Detecting 2009 pandemic influenza A (H1N1) virus infection: availability of diagnostic testing led to rapid pandemic response.

Diagnostic tests for detecting emerging influenza virus strains with pandemic potential are critical for directing global influenza prevention and control activities. In 2008, the Centers for Disease Control and Prevention received US Food and Drug Administration approval for a highly sensitive influenza polymerase chain reaction (PCR) assay. Devices were deployed to public health laboratories in the United States and globally. Within 2 weeks of the first recognition of 2009 pandemic influenza H1N1, the Centers for Disease Control and Prevention developed and began distributing a new approved pandemic influenza H1N1 PCR assay, which used the previously deployed device platform to meet a >8-fold increase in specimen submissions. Rapid antigen tests were widely used by clinicians at the point of care; however, test sensitivity was low (40%-69%). Many clinical laboratories developed their own pandemic influenza H1N1 PCR assays to meet clinician demand. Future planning efforts should identify ways to improve availability of reliable testing to manage patient care and approaches for optimal use of molecular testing for detecting and controlling emerging influenza virus strains.

Adaptation of a quantitative immunoassay for urine myoglobin. Predictor in detecting renal dysfunction.

Myoglobinuria, subsequent to rhabdomyolysis, may cause acute renal failure. For this reason, many qualitative and quantitative tests have been developed for the detection of myoglobin in urine. The authors describe the adaptation and optimization of the Stratus II serum myoglobin immunoassay to quantify urine myoglobin. In addition, the assay was used to accurately determine urine myoglobin concentrations in subjects at potential risk for myoglobin-induced renal dysfunction and the results obtained compared to conventional qualitative methods for urine myoglobin. The assay demonstrated with-in run and between-run coefficient of variations (CVs) of 6.2% and 7.2%, respectively, was linear from 0-950 micrograms/L, demonstrated good recovery, and was free from interference by hemoglobin, creatinine, and urea. Specimens were diluted with 0.1 mol/L phosphate buffer, pH 9.0 containing 3% bovine serum albumin before analysis. Myoglobin was assayed on urine obtained from 30 patients suspected of having myoglobinuria. Fifteen of 17 patients with serum creatinine greater than 1.4 mg/dL had myoglobin concentrations greater than 20,000 micrograms/L, whereas the remaining 31 patients with normal serum creatinine had urine myoglobin concentrations of less than 18,000 micrograms/L. If serum creatinine is used as an indicator of renal function, it would appear that accurate measurement of urine myoglobin may facilitate identification of patients with increased susceptibility to myoglobin-induced acute renal failure.

Stability of plasma lactate in vitro in the presence of antiglycolytic agents.

The use of plasma lactate to assess metabolic or circulatory impairment requires definition of critical preanalytical and analytical parameters. Stability has been documented for only 15 min after acquisition when samples were collected with fluoride and transported on ice. We examined time elapsed before analysis, storage temperature, and the antiglycolytic agent used to define preanalytical conditions. Plasma lactate was measured with a Kodak Ektachem 700XR analyzer. In controlled studies on volunteers, storage on ice slowed but did not eliminate the production of lactate; for samples collected with sodium fluoride (F) and potassium oxalate (OX), lactate increased by 0.2 mmol/L after 1 h, then changed little regardless of the storage temperature. For patients' samples collected in F/OX, the mean increase was only 0.15 mmol/L after 24 h. Samples with leukocytosis (neutrophil counts 23 x 10(9)-52 x 10(9)/L) were also stable, with a mean increase of 0.3 mmol/L at 8 h. Use of the antiglycolytic agents F and OX (at 60 and 12 mmol/L, respectively) maintained apparently stable lactate concentrations at room temperature for up to 8 h without special handling.

Intracellular magnesium content of mononuclear blood cells and granulocytes isolated from leukemic, infected, and granulocyte colony-stimulating factor-treated patients.

The intracellular magnesium (Mg) concentration of granulocytes and mononuclear blood cells (MBCs) was determined in cells isolated from patients with several disorders. The mean (+/-SD) Mg content of MBCs isolated from patients diagnosed with lymphocytic leukemia, myelocytic leukemia, or infection; from patients treated with granulocyte colony-stimulating factor (G-CSF); and from healthy volunteers (control group) was 2.3 (+/-0.6), 3.3 (+/-0.5), 4.1 (+/-0.8), 3.9 (+/-0.4), and 3.9 (+/-0.6) fmol/cell, respectively. The Mg content of MBCs isolated from patients with lymphocytic and myelocytic leukemia, but not those from patients with infection or receiving G-CSF treatment, were significantly lower (P < 0.001) than those from the control subjects. The mean Mg concentration of granulocytes obtained from lymphocytic leukemia, myelocytic leukemia, infection, and G-CSF patients and from the control group was 3.2 (+/-0.9), 3.4 (+/-0.5), 3.8 (+/-0.6), 4.5 (+/-0.6), and 4.6 (+/-0.6) fmol/cell, respectively. Granulocytes isolated from leukemic and infectious patients yielded lower intracellular Mg concentrations (P < 0.005) than those from patients receiving G-CSF and the control group. This study demonstrates that intracellular Mg content is altered in several pathological states. Several factors, including depleted Mg stores or altered intracellular Mg binding sites, could be responsible for these changes. Apparently, intracellular Mg content may be of use in assessing total body Mg status.