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Biomedical subjects

W Gerok

Publications and source records attributed to W Gerok.

At least 307 records · Page 17Linked to original sources
PubMed1982

Follow-up of treated adult celiac disease: clinical and morphological studies.

A follow-up study of 18 patients with celiac disease is reported. Adherence to the diet, blood chemistry and serum amino acid concentration were investigated in all patients. In addition, HLA blood group typing was performed. Ten patients agreed to undergo jejunal biopsy, xylose test and X-ray of the small intestine. The jejunal mucosa showed no complete restitution even in patients on a strict diet and function tests were abnormal, too. In this study HLA typing demonstrated an association with HLA-B8, HLA-DR3, and HLA-DR7. The results of the follow-up study are discussed with special reference to therapeutic aim and definition of therapeutic success of the gluten-free diet. In addition, a case of jejunal adenocarcinoma complicating celiac disease is presented.

Adenocarcinoma↗
PubMed1982

[Immunosuppressive therapy in patients with HBeAg-positive chronic active hepatitis B?].

The course of HBsAg-positive chronic active hepatitis was followed in 36 patients who were treated by immunosuppression and in 45 controls by means of serial determinations of HBeAg titers and by repeated biopsies of the liver. In the treated group remission occurred in 52% (HBeAg negative) resp. 48% (HBeAg positive); in the control group these percentages were almost identical, that is to say 61% resp. 41%. During therapy 5 out of 9 HBeAg positive patients and 7 out of 12 HBeAg negative patients developed cirrhosis of the liver as compared to 5 resp. 10, and 2 resp. 12 patients in the control group. Judging from these results it seems unlikely, that the course of HBsAg positive, chronic-active hepatitis in patients, whose serum shows a positive HBeAg titer by immunodiffusion, might be influenced in a positive way by immunosuppressive therapy.

Adolescent↗
PubMed1982

[Therapy of hepatic encephalopathy. Changes in the cerebrospinal fluid concentration of catecholamine neurotransmitters, ammonia and amino acids in the course of an infusion treatment with branched-chain amino acids].

Infusions containing branched-chain amino acids have recently been used for the therapy of hepatic coma. Their mode of action was attributed to a reduction in the intracerebral concentrations of the aromatic amino acids with resultant normalization of the neurotransmitters noradrenaline, dopamine and serotonin, synthesized from these amino acids. In order to further clarify this therapeutic mechanism an infusion solution consisting of branched-chain amino acids and ammonia-reducing amino acids was administered to patients with porto-systemic encephalopathy. The amino acid pattern, the ammonia in plasma and liquor, and the neurotransmitters noradrenaline, adrenaline and dopamine, in the liquor were determined before and after the course of treatment. Our studies show that the therapeutic effect of branched-chain amino acids in the therapy of hepatic encephalopathy is based on an effective intracerebral reduction of the ammonia concentration by 61%. The actual concentrations of the neurotransmitters were not significantly modified by the therapy. This opens to question the hypothesis that the neurotransmitters are responsible for the development of hepatic encephalopathy.

Amino Acids↗
PubMed1982

[Extraintestinal complications of Crohn disease, demonstrated in a patient].

A patient with different extraintestinal complications of Crohn's disease is demonstrated. The case allows a discussion of frequency and importance of such complications in Crohn's disease. Vitamin-und trace element deficiency, protein loss and renal complications are the main complications. Determination of vitamin and trace elements may early detect beginning extraintestinal complications and may induce a corresponding therapy.

Crohn Disease↗
PubMed1981

[Pathogenic significance of bile acids (author's transl)].

Because of their amphiphilic properties, bile acids have important physiological functions. However, they can also be pathogenetically active. Some recent findings on the biochemistry and enterohepatic circulation of bile acids are presented. In contrast to the adult liver where the only primary bile acids formed are cholic- and chenodeoxycholic acid, the foetal liver is able to synthesise a variety of "atypical" bile acids. Under certain circumstances, a retrograde differentiation is possible in the adult. The very effective transport systems in gut and in the sinusoidal and canalicular membrane of the liver cell limit the bile acids almost exclusively to the enterohepatic circulation. During transport in blood, through biomembranes and in the liver cytosol, bile acids are bound to carrier proteins. The carrier has been detected using photoaffinity labelling. Following biotransformation (sulphation and glucuronidation) pathogenetically active bile acids can be converted into derivatives which can be rapidly eliminated. Disturbances of these mechanisms result in functional defects and diseases. The pathological significance of bile acids in hepato-biliary diseases is represented with regard to the cholestatic and proliferative effect of individual bile acids. The significance of bile acids in chologenic diarrhea, steatorrhea and enteral hyperoxaluria are presented as examples of the pathogenetic effects of bile acids on the gut. In these diseases it is possible to recognise the specific effects of certain bile acids on the colon mucosa. Recent studies have demonstrated that bile acids are possibly of pathogenetic significance in the case of epidemiologically proven relationship between colon carcinoma and high fat, high cholesterol and low fibre diets.

