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Biomedical subjects

F W Schmidt

Publications and source records attributed to F W Schmidt.

At least 19 recordsLinked to original sources
PubMed1992

Energy expenditure and substrate oxidation in patients with cirrhosis: the impact of cause, clinical staging and nutritional state.

Many clinicians subjectively feel that cirrhotic patients frequently have clinical signs of hypermetabolism. However, it is unknown whether hypermetabolism is a constant feature of chronic liver disease, corresponds to liver destruction and repair or is of prognostic value. This article is about resting energy expenditure and substrate oxidation rates in 123 patients with biopsy-proven cirrhosis differing with respect to cause, duration of the disease, biochemical parameters of parenchymal cell damage, cholestasis, liver function, number of complications, clinical staging and nutritional state. Resting energy expenditure varied between 1,090 and 2,300 kcal/day and differed from the predicted values in 70% of the patients. Resting energy expenditure was closely related to fat-free mass, and 52% of the variability could be explained by fat-free mass, age and sex. Of all the patients, 18% were hypermetabolic and 31% were hypometabolic. Hypermetabolism showed no strict association with the cause of cirrhosis, the duration of the disease, liver function, cholestasis, cell damage, clinical staging, blood hemoglobin, plasma thyroid hormone levels or human leukocyte antigens. An increased resting energy expenditure was associated with significant losses of muscle, body cell mass and extracellular mass at unchanged body fat, whereas fat and fat-free mass were increased in hypometabolic patients when compared with normometabolic patients. Lipid oxidation was increased, but glucose oxidation was reduced in nearly all patients with cirrhosis. This was most pronounced at advanced stages of liver disease. Although similar with respect to liver function and clinical staging, 76.2% of hypermetabolic patients had transplants within the observation period, compared with only 16.7% and 8.1% in the normometabolic group and hypometabolic group, respectively. Posttransplantation mortality was independent of pretransplantation resting energy expenditure, but it increased significantly in patients with losses in body cell mass. In conclusion, hypermetabolism is not a constant feature of cirrhosis and results more from extrahepatic than from hepatic factors. It may cause malnutrition and contributes to the clinical outcome of patients with chronic liver disease.

Adult↗
PubMed1992

Mechanism of insulin resistance associated with liver cirrhosis.

Insulin-induced glucose metabolism was investigated in 26 patients with biopsy-proven liver cirrhosis and 10 control subjects. Two glucose clamp protocols together with continuous indirect calorimetry were performed to examine whether reduced rates of glucose oxidation and/or nonoxidative glucose metabolism explain insulin resistance in liver cirrhosis. Using a 4-hour, two-step protocol (0-2 hours, plasma glucose 5.2 mmol/L, plasma insulin 92 mU/L to test the half-maximum response; 2-4 hours, hyperglycemia 10.0 mmol/L, plasma insulin 442 mU/L to test the maximum cellular glucose disposal) liver cirrhosis reduced glucose disposal to 45% and 60% of control values, respectively. Simultaneously, insulin-induced increases in glucose oxidation, plasma lactate levels, and lipogenesis were normal, whereas nonoxidative glucose metabolism was reduced (-82% and -47% of controls, respectively). To determine whether reduced nonoxidative glucose metabolism was caused by reduced glucose disposal, glucose disposal was "matched" to normal values in a subgroup of cirrhotic patients. Nonoxidative glucose metabolism values were normal, but plasma lactate concentrations disproportionally increased (+96%) after "matching" glucose disposal. Insulin resistance was independent of the etiology of the cirrhosis, the biochemical parameters of parenchymal cell damage and liver function, and the clinical and nutritional state of the patients. It is concluded that liver cirrhosis impairs insulin sensitivity and maximum cellular glucose disposal. Reduced glucose disposal is caused by defective glucose storage. Insulin resistance is independent of the etiology of liver cirrhosis and of the clinical and nutritional state of the patient.

Adult↗
PubMed1992

Resting energy expenditure and the thermic effect of adrenaline in patients with liver cirrhosis.

