Biomedical subjects

J Toffaletti

Publications and source records attributed to J Toffaletti.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Changes in protein-bound, complex-bound, and ionized calcium related to parathyroid hormone levels in healthy donors during plateletapheresis.

In order to relate changes in protein-bound and complex-bound calcium to levels of citrate and secretion of parathyroid hormone during mild hypocalcemia, total, ultrafiltrable, and ionized calcium were measured in 13 apparently healthy donors during plateletapheresis. Carboxyl-terminal parathyroid hormone was measured in seven of the donors, and both amino-terminal and intact parathyroid hormone assays were done on one donor. Mean concentrations of total and ionized calcium decreased during most of the procedure, as did total protein, albumin, and phosphorus. Complexed calcium increased, which was attributed to the large increases in citrate levels. Protein-bound calcium decreased more than other forms of calcium, even allowing for the decrease expected from hemodilution. The carboxyl-terminal parathyroid hormone response varied among different donors, but on the average, decreased slightly before gradually rising during the citrate-induced hypocalcemia. These findings suggest that calcium citrate does not affect the secretion of parathyroid hormone, and that at least a portion of protein-bound calcium is readily exchangeable and possibly influenced by the hormone.

Blood Donors↗

PubMedDate not supplied

Plasma levels of ionized and total calcium during storage of citrated platelet concentrate.

Measurements of ionized and total calcium levels in supernatant plasma samples from citrated platelet concentrates (PCs) were made over 7 days of storage. Both ionized and total calcium increased significantly during the storage period: respectively, from 0.074 mM Ca2+ in fresh platelet-rich plasma to 0.084 mM in PCs stored for 7 days (p = 0.017), and from 1.94 mM total calcium to 2.06 mM (p = 0.014) over the same period. The increase in calcium was partially blocked by the addition of platelet activation inhibitors to the PCs. Platelet-poor plasma stored under similar conditions showed no significant change in ionized or total calcium, which indicated that the increases observed in PCs were due to the release of cellular calcium. Significant correlations (p less than 0.01) were found between ionized or total calcium levels and lactate concentration or pH, but not hypotonic shock recovery rate. The demonstration of non-zero levels of ionized calcium makes it likely that Ca2+-dependent enzyme systems such as calpain expression and thrombin generation are active in the plasma of citrated PCs and may contribute to the platelet storage lesion.

Alprostadil↗

PubMedDate not supplied

An overview of the laboratory diagnosis of lead poisoning.

Four tests for the evaluation of lead poisoning are reviewed from both the clinical and methodological aspects. Whole blood or erythrocyte lead measurements appear to provide the best means of assessing the bodily burden of lead with electrothermal and Delves cup flame atomic absorption spectorphotometric techniques providing accurate and precise results. Urine lead is less reliable as a screening test for lead poisoning but is excellent for monitoring the course of ethylenediamine tetraacetic acid (EDTA) therapy. Atomic absorption methods for urine are made difficult by the variable matrix of urine but satisfactory electrothermal and flame procedures have been described. Erythrocyte delta-aminolevulinic acid dehydratase activity is a very sensitive index of lead exposure,--perhaps too sensitive. Analytical procedures for measuring this enzyme are subject to errors and many complicating factors such as lack of stability of the specimen limit the usefulness of the test. Urine delta-aminolevulinic acid is of questionable value as a screening procedure and also is subject to analytical problems.

Clinical Enzyme Tests↗