Biomedical subjects
B Kommerell
Publications and source records attributed to B Kommerell.
[Studies on hypertriglyceridemia in liver diseases by means of measurements of hepatic triglyceride lipase and plasma lipoprotein lipase activity in the heparinized plasma].
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[Determination of total bile acids as a routine test for the evaluation of liver diseases].
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[Amounts, synthesis and turnover of sulfated and non-sulfated bile acids in patients with cholestasis].
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[Antibodies against HBs antigen in diabetics].
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[Treatment of hepatic coma by means of hemoperfusion].
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Intramural hematoma of the esophagus: a complication of carbon tetrachloride intoxication with acute renal failure.
Following a period of prolonged severe vomiting, an intramural esophageal hematoma could be demonstrated by endoscopy and by X-ray in a 21 year old patient with hepatic and renal failure after exposure to carbon tetrachloride. The hematoma resolved spontaneously. The intramural hematoma is thought to have developed from a microdissection of the esophageal wall in the presence of a hemorrhagic diathesis.
[Attempts at transmission of HBs-Ag positive viral hepatitis to rats and mini-pigs].
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A radioimmunoassay to determine the subtypes D and Y of the hepatitis-B surface antigen.
A radioimmunologic test system for determining the subtypes D and Y of the hepatitis-B surface antigen (HBs-Ag, Australia antigen, HAA) is described. This technique uses the immunoadsorption principle. The antigen to be subtyped is incubated with an antiserum which contains (125)I-labeled antibodies to the antigenic determinants a, d, and y. The specificity of the antibody which is not consumed in forming the antigen-antibody complex is determined by absorption on agarose to which HBs-Ag of subtypes D and Y is coupled. This specificity permits conclusions as to the subtype of the hepatitis-B surface antigen which is being investigated.
[Serum transaminases and bile acid concentrations in the serum of patients with biliary calculi during treatment with chenodeoxycholic acid].
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[Induction and activation of bile acid glucuronyl transferase in rat liver microsomes].
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[Proceedings: Clinical and epidemiological relevance of the subtypes D and Y of hepatitis-B-surgace-antigen].
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[Epidemiolgical significance of HBs-antigen subtypes D and Y in the Heidelberg area].
The HGsantigen subtypes D and Y were determined radioimmunologically in 220 HGsAg-positive patients from the Heidelberg area. The subtype D was significantly more frequent (D = 68%) in patients with chronic liver diseases (n = 45) and in healthy HGsAg carriers (n = 32) than in patients with acute viral hepatitis B (n = 143, D = 41%). The subtype distribution in patients with acute viral hepatitis was not constant in the years 1970--1974. An antigen drift from subtype D to subtype Y was shown in healthy HBsAg carriers from 1971 to 1974. The differing distribution of subtypes in persons with transient and persistent HGsAg finding can be explained unequivocally by the altered epidemiological situation at the time of the infection.
Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis.
In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.
A new radioimmunoassay for demonstrating the antibody to hepatitis-B-surface-antigen(HBs-Ag).
A new radioimmunological system for demonstrating the antibody to hepatitis-B-surface-antigen (HBS-Ag) based on the immunoadsorption principle is described. The optimal conditions for the test are given. False-negative and false-positive results could be excluded by specificity tests on sera from 100 voluntary blood donors. The sensitivity of the system is comparable to that of other more expensive radioimmunological methods.
Letter: Clinical significance of HBsAg subtypes D and Y in acute viral hepatitis B.
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[Proceedings: Elevation of transaminases following treatment with chenodeoxycholic acid: dependence on chenodeoxycholic acid dosage and on serum chenodeoxycholic acid concentration].
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Increased sulfation of lithocholate in patients with cholesterol gallstones during chenodeoxycholate treatment.
Chenodeoxycholate was administered to 13 patients with cholesterol gallstones. During the treatment period the bile composition changed markedly. Chenodeoxycholate increased from 42.9% of the total bile salts before treatment to 79.3% after 8 weeks of treatments. Ursodeoxycholate increased from 2.3 to 12.6% and lithocholate from 1.1 to 3.3%. In contrast, cholate decreased from 40.3% of the total bile salts to 3.1% and deoxycholate decreased from 12.5 to 2.5%. Less than 5% of chenodeoxycholate, ursodeoxycholate, cholate and deoxycholate in bile were sulfate esters. In contrast, considerable amounts of lithocholate were sulfated. The sulfation of lithocholate increased from 32.8% of the total lithocholate before treatment to 73.9% after 8 weeks of treatment. Sulfated lithocholate is more rapidly eliminated in feces and urine than the nonsulfated compound. Furthermore, sulfated lithocholate is less toxic. Therefore, the increase in the sulfation of lithocholate observed in most of our patients represents a protective mechanism.