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Biomedical subjects

W Schepp

Publications and source records attributed to W Schepp.

At least 19 recordsLinked to original sources
PubMed2006

[Is there a nonsurgical therapeutic approach to cholangiocellular carcinomas?].

Nonsurgical treatment aims at controlling disease and improving survival and quality of life in patients with nonresectable, recurrent metastatic cholangiocarcinomas. After R0 resection, percutaneous or intraluminal radiotherapy with adjuvant radiochemotherapy may improve survival. Available data, however, are still unsatisfactory, and the efficacy of adjuvant radiochemotherapy after R0 resection remains to be confirmed. Exclusive chemotherapy fails to improve survival postoperatively while, in adequate patients, neoadjuvant chemotherapy can improve R0 resection results. Palliative chemotherapy yielded improved survival and quality of life in only one small prospective randomized trial and cannot be generally recommended at present. Previous biliary stenting for relieving jaundice is mandatory. Beyond established regimens employing 5-fluorouracil/leukovorin and gemcitabine plus platin-based agents, ongoing trials are focussing on topoisomerase-and thyrosine kinase inhibitors. Palliative stenting of malignant bile duct stenoses may eliminate or at least relieve jaundice and pruritus. Single stenting is sufficient for distal bile duct stenoses. In patients with liver metastasis and life expectancy of <6 months, temporary plastic prostheses with 4-6-month patency are sufficient. When the prognosis is for >6 months, self-expanding permanent metal stents, with their significantly longer patency, are superior. In hilar tumors, obstruction of plastic prostheses occurs earlier than in distal bile duct stenoses. Thus, patients with Bismuth II-IV tumors benefit from self-expanding metal stents. These may be inserted by an endoscopic, retrograde approach, percutaneously, or by a combined rendez-vous maneuver. The superiority of bilateral vs unilateral stenting has yet to be proven in Bismuth II-IV tumors. Photodynamic therapy followed by stenting appears to improve survival rates by delaying stent occlusion rather than by regression of the tumoric disease itself.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

["Iatrogenic acute coronary syndrome"--59 year old patient with adenocarcinoma of ascending colon and stenocardia while receiving adjuvant chemotherapy with 5-fluorouracil].

Fluorouracil-associated cardiotoxic adverse events represent a relevant but underestimated problem in 5-fluorouracil treatment. After right hemicolectomy for adenocarcinoma of the rightsided colonic flexure a 59-year old patient was referred to our hospital for adjuvant chemotherapy according to MOSAIC-protocol with oxaliplatin and 5-fluorouracil. The patient's history was unremarkable for any cardiopulmonary disease and for any cardiovascular risk factors. 24 hours after completing the first cycle the patient was readmitted to our emergency department because of thoracic pain combined with significantly elevated cardiac enzymes and ischaemic changes in ECG. Coronary angiography was performed revealing no coronary artheriosclerosis. Clinical symptoms and pathological ischaemic serum parameters returned to normal range within 12 hours. Diagnosis of 5-FU-induced acute coronary syndrome could be made. Because of the high rate of recurring cardiotoxicity the patient's chemotherapy was modified to an alternative regimen containing raltitrexed instead of 5-fluorouracil. Immediate diagnosis of 5-FU-induced cardiotoxicity and differentiation from preexisting coronary heart disease is still a major problem in daily oncological practice.

Adenocarcinoma↗
PubMed2006

[Invasive and non-invasive diagnostic methods for evaluation of hypovolemia in acute pancreatitis].

