Journal of Laboratory and Clinical Medicine最新文献

Concentrations of C-reactive protein (CRP) and procalcitonin (PCT) have been suggested as markers of infection. The liver is believed to be a key source of CRP and PCT. For this reason we assessed the predictive value of these markers in patients with hepatic cirrhosis in a 31-bed university-hospital department of intensive care. Demographic, clinical, laboratory, and microbiologic data were collected prospectively over 9 months. Of 864 patients included in the study, 79 (9%) had hepatic cirrhosis. Patients with cirrhosis were more likely to have a medical than a surgical admission diagnosis (67 vs 47%, P = .03). They also had a higher rate of infection (48 vs 30%, P = .03) and higher mortality (44 vs 17%, P = .01) than did patients without cirrhosis. We detected no differences in CRP and PCT concentrations among patients with cirrhosis and different disease severity as assessed on the basis of Child-Pugh score. The serum CRP concentration (admission 11.2 ± 4.6 vs 13.0 ± 5.8, maximum 13.9 ± 6.4 vs 18.8 ± 7.3 mg/dL) and PCT (admission 1.3 ± 0.9 vs 2.0 ± 1.4, maximum 3.3 ± 1.8 vs 3.4 ± 2.1 ng/mL) were slightly lower in infected patients with cirrhosis than in infected patients without cirrhosis, but the differences were not statistically significant. Although the liver is considered the main source of CRP and a source of PCT, serum levels of these acute-phase proteins are not significantly lower in patients with cirrhosis than in other patients. Moreover, the predictive power of CRP and PCT for infection was similar for patients with and without cirrhosis.

Delayed sample analysis is not a rare circumstance in clinical and laboratory practice, especially when blood samples are shipped to distant centralized laboratories, when the analysis can not be readily performed, or when retesting is appropriate. In this study we sought to evaluate the stability of conventional and new hematologic parameters in blood specimens stored for as long as 24 hours at 4°C. Of the 21 hematologic parameters tested with the use of the Advia 120 hematologic analyzer (Bayer Diagnostics), means for paired samples of specimens differed significantly over the 24-hour storage period for hematocrit, main corpuscular volume, percentage of macrocytes, platelet count, main platelet volume, reticulocyte count and percentage, and reticulocyte hemoglobin content (all P < .01). We noted no significant changes in the other parameters tested or in the white blood cell differential. The overall distribution of the immature reticulocytes fractions remained substantially unchanged, though the high staining-intensity fraction showed a considerable shift from the baseline measure. Bland-Altman plots and limits-of-agreement analysis showed mean biases between −4.8% and 37.2% and relative coefficients of variations ranging from 0.4% to 32.7%. The 95% agreement interval in the set of differences was satisfactory and almost within the current analytic-quality specifications for desirable bias. The results of this investigation suggest that, within certain limitations for parameters derived or calculated from cellular volumes, blood specimens stored for as long as 24 hours at 4° C may be suitable for hematologic testing.

Background: Conflicting data exist as to what extent hypoalbuminemia reduces the anion gap; estimates range from 1.5 to 2.5 mM per g/dL decrease in serum albumin. Methods: We measured serum albumin, total protein, and electrolyte concentrations in 5328 consecutive patients aged 1 month to 102 years. Most patients (3750; 70%) had a normal albumin, but 1158 had hypoalbuminemia (≤3.4 g/dL); 420 had hyperalbuminemia (≥4.7 g/dL). Relationships between serum albumin or total protein and the anion gap were analyzed by linear regression. Results: 309 (27%) hypoalbuminemic patients had a decreased anion gap, and 257 hyperalbuminemic patients (61%) had an increased anion gap. Among the entire group of 5328 patients, there were highly significant correlations between either serum albumin or total protein and the anion gap (P < 0.001). The slope of the regression for albumin versus anion gap was 2.3 mM per g/dL. Using this slope, anion gap could be adjusted for abnormal serum albumin levels: anion gap_adjusted =anion gap + 2.3 (4-albumin). The initial assessment of an anion gap as being increased, normal, or decreased changed in 44% of the patients with hypo- or hyperalbuminemia once anion gap had been adjusted with this formula. Conclusions: Before considering whether a disorder associated with an increased or decreased anion gap is present, the anion gap should be first adjusted for abnormal serum albumin concentrations. Our data suggest that physicians use 2.3 times the change in serum albumin, whereas those of Figge et al suggest 2.5; either approach gives similar results.

