Aims Vanadium is currently undergoing clinical trials as an oral drug in patients with noninsulin-dependent diabetes mellitus. Furthermore, vanadium occurs in elevated concentrations in the blood of patients receiving intravenous albumin solutions containing large amounts of the metal ion as an impurity. The present study was performed to examine the pharmacokinetics of vanadium in humans following a single intravenous (i.v.) dose of a commercial albumin solution containing a high amount of vanadium. Methods The study was conducted in five healthy volunteer subjects who received intravenously 90 ml of a commercial 20% albumin infusion solution containing 47.6 m g vanadium as an impurity. Vanadium concentrations in serum and urine were determined by electrothermal atomic absorption spectrometry. Results Vanadium serum concentrations after i.v. administration were measured for 31 days. The data could be fitted by a triexponential function corresponding formally to a three-compartment model. There was an initial rapid decrease in serum concentrations with half-lives of 1.2 and 26 h. This was followed by a long-terminal half-life time of 10 days. The terminal phase accounted for about 80% of the total area under the serum concentration-time curve (AUC).

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In a previous clinical study it was found that patients with coronary heart disease and diabetics with peripheral artery disease often have an elevated erythrocyte aggregation value (AW) and that there is a positive correlation between AW and the number of risk factors found in a subject. In the present investigation we studied the relationship between AW and the serum concentration of high density lipoprotein cholesterol (HDL-C), which is known to be inversely associated with coronary heart disease (CHD) incidence. We found highly significant negative correlations between AW and HDL-C both in a subsample of the study population of a cross-sectional epidemiologic study on CHD risk factors (First Survey of the MONICA Project Augsburg) and in male patients with angiographically confirmed CHD. Correlation coefficients were -0.233 for normal men (P less than 0.01, n = 136), -0.261 for normal women (P less than 0.01, n = 117), and -0.745 for CHD patients (P less than 0.01, n = 14). The results support the concept that the erythrocyte aggregation value as an indicator of cardiovascular risk is consistent with established risk factor associations.

During a heterozygote screening of nearly 3000 persons, triosephosphate isomerase (TPI) deficiencies in erythrocytes were discovered in 11 unrelated persons, showing a residual activity between 39 and 76% of normal activity. Extensive genealogic studies were performed to confirm that these persons with TPI deficiency were heterozygous carriers. The total heterozygote frequency of triosephosphate isomerase deficiencies was 3.7/1000. The persons with heterozygous deficiency could be divided into two categories. Subjects of category I had a mean residual activity of 49% of the expected normal activity and were represented by a frequency of 1.3/1000. Subjects of category II had a mean residual activity of 67% of the expected normal activity and were represented by a frequency of 2.4/1000. None of the heterozygous persons showed an electrophoretic variant. The immunologic specific activity was normal with one exception. Therefore, we assume that in many cases of our heterozygous TPI-deficiencies a TPI protein with a normal specific activity is synthesized to a diminished degree.