The role of postmortem cardiac markers in the diagnosis of acute myocardial infarction.

Sudden cardiac deaths because of acute myocardial infarction (MI) constitute a significant percentage of the caseload for death investigators, coroners, and forensic pathologists. Clinicians use cardiac markers, highly sensitive and specific for myocardial damage, to screen living patients for acute MI; however, to this point, the utility of these markers in the autopsy setting has not been fully established. The current study included 10 decedents, five who died of acute MI, and five subjects who died of noncardiac disease. Samples of pericardial fluid and blood from multiple sites were tested for creatine kinase, creatinine kinase MB, and troponin-I. Three main conclusions were drawn: the levels of cardiac markers from all patients are significantly higher than the reference range for living patients, there are significant differences in cardiac marker levels between samples from different anatomic locations, and only three cardiac marker/anatomic site combinations were significantly different between the control and study groups.

Monitoring of mycophenolate acid in serum or plasma using LC tandem mass spectrometry.

Therapeutic drug management of patients receiving mycophenolic mofetil or mycophenolate sodium using mycophenolic acid (MPA) concentrations is controversial. Considered to be less toxic compared to many of the other drugs used in immunosuppression regimens, MPA is not tolerated by all patients. For these patients, monitoring is useful in achieving desired therapeutic targets, reducing adverse effects, and individualizing dosing. We describe an LC-MS-MS that permits the measurement of MPA and 7-O-glucuronide mycophenolic acid (MPAG) in serum or plasma.

An unusual cause of elevated serum total beta hCG.

Human chorionic gonadotropin (hCG), a heterodimeric hormone consisting of an alpha (alpha) and a beta (beta) subunit, is used as a marker for the diagnosis of pregnancy, congenital defects, and choriocarcinoma. After excluding the common causes of elevated serum hCG, laboratory identification of false-positive or true results assists in guiding clinical management. Options include testing urine for hCG, serum for heterophile antibodies, and serum hCG by different immunoassays. We report the case of a non-pregnant patient with chronic renal failure who had a positive urine hCG test, an elevated serum hCG level by two different assays but normal by a third assay, and persistently elevated serum hCG levels after ruling out the likelihood of heterophile antibodies. The discrepancies were explained by the patient's impaired renal clearance and the molecular forms of hCG that were measured by each assay. This case illustrates the importance of the laboratory's role in understanding the causes of elevated serum hCG.

Rapid method for beta2-transferrin in cerebrospinal fluid leakage using an automated immunofixation electrophoresis system.

BACKGROUND: Beta(2)-transferrin (beta-2 trf) is a desialated isoform of transferrin found only in cerebrospinal fluid (CSF), ocular fluids, and perilymph. In aural, nasal, and wound drainages, this protein is an important marker of CSF leakage. Immunofixation electrophoresis (IFE) on agarose gels is a widely accepted qualitative technique for detection of small amounts of beta-2 trf, but disadvantages include lengthy transfer immunoblotting techniques or the requirement of at least 2 mL of sample. METHODS: Using eight applications of unconcentrated sample on high-resolution agarose gels with an automated electrophoresis system (Helena SPIFE 3000), we developed a rapid method for beta-2 trf. Evaluation studies included reproducibility of migration distance (mm), limit of detection, specificity, and concordance of results compared with those reported by a reference laboratory. Neuraminidase-treated serum was the source of beta-2 trf for our sensitivity and specificity studies. Transferrin was measured by rate nephelometry. RESULTS: The 2.5-h procedure demonstrated reproducible migration (CV <2.5%) on five lots of gels. Detection of beta-2 trf at 0.002 g/L in an unconcentrated sample was attributed to reproducible application, quality of the anti-trf antiserum, and a sensitive acid violet stain. Our beta-2 trf findings (two negative and five positive) in seven available clinical samples agreed with the reference laboratory results. In 12 months after its inception, this test was ordered 48 times vs 13 in the previous year when testing was sent out. CONCLUSION: This method provides physicians with a rapid, reliable aid in the diagnosis of suspected CSF leakage, as described in a case report.

Evaluation of the i-STAT Portable Clinical Analyzer for point-of-care blood testing in the intensive care units of a university children's hospital.

We evaluated the analytical performance of the i-STAT Portable Clinical Analyzer (PCA), a point-of-care testing system consisting of a hand-held analyzer and single-use cartridges that measure different panels of electrolytes, metabolites, blood gases, and hematocrit in 65-100 microl of blood. Our objective was to determine whether PCA measurements at the bedside of patients in the neonatal and pediatric intensive care units of the MUSC Children's Hospital would be as reliable as those performed by the clinical laboratory's primary methods (Radiometer ABL 725 blood gas analyzer; Vitros 750 chemistry analyzer; and Coulter STKS hematology analyzer). Four cartridge types: (a) EC8+ (sodium; potassium; chloride; urea; glucose; pH; blood gases [PO2; pCO2]), (b) EC6+ (sodium; potassium; ionized calcium; glucose; hematocrit; pH), (c) G3+ (pH; PO2; pCO2), and (d) creatinine, were assessed for reproducibility, linearity, and method comparisons using aqueous samples, blood samples supplemented with several analytes, and -225 blood samples from patients. Reproducibility (CV) was good (< 2%) for electrolytes, glucose, urea, and pH, satisfactory (< 6.5%) for blood gases and creatinine, but poor (21%) for hematocrit. Linearity concentrations spanning the clinically relevant ranges were verified for all analytes. Method comparison studies with samples separated into 2 subgroups by patient age (> or < 3 mo) showed that agreement between the PCA and the primary methods was clinically acceptable. After the PCA was implemented for clinical testing, the observation of discrepant results of creatinine concentrations in neonatal blood samples that would have affected clinical management led to a second creatinine comparison study (59 additional samples) and to our eventual discontinuation of the PCA creatinine assay. This problem notwithstanding, the successful implementation of the PCA is attributed to careful analytical evaluations and ongoing communication with the clinical staff.