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Biomedical subjects

D Müting

Publications and source records attributed to D Müting.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Effect of arginine ketoglutarate on the detoxifying capacity of the liver in cirrhosis of the liver (author's transl)].

According to the present studies it is shown that arginine ketoglutarate in sufficiently high dosage (3x3 g daily by mouth) produces a significant lowering of plasma ammonia and free serum phenols with a high-protein diet in patients with liver cirrhosis, compared to a previous day without this substance. The ammonia reduction can be explained by a significant increase in urea synthesis, measured by the urea nitrogen content of the 24-hour urine. The simultaneous lowering of pathologically raised serum levels of free phenols can be explained by an improved oxidative decomposition of these substances. No stimulation of insulin secretion worthy of note occurred after oral administration of 9 g arginine ketoglutarate.

Adult↗
PubMed1977

[New aspects of the pathogenesis and therapy of alcoholic delirium (author's transl)].

Clinically, and especially biochemically, alcoholic delirium corresponds closely to an incipient but reversible exogenous hepatic coma. The blood levels of ammonia in particular, free phenols and lactate are greatly increased. These same metabolites increase slightly in the blood of persons with healthy livers after a single alcohol loading. The treatment of alcoholic delirium consists of optimal sedation with Distraneurin, which appears to have no side effects on the liver. There is even a lowering of the raised lactate level in the blood after a single administration of Distraneurin. Ammonia and phenols are reduced by ammonia-lowering aminoacids, lactulose and bifidum milk. Most important, however, is strict abstention from alcohol, which alone brings about a rapid improvement of pathological biochemical and morphological liver findings.

Alcohol Withdrawal Delirium↗
PubMed1977

[Clinical picture and therapy of portal-systemic encephalopathy (author's transl)].

The clinical syndrome of portal-systemic encephalopathy is caused by far advanced cirrhosis of the liver in most cases; it is characterized by increasing drowsiness, disturbances of mentation, flapping tremor and hyperreflexia. An early diagnosis can be established by testing writing and drawing abilities. Increased occurrence of spider nevi, a dry, deep red tongue, and hemorrhagic lesions of skin and mucous membranes are symptoms of incipient hepatic insufficiency. The syndrome is initiated in most cases by excessive intake of protein or alcohol, by intestinal bleeding, by diuretics, or by intercurrent infections. Therapy has to include elimination of causes, reduced intake of protein, enemas with acetate buffer solution and oral medication with lactulose, bifidum milk, and certain amino acids in order to lower hyperammoniemia; in serious cases neomycin has to be given. At the same time a normalization of fluid and electrolyte balance has to be achieved; replacement of potassium is especially important, when hypokalemia and alcalosis are present. In general prognosis of portal-systemic encephalopathy however is serious, depending primarily upon the fact, whether or not sufficient functional hepatic parenchyma is present.

Acetates↗
PubMed1975

[Monomeric igM in acute and chronic liver diseases (author's transl)].

Monomeric IgM could be found rather frequently in acute hepatitis and chronic aggressive hepatitis and occasionally also in chronic persistent hepatitis. Earlier it was reported in lympho-proliferative-, autoimmune diseases, some infectious diseases and in cirrhosis of the liver. The occurence of monomeric IgM in chronic aggressive hepatitis correlates with the detection of several autoantibodies (ANA, SMA, RF). The 7S-IgM-test may be used as an easily measurable additional criterium for diagnosis and course of chronic liver diseases.

Acute Disease↗