Rupture of double lumen Hickman catheter at time of removal by surgery--another potentially serious complication.
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Adult↗
Biomedical subjects
R Kramar
Publications and source records attributed to R Kramar.
[Vascular access, anticoagulation].
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Acute Kidney Injury↗
Clofibrate elevates enzyme activities of the tricarboxylic acid cycle in rat liver.
Activities of the tricarboxylic acid cycle enzymes were measured in subcellular fractions of liver from rats that had been fed clofibrate for 3 weeks. Large changes in these activities per gram tissue were found in the large particle fraction, which also showed an increase in total protein concentration of 76% under clofibrate treatment. The three regulatory enzymes of the cycle, namely citrate synthase, NAD(+)-linked isocitrate dehydrogenase, and 2-oxoglutarate dehydrogenase were significantly enhanced by 24% (P < 0.02), 54% (P < 0.02), and 153% (P < 0.005), respectively. Fumarase and malate dehydrogenase rose by 71% (P < 0.005) and 95% (P < 0.02), whereas succinate dehydrogenase remained unchanged. Enhancement of the citrate synthase, NAD-isocitrate dehydrogenase, and 2-oxoglutarate dehydrogenase may play a role in decreasing intracellular availability of acetyl-CoA for lipid metabolism.
Animals↗
Ventricular late potentials in haemodialysis patients and the risk of sudden death.
Cardiovascular diseases account for approximately 50% of deaths in patients on chronic haemodialysis. Therefore we prospectively studied 54 consecutive patients on dialysis for the presence or absence of ventricular late potentials (LP). LP, i.e. low-amplitude potentials in the terminal part of the QRS complex, have been shown to be highly indicative of life-threatening arrhythmias and sudden death. The results were correlated with echocardiographic studies and the clinical outcome during a follow-up period of 18 months. Fifty patients were suitable for evaluation (29 males, 21 females; mean age 55 years; mean time on dialysis 32 months; coronary artery disease present in 5) Our analysis revealed LP in seven of 50 patients only. Left ventricular hypertrophy, i.e. mean wall diameter > 12 mm, was present in 78%, a compromised left ventricular function, i.e. shortening fraction < 28%, was found in 28% of the patients. With respect to echocardiographic parameters, patients with and without LP were similar. During follow-up, sudden cardiac death was observed in three of 11 patients deceased. LP were detectable in one of the three only. From the remaining six patients with LP, four are still alive, and two patients died due to atherosclerosis and pulmonary embolism. Our data underline the crucial role of sudden cardiac death in dialysis patients. Ventricular late potentials, however, are of no prognostic relevance with respect to identification of dialysis patients at risk of sudden death.
Adolescent↗
Enhancement of NAD-linked isocitrate dehydrogenase activity in rat liver by clofibrate feeding.
After feeding rats for 3 weeks with clofibrate specific activities of the liver mitochondrial enzymes glycerol-3-phosphate dehydrogenase (G3PDH) and NAD-linked isocitrate dehydrogenase (NAD-ICDH) were found to be increased in a large particle fraction 6-fold and 1.6-fold, respectively, whereas the activity of NADP-linked isocitrate dehydrogenase (NADP-ICDH) remained unchanged. Possibly these effects contribute to the hypolipidemic action of clofibrate.
Animals↗
Papanicolaou test and enzyme-linked in-situ hybridization. A combined diagnostic system for papilloma virus infections with high prognostic value.
