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Biomedical subjects

H Gallenkamp

Publications and source records attributed to H Gallenkamp.

At least 19 recordsLinked to original sources

Caffeine elimination in cirrhotic and non-cirrhotic liver disease of different etiology.

Caffeine elimination was studied in 419 patients with cirrhotic and noncirrhotic liver disease of different etiology (hepatitis B virus infection n = 79; hepatitis NANB virus infection n = 74; ethanol-induced liver damage n = 143; primary biliary cirrhosis I-IV n = 63; cryptogenic liver cirrhosis n = 60) following oral administration of 366 mg caffeine. Caffeine clearance in the control group was 69 +/- 33 ml/min (age-matched healthy volunteers and patients without liver disease). Caffeine clearance in acute hepatitis B (70 +/- 60 ml/min) chronic persistent hepatitis B (81 +/- 56 ml/min), chronic aggressive hepatitis B (107 +/- 66 ml/min), posthepatitic liver cirrhosis B (84 +/- 62 ml/min), acute hepatitis NANB (94 +/- 69 ml/min), chronic persistent hepatitis NANB (122 +/- 60 ml/min), chronic aggressive hepatitis NANB (87 +/- 52 ml/min) and posthepatitic cirrhosis NANB (59 +/- 26 ml/min) is not reduced in comparison with controls. In patients with alcoholic fatty liver (127 +/- 71 ml/min, p < 0.05) caffeine clearance is enhanced, in alcoholic hepatitis (57 +/- 72 ml/min) comparable to controls and in alcoholic cirrhosis reduced (36 +/- 44 ml/min, p < 0.05). In primary biliary cirrhosis I-IV caffeine clearance is higher than in controls (117 +/- 59 ml/min, p < 0.05). In cirrhotic liver disease of different origin caffeine clearance is inversely related to the serum bilirubin level. However, the absolute value is determined in addition by the underlying disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Diagnostic problems in upper gastrointestinal bleeding.

In this editorial problems of different diagnostic procedures, the time of endoscopy, i.e. emergency endoscopy procedures, and its complications, are discussed. Criteria for a risk patient and possibilities of endoscopic therapy or operation are discussed.

Endoscopy

Post mortem changes in drug-metabolizing enzymes of rat liver and human liver.

The aim of this investigation was to obtain information on the time-dependent decrease of the drug-metabolizing system in autolysing rat liver, and also in human cadaver liver. Rat liver, divided into three parts, was tested immediately after removal and 6 and 12 hrs later. Parameters investigated were: microsomal protein, cytochrome P-450, NADPH cytochrome C reductase, glucose-6-phosphatase, aminopyrine-N-demethylation and aniline-p-hydroxylation. In human liver, samples taken from 0.5 up to 3.5 hrs after death, microsomal protein cytochrome P-450, NADPH cytochrome C reductase and phospholipids were tested. Nearly all parameters based on microsomal protein decrease during autolysis, but by different amounts. Interestingly, the cytochrome P-450 content of patients with signs of shock 12 hrs before death is significantly lower than in patients without shock.

Adult

[Methohexital clearance in patients with acute hepatitis (author's transl)].

Pharmacokinetics of methohexital were studied in patients with acute hepatitis and after a treatment period either with "essential phospholipids" or phenobarbital. During the acute phase the distribution of methohexital was significantly altered. No change had been observed in the methohexital clearance. During remission the distribution of methohexital was in a normal range. After treatment with phenobarbital the methohexital clearance increased significantly whereas no change was observed after treatment with "essential phospholipids".

Acute Disease

[Fiberendoscopic injection therapy of bleeding gastrointestinal lesions (author's transl)].

In 28 patients with acute gastrointestinal bleeding emergency fiberendoscopy was combined with aethoxysclerole (1%) injection of the bleeding lesion with purpose to controll haemorrhage. In 61% of 31 proceudres done in patients with oesophageal varices (n = 19) haemorrhage was controlled, and in further 16% deminuation of bleeding intensity was noted. In the remaining cases (n = 7) the procedure was ineffective. Only patients with Child C liver cirrhosis having oesophageal varices stages III and IV finally died because of uncontrolled haemorrhage. In 9 patients with bleeding from other lesions (gastric erosions and ulcers, Mallory-Weiss-Syndrome, erosio simplex Dieulafoy) haemorrhage was controlled in 8 patients. The method is practicable and efficient, but does not determine better the final outcome of patients with livercirrhosis Child C having oesophageal varices stages III and IV. In other cases tube treatment was avoided. The operation lethality within the series was 1,5%.

