Multicentre evaluation of performance of C-reactive protein analysis over a one-year period.

This communication deals with a longitudinal evaluation of C-reactive protein (CRP) analysis during a one-year period using a single lot of liquid control sera (3 levels) (BIOREF-CRP levels 1, 2 and 3) in different laboratories. A total of 652 sets of data were returned from 20 participating laboratories using 13 different reagent-measuring device combinations. The use of the control materials was defined in a standard operating procedure. Data was returned to the organizers on a monthly basis and questions could be asked or problems presented during the evaluation period. Although the performance of different reagents varied, the control materials were shown to be stable over the whole of the evaluation period when stored at 4-7 degrees C in a refrigerator/cold room. Typical problems were encountered, examples of which are presented here in graphical and tabular form.

Severe head trauma and the changes of concentration of neuron-specific enolase in plasma and in cerebrospinal fluid.

In nine patients with severe head trauma, the concentration of neuron-specific enolase in cerebrospinal fluid and in plasma was determined and compared with the activity of creatine kinase and alpha-hydroxybutyrate dehydrogenase, and with the concentration of lactate. In patients who died of the head trauma, a concentration of neuron-specific enolase of 6.8-64 micrograms/l in the plasma (reference range: 3.0-6.0 micrograms/l) and of 2.2-9.0 micrograms/l in the cerebrospinal fluid (reference range: 0.5-2.0 micrograms/l) was detected. Investigations of three patients showed that the changes of the concentration of neuron-specific enolase in plasma and in cerebrospinal fluid were independent of each other. Furthermore, the initial concentration of neuron-specific enolase in the plasma after the accident and the dynamics of its changes during the disease show a close relationship to the outcome.

Continuous determination of various enzymes and sodium concentration in urine. a usable method for diagnosis of kidney graft rejection.

We investigated changes in urinary enzyme activity and sodium concentration of kidney transplant patients. We found that the increase of the activity of brush border enzymes is one of the earliest signs of tubular damage following rejection. The decrease in the urinary sodium concentration points also to rejection episodes. Despite the unspecificity of both variables, their continuous determination and combined analysis of the results could improve the differential diagnosis of rejection after transplantation and might give important information about the pathogenesis of the graft damage.

[Biochemical parameters for determination of graft viability during the early postoperative period (author's transl)]. / Biochemische Parameter zur Feststellung der Lebensfähigkeit allogener Nierentransplantate.

In 54 patients with graft failure the changes of urine sodium concentration and of urinary enzyme activities (alanine aminopeptidase, AAP) were investigated. It was found that: (1) the kidneys with irreversible acute tubular necrosis are characterised by high urine sodium level, and low AAP activities. These changes correspond to the end stage of renal insufficiency. (2) Low concentration of sodium and extremely high AAP excretion are characteristic in grafts with severe rejection episodes. (3) If kidneys lost their function due to irreversible rejection, the biochemical variables showed the same changes as in the first group. We concluded that by continuous determination of sodium levels and enzyme activities in urine and by their correlation it is possible to detect the non-functioning grafts in the early posttransplantation period.

Changes of neuron-specific enolase concentration in plasma after cardiac arrest and resuscitation.

The concentration of neuron-specific enolase (NSE) was measured in plasma of 18 patients after cardiac arrest and resuscitation (14 nonsurvivors and 4 survivors). In all patients, the NSE concentration was significantly higher in comparison to reference values. The highest concentration was measured in nonsurvivors. Time-course investigation in the first 24 h after cardiac arrest was performed in five patients. Two nonsurvivors and one survivor of the five patients showed a significant rise, and a NSE peak concentration of 42.7 micrograms/L, 13.6 micrograms/L, and 10.5 micrograms/L, respectively, was found 10-19 h after cardiac arrest.

Lysosomal and ATP changes after renal-stalk clamping in rats. I. Protective action of Trasylol.

The action of Trasylol on the lysosomal and ATP changes after renal-stalk clamping in rats was examined. It was found that, in the presence of an effective Trasylol concentration, a distinct stabilization of the lysosomal membrane can be detected after 30 min of renal-stalk clamping. It was also found that there is only an indirect relationship between lysosomal changes and ATP metabolism under the action of Trasylol. The more rapid regeneration of the ATP is a result of the better microcirculation. The results confirm the earlier belief that Trasylol acts primarily on the lysosomal membrane.

