to seven days or by retrograde injection of a bile-trypsin taurocholate mixture into the opossum pancreatic duct. At selected times, groups of three animals each were examined by dynamic contrast-enhanced CT, and the abnormalities on the images were quantitated. Immediately following CT, the animals were sacrificed and the extent of necrosis was quantitated by morphometric analysis of tissue samples at the light microscope level. RESULTS: The CT severity score as well as the degree of nonenhancement on dynamic contrast-enhanced CT were both closely correlated with the extent of acinar cell necrosis (r = 0.91 and r = 0.97, respectively). CONCLUSIONS: The degree of pancreatic nonenhancement on dynamic contrast-enhanced CT can be used to quantitate the extent of pancreatic necrosis during acute necrotizing pancreatitis.

Acute Disease↗
PubMed1993

Inositol trisphosphate-independent agonist-stimulated calcium influx in rat pancreatic acinar cells.

CCK-JMV-180 is a cholecystokinin analog that stimulates digestive enzyme secretion from pancreatic acinar cells but does not cause either generation of inositol 1,4,5-trisphosphate or depletion of the inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ storage pool. We report that CCK-JMV-180 can accelerate Ca2+ influx into fura-2-loaded dispersed rat pancreatic acini and single acinar cells. Furthermore, CCK-JMV-180 accelerates Ca2+ influx into cells microinjected with the inositol 1,4,5-trisphosphate receptor antagonist heparin and into acini loaded with the Ca(2+)-chelating agent BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid). These results indicate that agonist-stimulated Ca2+ influx can occur (a) without depletion of the inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ storage pool, (b) without a rise in cytoplasmic free Ca2+ concentrations, and (c) after blockade of inositol 1,4,5-trisphosphate receptors. They suggest that depletion of an inositol 1,4,5-trisphosphate-independent intracellular Ca2+ storage pool and/or generation of a non-inositol 1,4,5-trisphosphate second messenger by CCK-JMV-180 may be a sufficient signal for acceleration of Ca2+ influx into rat pancreatic acinar cells.

Animals↗
PubMed1993

Endogenous somatostatin possibly controls pancreatic growth: further evidence for feedback regulation.

Specific inhibitors acting upon pancreatic proteinases in the gut can cause pancreatic hypertrophy ('growth'), which is probably mediated through a feedback mechanism utilizing cholecystokinin. We have proposed the involvement of somatostatin, and here test the hypothesis that endogenous somatostatin secreted into pancreatic juice may regulate pancreatic growth. Groups of rats were given the proteinase inhibitor camostate intragastrically for either 3, 7, 14, 28, or 56 days, when they were sacrificed. In some groups the pancreata were weighed and homogenized while in other groups isolated perfused pancreatic organ preparations were performed. Somatostatin was measured in the homogenates, pancreatic juice and portal vein effluents. In camostate-fed animals, pancreatic weights increased to a maximum at 28 days, while pancreatic somatostatin content increased significantly from the third day onwards, and somatostatin secretion into pancreatic juice increased progressively until day 28. In contrast, somatostatin secretion into portal blood remained unchanged from those of untreated controls over the duration of the experiment, and its concentration was lower than in pancreatic juice. These observations provide further evidence that endogenous pancreatic somatostatin may control pancreatic growth in rats.

Animals↗
PubMed1993

Effect of cysteamine on insulin release and exocrine pancreatic secretion in vitro.

Cysteamine is known to deplete somatostatin from pancreatic D cells. In the isolated perfused rat pancreas we investigated its effects on somatostatin and insulin release as well as exocrine pancreatic secretion in the presence of 16.7 mM glucose and 180 pM CCK-8. At a concentration of 0.1 mM, cysteamine had no significant effect on pancreatic endocrine and exocrine functions. At 10 mM, however, cysteamine released somatostatin (380 +/- 70 vs 100 +/- 20 fmol/20 min), inhibited insulin output (890 +/- 120 vs 13210 +/- 3260 mu units/20 min) and reduced exocrine pancreatic secretion (volume: 12 +/- 2 vs 20 +/- 2 microliters/20 min; lipase: 31 +/- 3 vs 60 +/- 7 units/20 min). We conclude that the complex changes induced by cysteamine are consistent with a physiological role of endogenous somatostatin in the regulation of insulin release. The reduction of exocrine pancreatic secretion, however, was at least in part, if not completely, mediated via the insuloacinar axis rather than a direct effect of cysteamine-released somatostatin on pancreatic acinar cells.

Animals↗
PubMed1993

Early ductal decompression prevents the progression of biliary pancreatitis: an experimental study in the opossum.

BACKGROUND: The value of early endoscopic or surgical interventions to remove bile duct stones and decompress the biliopancreatic ductal system in gallstone pancreatitis is controversial. METHODS: To evaluate this issue, acute hemorrhagic necrotizing pancreatitis was induced in opossums by obstructing the biliopancreatic ductal system with a balloon catheter for 1, 3, or 5 days. RESULTS: A progressive increase in the severity of pancreatitis, as manifested by inflammation, fat necrosis, hemorrhage, acinar cell vacuolization, in vitro lactate dehydrogenase release, and acinar cell necrosis, was noted in these obstructed animals. In contrast, decompression of the obstructed ductal system by removal of the balloon catheter after 1 or 3 days prevented the increase in severity of these parameters of pancreatic injury. CONCLUSIONS: We concluded that the severity of biliary pancreatitis in this model is dependent upon the duration of ductal obstruction and that decompression of the ductal system can prevent progression of the disease. These observations support the practice of early attempts to remove obstructing stones in clinical gallstone pancreatitis.

Animals↗