Endoscopy

[Metabolism of hexobarbital in patients with acute hepatitis and cirrhosis (author's transl)].

16 patients with acute hepatitis, 18 patients with cirrhosis and a total of 21 volunteers and patients with normal liver function received 7.32 mg/kg hexobarbital by linear intravenous infusion within 60 min. Hexobarbital was determined gaschromatographically in serial blood samples and the hexobarbital-clearance was calculated from the plasma concentration curve versus time. Additional experiments were performed in rats suffering from so called "galactosamine hepatitis". In half of the patients with acute hepatitis a normal hexobarbital clearance could be found. In the other patients this was distinctly reduced but not correlation was found to other liver function tests. Patients with cirrhosis were subdivided into two groups. The patients in group 1 were well compensated. The patients in group 2 had a decompensated state with ascites and oesophageal varices. In nearly all patients with cirrhosis the hexobarbital-clearance was diminished. This was more pronounced in group 2. Ketohexobarbital excretion in healthy subjects was in the range of 40-60% of dose. Patients with acute hepatitis excreted only 10-20% of dose and patients with liver cirrhosis only about 5% of dose. In rats with "galactosamine hepatitis" hexobarbital clearance in vivo was distinctly reduced and this could be explained by diminished microsomal cytochrome p 45- and hexobarbital oxidation rate.

Acute Disease

[Hexobarbital-oxidation in vivo and in vitro in rats after phenobarbital-pretreatment or after portacaval anastomosis (author's transl)].

Male rats were pretreated with phenobarbital for 5 days or received portacaval anastomosis 3 weeks before. Hexobarbital was applicated intravenously and hexobarbital plasma concentrations were followed up gaschromatographically in arterial blood samples. Hexobarbital clearance was calculated from the plasma concentration curve versus time. Liver microsomes were prepared and cytochrome P 450 and the hexobarbital oxidation rate was determined. After portacaval shunt the animals showed a small liver, a reduced cytochrome P 450 and diminished hexobarbital oxidation rate. Hexobarbital clearance in vivo was reduced, too. After phenobarbital pretreatment liver weight increased and cytochrome P 450 and hexobarbital oxidation rate were distinctly enhanced. The hexobarbital clearance in vivo were increased. Since the plot of hexobarbital clearance in vivo versus cytochrome P 450 or versus hexobarbital oxidation rate in vitro gave a good correlation, it is concluded that hexobarbital clearance in vivo may be a good estimate for hepatic cytochrome P 450 and hepatic hexobarbital oxidation rate.

Animals

Influence of d-galactosamine hydrochloride on lipids and their fatty acid composition in plasma and liver of guinea pigs.

48 hrs after i.v. applications of 1 g/kg b.w. galactosamine hydrochloride to guinea pigs the total lipids of plasma, liver homogenate and isolated liver microsomes were extracted and separated by dialysis and thin-layer chromatography. The fatty acid fractions of total lipids (plasma), neutral lipids and total phospholipids (liver homogenate) as well as phosphatidylcholines and remaining phospholipids (liver microsomes) were analyzed by gaschromatography. In plasma the concentration of total lipids was unchanged in the galactosamine group. A slight decrease of the C16- and an increase of the C161- fatty acids were observed. In total liver homogenate neutral lipids increased 9-fold, and phospholipids 2.5 fold after galactosamine application. Specially there was a relative and absolute increase of the C16-, C16(1)-, C18(1)-, and C18(3)-fatty acids in the neutral lipids, whereas the C18- and C18(2)-Fatty acids were relatively diminished. Similar changes within the fatty acid fractions could be found to a minor degree in the phospholipids. 48 hours after application of galactosamine the phospholipid content in isolated liver microsomes increased about 2-fold. Likewise there was an absolute increase of nearly all fatty acid fractions as well in phosphatidylcholines as in the other phospholipids. In both phospholipid fractions the percentage of the C18-fatty acids decreased and a relative increase in C16-fatty acids was observed. Contrary to the findings in total liver, in the isolated microsomes predominantly saturated fatty acids (C16, C18) were found.

Animals