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Biomedical subjects

C Niederau

Publications and source records attributed to C Niederau.

At least 73 records · Page 4Linked to original sources
PubMed1997

Solitary hepatic lesions with a hypoechoic rim: value of color Doppler sonography.

OBJECTIVE: A hypoechoic rim around a focal liver lesion as revealed by conventional sonography may be present in malignant liver lesions as well as in benign liver lesions. This study evaluated the potential of color Doppler sonography in differentiating various focal liver lesions with a hypoechoic rim. CONCLUSION: Color Doppler sonography may be helpful in distinguishing focal nodular hyperplasia (FNH) from other focal liver lesions. The characteristic finding of blood flow within the hypoechoic rim of FNH is most likely caused by small vessel abnormalities that have previously been described for FNH.

Case-Control Studies↗
PubMed1997

Vitamin E improves the aminotransferase status of patients suffering from viral hepatitis C: a randomized, double-blind, placebo-controlled study.

UNLABELLED: Vitamin E has been shown to protect against liver damage induced by oxidative stress in animal experiments. Based on our previous findings of diminished vitamin E levels in patients suffering from viral hepatitis, we treated 23 hepatitis C patients refractory to alpha-interferon therapy with high doses of vitamin E (2 x 400 IU RRR-alpha-tocopherol/day) for 12 weeks. STUDY DESIGN: pro-spective randomized double-blind crossover design. Clinical parameters including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined for monitoring the disease state, in parallel vitamin E plasma levels and plasma lipids were determined. The plasma levels of the alpha-tocopherol were increased about 2-fold in all 23 patients. In 11 of 23 patients the clinical parameters indicative of liver damage were improved during the phase of vitamin E treatment (48% responders). ALT levels in responders were lowered by 46% and AST levels were lowered by 35% after 12 weeks of vitamin E treatment. Cessation of vitamin E treatment was followed by a rapid relapse of ALT and AST elevation, whereas retreatment led to a reproducible ALT decrease by 45% and AST decrease of 37% after a 6 months followup. Since vitamin E is non-toxic even at elevated doses ingested over extended periods, we suggest the treatment of patients refractory to alpha-interferon therapy suffering from hepatitis C with vitamin E as a supportive therapy.

Alanine Transaminase↗
PubMed1997

[Hepatocellular carcinoma in Germany. Epidemiology, etiology, clinical aspects and prognosis in 100 consecutive patients of a university clinic].

Chronic hepatitis C and B are the main causes of hepatocellular carcinoma (HCC) worldwide. Little is known about the etiology of HCC in Germany which is regarded as a low-prevalence area for viral hepatitis C (HCV) and B (HBV). To assess the etiologic factors of HCC in Germany we have retrospectively analyzed the records of 100 consecutive patients with hepatocellular carcinoma in our clinic. HCC-patients with documented status on HCV/HBV-infection and daily alcohol intake (n = 55) had HCV antibodies in 53%, HBs-Ag in 20%, isolated chronic alcohol abuse in 11% and genetic hemochromatosis in 2%. In 13% of the HCC-patients no risk factor could be identified. Coinfections with HCV and HBV were not observed. Liver cirrhosis was present in 90% of the HCC-patients. In histologically confirmed HCC (n = 71) serum alpha-fetoprotein level was normal (< 8.5 ng/ml) in 20%, moderately elevated (8.5-300 ng/ml) in 48% and considerably elevated (> 300 ng/ml) in 32% of the patients. Only 31% of all patients presented with small single lesions (< or = 5 cm) without evidence for extrahepatic metastases or portal vein thrombosis. Only 30% of the HCC-patients could be treated with a curative intention (28 hepatic resections, one orthotopic liver transplantation). Patients who underwent resection had cumulative 6-month, 1-year, 2-year and 3-year survival rates of 83.8%, 65.9%, 54.3% and 24.8% respectively. Median survival time after resection was 24.8 months compared with 5.8 months in symptomatically treated patients with unresectable HCC (n = 39). Patients with hepatitis C-associated HCC were significantly older than patients with hepatitis B-associated HCC (mean values: 63.2 vs. 54.2 years). Frequency of cirrhosis, tumor stage, alpha-fetoprotein level and prognosis did not differ between groups. In conclusion hepatocellular carcinoma was predominantly associated with chronic HCV-infection. Most patients presented with normal or moderately elevated serum AFP-levels. Prognosis was poor even after hepatic resection.