Bile Acids and Salts↗
PubMed1981

[Approaches to a selective chemotherapy of hepatocellular carcinoma (author's transl)].

1. An improvement of the chemotherapy of hepatocellular carcinoma with adriamycin or 5-fluorouracil and a reduction of side effects has been achieved by intra-arterial administration of the drugs. This treatment provides a somewhat extended survival but no cure. 2. The treatment of hepatocellular carcinoma in patients by reduction of an inactive precursor of a cytocidal alkylating agent by azoreductase of the tumor showed no therapeutic effect. 3. A selective hepatocellular uptake of drugs coupled to asialoglycoproteins has been described. An application of this concept for the chemotherapy of hepatocellular carcinoma seems doubtful since a loss of binding proteins for desialylated glycoproteins during experimental hepatocarcinogenesis has been demonstrated. 4. The increased uptake of 5-fluorouridine in hepatomas after induction of a tissue-specific depletion of uridine 5'-triphosphate and cytidine 5'-triphosphate provides an effective experimental chemotherapy with limited side effects. A clinical use of this new concept for the chemotherapy of hepatocellular carcinoma may serve as a useful approach.

Antineoplastic Agents↗
PubMed1981

[Different effect of taurolithocholate and chenodeoxycholate on structure and function of isolated hepatocytes (author's transl)].

Alterations of cellular membranes under the influence of bile acids seem to be of pathophysiological importance in cholestasis. The effect of taurolithocholic acid (TLCA) and chenodeoxycholic acid (CDCA) on membrane structure and release of cellular enzymes was studied on isolated rat hepatocytes. The response of urea synthesis to glucagon was used as a parameter of membrane function. The threshold dose of TLCA, marked by rapidly increasing enzyme release, was about 100 micrometers, whereas that of CDCA was between 500 and 1,000 micrometers. Addition of albumin (1 g-%) increased the threshold dose of CDCA; this occurred for TLCA only 8 g-%. Electron-microscopical alterations of the endoplasmic reticulum and submembranous areas were found with concentrations below these threshold doses even in the presence of albumin. These alterations are interpreted as disturbance of cellular transport and energy metabolism. TLCA inhibited glucagon response of cells in concentrations below 100 micrometers. These results demonstrate an influence of the bile acids studied on structure and function of liver cell membranes, which may be of importance in the pathogenesis of cholestasis. The rough endoplasmic reticulum could be another cellular structure which is affected by these bile acids.

Animals↗
PubMed1981

[T-lymphocyte activation. Studies on the function of mediator proteins (author's transl)].

The functions of several mediator proteins involved in the T-cell blastogenesis have been investigated 1. Newly described is the Plasmatic Human IL-2 Inducing Protein (PHILIP), a glycoprotein from human serum with a molecular weight of about 85,000 D. Its presence is mandatory for the synthesis and/or secretion of Interleukin-2 (T-cell growth factor). The mediator protein can be distinguished from other known serum glycoproteins (e.g., transferrin and plasminogen) by affinity chromatography. Desialylation completely abolishes its biologic activity. 2. PMSF- and DFP-treatment of conditioned culture medium inhibit the blastogenesis in the peripheral mononuclear blood-cell fraction. However, the growth of a permanent T-cell line in the inhibitor-treated medium is not affected. This indicates the existence of a blastogenic factor with serine-protease activity.

Acute Disease↗
PubMed1981

Concanavalin A, a receptor protein with apparently co-operative binding characteristics.

Laser nephelometry is a suitable technique for the quantitative determination and differentiation of both lectins and glycoconjugates in the low-picomolar range. Simultaneously this method renders possible investigations on the specificity and mode of interaction between lectins and different ligands. The results demonstrate that the degree of co-operativity between concanavalin A and the respective glycoconjugate is dependent on the presence of hydrophobic binding sites and can be substantially altered by conformational changes of the ligand. The transition from apotransferrin to Fe3+-transferrin induces a transformation of the sigmoidal-shaped binding curve to a hyperbolic one. Hence, at low concentrations, Fe3+-transferrin is bound far better than apotransferrin, whereas maximal binding is nearly identical. After removal of N-acetylneuraminate, concanavalin A is less efficient in differentiating between the Fe3+-charged and Fe3+-free (apo) forms of transferrin.