Severe acute pancreatitis leads to a dramatic fluid loss in the intraperitoneal space which may result in circulatory decompensation. Sequestration of fluid can amount up to 40 percent of the circulating blood volume. The amount of fluid and electrolyte replacement is often misjudged leading to a higher rate of complications and a higher mortality rate of the disease. Furthermore, subsequent and adequate fluid resuscitation seems to influence the prognostic course of the disease by improving the perfusion and oxygenation of the pancreas. Otherwise volume overload may cause cardiopulmonary decompensation in the case of synchronous cardiopulmonary comorbidities. Therefore, an important part of treatment relies on careful haemodynamic monitoring, if necessary managed in an intensive care unit. Usually most patients with acute pancreatitis will be treated on a non-intensive medical ward which allows a differentiated and continuous haemodynamic monitoring only to a limited extent. Apart from monitoring circulatory parameters and measuring central venous pressure, there are other clinical methods, laboratory tests and radiological diagnostic procedures to determine the amount of intravascular fluid deficit and the individual volume demand of patients with acute pancreatitis. Prospective clinical trials for evaluation of pancreatitis-specific volume management do not exist so far. The aim of this review is to provide background information on invasive and non-invasive diagnostic methods for detection of circulatory hypovolemia in acute pancreatitis.

Blood Volume↗
PubMed2005

[Severe intrahepatic cholestasis in a 66-year old male patient with medically treated atrial fibrillation].

A 66-year-old male was admitted to hospital due to painless jaundice. Because of ischemic cardiomyopathy with paroxysmal atrial fibrillation as well as recurrent ventricular tachycardias and fibrillation he was treated with phenprocoumon and amiodarone (200 mg per day) for 2 years. Laboratory tests revealed significant elevation of the parameters of cholestasis and aminotransferase activity. Serological tests excluded infectious, autoimmune or metabolic liver diseases. Abdominal ultrasound and ERCP showed no mechanic cholestasis nor tumor of the pancreas. Cardiac congestive disease was also excluded. Severe intrahepatic cholestasis, consistent with drug-induced hepatotoxic damage, was diagnosed histologically. After discontinuing phenprocoumon the liver enzymes further increased. When amiodarone was stopped, however, laboratory parameters showed a continuous downward tendency. For prevention of malignant cardiac arrhythmia the patient received an atrioventricular defibrillator. Intrahepatic cholestasis is a rare presentation of amiodarone-induced hepatic toxicity. Liver damage can even occur after the drug has been taken for prolonged periods without any problems.

Aged↗
PubMed2005

[A 67-year-old patient with diarrhoea and constipation without any pathological findings in virtual colonoscopy].

Virtual colonoscopy provides a computer-simulated endoluminal perspective of the air-filled, distended colon using modern CT scanning (spiral CT). According to recent studies the sensitivity and specificity of this technique are high for adenomatous polyps > or = 10 mm. A 67-year-old patient was admitted to our hospital because of diarrhoea and constipation, associated with abdominal pain in the lower right abdomen. Prior to admission the patient had undergone virtual colonoscopy in a specialised radiological practice which had detected no abnormalities apart from colonic diverticulosis. However, conventional video-colonoscopy revealed a subtotal circular malignant stenosis in the region of the right colonic flexure. A poorly differentiated adenocarcinoma was diagnosed histologically. Staging showed peritoneal carcinosis with infiltration of the right ureter and lymphangiosis carcinomatosa of the pectoral lobe of the left lung. After right hemicolectomy because of metastasised carcinoma of the ascending colon (pT4pN1pM1) we started palliative chemotherapy with oxaliplatin, 5-fluorouracil and leucovorin. The risk of misdiagnosis by virtual colonoscopy is clearly increased in patients with subtotal tumour stenosis of the ascending colon. Conventional video-colonoscopy remains the gold standard for the diagnosis of colorectal carcinoma.

Adenocarcinoma↗
PubMed2003

[Acrocyanosis: crucial symptom in a case of chronic diarrhea and weight loss].

The patient reported here was admitted because of severe dehydration caused by watery diarrhea. As underlying disease we found bacterial overgrowth of the small bowel due to myopathic dysmotility of the small bowel as a manifestation of CREST syndrome. An important clue to the diagnosis was the result of a ward round: the patient showed Raynaud's phenomenon when exposed to the cold at an open window airing the room. A leading tool for diagnosis and therapy proved to be small bowel manometry which is further discussed in this case report.

