Acid freezes uricolysis in addition to glycolysis: Utility of fluoride-EDTA-citrate tube in the measurement of uric acid for patients administered rasburicase

Author(s):  
Tejas Kalaria ◽  
Jonathan Fenn ◽  
Richard Whitmill ◽  
Clare Ford ◽  
Rousseau Gama

Background In samples from patients administered rasburicase, ex vivo uricolysis leads to spuriously low uric acid results. The manufacturer’s recommendation of storing the sample in ice-water until analysis, however, does not fully arrest uricolysis. Since uricase activity is affected by pH and metal chelators, we assessed uricolysis inhibition in sodium fluoride-ethylenediaminetetraacetic acid (EDTA)-citrate sample tube (FC Mix tube, Greiner) used primarily for plasma glucose. Method A serum pool was spiked with rasburicase and uric acid measured at 15, 45, 90, 150, 240 and 1080 min in a lithium heparin tube in ice-water, plain tube at room temperature (RT), EDTA tube at RT, FC Mix tube in ice-water, FC Mix tube at RT and FC Mix tube at RT prepared by dissolving FC Mix in serum. Results The rate of urate decay was lowest in the FC Mix tube independent of temperature, then lithium heparin tube in ice-water, then EDTA tube at RT and highest in the plain tube at RT. Uric acid concentrations in the prepared FC Mix tube at RT and heparin tube in ice-water were, respectively, 98.2% and 93.8% of control values at 90 min, 97.1% and 89.3% of control values at 4 h, and remained higher in the prepared FC Mix tube at all time points. Conclusion NaF-EDTA-citrate mixture largely arrested rasburicase mediated ex vivo uricolysis without the need for sample cooling. We propose that sample tubes containing NaF-EDTA-citrate be used for the measurement of uric acid in patients administered rasburicase.

1992 ◽  
Vol 68 (02) ◽  
pp. 214-220 ◽  
Author(s):  
C Weber ◽  
J R Beetens ◽  
F Tegtmeier ◽  
P Van Rooy ◽  
E Vercammen ◽  
...  

SummaryThe effects of ridogrel, a dual thromboxane A2 (TXA2) synthase inhibitor and TXA2/prostaglandin (PG) endoperoxide receptor antagonist, on systemic and renal production of prostaglandins and on platelet TXA2/PG endoperoxide receptors was evaluated upon chronic administration (300 mg b. i. d. orally, for 8 and 29 days) to man. Such a medication with ridogrel inhibits the systemic as well as the renal production of TXA2 as measured by the urinary excretion of 2,3-dinor-TXB2 and TXB2 respectively without inducing significant changes in systemic or renal PGI2 production. Simultaneously with the latter effects, the production of TXB2 by spontaneously coagulated whole blood ex vivo is inhibited (>99%) while that of PGE2 and PGF2α is largely increased. Administration of ridogrel causes a three- to five-fold shift to the right of concentration-response curves for U46619 in eliciting platelet aggregation; no tachyphylaxis is observed after 29 days of treatment in this respect. Apart from a reduction of serum uric acid levels with a concomitant increase in urinary uric acid excretion during the first days of treatment, no clinically significant changes in hematological, biochemical, hemodynamic and coagulation parameters occur during the 8 days or 29 days study. The study demonstrates that ridogrel is a potent inhibitor of the systemic as well as renal TXA2 synthase and an antagonist of platelet TXA2/PG endoperoxide receptor in man, covering full activity during 24 h at steady-state plasma level conditions without tachyphylaxis during 29 days of medication. The compound is well tolerated, at least during 1 month of administration.


2019 ◽  
Vol 45 (4) ◽  
pp. 1092-1099
Author(s):  
Roberto Cannella ◽  
Mohammed Shahait ◽  
Alessandro Furlan ◽  
Feng Zhang ◽  
Joel D. Bigley ◽  
...  

1985 ◽  
Vol 229 (1) ◽  
pp. 241-249 ◽  
Author(s):  
J A Salas ◽  
K Johnstone ◽  
D J Ellar

The likelihood that uric acid was the only compound capable of triggering germination of Bacillus fastidiosus spores was reinforced by the finding that ureidoglycollic acid, urea, NH4Cl, 2,8-dihydroxypurine and a combination of L-alanine and O-carbamoyl-D-serine were ineffective as germinants. Uric acid-triggered germination of B. fastidiosus was prevented by a range of inhibitors that also inhibited uricase activity in dormant spore extracts. O2 uptake during germination started immediately after addition of uric acid, possibly as a consequence of the oxidation of uric acid by the enzyme uricase. Germination showed a dependence on uric acid concentration, with a relatively high Km (4-5 mM). During the first 10 min of germination of heat-activated spores there was no detectable change in the number of spore-cortex reducing groups, indicating that selective cortex hydrolysis is not involved in the trigger mechanism of germination of B. fastidiosus. On the basis of the results, a model is proposed in which re-initiation of uricase activity is the mechanism by which B. fastidiosus spores are triggered to emerge from the dormant state.


1966 ◽  
Vol 12 (1) ◽  
pp. 18-24 ◽  
Author(s):  
Wendell T Caraway ◽  
Herman Marable

Abstract A colorimetric carbonate procedure for the determination of uric acid has been modified to include incubation of serum with uricase to destroy uric acid. Residual nonurate chromogens are subtracted from total chromogens to obtain the concentration of "true" uric acid. Result obtained by the carbonate and the uricase-carbonate methods were in good agreement. The mean concentration of nonurate chromogens in serum is approximately 2% of the true uric acid values. Recovery of uric acid added to serum is essentially quantitative. Formaldehyde markedly inhibits uricase activity and interferes with recoveries. The uricase-carbonate method is applicable to hemolytic serum and to serums from patients with uremia or those receiving high doses of salicylate in which excess concentrations of nonurate chromogens may be encountered.