Adolescent↗
PubMed1996

Long-term follow-up of HBeAg-positive patients treated with interferon alfa for chronic hepatitis B.

BACKGROUND: In patients with chronic hepatitis B, treatment with interferon alfa and the consequent loss of hepatitis B e antigen (HBeAg) from the blood leads to a reduction in inflammatory activity, but the clinical benefits of this treatment have not been established. We evaluated whether HBeAg seroconversion induced by interferon alfa improves clinical outcome. METHODS: We studied prospectively a cohort of 103 patients treated with interferon alfa for chronic hepatitis B; the mean (+/- SD) follow-up was 50.0 +/- 19.8 months. Fifty-three untreated patients served as controls. RESULTS: After treatment with interferon alfa, 53 of 103 patients no longer had detectable HBeAg or hepatitis B virus DNA, although only 10 patients became seronegative for hepatitis B surface antigen (HBsAg) (Kaplan-Meier estimates of cumulative clearance rates at five years, 56.0 percent for HBeAg and 11.6 percent for HBsAg). Of the 53 untreated patients, only 7 spontaneously eliminated HBeAg (28.1 percent at five years), and all remained positive for HBsAg (p < 0.001 for the Comparison with the treated patients, by the proportional-hazards model). During follow-up, 6 of the 103 treated patients died of liver failure, and 2 needed liver transplantation, all 8 were persistently positive for HBeAg. In another eight treated patients, complications of cirrhosis developed; all but one of these patients remained positive for HBeAg. Overall survival and survival without clinical complications were significantly longer in patients who were seronegative for HBeAg after therapy with interferon alfa than in those who remained seropositive (P = 0.004 and P = 0.018, respectively). In a regression analysis, clearance of HBeAg was the strongest predictor of survival. Of the 53 untreated patients, 13 had severe complications (including 4 deaths and 1 need for liver transplantation); all 13 continued to be HBeAg-positive. CONCLUSIONS: In patients with chronic hepatitis B infection, the clearance of HBeAg after treatment with interferon alfa is associated with improved clinical outcomes.

Antiviral Agents↗
PubMed1996

Oxidative injury to isolated rat pancreatic acinar cells vs. isolated zymogen granules.

This study compares the susceptibility of pancreatic acinar cells and zymogen granules against oxidative injury and analyzes the mechanisms involved. Zymogen granules and acinar cells, isolated from rat pancreas, were exposed to a reaction mixture containing xanthine oxidase, hypoxanthine, and chelated iron. Cell function and viability were assessed by various techniques. Trypsin activation was quantified by an Elisa for trypsinogen activating peptide. Integrity of granules was determined by release of amylase. The reaction mixture rapidly generated radicals as assessed by deoxyribose and luminol assays. This oxidative stress caused lysis of granules in a matter of minutes but significant cell death only after some hours. Nevertheless, radicals initiated intracellular vacuolization, morphological damage to zymogen granules and mitochondria, increase in trypsinogen activating peptide, and decrease in ATP already after 5-30 min. Supramaximal caerulein concentrations also caused rapid trypsin activation. Addition of cells but not of granules reduced deoxyribose oxidation, suggesting that intact cells act as scavengers. Caerulein pretreatment only slightly increased the susceptibility of cells but markedly that of granules. In conclusion, isolated zymogen granules are markedly more susceptible to oxidative injury than intact acinar cells, in particular, in early stages of caerulein pancreatitis. The results show that oxidative stress causes a rapid trypsin activation that may contribute to cell damage by triggering autodigestion. Zymogen granules and mitochondria appear to be important targets of oxidative damage inside acinar cells. The series of intracellular events initiated by oxidative stress was similar to changes seen in early stages of pancreatitis.

