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Biomedical subjects

W Stremmel

Publications and source records attributed to W Stremmel.

At least 19 recordsLinked to original sources
PubMed1992

[Diagnosis and therapy of hepatorenal syndrome].

Hepatorenal syndrome (HRS) is defined as severe vasoconstriction of renal cortical vessels with critical impairment of glomerular filtration rate, initiated by deteriorating liver function. In addition, systemic vasodilation, predominantly of splanchnic vessels is present. Although the urinary status is basically normal, during the course of HRS kidneys are loosing their ability to concentrate and at an urinary production rate of less than 100 ml/day the urinary osmolarity and Na(+)-concentration drops significantly. Because HRS can not be improved by conventional medical treatment regimens, its prophylaxis is of major importance. Besides improvement of liver function and avoidance of drastic volume depletion (bleeding, paracentesis, high dose diuretic therapy) and sepsis, the therapeutic goal is to reverse systemic vasodilation and to achieve a concomitant relaxation of renal arteries. Expansion of plasma volume and application of renal vessel dilating prostaglandins is one strategy. Alternatively, therapy with ornipressin was shown to be successful, which improves renal perfusion and normalizes the hyperdynamic state of systemic circulation.

Algorithms↗
PubMed1992

Identification and characterization of a monoclonal antibody to the membrane fatty acid binding protein.

A monoclonal antibody to the rat liver membrane fatty acid binding protein (MFABP) was prepared by immunizing mice with purified MFABP isolated from solubilized rat liver plasma membrane proteins by oleate-agarose affinity chromatography technique. The monoclonal antibody K15/6 identified a single 40 kDa protein in rat liver plasma membranes with pI values of 8.5, 8.8 and 9.0, which is identical to the authentic MFABP, but clearly distinct from rat mitochondrial GOT. The antibody K15/6 selectively inhibited cellular influx as well as membrane binding of fatty acids, but not of cholesterol or vitamin E. The same antibody was used in immunofluorescence, ELISA and Western blot analysis to determine the subcellular and organ distribution pattern of MFABP. The protein was identified in rat liver plasma membranes and mitochondria, but in no other cell compartment. It was detectable in homogenates of rat liver but not in homogenates of other organs. Therefore, the monoclonal antibody K15/6 represents an organ specific antibody to MFABP which reveals inhibitory action on membrane binding/transport of fatty acids.

Animals↗
PubMed1992

Testosterone treatment of men with idiopathic hemochromatosis.

Patients with chronic liver disease usually exhibit low plasma levels of testosterone with loss of libido and potency; this is also valid in male patients suffering from idiopathic hemochromatosis (IHC), in whom nowadays the diagnosis is made at an earlier age. Therefore, the effect of testosterone treatment was studied in 10 patients with IHC. After the application of 250 mg testosterone enanthate i.m., the plasma testosterone (from 2.4 +/- 1.9 to 20.1 +/- 7.4 ng/ml) and estradiol (from 17.4 +/- 6.3 to 38.5 +/- 14.2 pg/ml) levels increased significantly. The rise of estradiol was in the range of controls and smaller than reported in other chronic liver diseases. In a long-term study, 250 mg testosterone enanthate was given 4-weekly for 33-96 months to 5 patients with IHC. General well-being, libido, and potency recovered almost immediately. Over a treatment period of 27.3 patient years, symptoms of hyperestrogenism (gynecomastia) or (portal vein) thrombosis were not seen, both of which had been described in patients with alcoholic liver cirrhosis. There was no deterioration of liver function. The effect of testosterone treatment on the patients' well-being and plasma hormone concentrations remained unchanged over the whole period of testosterone treatment. Thus, in male patients with IHC and lowered plasma testosterone, treatment with testosterone enanthate may be instituted. Because of the positive effects on general well-being, liver regeneration capacity, and potency, testosterone should especially be administered to younger subjects suffering from IHC.

Adult↗
PubMed1992

Prospective randomized controlled trial of sequential treatment with corticoids and alpha-interferon versus treatment with interferon alone in patients with chronic active hepatitis B.