Aged↗
PubMed2001

Differential expression of CD95, Bcl-2, and Bax in rat gastric chief and parietal cells.

Apoptotic cell death is common in the inflamed gastric mucosa, but its role in the regulation of cell homeostasis in normal gastric mucosa is unknown. We investigated the expression of CD95, Bcl-2, and Bax and their roles in the regulation of apoptosis in normal rat gastric mucosa and in cultures of highly enriched rat chief and parietal cells by immunostaining, Western blotting, and FACS. In intact tissue CD95, Bcl-2, and Bax were localized predominantly in the glandular base region in chief cells. In freshly isolated cells, expression of CD95, Bcl-2, and Bax was much more pronounced in chief cells than in parietal cells. A lower intracellular Bcl-2/Bax ratio suggesting a higher susceptibility to apoptosis was noticed in chief rather than in parietal cells. In extended cultures of parietal and chief cells, Bax expression was upregulated and Bcl-2 expression was downregulated. These regulatory changes, presumably caused by in vitro effects, were not associated with an increase in spontaneous apoptosis. Treatment of chief and parietal cells with Fas-ligand induced apoptosis of all CD95 expressing cells. Expression of CD95, Bcl-2, and Bax predominantly in chief cells suggests that in this cell type regulation of apoptosis may differ from that in parietal cells. Binding of FasL with functionally active CD95 receptors on chief and parietal cells may be relevant for induction of apoptosis in inflamed gastric mucosa.

Animals↗
PubMed2001

Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesin during chronic gastric inflammation.

Helicobacter pylori has been assigned as a class I carcinogen because of its relation to gastric adenocarcinoma. Chronic H. pylori infection may lead to severe gastritis, glandular atrophy (AT), and intestinal metaplasia (IM). Strains secreting the vacuolating toxin VacA and producing the cytotoxin-associated antigen CagA (type 1 strains), as well as the blood group antigen binding adhesin (BabA) targeting Lewis(b) antigens, have been associated previously with distal gastric adenocarcinoma (M. Gerhard et al., Proc. Natl. Acad. Sci. USA, 96: 12778-12783, 1999) and may therefore also be related to lesions preceding gastric cancer. Antral and corpus biopsies were collected from 451 patients; 151 were H. pylori positive, as determined by PCR. Gastric biopsies were histologically evaluated for activity of gastritis (G0-G3, granulocyte infiltration), chronicity of gastritis (L1-L3, lymphocyte infiltration), and the presence of IM and/or AT according to the Sydney classification. Simultaneously, the presence of bacterial genes encoding virulence and adherence factors (racAs1/s2, cagA, and babA2) was determined by PCR. The presence of cagA+ and vacAs1 (alone or combined) both correlated with activity and chronicity of gastritis (P < 0.05); however, the overall prevalence of these genes was 60 or 72%, respectively, and was thus relatively frequent. The babA2 gene, encoding the adhesin BabA, was detected in 38% of infected patients and was correlated with the activity of gastritis in antrum and corpus (P < 0.005). cagA+/vacAs1+ strains (suggesting the presence of type 1 strains) that were also babA2 positive were detected more frequently in patients with severe histological alterations (such as G3, IM, or AT) compared with subjects without these changes (P < 0.01). cagA+/vacAs1+ strains that were babA2 negative, however, lacked a significant correlation with severe histological changes, activity, or chronicity of gastritis in antrum and corpus. Adherence of H. pylori via BabA appears to be of importance for efficient delivery of VacA and CagA and may play a special role in the pathogenesis of severe histological changes.