1978 ◽  
Vol 234 (4) ◽  
pp. E421
Author(s):  
M Y Dju ◽  
T F Yü

The homozygous muscular dystrophic mice (dydy) were found to have significantly higher plasma uric acid than their heterozygous littermate controls (Dydy), and the Swiss albino mice. Because the rate of uric acid excretion did not compensate for the elevated plasma levels, U/P (urine/plasma) urate was lower in dydy mice. With RNA supplement, plasma and urinary urate were increased in both dydy and Dydy mice; again U/P urate was lower in dydy mice. It appears that the dydy mice to a certain extent are comparable to some gouty subjects, whose hyperuricemia is not accompanied by a corresponding increase in urinary uric acid. There was no difference in converting uric acid to allantoin either on basal diet alone or with RNA supplement. Oxonic acid effectively, though transiently, blocked the uricase activity in both dydy and Dydy mice resulting in hyperuricemia and hyperuricosuria with decreased allantoin. Uric acid content was increased markedly in the kidney without histological evidence of urate deposition, apparently related to the unsustained effect of oxonic acid, which was rapidly excreted.


2008 ◽  
Vol 36 (3-4) ◽  
pp. 133-138 ◽  
Author(s):  
Paul Stolzmann ◽  
Hans Scheffel ◽  
Katharina Rentsch ◽  
Thomas Schertler ◽  
Thomas Frauenfelder ◽  
...  

2011 ◽  
Vol 196 (6) ◽  
pp. 1279-1287 ◽  
Author(s):  
Mingliang Qu ◽  
Juan C. Ramirez-Giraldo ◽  
Shuai Leng ◽  
James C. Williams ◽  
Terri J. Vrtiska ◽  
...  

1997 ◽  
Vol 35 (6) ◽  
pp. 577-585 ◽  
Author(s):  
PAOLO ENRICO ◽  
GIOVANNI ESPOSITO ◽  
MARIA A. MURA ◽  
ROSSANA MIGHELI ◽  
PIER ANDREA SERRA ◽  
...  

2018 ◽  
Vol 56 (2) ◽  
pp. 249-255 ◽  
Author(s):  
Stan R. Ursem ◽  
Marc G. Vervloet ◽  
Jacquelien J.G. Hillebrand ◽  
Renate T. de Jongh ◽  
Annemieke C. Heijboer

Abstract Background: Posttranslational oxidation of parathyroid hormone (PTH) modifies its biological activity. Measurement of non-oxidized PTH (n-oxPTH) could be an improvement in assessing PTH status, as intact PTH may rather reflect oxidative stress. However, it is debated whether oxidation of PTH occurs in vivo, or whether it is mainly an in vitro artifact. The aim of this study was to investigate the influence of different preanalytical conditions on the oxidation of PTH within a wide range of plasma PTH concentrations and oxidation propensity. Methods: n-oxPTH was separated from its oxidized form using an affinity column capturing the oxidized PTH. n-oxPTH was measured in eluate using commercially available PTH assays. The study included ethylenediaminetetraacetic acid plasma samples from 17 patients undergoing hemodialysis and 32 healthy subjects. We determined effects of storage temperature, time until centrifugation and freeze-thaw cycles. PTH and n-oxPTH concentrations were measured in each sample using six different immunoassays. Results: n-oxPTH concentrations remained unchanged up to 180 min until centrifugation, two freeze-thaw cycles or after storage at −20°C or −80°C up to 79 days. Various methods for n-oxPTH and PTH measurements yielded highly comparable results, apart from standardization differences between various PTH and n-oxPTH assays. Conclusions: n-oxPTH concentrations were stable under our study conditions, indicating negligible ex vivo oxidation of PTH. In addition, PTH immunoassays have a different sensitivity for n-oxPTH than for total PTH. For this reason, the n-oxPTH/total PTH ratio cannot be used in absence of a n-oxPTH standard. Clinical implications of determining n-oxPTH require additional study.


1999 ◽  
Vol 277 (4) ◽  
pp. L719-L726 ◽  
Author(s):  
Henryk Zielinski ◽  
Ian S. Mudway ◽  
Kelly A. Bérubé ◽  
Samantha Murphy ◽  
Roy Richards ◽  
...  

Oxidative stress may be a fundamental mode of injury associated with inspired particles. To examine this, we determined the ability of three carbon black particles (CBPs; M120, M880, and R250) and two forms of silicon dioxide, amorphous (Cabosil) and crystalline (DQ12) quartz, to deplete epithelium lining fluid antioxidant defenses. Single and composite antioxidant solutions of uric acid, ascorbic acid (AA), and reduced glutathione (GSH) were examined in the presence of particle concentrations of 150 μg/ml. Uric acid was not depleted by any particle considered. AA was depleted in a near-linear fashion with time by the three different CBPs; however, AA depletion rates varied markedly with CBP type and decreased in the presence of metal chelators. An initially high GSH depletion rate was noted with all CBPs, and this was always accompanied by the appearance of oxidized glutathione. Exposure to Cabosil or DQ12 did not result in the loss of GSH. Together, these data demonstrate that particle type, size, and surface area are all important factors when considering particle-antioxidant interactions in the airways.


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