M Römer, R Haeckel, P Bonini, G Ceriotti, A Vassault, P Solere, P Morer
{"title":"European Multicentre Evaluation of the ESAT 6660.","authors":"M Römer, R Haeckel, P Bonini, G Ceriotti, A Vassault, P Solere, P Morer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The analytical performance of the glucose analyser ESAT 6660 from Eppendorf was studied according to the ECCLS guidelines and partly according the SFBC protocol in a multicentre evaluation involving laboratories from three European countries. The glucose determination in serum and in haemolysate was studied. The following results were obtained. 1. The precision was as good as or better than the precision of the comparison instruments. The coefficients of variation were between 1.1 and 3.4% for the between-days imprecision and between 0.35 and 1.45% for the within-run imprecision experiment. 2. The recovery of control sera values compared with the hexokinase method was between 94.3 and 102.6%. 3. With patient specimens as good agreement was found between the results obtained with the ESAT 6660 and the different comparison instruments (ASTRA, Hitachi 737 and ACP 5040). 4. A drift effect of 1.1-2.3% occurred in 5 of 21 experiments, depending on the individual enzyme membrane. 5. Sample carry-over was not observed. 6. A linearity between 0.5 and 50 mmol/l was found, exceeding the manufacturer's claims. 7. Several different endogenous and exogenous interferences were investigated. No interfering effect was detected for endogenous substances. A positive interference was observed by ascorbic acid at a concentration above 350 mg/l. 8. The practicability of the instrument was judged as very good. It was considered as a disadvantage that the instrument is not capable of piercing sample lids. Also the numeration of samples is not very convenient.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"435-43"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L Kochhan, S Janssen, D Knorr, K Olek, F Bidlingmaier
{"title":"HLA class I-, complement C4- and 21-hydroxylase probes in the genetic analysis of 21-hydroxylase deficiency.","authors":"L Kochhan, S Janssen, D Knorr, K Olek, F Bidlingmaier","doi":"10.1515/cclm.1990.28.6.413","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.413","url":null,"abstract":"<p><p>In order to develop an optimal strategy for the prenatal diagnosis of steroid 21-hydroxylase (EC 1.14.99.10) deficiency, we investigated 16 affected families with salt wasting syndrome. Genomic DNA derived from peripheral white blood cells was digested with 6 different restriction enzymes. Hybridisation was carried out with DNA-probes of the HLA class I region, the 21-hydroxylase- and the complement C4 genes. All the families were informative in at least three different loci. Twelve out of the 16 families were informative by neutral polymorphisms or disease related variants of the 21-hydroxylase gene or the adjoining C4 locus. The reliability of prediction in these cases exceeded 99%. The remaining 4 families were informative only in the HLA class I region, tantamount to a reliability of prediction of about 98%. In none of the cases did we have to fall back on semiquantitative gene dose assessments. We further describe new polymorphisms in the 21-hydroxylase region for the enzyme Pvu II and EcoR V.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"413-7"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.413","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The clinical evaluation of cobalamin deficiency by determination of methylmalonic acid in serum or urine is not invalidated by the presence of heterozygous methylmalonic-acidaemia.","authors":"K Rasmussen, E Nathan","doi":"10.1515/cclm.1990.28.6.419","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.419","url":null,"abstract":"<p><p>It is well established that accumulation of methylmalonic acid may provide an early clue to the existence of tissue cobalamin (vitamin B12) deficiency. To verify whether methylmalonic acid accumulates in adult heterozygotes for inherited methylmalonic-acidaemia and thereby gives \"false\" positive test results for cobalamin deficiency, we measured the concentration of methylmalonic acid in serum and its urinary excretion in six patients of three children with severe methylmalonic-acidaemia. We found levels of methylmalonic acid similar to those in normal subjects. In serum, the concentrations of methylmalonic acid ranged from 0.12 to 0.39 mumol/l (reference range: 0.05-0.44 mumol/l). In urine, the values ranged from 1.18 to 2.48 mmol per mol of creatinine (reference range: 0.58-3.56). We conclude that the 2% of carriers of inherited methylmalonic-acidaemia in the general population do not invalidate the usefulness of measurement of methylmalonic acid in serum or urine for the clinical evaluation of cobalamin deficiency.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"419-21"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.419","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A colorimetric assay for the determination of acid nucleoside triphosphatase activity.","authors":"M Kirchgesser, N Dahlmann","doi":"10.1515/cclm.1990.28.6.407","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.407","url":null,"abstract":"<p><p>A photometric method for the determination of the acid nucleoside triphosphatase (EC 3.6.1.-) is described, in which inorganic phosphate is liberated from ATP or other nucleoside triphosphates. Colorimetric determination of liberated phosphate is based on the formation of a green complex of phosphomolybdate and malachite green hydrochloride. Optimal test conditions were evaluated as well as the sample preparation. The enzyme activities measured in 100 normal human sera are in the range of 0.5 to 9.0 U/l with an average of 4.0 U/l for men and 3.8 U/l for women.