A combined diagnostic system for human papilloma virus (HPV) infections comprising the Papanicolaou test and in-situ hybridization assay was evaluated. Cervical smears from 259 women obtained with a "Cytobrush" were screened. Human papilloma virus genotypes 6/11, 16/18, 31/35/51 were detected by biotin in-situ hybridization in conjunction with a streptavidin-alkaline phosphatase detection complex. The diagnostic sensitivity of this assay was tested by human papilloma virus-DNA-positive human cervical carcinoma cell lines. According to the cytological (Bethesda system) and colposcopical criteria a random control group (n = 80) and prevention (n = 179) were chosen. Compared with Papanicolaou tests the frequency of human papilloma virus-DNA-positive cervices rose with the severity of cell abnormalities. The detection rate of human papilloma viruses-16/18 and human papilloma viruses-31/35/51 and of concomitant infections with human papilloma viruses-6/11 and human papilloma viruses-16/18 and/or human papilloma viruses-31/35/51 increased with the severity of cell dysplasia, whereas the rate of human papilloma virus-6/11 DNAs decreased. The incidence of oncogenic human papilloma virus types 16/18 and 31/35/51 rose with the age of the patients. A follow-up study by Papanicolaou tests of patients with mild (slight) and moderate dysplasias six months after human papilloma virus-DNA-hybridization indicates that human papilloma virus-16/18 DNA-positive lesions are more likely to persist or to progress than human papilloma virus-6/11 DNA-positive cell changes. Human papilloma virus-31/35/51 DNA-positive cell smears exhibited persistent behaviour. Our findings demonstrate that the Papanicolaou test combined with in-situ hybridization is suitable for early diagnosis and prevention of intraepithelial neoplasias and carcinomas of the uterine cervix.
Adolescent↗
Response to thyroxine of lamellar bodies, peroxisomes and peroxisomal enzymes in the adult rat lung.
Adult male rats were fed a standard diet containing 25 mg/kg L-thyroxine for 2 weeks. The hyperthyreotic condition of the animals was checked by monitoring the metabolic rates and liver glycerol-3-phosphate dehydrogenase. In the postnuclear fraction of the lung the activity of fatty acyl-CoA oxidase, the enzyme responsible for the rate limiting first step of peroxisomal fatty acid beta-oxidation, showed a twofold increase. Catalase, the marker enzyme of peroxisomes, showed a similar increase. Electron microscopic examination of alveolar type II cells did not reveal changes in the number and distribution frequency of peroxisomes and lamellar bodies. Similarly the content of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (dipalmitoyl phosphatidylcholine), the main constituent of alveolar surfactant, was not altered significantly by thyroxine feeding. On the other hand the volume density of the peroxisomal compartment was found to be doubled according to the measured increase of catalase and acyl-CoA oxidase. Our data suggest that the induction of peroxisomal matrix enzymes, such as catalase and fatty acyl-CoA oxidase, does not influence the surfactant content.
Acyl-CoA Oxidase↗
Detection of prune-belly syndrome in a 35-year-old man: a rare cause of end-stage renal failure in the adult.
The clinical entity of prune-belly syndrome is mainly encountered in childhood. Here we present the case of a 35-year-old male patient with end-stage renal failure, the underlying cause of which being prune-belly syndrome. Apart from the typical triad of abdominal muscle deficiency, severe urinary tract abnormality, and cryptorchidism, a multitude of other abnormalities and malformations existed, especially of the skeletal and gastrointestinal systems. The major hypotheses regarding etiology and pathogenesis of the syndrome are briefly discussed.
Adult↗
[Calcium-free hemodialysis--value in therapy of hypercalcemic crisis].
If conservative treatment of hypercalcemic crises is ineffective, low calcium bath or zero calcium bath hemodialysis represent good alternatives. We report 5 patients (from 54 to 82 years old) treated with calcium free acetate hemodialysis because of hypercalcemic crises due to breast cancer with bone metastases, thiazids' medication and immobilisation, liver cirrhosis, hepatocellular carcinoma and hyperparathyroidism. By 3 hours' therapy calcium concentration could be reduced from a mean value of 3.74 mmol/l (3.13-4.46) to 2.47 mmol/l (1.38-3.12). In 3 cases rapid clinical improvement was achieved and in 4 cases the subsequent conservative therapy was sufficient to maintain serum calcium levels within reference range. In accordance to other investigators we consider hemodialysis as an effective method of low risk in hypercalcemic crises. Calcium rebound may occur in patients with hyperparathyrodism.
Aged↗
Calcium free hemodialysis: an effective therapy in hypercalcemic crisis--report of 4 cases.
