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Biomedical subjects

L Ranek

Publications and source records attributed to L Ranek.

At least 37 records · Page 2Linked to original sources
PubMed1986

Halothane hepatitis in a prospective study of postoperative complications.

In a prospective study comprising 2609 consecutive surgical patients, of whom 1166 were anesthetized with halothane, four cases of hepatitis were encountered. The incidence of hepatitis among those who received halothane was 1:292 in our material. The high incidence may be explained by the recognition of milder forms of hepatitis and by the selection of the series (over 40 years). Serum alanine aminotransferase should be investigated in all patients with postoperative pyrexia of unknown origin if mild forms of halothane hepatitis are to be discovered. The patient's history should be carefully examined for previous postoperative pyrexia of unknown origin following halothane anesthesia, in which case other anesthetics should be chosen.

Aged↗
PubMed1986

Reye's syndrome in Denmark. A retrospective study.

We tried to determine the incidence of Reye's syndrome (RS) in Denmark in a retrospective study. As RS is often preceded by influenza B, we chose the year 1979, where an epidemic of influenza B was registered in Denmark. All children aged 1 month to 18 years, who died, were identified, excluding children who died from accidents or malignant diseases. Two hundred and forty-two children died in hospital. Review of the records revealed one case of RS. One hundred and five died outside hospital. Reviewing death certificates and autopsy reports, none of these fulfilled the criteria for RS. All paediatric departments were asked if they had made a diagnosis of RS. None had. In 1979 approximately 1.1 mill. children aged 1 month to 14 years lived in Denmark. This gives an incidence of 0.09 per 100 000 for 1979. Although this is a minimum figure, the incidence of RS in Denmark, for unknown reasons, seems very low.

Adolescent↗
PubMed1986

Fatal familial cholestatic syndrome in Greenland Eskimo children.

A syndrome of intrahepatic cholestasis leading to death in early childhood was studied in 16 Greenland Eskimo children. The pedigrees are compatible with autosomal recessive inheritance. Jaundice, bleeding, pruritus, malnutrition, steatorrhoea, osteodystrophy and dwarfism were typical clinical features. Eight had died between the ages of six weeks and three years due to bleeding or infections. Hyperbilirubinaemia, profound hypoprothrombinaemia, thrombocytosis and elevated alkaline phosphatase levels were evident. Serum calcium, phosphate and parathyroid hormone levels indicated a secondary hyperparathyroidism. Hepatic fibrosis developed with increasing age. Follow-up of the surviving patients was 4 to 30 months. The aetiology of the disease is unknown. The syndrome has some features in common with previously described patients with familial intrahepatic cholestasis. No specific treatment is available. Genetic counselling is essential.

Celiac Disease↗
PubMed1985

Beneficial effect of azathioprine and prediction of prognosis in primary biliary cirrhosis. Final results of an international trial.

The effect of azathioprine on survival of patients with primary biliary cirrhosis was studied prospectively in a multinational, double-blind, randomized clinical trial including 248 patients of whom 127 received azathioprine and 121 placebo. There were 57 deaths in the azathioprine group and 62 in the placebo group. The actual survival was slightly longer during azathioprine than during placebo treatment. Using Cox multiple regression analysis and adjusting for slight imbalance between the two treatment groups, the therapeutic effect of azathioprine was statistically significant (p = 0.01), with azathioprine reducing the risk of dying to 59% of that observed during placebo treatment (95% confidence interval 40%-90%) or improving survival time by 20 mo in the average patient. Furthermore, azathioprine slowed down progressing incapacitation. Side effects of azathioprine were relatively few. The analysis revealed that the following five variables independently implied poor prognosis: high serum bilirubin, old age, cirrhosis, low serum albumin, and central cholestasis. These factors were combined to a "prognostic index" for prediction of outcome in new patients. The index was validated on independent patient data. On the basis of these results we recommend azathioprine as a routine treatment of primary biliary cirrhosis.

Actuarial Analysis↗
PubMed1985

Double blind controlled trial of d-penicillamine in patients with primary biliary cirrhosis.

One hundred and eighty nine patients with primary biliary cirrhosis were entered into a double blind, placebo controlled randomised trial starting in January 1978 to assess the therapeutic value of d-penicillamine 1200 mg daily. Eighteen of the 98 patients receiving d-penicillamine and 22 of the 91 placebo treated patients died during the study. Thirty six per cent of those on d-penicillamine and 8% of those on placebo were withdrawn from the study. No difference in overall survival was noted between the two groups of patients whether the results were analysed for the entire period of observation or only during the period in which the patients were receiving therapy. The mortality rate of those receiving d-penicillamine in histological stage I to II, however, was one third of that of the placebo group although this difference did not reach statistical significance. Using the occurrence rate ratio as the statistical method of analysis, no effect of d-penicillamine was noted on any clinical, biochemical or histological features examined, except the serum alanine aminotransferase activity which was greater in those on active treatment. In this trial we have been unable to establish any therapeutic benefit from the drug.

Clinical Trials as Topic↗
PubMed1984

Isolated liver damage in chemical workers.

During a period of 18 months three workers were admitted to hospital with jaundice that had developed two to four months after beginning work at a chemical plant. Liver biopsies showed severe centrilobular, haemorrhagic liver cell necrosis. The pathological changes resolved within six to 18 months. No damage to other organs was observed. The only worker who resumed work at the plant developed clinical and biochemical evidence of relapse of liver damage. Exposure to carbon disulphide, isopropanol, toluene, and acrylonitrile among others was shown, but liver damage may have been caused by a synergistic, hepatotoxic reaction mediated through the hepatic microsomal enzyme system. It was not possible to decide which chemical was responsible.

