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Prostate-specific antigen (PSA) is a widely used biochemical marker for prostate cancer (1). PSA, a serine protease, forms complexes with serine protease inhibitors such as α2-macroglobulin and α1-antichymotrypsin (ACT) (2). The major immunoreactive forms of serum PSA are PSA-ACT complex and free PSA. PSA complexed to α2-macroglobulin is not measured by current immunoassays (3). Because the proportion of PSA complexed to ACT is higher in men with prostate cancer than in men with benign prostatic hyperplasia (BPH) (3)(4), the use of a ratio of free-to-total PSA may improve discrimination between men with BPH and prostate cancer (5)(6). Results obtained with different PSA immunoassays are not interchangeable (7)(8)(9)(10). The variation among immunoassays reflects, in large part, the specificity of different PSA antibodies (7). To a lesser extent, the composition of the calibrator, the PSA values assigned to the calibrator, the test diluent, and the physical design of the immunoassays contribute to intermethod differences (6)(7). Assays using a monoclonal-monoclonal sandwich format yield, in general, an equimolar response to free and ACT-complexed PSA, whereas monoclonal-polyclonal formats tend to yield higher values for samples containing greater proportions of free PSA (8). We have recently described the Bayer Immuno 1TM PSA Assay (Bayer Corporation), which uses a monoclonal-polyclonal antibody format that yields an equimolar response to varying proportions of free and complexed PSA (11). This has now been found to be a result of the unique binding properties of the monoclonal antibody used for the capture of PSA (manuscript in submission). Proficiency testing among clinical laboratories has indicated large intermethod variability in the quantitation of total PSA (12). The aim of this study was to determine the magnitude and cause of this intermethod variation. Here we report our multi-site analysis of …

To determine the degree of damage occurring during preparation and storage of platelet concentrates, the percent release of B-thromboglobulin (BTG) and percent leakage of the cytosolic protein lactic dehydrogenase was determined sequentially from phlebotomy to the end of storage for 72 h at 20-24 degrees C. The effect of storage temperature, pH, and radiation was also evaluated. The results showed that during preparation of platelet concentrate a large degree of release was found after resuspension of the platelet button formed after the high-speed centrifugation. During storage the percent BTG release increased from 18.1 to 40.2% (p less than 0.05). The percent release seen during storage at 4 degrees C (72 h) was 19.2%, while that seen for platelets subjected to temperature cycling at 4-37 degrees C was 24.9%. Both of these values were significantly less (p less than 0.05) than that seen for concentrates stored at room temperature. A negative correlation between pH and BTG release was found (r = -0.64). Irradiation to 10,000 rad did not induce the release reaction or lactic dehydrogenase leakage. We conclude that the degree of in vitro platelet release is dependent on the preparative manipulations, and gentler protocols for preparation and storage of platelets should be investigated.

A 40-year-old man with jejunoileal bypass developed a syndrome of bizarre behavior, slurred speech, ataxic gait, and inappropriate affect, associated with a metabolic acidosis characterized by an increase in the anion gap. Serum L-lactate level was normal, but high-resolution proton nuclear magnetic resonance spectrums of the patient's serum showed a high concentration of lactate. A diagnosis of D-lactic acidosis was confirmed by a specific enzymatic assay for D-lactate. The D-lactic acidosis was cleared using antibiotic therapy, suggesting that D-lactate is produced from fermentation of ingested carbohydrate by colonic bacteria. Nuclear magnetic resonance spectroscopy is a rapid screening test for identifying organic acids in patients with unexplained acidosis. Neuropsychiatric symptoms in patients with short bowel syndrome may be associated with D-lactic acidosis.

We have recently seen two cases of propranolol poisoning. In both instances, plasma propranolol levels were elevated. Both patients experienced generalized seizures and had a transient intraventricular conduction defect on electrocardiogram. The literature on intoxication of propranolol and other beta-adrenoceptor blocking drugs suggests that the effects of massive propranolol intoxication observed in our patients can be explained on the basis of the pharmacologic properties of propranolol. Therapy consisted of gastric lavage and agents to antagonize the beta-adrenoceptor blockade effect. Both patients recovered.