PubMed Health⌕ Search

Biomedical subjects

D Müting

Publications and source records attributed to D Müting.

17 recordsLinked to original sources
PubMed1991

Limited hepatic resection for selected cirrhotic patients with hepatocellular or cholangiocellular carcinoma: a prospective study.

From 1 January 1983 to 1 January 1989 123 cirrhotic patients with hepatocellular cancer (n = 122) or cholangiocarcinoma (n = 1) were screened using liver function tests, alpha-fetoprotein determination, ultrasonography with biopsy (and in selected cases computed tomography or nuclear magnetic resonance), laparoscopy and angiography, Child-Pugh classification and urea-nitrogen synthesis rate. Twenty-three patients were selected for surgical resection because the tumour was smaller than 5 cm, not centrally located and at least 1 cm away from main structures; there was no evidence of multicentricity or metastatic disease; and the Child-Pugh classification was A or B and the urea-nitrogen synthesis rate at least 6 g/day. Upper gastrointestinal endoscopy was used routinely to identify oesophageal varices which were present in 17 cases; ten patients with a history of variceal haemorrhage (43 per cent) had preoperative endoscopic sclerotherapy. In cases with recurrent haemorrhage, surgery was used to prevent intraoperative and postoperative bleeding. Tumour resection was carried out using controlled hypotension and hepatoduodenal ligament clamping. Twelve bisegmentectomies, ten segmentectomies and one atypical resection were performed. The operative mortality rate was 13 per cent with liver failure and sepsis as the causes of death. The 'recurrence rate' was 26 per cent and the late mortality rate for the whole group up to 1 January 1990 was 30 per cent; 13 patients were still alive. The 12-month survival rate was 77 per cent and after 5 years it was 49 per cent. Thus, surgical resection of small liver tumours is the treatment of choice in this selected group of patients.

Adenoma, Bile Duct↗
PubMed1979

[Eliciting factors and clinical picture of hepatic coma in 152 patients with cirrhosis of the liver (author's transl)].

Exogenous hepatic coma was found 102 times (group A) and a combination of exogenous and endogenous hepatic coma 50 times (group B) in 152 patients with hepatic coma. The most frequent eliciting factors in group A were too high a protein supply and gastrointestinal hemorrhage and diuretics, in group B necrotic exacerbations and infections, 2/3 of them having severe portal hypertension with ascites and esophageal varices at the same time. A typical fetor hepaticus was found in only 25% of group A and 50% in group B. 10% had a primary liver cell carcinoma. The prognosis depends largely on the stage of the coma and the treatment of the eliciting factors. Altogether 50 of the 152 hepatic coma patients died. The most frequent complication was a terminal renal failure which no longer responded to therapy.

Acute Kidney Injury↗
PubMed1977

[Therapy of hepatic insufficiency].

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.

Alcoholism↗
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↗