Adult↗
PubMed1984

The effect of continuous vasopressin infusion on splanchnic blood flow, liver function, and portal and central venous pressures in patients with cirrhosis.

Continuous vasopressin infusion has been shown to control bleeding from oesophageal varices in patients with cirrhosis of the liver. The mortality, however, has not been changed. To investigate whether reduction of portal blood flow over a period of hours deteriorates the liver function, we measured the splanchnic blood flow and galactose and oxygen consumption in five cirrhotic patients during liver vein catheterization. Vasopressin was given as a continuous infusion of 0.2 units per min for three h. The splanchnic blood flow was reduced to 70% of control values and remained so throughout the infusion. After three h no impairment of the liver function was found. The wedged hepatic pressure (portal pressure) rose slightly, probably due to the increase of the central venous pressure reflecting impaired cardiac function. The reported beneficial effect of vasopressin on varix bleeding probably depends on the reduced portal flow per se.

Adult↗
PubMed1983

Liver damage associated with occupational exposure to organic solvents in house painters.

Among 156 patients admitted to hospital because of suspected solvent intoxication or dementia following long-term occupational exposure to organic solvents, twenty-three had elevated aminotransferases in serum. In thirteen of these no particular cause of this elevation could be found and the chronic exposure to aliphatic and aromatic organic solvents is therefore likely to have played a pathogenetic role and a liver biopsy was performed. Liver histology revealed significant steatosis in eleven patients and in six of these focal necroses were also observed. Moreover, six of the biopsies showed enlarged portal tracts with fibrosis. Necrosis was only observed in liver specimens from patients who recently had been exposed to solvents. A causal relation between occupational exposure to aliphatic and aromatic organic solvents such as white spirit, xylene, toluene and styrene, and toxic liver injury is suggested by this descriptive study but needs confirmation.

Adult↗
PubMed1983

Splanchnic galactose uptake in patients with cirrhosis following single injection.

The galactose elimination capacity is used as a quantitative liver function test and is supposed to express the functioning liver cell mass. Clinical observations indicate, however, that the galactose elimination capacity overestimates functioning liver cell mass, and we therefore compare hepatic (splanchnic) and extrahepatic, extrarenal galactose elimination after a single injection of galactose in 23 patients with reduced liver function. The galactose elimination capacity was consistently greater than the hepatic (splanchnic) galactose elimination rate, estimated during liver vein catheterization. The difference was on the average 0.68 mmol min-1 (SD +/- 0.19, P less than 0.001) or about 40% of the galactose elimination capacity. If this difference, partly or fully, is due to extrahepatic extrarenal elimination, the clinical test for galactose elimination needs a correction (of the order of magnitude of 0.7 mmol min-1) to serve as an absolute measure of the hepatic functional capacity, but since the hepatic uptake rate may be underestimated following a single injection, the correction may be smaller.

Catheterization↗
PubMed1983

Splanchnic galactose uptake in patients with cirrhosis during continuous infusion.

The galactose elimination capacity (GEC) is considered a test of functional liver cell mass. The main uncertainties of the method are the effects of extrahepatic elimination and of uneven distribution in the body on the calculated maximal elimination rate of galactose. This has been evaluated by hepatic and renal venous catheterization during continuous infusion of galactose at two arterial concentration levels (mean 6.0 and 8.7 mmol l-1) in 10 patients with reduced liver function. Hepatic and renal blood flow were measured by constant infusions of Indocyanine Green and 131I Hippuran. Hepatic galactose elimination rate was identical (mean 1.36 and 1.32 mmol min-1, P greater than 0.4) at the two arterial concentration levels studied, indicating that hepatic galactose elimination rate was maximal (Vmax). The total body galactose elimination rate, calculated as amount infused during steady state, was 1.4 times greater than the hepatic elimination rate, calculated as arterio-hepatic venous concentration difference times hepatic blood flow. Within the experimental error, the extrahepatic (i.e. total minus hepatic) galactose elimination could be accounted for by renal elimination. The steady state studies show that the galactose elimination capacity, estimated from single injection, overestimates the hepatic Vmax by about 25%. The reason for this is probably mainly distribution phenomena and insufficient correction for urinary loss, but extrahepatic metabolism of galactose cannot be excluded.

Catheterization↗
PubMed1983

Cholic acid conjugation test and quantitative liver function in acute liver failure.

In 33 patients with acute hepatic encephalopathy due to toxic or viral hepatitis the following analyses were performed: (24-14C)cholic acid conjugation and sulfation, plasma phenazone clearance, galactose elimination capacity, and concentrations of glycocholic acid and glycolithocholic acid sulfate in plasma. The (24-14C)cholic acid conjugation in patients with viral hepatitis was significantly lower in fatal cases than in patients who survived (p less than 0.002). In these patients the galactose elimination capacity and the plasma phenazone clearance were insignificantly lower. Tauro-(24-14C)cholic acid was the predominant metabolite of (24-14C)cholic acid in six patients, but in four patients with toxic hepatitis this metabolite was only found in trace amounts. Sulfation after 3 h of (24-14C)cholic acid accounted for 0-8.2% of the administered dose. The sulfate of glycolithocholic acid was found in the plasma of all patients. No survival limit with regard to the capacity for the (24-14C)cholic acid conjugation could be defined.

Acute Disease↗