Patterns of add-on tests for hospitalized and for private patient populations.

CONTEXT: The policy of storing clinical samples in a pathology laboratory is based on long-standing practice rather than on objective data regarding the actual use of the stored samples. OBJECTIVE: To determine the time after initial order that requests for add-on tests are submitted to the laboratory. These data might be useful for improving the efficiency of sample storage. DESIGN: Two hundred sixteen add-on requests evenly divided between inpatients and private practice patients were reviewed for types of tests added on and the time of the requests. RESULTS: Ninety-five percent of add-on test requests for inpatients were made by 0.75 day after the initial order (range, 0.01-4.3 days). However, the 95th percentile for private practice patients' add-on requests did not occur until 5.6 days later (range, 0.01-7.0 days). The pattern of add-on tests for hospitalized patients also differed from those for private practice patients. Most add-on tests for hospitalized patients were for routine hospital tests, and the private practice add-on requests were for assays that were not as routine, frequently for testing referred to the reference laboratory. This difference affected the rapidity of completing the add-on tests. CONCLUSIONS: Samples for hospitalized patients can be stored for 3 days, but samples from patients in private practices should be held for 7 days. This change of "usual" storage practice would increase the efficient use of laboratory space and personnel. Screening all requests for add-on tests for hospitalized patients might reduce the frequency of unnecessary add-on requests, further increasing the efficiency of the laboratory.

Reducing substances in urine: a paradigm for changes in a standard test.

Detection of reducing substances in urine has been a standard laboratory procedure for about 50 yr. It is used as a screening test for inborn errors of carbohydrate metabolism. Although the test has poor specificity and most states perform mandatory newborn screening for the common genetic defects, most clinical laboratories still perform this as a reflex test on all pediatric urine samples. We suggest that laboratories should perform this test only at the specific order of a physician and that they should review their test menu frequently to delete tests that no longer have a clinical rationale.

A model for troponin I as a quantitative predictor of in-hospital mortality.

OBJECTIVES: We evaluated log-transformed troponin I as a predictor of mortality in 2 independent populations. BACKGROUND: The troponin I result is typically dichotomized by a single diagnostic cutoff. Its performance as a continuous prognostic variable has not previously been well-characterized. METHODS: We studied the first troponin I sent from the emergency department (ED) as a predictor of all-cause inpatient mortality, with retrospectively gathered data. We performed our study in 2 stages, deriving our model with data from a single medical center and validating it with data from another. Subjects included every patient who had a troponin I sent from the ED during the period from November 2002 to January 2005. We assessed prognostic independence by including other potential confounders in nested logistic regression models. The troponin assay was identical at both sites (Ortho-Clinical Diagnostics, Rochester, New York). RESULTS: There were a total of 34,227 patients (12,135 derivation and 22,092 validation). Odds ratio for mortality as a function of log10-troponin was 2.08 (95% confidence interval [CI] 1.85 to 2.32) in the derivation set and 2.07 (95% CI 1.92 to 2.24) for the validation set. Troponin I remained a strong predictor after inclusion of age, electrocardiogram normality, renal insufficiency, arrival mode, chief complaint, admission diagnosis, and abnormal vital signs into bivariate and nested multivariate models. CONCLUSIONS: The presence of any detectible troponin I at ED presentation is associated with increased inpatient mortality. In 2 distinct clinical populations, the odds of death approximately doubled with any 10-fold increase in troponin result. This held true at levels below current diagnostic cutoffs. The placement and utility of dichotomous cutoffs might merit reconsideration.

Multicenter evaluation of the Bayer ADVIA Centaur HIV 1/O/2 enhanced (EHIV) assay.

BACKGROUND: It is important that serological assays detect antibodies to human immunodeficiency virus (HIV) in all infected individuals, including those infected with less prevalent, more diverse subtypes. METHODS: Performance of the ADVIA Centaur HIV 1/O/2 Enhanced (EHIV) Assay was tested on 1344 samples from HIV-positive subjects, 6061 samples from groups at low-risk for HIV infection, and 1042 samples from groups at high-risk for HIV-1 and HIV-2 infection. Results were compared with those of an FDA-approved predicate assay. RESULTS: The ADVIA Centaur EHIV Assay showed good precision with a diagnostic specificity of 99.9% and diagnostic sensitivity of 100%. HIV seroconversion was detected earlier in 6 panels, at the same time in 13 panels and later in only 1 of the panels when compared to the predicate assay, thereby narrowing the window period between infection and antibody detection. Of clinical significance, a blood donor sample that was indeterminate by HIV-1 Western blot and non-reactive by the predicate assay was repeatedly reactive in the ADVIA Centaur Assay and confirmed as positive by HIV-2 immunoblot. CONCLUSIONS: The ADVIA Centaur EHIV Assay is useful as an aid in the diagnosis of individuals infected with HIV-1 and/or HIV-2.

Establishing a new target range for unfractionated heparin for acute coronary syndromes.

INTRODUCTION: The target activated partial thromboplastin time (aPTT) range of 1.5 to 2.5 times the control value or 45 to 75 seconds recommended by the ACC/AHA for patients receiving unfractionated heparin (UFH) for acute coronary syndromes (ACS) is vulnerable to variation in test reagents. Rather than use the standard target aPTT range, it has been recommended that each institution establish its own target aPTT range based upon anti-factor Xa heparin levels. As a quality assurance project, we evaluated our institution's therapeutic aPTT range by examining the correlation between aPTTs and anti-factor Xa heparin levels and established a new target aPTT range with a new thromboplastin reagent based upon the therapeutic anti-factor Xa heparin levels. METHODS: Sixty-two plasma samples from 26 consecutive patients receiving UFH for ACS were analyzed. Plasma aPTTs measured with a thromboplastin reagent and a new thromboplastin reagent and anti-factor Xa heparin levels were obtained on each plasma sample. Linear regression analysis was performed to establish a new target aPTT range from corresponding therapeutic anti-factor Xa heparin levels. RESULTS: Thirty-two percent of patients with our institution's target range aPTTs of 61 to 100 seconds had anti-factor Xa heparin levels below 0.35 to 0.7 U/mL while 68% of patients had therapeutic anti-factor Xa heparin levels (positive predictive value = 68%). When the same blood was tested with a new thromboplastin reagent lot, only 9% of patients with target range aPTTs had anti-factor Xa heparin levels below 0.35 U/mL while 91% of patients had therapeutic anti-factor Xa heparin levels (positive predictive value = 91%). The Pearson correlation coefficient ( r ) for the new thromboplastin reagent lot was 0.93. The target aPTT range established with the new thromboplastin reagent lot was 61 to 100 seconds. CONCLUSION: Monitoring aPTTs without standardizing the thromboplastin reagent may not adequately reflect therapeutic heparin levels. Despite apparently target aPTTs, patients treated with UFH may be under-anticoagulated. Our new anti-Xa-adjusted target aPTT range shows an increase in the positive predictive value of aPTTs. Large-scale clinical studies are needed to determine the optimal anti-factor Xa range for ACS patients treated with UFH, with further refinements if glycoprotein IIb/IIIa inhibitors are concomitantly used and to show a benefit in clinical outcomes for monitoring plasma heparin levels with anti-factor Xa heparin levels. Institutional standardization of the aPTT is necessary to ensure optimal patient care when changing thromboplastin reagents.