OBJECTIVES: A randomized controlled trial was conducted to prospectively compare the efficacy of sequential treatment with corticoids and alpha-interferon versus treatment with interferon (IFN) alone in patients with chronic hepatitis B. METHODS: Sixty patients with chronic active hepatitis B and positive serum HBV-DNA were randomized into two treatment groups (n = 20, respectively) and one control group (no treatment; n = 20). In one treatment group, patients received first an oral corticoid (2 weeks 40 mg/day and further 2 weeks 20 mg/die prednisolone); thereafter interferon-alpha (Intron A, Essex) was given as three subcutaneous injections of 2 million units per week for 3 months. In patients in whom therapy did not eliminate HBe-Ag and HBV-DNA two months after its end, a similar sequential treatment was given with the same corticoid dose but a higher IFN dose of 5 MU. In the other treatment group patients were given three subcutaneous injections of 5 MU IFN per week for 4 months. The sequential corticoid/IFN treatment at a dose of 3 x 2 MU IFN resulted in seroconversion of HBe-Ag in only 4 of 20 patients (20%). Of the remaining 16 patients 14 subjects received a repetitive corticoid/IFN therapy with the same corticoid dose but with a 3 x 5 MU dose of IFN. RESULTS: With the higher IFN dose, 6 of 14 patients had a seroconversion of HBe-Ag. Therapy with 3 x 5 MU IFN without prior corticoids resulted in a seroconversion in 8 of 20 patients (40%). Calculated for both doses, the sequential corticoid/IFN therapy eliminated HBe-Ag and HBV-DNA in 10/20 patients (50%); therapy with IFN alone was almost as effective (40% seroconversion) (p > 0.05 for comparison of seroconversion rates by chi 2-test). Seroconversion of HBe-Ag and elimination of HBV-DNA occurred in parallel and were associated with a decrease of serum transaminases and a regression of inflammatory activity on rebiopsy. In the control group there was no spontaneous seroconversion of HBs-Ag, HBe-Ag or HBV-DNA. CONCLUSIONS: The present results show that in many patients who failed to respond to a sequential therapy with corticoids and 2 MU IFN, the higher IFN dose of 5 MU effectively eliminated HBe-Ag and HBV-DNA. Sequential corticoid/IFN therapy and therapy with IFN alone eliminated HBe-Ag and HBV-DNA in a similar percentage of patients. Further statistical analysis showed that, in particular, patients with low transaminases benefit from prior corticoid treatment. In all groups, patients with low serum HBV-DNA and a short history of infection had the best treatment results.

Adolescent↗
PubMed1992

[Liver function tests in a clinical comparison].

Various liver function tests were evaluated in regard to a quantitative estimation of the impairment of liver function related to the Child-Pugh classification in 32 patients with cirrhosis. Only the ICG-test revealed significant differences between healthy subjects and cirrhotic patients in stadium Child A, B and C. When ICG-dye retention values were plotted as a function of the individual score units of the Child-Pugh classification, a linear relationship with a correlation coefficient of 0.7 was obtained. In contrast to the ICG-test, the MEGX- and galactose elimination capacity (GEC)-test as well as static parameters of liver function (cholinesterase activity, prealbumin concentration, coagulation factor V and VII) resulted in less significant differentiation of the various Child classes. The MEGX-test, GEC, concentration of prealbumin, coagulation factor V and VII were only weakly correlated to the score units of the Child-Pugh index. The results of this study indicate that of all evaluated parameters only the ICG-test is suitable for objective and graduated analysis of liver function in patients with cirrhosis.

Cholinesterases↗
PubMed1992

[Pathogenesis of Wilson's disease].

Wilson disease is due to a genetically determined impairment of copper excretion from liver into bile resulting in copper overload of the organism. The chromosomal defect and the primary defect of copper metabolism is not yet defined. When during the course of the disease the cytoplasmatic copper binding sites of hepatocytes are saturated, excess of "free" copper is accumulating. It induces liver cell damage and necrosis followed by the development of fibrosis and cirrhosis. The accumulation process of excess free copper in hepatocytes is accompanied by a redistribution into the lysosomal compartment of the cells as well as by release of free copper into blood. This increase of the free serum copper concentration leads during the course of the disease to an elevated copper burden of other organs. This results in a variety of symptoms, of which liver disease and neurologic disturbances are of major significance in regard to clinical presentation and prognosis of the patients.

Ceruloplasmin↗
PubMed1991

Wilson disease: clinical presentation, treatment, and survival.

OBJECTIVE: To evaluate the diagnostic features, clinical course, and overall long-term survival of patients with Wilson disease. DESIGN: Retrospective cohort study with a mean follow-up period of 14.2 years. SETTING: A university medical center and a community hospital. PATIENTS: Fifty-one consecutive patients with Wilson disease were evaluated between 1957 and 1989. INTERVENTIONS: Patients were treated with D-penicillamine (600 to 1800 mg/d). Two patients with end-stage liver disease had liver transplantation. MAIN RESULTS: Initial symptoms occurred at a mean age of 15.5 years. At diagnosis, the most common neurologic signs were dysarthria, tremor, writing difficulties, and ataxia followed by hypersalivation and headache. Somatic symptoms included abdominal pain, hepatomegaly, splenomegaly, cirrhosis of the liver, and thrombocytopenia. The mean serum concentrations of ceruloplasmin and copper were 44 mg/L and 4.7 mumol/L, respectively. The mean basal urinary copper excretion was 5.5 mumol/d, and the mean hepatic copper concentration was 19.6 mumol/g dry weight. Free serum copper concentration (mean, 2.7 mumol/L) was a reliable indicator of disease and was useful in assessing the effectiveness of therapy (values less than 1.6 mumol/L). Treatment with D-penicillamine improved most of the hematologic and neurologic abnormalities but had little effect on hepatomegaly and splenomegaly and did not reverse cirrhosis. Two patients died of fulminant hepatic failure during the observation period, whereas two others with end-stage liver disease had successful liver transplantation and remain asymptomatic. Long-term survival of patients with Wilson disease was similar to that of age- and sex-matched controls. CONCLUSION: Our results suggest that long-term treatment of patients with Wilson disease with D-penicillamine can relieve symptoms and improve prognosis.