Hypercalcemic crisis represents a medical emergency. If conservative treatment is ineffective, low calcium bath or zero calcium bath hemodialysis are good alternatives. We report 4 patients treated with calcium free acetate hemodialysis because of hypercalcemic crisis due to breast cancer, hepatocellular carcinoma, cirrhosis of the liver and immobilisation with hydrochlorothiazids' medication. Following 3 h of hemodialysis, serum calcium concentrations fell from a mean value of 3.96 (range 3.53-4.46) mmol/l to 2.71 (2.28-3.12) mmol/l. In 2 patients rapid clinical improvement was achieved and in one oliguric patient diuresis started spontaneously during hemodialysis. One patient died from gram-negative sepsis. In 3 cases the subsequent conservative treatment was sufficient to maintain serum calcium levels within the normal range. Together with the previously reported cases (5 patients treated by hemodialysis with low dialysate calcium and 3 patients by hemodialysis with calcium free dialysate) our experience indicates that hemodialysis is an effective and safe therapy for hypercalcemic crisis.
Aged↗
Peroxisomal oxidation of pipecolic acid in the rat.
Postnuclear fractions from rat liver and kidney oxidize L-pipecolic acid, a by-product of lysine catabolism, in a hydrogen peroxide-producing reaction. This pipecolate oxidase2) activity is enhanced in preparations from animals treated with clofibrate and thyroxine, substances known to act as peroxisome proliferators and inducers of the peroxisomal fatty acid beta-oxidation. The enzymatic activity co-purified with the peroxisomal marker fatty acyl-CoA oxidase2) rather than with the mitochondrial marker glycerol-3-phosphate dehydrogenase2). Thus the degradation of L-pipecolic acid may start in the rat with a peroxisomal oxidase comparable to other hydrogen peroxide-producing oxidases found in peroxisomes. These findings provide indirect evidence that the marked hyperpipecolinaemia described in a group of human genetic disorders connected with peroxisomal defects such as Zellweger syndrome might be due to the absence of peroxisomal L-pipecolate oxidase.
Animals↗
Severe sublimate intoxication in the rat. Influence of thyroxine on renal enzymes of fatty acid degradation and on the survival rate of intoxicated rats.
1. The influence of thyroxine pretreatment on prognosis and some renal enzymes of fatty acid degradation of mercuric chloride intoxicated rats was studied. 2. Survival rates as observed over 10 d after 1.5 to 6.0 mg mercuric chloride/kg i.p. were not influenced by thyroxine pretreatment. 3. A quarter of survivors of both groups developed renal hypertrophy more pronounced in animals not treated with thyroxine. 4. Fatty acyl-CoA oxidase, the rate limiting enzyme of peroxisomal beta-oxidation was found to be depressed by about 50% 2 d after intoxication. This effect was prevented by thyroxine pretreatment. The other enzyme activities (carnitine acetyltransferase, carnitine-palmitoyltransferase and crotonoyl-CoA dependent NAD+ reduction) are essentially not influenced neither by intoxication nor by thyroxine pretreatment. 5. It is concluded that the prognosis of the intoxication is not correlated with fatty acid degradation enzymes.
Acute Kidney Injury↗
["Diabetic" proliferative retinopathy and nodular glomerulosclerosis without diabetes mellitus].
A 65-year-old woman of normal weight, hospitalized because of pleuritis, was found to have chronic renal failure (creatinine clearance 20 ml/min). Renal biopsy (light and electron-microscopy) revealed nodular glomerulosclerosis (Kimmerstiel-Wilson disease), described as a diabetes-specific renal change. Fundoscopy discovered bilateral proliferative retinopathy as seen in diabetes. But oral and intravenous glucose tolerance tests were normal, excluding a manifest diabetic metabolic disorder. No other cause of the glomerulosclerosis (such as amyloidosis or multiple myeloma) was found. The patient had been overweight for a time when younger, reversed by dieting. It is suggested that the "diabetic" changes in the kidneys and eyes without diabetes could be the result of a transitory disorder of glucose tolerance during the period of obesity.
Aged↗
Clinical biochemistry of peroxisomal disorders.