1. Resting energy expenditure and the metabolic responses to adrenaline (infusion rate: 0.03 micrograms min-1 kg-1 fat-free mass for 1 h) were investigated in 25 patients with liver cirrhosis. The patient group was heterogeneous and varied with respect to the aetiology of cirrhosis, the clinical condition (i.e. Child A or B), the nutritional status and the degree of hyperinsulinaemia. 2. When compared with 10 healthy control subjects the basal plasma adrenaline and noradrenaline concentrations were both increased in cirrhosis and remained elevated during adrenaline infusion (+39% and +31%, respectively; P < 0.05). Concomitantly, the peripheral plasma insulin concentration and the molar C-peptide/insulin ratio were increased in liver cirrhosis (+96% and +30%, respectively; P < 0.05). Hyperinsulinaemia was more pronounced in patients with ethanol-induced liver cirrhosis. 3. When expressed per kg fat-free mass, resting energy expenditure was enhanced in liver cirrhosis (+21%; P < 0.05) and was more pronounced (i.e. resting energy expenditures of +35% to +49% above estimated values) in patients with ethanol-induced cirrhosis, at advanced stages of the disease and in association with decreased body cell mass. 4. Infusion of adrenaline increased heart rate, O2 consumption and the plasma concentrations of glucose, lactate, free fatty acids, glycerol and 3-hydroxybutyrate, and similar transient increases and subsequent decreases in the respiratory quotient were observed in both groups. However, the lipolytic, ketogenic and thermic responses were reduced in cirrhotic patients. Reduced metabolic responses were more pronounced in hyperinsulinaemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Bismuth subsalicylate in the treatment of H2 blocker resistant duodenal ulcers: role of Helicobacter pylori.

Fifty nine patients with Helicobacter pylori positive duodenal ulcers that failed to heal after a six week course of treatment with H2 blockers were randomly assigned to one of the following three regimens: (i) bismuth subsalicylate, 600 mg three times daily (n = 19), (ii) ranitidine, 300 mg at night (n = 20), (iii) bismuth subsalicylate plus ranitidine (n = 20). Cumulative ulcer healing rates after four and eight weeks respectively were as follows: bismuth subsalicylate 74% (14/19) and 95% (18/19), ranitidine 40% (8/20) and 65% (13/20), bismuth subsalicylate plus ranitidine 80% (16/20) and 95% (19/20). Bismuth subsalicylate treatment was better than ranitidine at both four and at eight weeks (p less than 0.05). The clearance rates for H pylori after four weeks were: bismuth subsubsalicylate 58%, ranitidine 0%, bismuth subsalicylate plus ranitidine 55%. After stopping bismuth therapy bacterial recrudescence frequently occurred. After bismuth treatment 86% (19/22) of ulcers had healed if H pylori had been cleared, whereas only 65% (11/17) had healed if H pylori persisted (NS). This study shows that bismuth subsalicylate is more effective in the treatment of resistant duodenal ulcers than standard dose ranitidine. It may be that suppression of H pylori by bismuth subsalicylate promotes ulcer healing.

Bismuth↗
PubMed1992

[Chemoembolization of hepatocellular carcinoma in cases of isolated liver involvement].

Chemoembolization is an effective treatment for hepatocellular carcinoma, giving results equally as good as surgical therapy for T2 tumours. Survival can be prolonged and side-effects can be reduced by combining Lipiodol and Gelfoam for chemoembolization, employing a modified technique, with repeated procedures, and using appropriate follow-up treatment. The toxicity of the procedure is acceptable, but it requires supportive therapy necessitating an intense interdisciplinary co-operation.

Aged↗
PubMed1991

The influence of colostral leukocytes on the immune system of the neonatal calf. IV. Effects on bactericidity, complement and interferon; synopsis.

The influence of colostral leukocytes on the bactericidity of whole blood of calves against a strain of E. coli and on the activities of haemolytic complement and interferon-alpha (the antiviral activity of sera resisting an acidic treatment at pH 2 for 6 h) in the serum was investigated during a period of 4 weeks using 4 experimental groups. The calves received either complete colostrum (COL+, n = 16), cell-depleted colostrum (COL-, n = 16), cell-supplemented milk substitute (MS+, n = 7) or pure milk substitute (MS-, n = 6) during their first three days of life. The bactericidity of whole blood of the COL+ group was significantly higher on the second and third days of life while the activity of haemolytic complement was lower after the first week as compared to the COL- group. No interferon-alpha was detectable in the sera of both COL groups. The bactericidity of the MS groups was significantly lower than that of the COL groups after the first day of life. It was significantly lower in the MS+ group after one week of life while the activity of haemolytic complement was higher than that of the MS- group. Three out of 5 MS- and only one out of 7 MS+ calves had low titres of interferon-alpha in their sera on the third day. Three out of 6 MS- calves died and 5 out of 7 MS+ animals. The mean day of death was 4.0 in the MS- and 8.4 in the MS+ group. Based on the in vitro results of this and the previous three communications it can be concluded that leukocytes which are an integral part of normal bovine colostrum, influence immunological reactions of the calf and that they may enhance its defence against infection. Colostral leukocytes in the absence of humoral components of the colostrum are not able to prevent fatal losses in the calves due to natural infection, although their influence on immune responses of the calves was detectable in vitro.