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"407-11"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.407","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13323398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The use of cluster analysis in clinical chemical diagnosis of liver diseases.","authors":"U Folkerts, D Nagel, W Vogt","doi":"10.1515/cclm.1990.28.6.399","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.399","url":null,"abstract":"<p><p>Diagnostic judgement is usually based on recognition of patterns. Unfortunately more than three quantitative data cannot be judged simultaneously without help of mathematical methods. Working on laboratory reports, a clinician usually goes linearly through the columns and reduces quantitative to qualitative data. Therefore the medical decision process should be improved if data reduction is performed with the aid of mathematical methods for pattern recognition. A total of 191 consecutive outpatients with a tentative or proven diagnosis of hepatobiliary disease were examined clinically, clinically chemically and partly histologically. Nineteen clinical chemical parameters were determined. Prior to pattern cognition, a principal component analysis was performed. Using six factors, accounting for 72.4% of total variance, cluster analysis was done, applying a hierarchical algorithm for ascertaining a starting partition, followed by the k-means algorithm. The validity of the solution was scrutinized, and a stable structure was found with nine clusters. Patients with a rejected suspect of liver disease were mainly located in clusters 1, 6 and 7. Cluster 1 also contains patients with compensated cirrhosis without inflammation, idiopathic hyperbilirubinaemia, focal nodular hyperplasia and haemangioma of the liver. In contrast, one third of cirrhoses, all with inflammatory activity were assigned to cluster 5. Patients with primary biliary disease were distributed among clusters 2, 3 and 4. All malignant neoplasias were assigned to cluster 9. More than 50% of fatty livers were classified to cluster 7. Cluster 2 and 8 contain only one patient with primary biliary cirrhosis (cluster 2) and fatty liver hepatitis (cluster 8). The follow-up of 66 patients also showed clinically meaningful changes of cluster assignment.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"399-406"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.399","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Kits for the diagnosis of infectious mononucleosis compared with the Paul-Bunnell test.","authors":"A Uldall, B S Jensen, J Henrichsen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We compared the results obtained with six different test kits for infectious mononucleosis with those obtained with the Paul-Bunnell test. The investigation was carried out in one laboratory using 149 selected pools of patient sera. Each pool was tested three times with the Paul-Bunnell test and once with each kit. The results obtained with the kits were grouped according to the titre found with the Paul-Bunnell test. The percentage of positive results within each group was calculated for each kit. The Paul-Bunnell titre, which would have classified 50% of the specimens as positive, was estimated for each kit and this was designated the 50% cut off value. In general, there was good agreement. However, false positive test results were found rather frequently with one kit (19%) and the 50% cut off values differed. One kit showed a 50% cut off value at about 8, another at about 16, and the rest at between 16 and 32. We suggest the introduction of improved internal quality control combined with external quality assessment.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"423-5"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G Hintze, E Briehl, D Jaworek, A Kunst, J Köbberling
{"title":"Evaluation of a new enzyme immunoassay system for free thyroxine (Enzymun-Test FT4).","authors":"G Hintze, E Briehl, D Jaworek, A Kunst, J Köbberling","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Free thyroxine (FT4) represents the metabolically active fraction of the circulating thyroid hormone thyroxine (T4). In this paper the results of the evaluation of a newly developed FT4 assay are reported. This assay system is based on an enzyme-labelled one-step immunoassay. The within-run imprecision, checked using serum pools and several commercial reference materials, showed a coefficient of variation (CV) of between 0.8 and 9.8%, depending on the reference material used. The between-run imprecision showed a CV of between 1.0 and 13.2%. Accuracy experiments yielded values between 80 and 116%. When the new FT4 was compared with the calculation of an index for free thyroxine (FT4I; derived from either the ratio of T4/thyroxine binding coefficient of from T4/thyroxine binding globulin) in a number of samples in the hypo-, eu- and hyperthyroid range, a good correlation was obtained. The same was true when the new FT4 assay was compared with a widely used two-step radioimmunoassay (y = -0.146 + 0.943 x). In euthyroid subjects the measured FT4 concentration was 10.3-25.8 pmol/l. No effect was evident when the influence of EDTA and citrate was investigated, whereas addition of heparin led to an increase in FT4 concentration of about 12 to 15%. Investigation of the possible influence of a large number of drugs showed that probenezid, carbamazepine and furosemide led to an increase in the measured FT4 concentration. Dialysis increased the FT4 concentration, as measured in patients before and after haemodialysis. No effect of alteration in protein concentration and/or protein distribution of FT4 concentration could be detected. In pregnancy, FT4 values were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"427-33"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D Ratge, A Wiedemann, K P Kohse, H Klar, K Hellberg, H Wisser