Changes in serum and urine lysozyme activity after kidney transplantation: influence of graft function and therapy with azathioprine.

We investigated changes in lysozyme activity in serum and urine of kidney-transplant patients, and found that the production and catabolism of lysozyme in such patients differs markedly from that in normal subjects. Resumption of graft function decreases the high serum lysozyme activity by increasing the rate of catabolism in the transplant; at the same time, however, the production is inhibited by therapy with azathioprine. Changes in serum lysozyme activity correlate well with leukocyte count; thus its determination might be useful in monitoring immunosuppression. The urinary excretion of the enzyme, although not specific to rejection, is a good index of the degree of tubular damage.

The concentration of hypoxanthine and lactate in the blood of healthy and hypoxic newborns.

This work examines the correlation between the concentration of hypoxanthine and lactate, the clinical course, and the parameters of the acid-base metabolism in newborns. In order to obtain normal values in mature, healthy newborns (Group A) 136 determinations of hypoxanthine and 126 determinations of lactate in blood were performed in the first five postnatal days. In well prematures (Group B) hypoxanthine was determined 18 times and lactate 16 times. In newborns requiring oxygen therapy including ventilator support (Group C) hypoxanthine and lactate were determined 36 and 31 times respectively. Hypoxanthine levels in the blood of mature healthy newborns decreased with increasing age. A similar course is known for lactate levels. In the group of well prematures (Group B), hypoxanthine and lactate levels have an age dependent course similar to that in group A. Correlations between hypoxanthine and lactate concentrations were observed in all three groups but were not noted to be as well defined as has been seen experimentally (e.g., by SAUGSTAD) and thus confirm the clinical results of other authors. Among the newborns requiring oxygen therapy (Group C) 7 of 36 hypoxanthine values were more than two standard deviations above those in the normal group. For lactate group C infants were in 12 of 31 cases above the two standard deviation range. The hypoxanthine and lactate concentrations of group C newborns were correlated with clinical and biochemical indicators of hypoxia. Infants with unequivocal signs of hypoxia showed elevated as well as normal hypoxanthine and lactate levels. Conversely, infants without clinical, pathological or biochemical hypoxia indicators showed in some cases elevated hypoxanthine and lactate values.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuron specific enolase in amniotic fluid--a possible indicator for fetal distress and brain implication.

It can be suggested that a NSE concentration in body fluids above the normal range may indicate brain damage, because NSE is found in neurons and neuroendocrine cells only. In this paper the concentration of the neuron specific enolase (NSE) in the amniotic fluid of normal and high risk pregnancies was investigated. Sixty-three samples of amniotic fluid were collected from 55 pregnant women and women in labor between the 19th and the 42nd gestational week. In 24 normal pregnancies 1.02 +/- 0.31 microgram NSE/L (mean +/- SD) were found. A relationship of NSE concentration was not found for gestational age, uterine contractions, age and parity of the mother, infant's birth weight or 1 min Apgar score. Maternal diseases such as diabetes mellitus, hypertension and others do not result in any increase of NSE concentration in the amniotic fluid (N = 20; 1.06 +/- 0.24 microgram NSE/L). Fetal and birth related high risk factors such as meconium stained amniotic fluid, cord around the neck, severe decelerations of the fetal heart rate or combinations of these factors caused the NSE concentration to exceed significantly normal values (N = 17; 2.22 +/- 0.87 microgram NSE/L). Due to its high organ and cell specificity, NSE may be a possible parameter for brain damage due to hypoxia in the fetus and newborn; however, only subsequent neurological and psychological examinations of these children can indicate the prognostic value of an elevation of NSE concentration in amniotic fluid.

[Psychomotor development of newborn infants at risk with reference to the neuron-specific enolase]. / Psychomotorische Entwicklung von Risikoneugeborenen unter Berücksichtigung der Konzentration der neuronenspezifischen Enolase.