Animals↗
PubMed1990

Progress in the enzyme diagnosis of liver disease: reality or illusion?

This paper discusses the progress of enzyme diagnosis by different examples. These include: the requirement for improved enzymological screening, despite the introduction of a test for hepatitis C; the imbalance between the popularity of "unexplained chronic aminotransferase elevations" and efforts to solve the inherent problems; the inadequate attempts to use the metabolic changes in the hepatocytes to improve diagnosis, prognosis, and pathophysiological understanding of viral liver diseases; the remarkable investigations into the 2'-5'-oligoadenylate synthetase for better control of interferon therapy in chronic viral hepatitis; the use of enzymes as markers of etiology, particularly for the detection of alcohol induced liver diseases; the continuing preference for the aminotransferases in this scenario although the ratios of aspartate aminotransferase over alanine aminotransferase, or of mitochondrial aspartate aminotransferase over total aspartate aminotransferase activity, largely depend on the severity and intralobular localization of damage and the stage of the liver disease.

Clinical Enzyme Tests↗
PubMed1990

Neurophysiological assessment of early hepatic encephalopathy.

The spontaneous EEG, pattern reversal VEPs, and the P300 wave were studied in patients with liver cirrhosis and early stages of hepatic encephalopathy (HE). The sensitivities of the different neurophysiological methods in the early stages of hepatic encephalopathy were compared with each other and with several neuropsychological tests. P300 latency was shown to be the most appropriate neurophysiological method for detection of early HE. The diagnostic sensitivity of the P300 latency resembled that of the number connection test (NCT). These results are discussed with regard to methodological considerations and the clinical use of both methods.

Adult↗
PubMed1979

Total body water, extracellular water, plasma volume, and total body potassium in cirrhosis of the liver.

Extracellular water (EWC; 82-bromide), total body water (TBW; 3-THO), intracellular water (ICW = TBW-ECW), plasma volume (PV; 51-Cr), and total body potassium (TBK; 40-K) were studied in patients with cirrhosis of the liver (n = 12) and in controls (n = 12). ECW (39%), TBW (28%), ICW (19%), and PV (24%) increased, TBK (28%) however, decreased in cirrhosis. The results indicate that it is less the lean body mass, but rather the intracellular potassium concentration that is lowered (cirrhosis: 84 +/- 21 mmol/l ICW; controls: 115 +/- 23 mmol/l ICW). Decreased potassium per cell (mmol) and increased intracellular water are discussed as possible reasons for this. The correlation between TBK (%) and serum potassium (mmol/l) was found to be r = 0.56 (p less than 0.002). Correlations between the biochemical parameters gamma-globulins, cholin esterase, serum sodium and serum albumin (g/l PV) and characteristic fluid disturbances in cirrhosis are highly significant whereas albumin (g/kg bodyweight) was the same in both groups. We can support the 'overflow theory' of ascites formation.

Adult↗
PubMed1979

Evaluation of one dimensional profile scans with a whole body counter--82bromide space in liver cirrhosis: concise communication.

One dimensional profile scans with a whole body counter are refocused with a linear space invariant filter in the frequency domain, 'Hanning' window and inverse system transfer function. Artifacts are eliminated in a way that a clinically applicable method is developed. Topographic information is achieved with the highly energetic nuclide 82bromide. The bromide space (extracellular volume) in patients with liver cirrhosis (n = 9) compared to normal subjects (n = 10) is increased most in the upper abdominal thoracic region.

Adult↗
PubMed1979

Effect of liposome-entrapped methotrexate on Ehrlich ascites tumor cells and uptake in primary liver cell tumor.