{"title":"Magnitude and kinetics of alterations in plasma catecholamines and leukocyte beta-adrenergic receptors in response to anaesthesia and surgery.","authors":"D Ratge, A Wiedemann, K P Kohse, H Klar, K Hellberg, H Wisser","doi":"10.1515/cclm.1990.28.6.391","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.391","url":null,"abstract":"<p><p>We studied the response of the sympatho-adrenal system to varying intensities of different stimuli. Concentrations of norepinephrine and epinephrine in plasma as well as densities of beta 2-adrenergic receptors on mononuclear leukocytes were determined in patients subjected to operations of varying complexity and different types of anaesthesia. In patients undergoing hysterectomy (n = 9), the maximal increases in plasma norepinephrine and epinephrine were 2.7- and 2.8-fold, respectively, corresponding to a post-operative decrease of the mononuclear leukocyte beta 2-adrenergic receptors of 27% after 4 hours. Patients with coronary revascularization (n = 17) were randomly selected to receive either enflurane/N2O or neurolept anaesthesia. During intraoperative periods of stress, such as cardiopulmonary bypass and hypothermia, norepinephrine and epinephrine levels were 2-3 times higher in the neurolept patients, compared with the enflurane patients. In the former group, the respective maximal norepinephrine and epinephrine concentrations were 9.7 and 28 times the vasal values of the non-anaesthetized patients. One day postoperatively, the mononuclear leukocyte beta 2-receptor density decreased maximally by 45 +/- 11% in the enflurane patients, and by 53 +/- 6% in the neurolept patients. As early as two to five days after cardiac surgery, beta 2-receptor densities were no longer distinguishable from the preoperative values. Significant correlations between the increases in catecholamine concentrations and the decreases in beta 2-receptor densities did not exist. It is concluded that enflurane blocks the sympatho-adrenal response to surgical stress more effectively than neurolept anaesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"391-8"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13134707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cholecystokinin and glucose-induced insulinaemia in dogs with and without pancreatic acinar atrophy.","authors":"R H Meister, I H Berger, P O Schwille","doi":"10.1515/cclm.1990.28.6.379","DOIUrl":"https://doi.org/10.1515/cclm.1990.28.6.379","url":null,"abstract":"<p><p>The entero-insular hormonal axis was studied in eleven conscious Beagle dogs, loaded with glucose orally and intravenously. In five of them, exocrine pancreatic atrophy was induced by pancreatic duct occlusion with prolamine, and documented by means of the p-amino-benzoic acid test. After oral glucose, the duct-occluded dogs displayed higher blood glucose (log area 4.12 +/- 0.07 versus 3.76 +/- 0.10; p less than 0.01), less plasma insulin (log area 3.56 +/- 0.08 versus 3.99 +/- 0.08; p less than 0.01) and less cholecystokinin-like immunoreactivity (log area 2.64 +/- 0.09 versus 3.10 +/- 0.14; p less than 0.01) than controls. In controls, the peripheral venous insulin concentrations were higher after oral than after isoglycaemic intravenous glucose, and this difference was no longer demonstrable in duct-occluded dogs. In the latter, gel permeation chromatography of pool plasma after oral glucose revealed a relative decrease of cholecystokinin-like immunoreactivity species, which eluted at the positions of sulphated cholecystokinin octapeptide, cholecystokinin-33 and cholecystokinin-39, and at a position intermediate between these two. Also in the duct-occluded animals, intravenous infusion of sulphated cholecystokinin octapeptide, in addition to oral glucose, resulted in an increase in plasma insulin (log area 3.83 +/- 0.10 versus 3.64 +/- 0.06; p less than 0.01) and an improvement in oral glucose tolerance. It is concluded that in the dog 1) the absence of pancreatic acinar tissue is associated with a loss of gastrointestinal factors mediating glucose-induced insulin secretion, and 2) reduction of circulating endogenous cholecystokinin species may account at least in part for this defect.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 6","pages":"379-90"},"PeriodicalIF":0.0,"publicationDate":"1990-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/cclm.1990.28.6.379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13364975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of the kidney in carnitine metabolism.","authors":"W G Guder, S Wagner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The kidney plays a major role in carnitine biosynthesis, excretion and acylation. Unlike in the rat, human kidney contains all enzymes needed to form carnitine from trimethyllysine in activities exceeding those of the liver. This carnitine precursor is found to be increased in plasma of patients with chronic renal failure. Free carnitine formed in the kidney as well as carnitine reabsorbed from the glomerular filtrate may be acylated in the proximal tubule. Isolated rat cortical tubule suspensions contain total carnitine concentrations of 2.85 mumols/g protein. During incubation over 60 min the acylcarnitine/carnitine ratio decreased, indicating deacylation of acylcarnitine in proximal tubules. Exogenous carnitine was acylated at a rate of 35 mumols/h.g protein. Besides pyruvate and acetate, ketone bodies stimulated the acylation rate severalfold, indicating that these substrates are a major source of acetyl-CoA for the acylation reaction. This may explain the higher acetylcarnitine/carnitine ratio found in urine under ketotic conditions.</p>","PeriodicalId":15649,"journal":{"name":"Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie","volume":"28 5","pages":"347-50"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13352754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}