Adolescent↗
PubMed1991

Antiarrhythmic drugs impair hepatic uptake and secretory function by different mechanisms in the isolated perfused rat liver.

In the present study the effect of various antiarrhythmic drugs on hepatic perfusion parameters, uptake capacity of organic anions and biliary secretion using the isolated perfused rat liver was examined. Infusion of verapamil (VP), diltiazem, N-propyl-ajmaline (NPAB), and quinidine at pharmacological doses induced consistently a 1.4-1.6-fold increase in portal pressure accompanied by a approximately 60% decrease in bile flow and a approximately 65% inhibition of biliary taurocholate (TC) excretion. Furthermore, hepatic uptake of oxygen, bromosulphthalein (BSP), and TC was significantly reduced. All these effects were dose-dependent and reversible upon withdrawal of the drugs. Studies of the hepatic circulation using a Trypan blue staining technique demonstrated a patchy perfusion pattern during infusion of the antiarrhythmic drugs as compared to the homogenously stained control organ. The hemodynamic alterations and the impairment of the hepatic initial uptake function could be entirely prevented by concomitant administration of the vasodilator papaverine. Bile flow and biliary TC excretion, however, were still inhibited under these conditions. The present results indicate that antiarrhythmic drugs produce cholestasis in the isolated perfused rat liver independently of their adverse effect on hepatic hemodynamics.

Animals↗
PubMed1991

Fatty acid uptake in normal human myocardium.

Fatty acid binding protein has been found in rat aortic endothelial cell membrane. It has been identified to be a 40-kDa protein that corresponds to a 40-kDa fatty acid binding protein with high affinity for a variety of long chain fatty acids isolated from rat heart myocytes. It is proposed that this endothelial membrane fatty acid binding protein might mediate the myocardial uptake of fatty acids. For evaluation of this hypothesis in vivo, influx kinetics of tracer-labeled fatty acids was examined in 15 normal subjects by scintigraphic techniques. Variation of the plasma fatty acid concentration and plasma perfusion rate has been achieved by modulation of nutrition state and exercise conditions. The clinical results suggest that the myocardial fatty acid influx rate is saturable by increasing fatty acid plasma concentration as well as by increasing plasma flow. For analysis of these data, functional relations describing fatty acid transport from plasma into myocardial tissue in the presence and absence of an "unstirred layer" were developed. The fitting of these relations to experimental data indicate that the free fatty acid influx into myocardial tissue reveals the criteria of a reaction on a capillary surface in the vicinity of flowing plasma but not of a reaction in extravascular space or in an unstirred layer and that the fatty acid influx into normal myocardium is a saturable process that is characterized by the quantity corresponding to the Michaelis-Menten constant, Km, and the maximal velocity, Vmax, 0.24 +/- 0.024 mumol/g and 0.37 +/- 0.013 mumol/g(g.min), respectively. These data are compatible with a nondiffusional uptake process mediated by the initial interaction of fatty acids with the 40-kDa membrane fatty acid binding protein of cardiac endothelial cells.

Animals↗
PubMed1991

Epidemiology, clinical course and treatment of chronic viral hepatitis.

Chronic hepatitis may take the form of a hepatitis B infection, a delta virus infection, or a non-A, non-B hepatitis including hepatitis C. All the viruses involved are transmitted predominantly by parenteral or sexual routes. New insights into the structure of the hepatitis B virus (HBV) and the immune response mechanisms of the organism permit a clear definition of the replicative state of the virus, and allow predictions to be made about the outcome of the disease. Development of cirrhosis and hepatocellular carcinoma are the major complications associated with impaired life expectancy. Recently, the hepatitis C virus (HCV) was identified as the agent responsible for most cases of chronic non-A, non-B hepatitis. The development of an assay for the detection of HCV-antibodies facilitated the diagnosis of this type of hepatitis. Moreover, the use of screening tests for hepatitis B and hepatitis C in blood donors will decrease the risk of acquiring hepatitis via contaminated blood products. Treatment of chronic hepatitis B and C with alpha-interferon has shown promising results. However, the dosage schedule, the period of treatment, and the selection of patients needs to be evaluated in further studies.

Hepacivirus↗