Adhesins, Bacterial↗
PubMed2001

Primary low-grade B cell non-Hodgkin's lymphoma of MALT type simultaneously arising in the colon and in the lung: report of a case.

zone B cell lymphoma of mucosa-associated lymphoid tissue type according to the Revised European American Lymphoma classification). Other mucosa-associated lymphoid tissue-type lymphomas arise in the salivary glands, thyroid gland, and in the lung (bronchus-associated lymphoid tissue). Here, we report the first case of a monoclonal mucosa-associated lymphoid tissue lymphoma with simultaneous manifestation in the colonic and bronchial mucosa in a 62-year-old patient. With mitoxantrone, chlorambucil, and prednisone polychemotherapy, a complete year-long remission was achieved.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Effect of caloric density of a meal on lower oesophageal sphincter motility and gastro-oesophageal reflux in healthy subjects.

BACKGROUND: Patients with gastro-oesophageal reflux disease are advised to avoid the ingestion of large meals. In healthy volunteers, a relationship between the amount of postprandial gastro-oesophageal reflux and the volume of a liquid meal has been demonstrated. AIM: To evaluate whether the amount of postprandial gastro-oesophageal reflux is also related to the calorie content of a meal, a second parameter that will be reduced by avoidance of the ingestion of large meals. METHODS: Twelve healthy volunteers (six female, 19-31 years) received two solid-liquid meals with either 842 kcal (solid 582 kcal, liquid 260 kcal) or 582 kcal (31% reduction) in a randomized order. The nutritional components (10% fat, 76% carbohydrates, 14% protein) and the volume of the meals were identical in both meals. The lower oesophageal sphincter pressure was measured continuously in the first postprandial hour with a Dent sleeve, and pH-metry was performed for 3 h postprandially with a glass electrode in the distal oesophagus. Blinded to the type of ingested meal, we calculated the mean lower oesophageal sphincter pressure, the frequency of transient lower oesophageal sphincter relaxations, the number of reflux episodes, and the fraction of time for which pH < 4. RESULTS: A similar decrease in lower oesophageal sphincter pressure was observed after ingestion of the high calorie meal (median 10.9 mmHg, range 4.8-16.7 mmHg) and low calorie meal (median 9.9 mmHg, range 3.9-18.4 mmHg). No difference in the number of transient lower oesophageal sphincter relaxations (high calorie: median 9 per hour, range 5-13 per hour; low calorie: median 7 per hour, range 0-14 per hour) and of reflux episodes (high calorie: median 12 in 3 h, range 3-22 in 3 h; low calorie: median 12 in 3 h, range 3-30 in 3 h) was registered after intake of both types of meal. Additionally, no difference was identified regarding the fraction of time for which pH < 4 between the high calorie (mean 2.3%, 0.2-23.7%) and low calorie meal (3.3%, 0.5-17.8%). CONCLUSION: Reducing the caloric density of a meal neither influences postprandial lower oesophageal sphincter pressure nor decreases gastro-oesophageal reflux in healthy volunteers. Thus, the amount of gastro-oesophageal reflux induced by ingestion of a meal seems to depend on the volume but not on the caloric density of a meal.

Adult↗
PubMed2001

Neuronal nitric oxide synthase: expression in rat parietal cells.

Nitric oxide synthases (NOS) are enzymes that catalyze the generation of nitric oxide (NO) from L-arginine and require nicotinamide adenine dinucleotide phosphate (NADPH) as a cofactor. At least three isoforms of NOS have been identified: neuronal NOS (nNOS or NOS I), inducible NOS (iNOS or NOS II), and endothelial NOS (eNOS or NOS II). Recent studies implicate NO in the regulation of gastric acid secretion. The aim of the present study was to localize the cellular distribution and characterize the isoform of NOS present in oxyntic mucosa. Oxyntic mucosal segments from rat stomach were stained by the NADPH-diaphorase reaction and with isoform-specific NOS antibodies. The expression of NOS in isolated, highly enriched (>98%) rat parietal cells was examined by immunohistochemistry, Western blot analysis, and RT-PCR. In oxyntic mucosa, histochemical staining revealed NADPH-diaphorase and nNOS immunoreactivity in cells in the midportion of the glands, which were identified as parietal cells in hematoxylin and eosin-stained step sections. In isolated parietal cells, decisive evidence for nNOS expression was obtained by specific immunohistochemistry, Western blotting, and RT-PCR. Cloning and sequence analysis of the PCR product confirmed it to be nNOS (100% identity). Expression of nNOS in parietal cells suggests that endogenous NO, acting as an intracellular signaling molecule, may participate in the regulation of gastric acid secretion.