Animals↗
PubMed1996

Long-term survival in patients with hereditary hemochromatosis.

BACKGROUND & AIMS: The course of hereditary hemochromatosis may depend on the degree of iron overload and the time of therapeutic intervention. This analysis evaluates the impact of early diagnosis and iron removal on survival and complications in hereditary hemochromatosis. METHODS: A Cohort of 251 patients with hemochromatosis was followed up for 14.1 +/- 6.8 years. RESULTS: Survival was reduced in the total group of patients when compared with a matched normal population. Survival in noncirrhotic and nondiabetic patients and in patients diagnosed between 1982 and 1991 was identical with rates expected. Survival was reduced in patients with severe iron overload vs. those with less severe overload. The percentage of early diagnoses increased threefold between 1947 and 1969 to that between 1970 and 1981; there was only a further 20%-25% increase in the last decade. Deaths caused by liver cancer, cardiomyopathy, liver cirrhosis, and diabetes mellitus were increased as compared with expected rates. Liver cancers were associated with cirrhosis and amount of mobilizable iron but not with hepatitis B or C markers. CONCLUSIONS: Prognosis of hemochromatosis and most of its complications, including liver cancer, depend on the amount and duration of iron excess. Early diagnosis and therapy largely prevent the adverse consequences of iron overload.

Adolescent↗
PubMed1996

Diminished plasma levels of vitamin E in patients with severe viral hepatitis.

RRR-alpha-Tocopherol (Vitamin E) was assayed in plasma of 48 patients with viral hepatitis and of 32 healthy controls. In patients with highly elevated serum transaminases (ALT > 100 U/L) vitamin E plasma levels were significantly lower (17.5 +/- 4.8 mumol/L) than in controls (22.7 +/- 4.2 mumol/L, p < 0.01). The vitamin E/lipid ratios (3.12 +/- 0.63 mumol/g) in these patients were 33% lower than those of the controls (4.68 +/- 0.54 mumol/g). The lowered vitamin E levels in patients with acute or chronic viral hepatitis with high activity of disease may be due to free radical-mediated liver injury.

Acute Disease↗
PubMed1996

-Cardiomyopathy as the cause of death in genetic hemochromatosis-.

Hemochromatosis is an autosomal-recessive disease which causes iron-overload of various organs including liver, pancreas and heart. This report analyzes the course of hemochromatosis in two patients (a 28-year-old man and a 57-year-old woman) in whom hemochromatosis was detected because of severe cardiomyopathy. Initial symptoms were edema, anasarca and dyspnea. Further examinations showed pleural effusion, decreased left-ventricular-function, skin pigmentation, diabetes mellitus and liver cirrhosis. Although phlebotomy treatment and iron-chelation therapy with deferoxamine initially resulted in some improvement, both patients died from cardiomyopathy three months after diagnosis. The reports of these two cases underline that hemochromatosis-associated cardiomyopathy is often irreversible if severe congestive heart failure is present. In cardiac decompensation heart transplantation has to be considered as early as possible.

Adult↗
PubMed1996

[Diagnosis and therapy of chronic viral hepatitis].

Recent advances in our understanding of viral hepatitis involve the discovery and further characterization of the hepatitis C virus and the interferon treatment of patients with chronic viral hepatitis. Liver cirrhosis and primary hepatocellular carcinoma can develop after some years of disease. Interferon is the only effective treatment, which may improve symptoms and prognosis in some patients. Long-term responses with termination of viral replication are seen in 40% of patients with hepatitis B and 15-25% of patients with hepatitis C. In some patients complete elimination of the virus occurs. Higher response rates are achievable in subgroups of patients with favourable prognostic constellations. Patients have to be informed about side-effects and risks of interferon therapy. Treatment in uncomplicated cases is performed on an outpatient basis. The present paper reviews diagnosis, indications, contraindications and practical considerations concerning interferon treatment in patients with chronic viral hepatitis.

Hepatitis, Chronic↗
PubMed1995

[Diagnosis and therapy of Gaucher disease].