Peroxisomes have been shown to participate in a variety of pathological processes. Peroxisomal anomalities are central features of Zellweger's cerebro-hepato-renal syndrome, neonatal adrenoleukodystrophy, infantile Refsum's disease and several other genetic metabolic disorders (pseudo-Zellweger syndrome, Leber congenital amaurosis, cerebrotendinous xanthomatosis, rhizomelic chondrodysplasia punctata). In disorders with general loss of peroxisomal functions (Zellweger syndrome, neonatal adrenoleukodystrophy, infantile Refsum's disease) an accumulation of very long-chain fatty acids and pathological bile acids are found. Patients have a defective synthesis of plasmalogens and show increased excretion of dicarboxylic acids of medium chain length and of pipecolic acid in the urine. These anomalities which are due to the lack of peroxisomal enzymes, supply the basis for clinical laboratory tests. The study of these peroxisomal disorders has presented valuable information on the normal function of peroxisomes.
Humans↗
[Reparative giant cell granuloma as a manifestation of primary hyperparathyroidism in jaw area].
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Granuloma, Giant Cell↗
Fatty acyl-CoA oxidase in rat kidney and liver after application of thyroxine.
Male rats were fed a standard diet containing 2.5 mg% L-thyroxine. After 10 and 20 days, in postnuclear fractions of the kidney the specific activity of fatty acyl-CoA oxidase, the enzyme responsible for the rate-limiting first step of peroxisomal fatty acid beta-oxidation, was increased by 100 and 160%, respectively. A similar effect was found in the liver. It is suggested that thyroxine essentially affects only this step of the fatty acid beta-oxidation sequence. Presumably the elevation of fatty acyl-CoA oxidase is one reason for the beneficial action of thyroid hormones in toxic lesions of the kidney.
Acyl Coenzyme A↗
[The contribution of peroxisomes to lipid metabolism].
Peroxisomes are ubiquitous subcellular organelles. They contain catalase and hydrogen peroxide-producing oxidases like fatty acyl-CoA oxidase. The latter enzyme is part of a special fatty acid beta-oxidation system which shortens long-chain fatty acids. The middle-chain acids formed are subsequently degraded by mitochondria. The capacity to remove very long fatty acids and trans-unsaturated acids found in hydrogenated oils is restricted to peroxisomes. Essentially, the peroxisomal beta-oxidation system is not constitutive but inducible by certain hypolipidaemic compounds which are distinguished by their capacity to lead to proliferation of peroxisomes. Thyroid hormones as well as prolonged exposure to cold and high fat diets, esp. with long-chain unsaturated fatty acids, also induce beta-oxidation and peroxisome proliferation. Two other beta-oxidative reactions namely the removal of the cholesterol side-chain, leading to the formation of bile acids, and the degradation of dicarboxylic acids as formed by omega-oxidation of fatty acids were shown to be connected with peroxisomes. Presumably also 3-hydroxy-3-methyl-glutaryl-CoA reductase, the key enzyme of cholesterol biosynthesis exists in a peroxisomal moiety. NADPH consumed in this reaction (and in the dihydroxyacetone phosphate pathway of glycerolipid synthesis) might be provided by glucose-6-phosphate dehydrogenase which was recently also found in peroxisomes. Peroxisomes are indispensable in forming saturated ether lipids and plasmalogens because alkyldihydroxyacetone phosphate synthase is a membrane enzyme exclusively located in peroxisomes. Certain other enzymes of the dihydroxyacetone phosphate pathway of glycerolipid synthesis are also found in peroxisomes. Because of the combination of oxidases like fatty acyl-CoA oxidase and catalase and the feasibility of reoxidising NADH within the peroxisomes the aerobic metabolism of peroxisomes is energy-wasting. Therefore they might be important in chemical thermogenesis and in the control of body weight. For all these reasons peroxisomes must be essential for human metabolism. This is further demonstrated by genetically caused disorders: Total absence of peroxisomes is connected with the fatal cerebro-hepatorenal Zellweger syndrome. Defective peroxisomal beta-oxidation is manifested in Schilder's disease (adrenoleukodystrophy) characterized by accumulation of very long fatty acids. Peroxisomes perform a number of complementary and auxiliary reactions in general cell metabolism, in particular the cata- and anabolism of certain lipids, and therefore deserve consideration in clinical chemistry.
Bile Acids and Salts↗