Animals↗
PubMed2000

Expression of intrinsic factor in rat and murine gastric mucosal cell lineages is modified by inflammation.

Intrinsic factor is produced primarily by chief cells in rat and mouse, but 4 to 11% of isolated rat parietal cells also contain intrinsic factor. To test whether local conditions could alter the distribution of intrinsic factor expression, two rodent models of chronic lymphocytic gastric inflammation were examined. Immunocytochemistry was performed using antiserum against human intrinsic factor and H/K ATPase (a parietal cell marker), counting the percent of intrinsic factor-positive parietal cells. HLA-B27 transgenic rats develop chronic gastritis at age 3 months. Congenic controls expressed intrinsic factor in 8.9 +/- 3.8% (mean +/- SD) of parietal cells; in inflamed areas of transgenic rats 21 +/- 5.2% (P < 0.0001) of parietal cells were positive. In adjacent areas without inflammatory infiltrate 16 +/- 3.6% of parietal cells contained intrinsic factor. C57BL/6 mice inoculated with Helicobacter felis develop gastritis by 4 weeks. After 4 and 8 weeks of infection, intrinsic factor-positive parietal cells increased from 7.8 +/- 2.8% in the congenic controls to 17.6 +/- 4.1% in the inflamed gastric body (P < 0.0001). Isolated rat parietal cells incubated with interleukin-1beta demonstrated a twofold increase in intrinsic factor-positive parietal cells. These studies are consistent with the concept that intrinsic factor expression is both predetermined in chief cells and can be expressed in parietal cells in response to local inflammatory factors. The differences between inflamed and adjacent noninflamed areas in the rat model suggest a tissue gradient of soluble inducer(s), possibly cytokines.

Animals↗
PubMed2000

[Successful therapy of hepatorenal syndrome with norepinephrine].

A 39-year-old female with alcoholic cirrhosis was admitted with signs of an alcoholic hepatitis. Within one week a hepatorenal syndrome (HRS) (Creatinin 5.83 mg/100 ml, Harnstoff 235 mg/100 ml) evolved in the absence of additional causes. She had a diminished water (urine volume 31 ml/h) and sodium excretion (10 mmol/l). Urine flow was increased to 131 ml/h by plasma expansion with i.v. infusion of volume and albumin and with infusion of dopamine (3 micrograms/kg/min) and, as there was no diuretic pretreatment and thus, no HRS secondary to diuretic treatment, furosemide (500 mg/24 h). However, impairment of renal function remained unchanged with this therapy. Therefore, norepinephrine (NE) therapy was initiated. A dosage of 0.1-0.12 microgram/kg/min was necessary to achieve the desired increase in the mean arterial pressure of 10-20 mm Hg. During the NE infusion the urine volume increased further to 231 ml/h, the sodium excretion raised to 44 mmol/l, and serum levels of creatinine and urea decreased to 1.91 mg/100 ml and 141 mg/100 ml, respectively. With recovering liver function the NE infusions could be discontinued after 5 days without recurrence of a HRS until discharge after 3 weeks. Beside the vasopressin analogon ornipressin, the combination of norepinephrine and dopamine seems to be useful for the therapy of HRS. Norepinephrine has the advantage of an easy accessibility in ICUs and seems to exert less side effects.

Adult↗