Apoproteins↗
PubMed1981

[Therapy of aminoacid and protein metabolism disturbances in liver disease (author's transl)].

1. The role of the liver in synthesis and metabolism of proteins, in the metabolism of certain aminoacids, and in urea synthesis is described. 2. In the liver disease protein synthesis may be reduced. The activity of lysosomal proteases is enhanced during acute hepatitis and in cirrhosis. Diseases of the liver may be associated with various derangements in the metabolic pathways of particular aminoacids. Synthesis of urea is decreased in chronic liver disease. 3. Nutrition for patients with chronic liver disease needs to include sufficient calories and has to be well balanced. Parenteral nutrition and diet in patients with edema and ascites deserves special attention. Dietary treatment of patients with cirrhosis of the liver and impending or already existing hepatic encephalopathy is outlined.

Amino Acids↗
PubMed1980

Spontaneous cholecystocolonic fistula: a model situation for bile acid diarrhea and fatty acid diarrhea as a consequence of a disturbed enterohepatic circulation of bile acids.

Fistulas between the biliary and gastrointestinal tract complicate 12% of cases with cholecystitis. Communications of the biliary tract occur with decreasing frequency into the duodenum, colon and stomach. Clinical symptoms of cholecysto-colonic fistulas are chills and temperature elevation indicating ascending cholangitis. As bile acids bypass the small intestine, diminished fat absorption results. The unusual amount of bile acids in the colon delays water absorption, causing bile acid diarrhea. A pneumocholangiogram is seen in only 50% of the cases. Barium enema will visualize the fistula most often.

Aged↗
PubMed1979

Solid-phase radioimmunoassay for hepatitis Be antigen (HBeAg).

A solid-phase radioimmunoassay was developed for the detection of HBeAg and anti-HBe in sera or serum fractions. HBe/sAg positive sera, partially purified HBeAg, partially purified HBsAg, and HBe/sAg negative sera were polymerized in polyacrylamide and compared for their ability to bind 125I-IgG (anti-HBe). Only gels containing HBeAg reacted specifically with the iodinated antibody. The specificity of the binding was confirmed by blocking and inhibition tests using anti-HBe, HBeAg, HBsAg, and negative control sera. The radioimmunoassay allows the specific and quantitative detection of HBeAg and anti-HBe even in the presence of detergents and high salt concentrations.

Binding, Competitive↗
PubMed1979

Activities of urea-cycle enzymes in chronic liver disease.

The activities of urea-cycle enzymes were measured in liver biopsies of patients suffering from chronic-persistent hepatitis (CPH), chronic-active hepatitis (CAH) and liver cirrhosis. Most of the activities of urea-cycle enzymes did not differ in the case of CPH as compared to controls. Chronic-active hepatitis and liver cirrhosis are associated with a significant (p less than 0.05) decrease of enzyme activity as compared to normal persons. Most of the urea-cycle enzymes are significantly decreased in patients with CAH in comparison with CPH. No significant differences can be demonstrated in the case of CAH as compared to patients with complete cirrhosis. In conclusion, progression of chronic liver disease is associated with increasing alterations of enzyme activities catalyzing a liver specific metabolic pathway. The decrease of the activities of the key enzymes of the urea cycle (Carbamylphosphate-Synthetase and Arginino-succinate-Synthetase) is nearly identical both in CAH and liver cirhosis, although CAH may be a reversible disease. Therefore, marked alterations in the metabolic pathway of ammonia detoxification seem to preceed the histological manifestation of irreversible liver damage.

Arginase↗
PubMed1979

[Cell receptor defects as the cause of endocrine and metabolic diseases (author's transl)].

The following pathogenetic mechanisms, exemplified by three diseases (diabetes mellitus, hyperthyroidism and familial hypercholesterolemia), are discussed: 1. The impaired interaction between a chemical signal and a specific receptor can be the cause of a disease. 2. The cause for an imparied interaction can be a defect of the receptor, i.e., a reduced number of receptors or an altered receptor affinity, or a wrong signal. 3. A defect of the receptor can be induced by exogenous influences or it can be determined genetically. 4. The receptor and the signal can be modified by their interaction: the number of receptors is reduced by high concentrations of the chemical signal or by increased degradation due to binding to the receptor. 5. The receptor concept opens new perspectives for the pathogenetic understanding, diagnosis and therapy of some diseases.

Adult↗