In a prospective study the psychomotor development of an unselected collective of risk newborn infants up to the end of the second year of life was examined. 199 children have developed normal, 21 showed developmental abnormalities, 84 light to moderate disturbances, and 30 severe disabilities. Already in the newborn period the concentration of neuron-specific enolase in the serum was evaluated. The NSE could be an indicator of brain damage. The determined values of NSE showed a log-normal-distribution at the three times (cord-blood, first or second day of life, third or fourth day of life, and ninth to eleventh day of life). Significant relationship between the psychomotor development during the first two years of life and of NSE-concentration was not found. Nevertheless the diagnostic value of the NSE is better with a specificity of 47.7% and a sensitivity of 80.0% than those of the results of intracranial ultrasound examination or of the erythrocytic-density-test. In contrast to these results the use of the neuron-specific enolase alone for the prediction of individual prognosis of children is not be recommended.

[Significance of LDH determination in renal perfusions as criterion of vitality in kidney transplantations (author's transl)]. / Die Aussagefähigkeit der LDH-Bestimmung im Perfusat als Vitalitätskriterium bei Nierentransplantation

The activity of LDH in perfusate on human kidney and in experiments on dog kidney was investigated during the preservation by the Gambro perfusion apparatus. The enzyme activity of perfusate was characterized by a quotient of volume activity in relation to the perfusion flow rate. With this method we are able to distinguish the values of damaged and normal kidneys. A correlation was established between this quotient and the function resumption day in human kidney transplantation.

[Enzyme immunoassays for the quantification of human gamma-gamma-enolase (NSE)]. / Enzym-Immunoassays zur Quantifizierung humaner gamma-gamma-Enolase (NSE).

A direct two-site binding assay on the basis of antibodies from sheep for the quantification of human gamma-gamma enolase is described. The antibody was produced by immunization with human NSE coupled to horse spleen ferritin. The assay shows two feature: a decreased reactivity with NSE from rat and NSE from human serum in spite of 100% recovery of purified human brain NSE. The sheep antibody seems to react with epitopes less accessible on the rat NSE and on the NSE of human serum. The assay is characterized by gamma-gamma enolase specificity, a high sensitivity (2 pg) and a precision of CV = 3-7%.

[Intracerebral hemorrhage and neuron-specific enolase in premature and full-term infants--a clinical study]. / Intrazerebrale Blutungen und neuronenspezifische Enolase bei Früh- und Termingeborenen--Eine klinische Studie.

In a prospective study 199 risk newborn infants were examined by means of cerebral ultrasound scanning and after this the influence of diagnosed intracerebral events on the concentration of neuron-specific enolase (NSE) was determined. The NSE may be valid as an indicator of intracerebral damage. A significant relationship between increased concentration of NSE and intracerebral haemorrhage of type II could be found only for the NSE-1 (determination from cordblood or from blood of the first or second day of life). The same relationship results for intracranial cystic rebuildings, destructions and enlargements of ventricles. The diagnostic tests of NSE-1 for intracerebral haemorrhages don't prove with a validity of 57.4% high prognostic value. Not until a NSE-1-level of 16.0 micrograms/l a predictive value of the positive test of 100% was calculated.

Development of enolase isoenzymes in various regions of the human brain.

Various brain regions from 4 fetuses (21st to 28th gestational week) and from a 3-month-old infant were investigated for the total enolase activity and their isoenzyme distribution. In the brain tissue from a 3-month-old infant, the activity of the so-called neuron-specific enolase amounted to about 50% of the total enolase activity. In various brain regions different developmental patterns emerged for nonneuronal (NNE) and neuron-specific enolase (NSE). By the 21st gestational week the medulla, pons and thalamus had already reached a relatively high NSE activity (about 60-90% of that of the 3-month values), whereas the cortex regions had 10-30% only. It is concluded that in phylogenetically old regions, the switch from NNE to NSE-subunits appears before the 21st gestational week, in the phylogenetically young regions between the 21st and 28th gestational week.

[A staged plan for laboratory diagnosis of hereditary metabolic diseases]. / Stufenplan zur Labordiagnostik hereditärer Stoffwechselerkrankungen.

When clinical evidence provides grounds for suspecting inborn errors of metabolism it is urgent to perform the necessary, relevant, specific laboratory investigations in good time and with a view to quality. Normally, the realization depends on individual initiatives and the use of laboratories mainly designed for pediatrics and human genetics. Consequently the results are equally a matter of chance. Nothing in this situation can be changed in principle by using the catalogue of services of the Society for Human Genetics of the GDR. Central administrative provisions are necessary to improve the present unsatisfactory situation. Proposals for regulations, division of responsibility and a graduated programme of parameters are discussed here with a view to establishing uniform procedures.