The Ets-1 oncoprotein and the heme-catabolizing enzyme heme oxygenase (HO)-1 have been implicated in the pathogenesis of renal disease. We investigated the role of the putative Ets-binding sites (EBSs) in the transactivation of the proximal promoter of rat heme oxygenase 1 (hmox1) gene by the Ets oncoproteins Fli-1, Erg-2, and Ets-1 in mesangial cells. We examined several rat hmox1-chloramphenicol acetytransferase (CAT) constructs and EBS mutant constructs in an effort to assess the effect of ETS oncoproteins on transactivation of the rat hmox1 proximal promoter in renal glomerular mesangial cells. CAT assays demonstrated that the proximal promoter region (−1387 to −40) contains positive and negative regulatory regions and that the EBS-2, 3, and 4 play a role in basal promoter activity. Overexpression of Fli-1 and Erg-2 proteins showed a significant increase in promoter activity, whereas Ets-1 showed no effect on promoter activity. The Fli-1–induced transcriptional activation was not altered by mutation of EBSs, either independently or in combination. However, mutation of EBS-4 independently or a combined mutation of sites 3 and 4 led to a 50% reduction in Erg-2–induced transcriptional activation. Furthermore, mutation of EBS-2 and 4 completely abolished Erg-2–mediated promoter activation. Our results support a role for Ets transcription factors in the regulation of rat hmox-1 gene expression in mesangial cells.

Heparin-induced thrombocytopenia (HIT) is usually caused by platelet-activating antibodies of immunoglobulin G class that recognize platelet factor-4 (PF4) bound to heparin or certain other polyanions. Commercial enzyme immunoassays (EIAs) for PF4/polyanion-reactive antibodies detect two immunoglobulin classes (IgA and IgM) besides IgG. To investigate whether the additional detection of these antibody classes improves or worsens assay operating characteristics, we compared the sensitivity and specificity of EIAs that detect these 3 immunoglobulin classes individually with that of a commercial EIA (Genetic Testing Institute, GTI), as well as a platelet-activation assay, the serotonin-release assay (SRA). We compared the operating characteristics of these 5 assays by evaluating 448 patients, in 14 of whom clinical HIT developed, who received either unfractionated or low molecular weight heparin in prospective studies that included systematic platelet-count monitoring and serologic evaluation for anti-PF4/polyanion antibodies. We found that the SRA and IgG and commercial EIAs had similar high sensitivity for HIT; however, diagnostic specificity (for unfractionated and low molecular weight heparin, respectively) varied considerably, as follows: SRA (95.1%, 97.2%) > IgG EIA (89.0%, 93.7%) > GTI EIA (74.2%, 87.6%). Additional detection of IgA and IgM antibodies by the GTI EIA worsened test specificity by detecting numerous nonpathogenic antibodies. Moreover, the frequency and magnitude of IgA and IgM antibody formation in non-HIT immune responses did not differ from that exhibited by patients in whom clinical HIT developed. We conclude that an EIA that detects anti-PF4/polyanion antibodies of only the IgG class has greater diagnostic usefulness in revealing clinical HIT than does an assay that also detects IgA and IgM class antibodies.

The Rhesus (Rh) blood group is the most polymorphic human blood group system, and it is clinically significant in transfusion medicine. About 15% of Caucasoid people are RhD-negative, whereas in the Asian population, the RhD-negative blood type only occurs in 0.1% to 0.5%. However, approximately 30% of apparently RhD-negative Taiwanese people actually were RhD_el. Traditionally, we verify RhD_el by a serologically adsorption-elution procedure with polyclonal anti-D. In our recent report, RhC phenotype is highly associated with RhD_el, and RHD1227A is a useful genetic marker for RhD_el. For setting up a rapid protocol to detect RhD_el in clinical laboratory, a total number of 395 Taiwanese serological RhD-negative blood samples, those with RhC (+) phenotypes as selected by serological tests, were further screened by adsorption/elution tests and RHD1227A allele by specific sequence primer-polymerase chain reaction (SSP-PCR) for RhD_el. Among 395 blood samples collected from RhD-negative subjects, the incidence of RhC (+) was 43% (171/395). One hundred and twenty six of the 171 RhC (+) samples were positive for both adsorption/elution for RhD detection and SSP-PCR assay for RHD1227A. The sensitivity and specificity were 96.9% and 97.5%, respectively, for RHD1227A detection as compared with the traditional adsorption/elution test. Our results also indicated that RHD1227A was highly linked to Ce haplotypes (95.2%). In conclusion, combined RhC (+) phenotyping and RHD1227A analysis can be a simple and accurate laboratory screening protocol for RhD_el detection in RhD-negative population.