A therapeutically useful concentration (0,5 mg/ml) of Methotrexate was prepared in negatively charged artificial liposomes (lecithine: cholesterol: dicetylphosphate=5:5:1 molar ratios). Entrapment yield after separation on Sepharose 6B is nearly 100%. In contrast to free Methotrexate the liposome entrapped folic acid antagonist is eliminated only slowly by the kidneys and after intravenous application it is unevenly distributed in the body of mice, the highest concentrations being found in liver and spleen. Daily injections (7.5 mg/kg/day) of entrapped Methotrexate for 5 days into the tail vein of Ehrlich ascites tumor bearing mice reduced both tumor cell count and the production of ascites fluid about fourfold as compared to mice receiving the same dose of Methotrexate in the free form. Six hours after intravenous application of liposome entrapped Methotrexate the tissue concentration in normal liver is ca. 20-fold higher than when the same amount is applied in the free state. On the other hand, only a little uptake of liposome entrapped Methotrexate was detected in the tissue of nitrosamine-induced primary liver tumor when compared to normal liver tissue of rats.

Animals↗
PubMed1979

Sensitivity of bile acid breath test in the diagnosis of bacterial overgrowth in the small intestine with and without the stagnant (blind) loop syndrome.

The bile acid breath test was studied to examine its sensitivity for establishing the diagnosis of bacterial overgrowth in comparison to that of the Schilling test and small-intestinal cultures in 12 patients with a stagnant (blind) loop syndrome, as well as in 38 patients who had other conditions with suspected bacterial contamination of the small intestine. The presence of bile acid malabsorption was excluded in all 50 patients by studies of fecal excretion of radioactively labeled bile acids. The bile acid breath test was positive in 100% (12/12) of the patients with a stagnant (blind) loop syndrome, whereas 92% (11/12) had a positive Schilling test and 75% (9/12) a positive small-intestinal culture. The abnormal tests improved only in 2 of 4 patients treated with tetracycline. In the group of 38 patients without demonstrable dilated or blind loops of small bowel who were suspected of having bacterial contamination of small bowel, the bile acid breath test was positive in 53% (20/38), the Schilling test in 39% (15/38), and the small-intestinal culture in 45% (17/38). The difference in the incidence of positive results between the tests in the two patient groups was statistically not significant. The findings of these studies have the following diagnostic implications: (1) Bile acid breath test, Schilling test, and cultures of aspirates from the upper small bowel are of comparable sensitivity in the detection of bacterial overgrowth in the small intestine. (2) A negative bile acid breath test makes the diagnosis of a stagnant (blind) loop syndrome very unlikely.

Bacteria↗
PubMed1979

Creatine kinase (EC-No.2.7.3.2) and creatine kinase isoenzymes during pregnancy and labor and in the cord blood.

Total CK and CK isoenzyme activity in serum was investigated during pregnancy, labor and after delivery as well as in cord blood. Total CK was decreased in the second trimester of pregnancy but increased in late pregnancy. Low CK-MB activity in serum was found in patients with early labor pains. CK-BB activity could never be detected during pregnancy. Total CK and isoenzyme activity increased after delivery. The rise of total CK and CK-MB in maternal serum is directly correlated with the following: type of delivery, duration of labor, parity of the mother, and birth weight. From this it can be deduced that postpartum CK levels depend on skeletal muscle activity as well as on the activity of uterine muscle. Prematures and infants "small for date" have significantly lower total CK and slightly more elevated CK-BB activity in cord blood than children of normal maturity. CK-BB activity is much more pronounced in high risk patients with low Apgar score.

Creatine Kinase↗
PubMed1979

Thiols and hepatic coma.

The plasma concentrations of methane and ethane thiols have been determined during the course of acute liver failure by a gas-chromatographic technique, and a prognostic evaluation is possible using this analysis. Further, the effects of some therapeutic measures, notably hemoperfusion, on the thiol levels have been investigated. It is concluded that these toxins, which are to a large extent covalently protein-bound, are extremely difficult to remove in an extracorporeal liver support system. Since the cause of the pathological thiol concentrations is probably the elevated plasma methionine levels associated with severe liver disease, it is suggested that the most hopeful course of action against the accumulation of thiols in the body might be a preventative therapy involving the normalization of methionine at an early stage of the disease.

Charcoal↗