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U Leonhardt

Publications and source records attributed to U Leonhardt.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Individual therapeutic procedure in metastatic carcinoid of the small intestine].

Actually, the therapeutic goal in a metastasized carcinoid tumor is rather symptomatic than curative. Here we report the case of a 53 year old woman with a hepatic and pulmonal metastasized carcinoid tumor of the small intestine. We will discuss current therapeutic options and the approach to the individual patient. After treatment with the standard therapeutics Octreotide and Interferon alpha we could achieve a remarkable and persistent remission by applying the rather unusual drug Dacarbacine in this patient. This is an example for the frequently occurring clinical situation in the treatment of patients with rare tumors requiring the application of individually modified therapeutic regimens. Furthermore, the potency of Dacarbacine in the treatment of carcinoid tumors seems to be underestimated up to now.

Carcinoid Tumor↗
PubMed1995

Effect of a platelet-activating factor antagonist on pancreas perfusion after 24 h of ischemia.

Platelet-activating factor (PAF) is a strong mediator of inflammation that is present in many mammalian tissues and cell types. In the pancreas, PAF can be synthesized in acinar cells after stimulation with secretagogues. The present study uses a perfused porcine pancreas model to investigate the role of PAF in pancreatic ischemia and the effect of the PAF antagonist bepafant on pancreas preservation. Pancreata were preserved with or without bepafant, stored for 24 h at 4 degrees C, and then reperfused at 37 degrees C in a perfusion chamber. Reperfusions were significantly improved by the addition of bepafant. This was indicated by a significantly increased arteriovenous volume flow (16.54 +/- 1.88 ml/min versus controls 8.54 +/- 1.31 ml/min; p = 0.0068; bepafant, n = 7; controls, n = 12) and a reduced vascular resistance (p = 0.0068; bepafant, 1.95 +/- 0.22 mm Hg * min/ml versus controls 4.08 +/- 0.56 mm Hg * min/ml). Radioimmunological quantification of PAF in pancreatic tissue revealed that PAF levels remain unchanged during storage in a cold protective solution at 4 degrees C but increase significantly during surgical pancreas preparation under general anesthesia (from 142.1 +/- 21.2 to 368.8 +/- 52.5 pg/g; n = 15; p = 0.0007). The present study shows that bepafant improves pancreas preservation after cold ischemia. The beneficial effect might be explained by antagonizing inflammatory and vasoconstrictory responses to PAF synthesized during surgical pancreas preparation.

Animals↗
PubMed1995

Treatment of metastasized midgut carcinoids with dacarbazine.

Seven patients with metastasized midgut carcinoids were treated with intravenous infusion of dacarbazine [dimethyltriazenoimidazole carboxamide (DTIC)] (650 mg/m2) every 4 wk. After 2 wk, white blood cell counts decreased transiently in three patients. No other DTIC-associated side effects occurred. Biochemical markers of disease activity decreased significantly in four patients for 4-20 months (mean duration, 12 months). Size of hepatic metastases was reduced or remained unchanged in six patients for 6-20 months (mean duration, 10 months). Clinical symptoms such as cutaneous flush, diarrhea, abdominal pain, constipation, night sweat, or weight loss improved in six of seven patients. We conclude that DTIC represents a useful therapeutic option in the treatment of advanced and metastasized carcinoid tumors.

Adult↗
PubMed1993

Hydroxyethyl starch does not improve pancreas preservation with HTK.

The effect of hydroxyethyl starch on pancreas preservation with cardioplegic histidine-tryptophan-ketoglutarate solution (HTK) was investigated. The study was performed using an in vitro reperfusion system of the porcine pancreas. During organ preservation pancreatic weight, arterial pressure, volume flow, and washout of amylase and lactate were quantified. Addition of hydroxyethyl starch did not affect arteriovenous volume flow or washout of amylase and lactate during protective perfusion after pancreas preparation. However, hydroxyethyl starch in HTK prevented an increase in pancreatic weight at the end of the protective perfusion (102.2 +/- 4.55% vs 127.8 +/- 4.62% in controls; p < 0.005) and after 24 h cold ischemia (72.9 +/- 3.91% vs. 83.5 +/- 3.49% in controls; p < 0.05). Hydroxyethyl starch did not affect postischemic organ quality assessed during reperfusion in a perfusion chamber by pancreatic vascular resistance, amylase and lactate release, insulin secretion, and oxygen consumption. We conclude that hydroxyethyl starch does not bring about any further improvement in immediate postischemic organ quality assessed in an in vitro reperfusion system.

Amylases↗
PubMed1993

Effect of camostate administration for two weeks on experimental pancreatitis in mice and rats.

The present study investigates the effect of oral pretreatment with the protease inhibitor camostate on the outcome of pancreatitis in three experimental models. In pancreatitis induced by overstimulation with cholecystokinin (CCK) in rats, pancreatic enzymes and the histological degree of pancreatitis were quantified; in pancreatitis induced by a choline-deficient ethionine-supplemented (CDE) diet in mice, the effect on survival was monitored; and in bile-induced pancreatitis in rats, the effect on survival, pancreatic enzymes, and histology was studied. Feeding of camostate (200 mg/kg/day) for 2 weeks worsened the histological degree of pancreatitis induced by overstimulation with CCK or by injection of taurocholate. The concentration of amylase in the pancreas and in serum was significantly lower after pretreatment with camostate, both in cerulein-induced pancreatitis and in bile-induced pancreatitis, while the concentration of trypsin in the pancreas was significantly increased in the camostate-treated animals. Pretreatment with camostate significantly lowered survival. In pancreatitis induced by a CDE diet, 3 of 20 mice survived the observation period, while 9 of 20 control animals survived (p < 0.05). In taurocholate-induced pancreatitis, 5 of 29 rats were alive after 3 days versus 18 of 30 animals in the control group (p < 0.001). CCK levels were not elevated in camostate-treated rats, when pancreatitis was induced 24 h after finishing camostate feeding. It is concluded that camostate induced pancreatic hypertrophy and increased concentration of proteolytic enzymes aggravate experimental panceatitis and that this is not mediated by increased CCK levels.

Administration, Oral↗