BACKGROUND: Since 3 years there is an effective enzyme replacement therapy for patients with Gaucher's disease which is the most prevalent sphingolipid storage disease. Also the diagnostic procedures have recently been improved. This study reports about the results of longterm enzyme replacement therapy and the diagnostic workup in 18 patients with Gaucher's disease. PATIENTS AND METHODS: Since June 1991, 18 patients with moderate to severe degree of Gaucher's disease were treated by administration of modified human glucocerebrosidase on regular bases in the University Hospital Düsseldorf. According to the severity of the disease, glucocerebrosidase infusion was performed every 2 weeks. The dosage was individually chosen according to the severity of the disease. RESULTS: Within 3 to 4 months all patients showed an improvement of laboratory findings, of hepatosplenomegaly and of their general well-being. CONCLUSIONS: The advances in our understanding of this disease need to be publicized because an early diagnosis and timely enzyme replacement guarantees almost all patients with the adult type of Gaucher's disease to live a normal life without complaints and complications.

Adult↗
PubMed1995

Effects of C1-esterase inhibitor in three models of acute pancreatitis.

The present studies were done to evaluate the therapeutic potential of C1-esterase inhibitor in three different models of acute pancreatitis: (1) Edematous pancreatitis with acinar cell necrosis was induced by 7-h ip injections of 50 micrograms/kg cerulein in mice; (2) Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet in mice; and (3) Hemorrhagic pancreatitis was induced by retrograde infusion of 0.6 mL 5% sodium-taurocholate into the pancreatic duct in rats. C1-esterase inhibitor was given at 100 mg/kg iv before the onset of pancreatitis and at certain intervals thereafter. The severity of pancreatitis was assessed at various times after its onset by determination of serum amylase, by grading of histological alterations, and by determination of survival (survival determined only in models of hemorrhagic pancreatitis). In some of the models, C1-esterase inhibitor slightly ameliorated the degree of histological alterations; the increase in serum amylase was reduced by C1-esterase inhibitor only in CDE diet-induced pancreatitis. In all three models, C1-esterase inhibitor, however, failed to cause major beneficial effects and also failed to improve survival in taurocholate- and diet-induced pancreatitis. Additional studies in 12 patients with acute pancreatitis showed that C1-esterase inhibitor activity was markedly increased in serum of all patients during the first 9 d of the disease, suggesting that C1-esterase inhibitor behaves like an acute phase protein. Taken together the results from the animal and the human studies, C1-esterase inhibitor appears to only have a limited potential for treatment of acute pancreatitis.

Acute Disease↗
PubMed1995

Influence of ductal pressure and infusates on activity and subcellular distribution of lysosomal enzymes in the rat pancreas.

BACKGROUND & AIMS: Subcellular redistribution of lysosomal enzymes into the zymogen-enriched fraction (cosedimentation) in pancreatic homogenates occurs after different pancreatic injuries and has been proposed to be the trigger event for acute pancreatitis. This phenomenon is now studied in models of biliary pancreatitis. METHODS: The bile-pancreatic duct in rats was either obstructed or retrogradely infused at different degrees of pressure and with solutions of various injurious potential. Controls were untreated or sham operated. Six hours later, the pancreas was analyzed for the total activity of cathepsin B and beta-galactosidase and their distribution among subcellular fractions. RESULTS: In control animals, 17% and 29%, respectively, of these lysosomal enzymes were found in the zymogen fraction. Redistribution occurred after all duct manipulations, including obstruction. In contrast to sham operation and duct obstruction, all modes of duct infusion resulted in marked increases in the total activity of lysosomal enzymes. CONCLUSIONS: Increased lysosomal activity in models of biliary pancreatitis might contribute to acinar injury or represent a cellular repair mechanism. Cosedimentation at a certain extent is a physiological event. Redistribution reflects a uniform response to a range of perturbations, some of which do not cause pancreatitis. Thus, it seems unlikely that redistribution is the trigger event for acute pancreatitis.

Acute Disease↗