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Biomedical subjects

M Leclercq

Publications and source records attributed to M Leclercq.

At least 127 records · Page 7Linked to original sources
PubMedDate not supplied

Detection of p30 antigen in sexual assault case material.

A sandwich enzyme immunoassay for the detection of p30 prostate specific antigen was applied in 52 forensic cases. In each case, immunoassay results were compared with those of the search for spermatozoa and prostatic acid phosphatase analysis. The results indicate that the p30 assay gave no false positive and fewer false negative reactions than the acid phosphatase test. The sensitivities compared to the search for spermatozoa as a reference method were 94.8% for the p30 assay and 84.4% for the acid phosphatase test; the specificities were 95.6% and 90.0% respectively.

Acid Phosphatase↗
PubMedDate not supplied

Vitamin K metabolism in a patient resistant to vitamin K antagonists.

We investigated various pharmacokinetic and pharmacodynamic parameters in a 63-year-old man, resistant to warfarin, fluindione, acenocoumarol and phenprocoumon. Daily doses of up to 30 mg of the long-acting phenprocoumon yielded a drug concentration of 85 mg/l (usual range 1-5 mg/l) but the international normalized ratio remained around 1. The plasma half-life of phenprocoumon was approximately 350 h (normal 120-150 h). Thus, the resistance was not due to malabsorption or to an accelerated metabolism of the drug. The level of vitamin K1 (1,202 ng/l) was insufficient to induce resistance. Decarboxyprothrombin concentrations were low, demonstrating that the gamma-carboxylation of the precursors of the vitamin K-dependent coagulation factors was not effectively reduced. The concentration of vitamin K epoxide, normally increased under oral anticoagulation, correlated to the vitamin K concentration (r2 = 0.77) but the quotient epoxide/vitamin K remained 4-fold lower than that of 22 warfarin-sensitive patients, suggesting an absence of blockade of the vitamin K reductase by phenprocoumon. This resistance to all the molecular forms of the vitamin K antagonists is most likely due to a reduced affinity of the drugs to a mutant vitamin K reductase.

Drug Resistance↗
PubMedDate not supplied

Is vitamin K1 supplementation necessary in long-term parenteral nutrition?

BACKGROUND: I.v. lipid emulsions contain vitamin K in substantial quantities and in 1989, we therfore stopped supplying vitamin K1 to patients receiving home parenteral nutrition (HPN). METHODS: Nine patients (group I) receiving HPN before 1989 (10 mg i.v. vitamin K1 supplementation weekly until 1989, which was discontinued thereafter) and six patients with an initial low plasma vitamin K1 concentration (related to their malabsorption) (group II) receiving HPN after 1989 were studied. Prothrombin time (PT), plasma vitamin K1 concentration, and vitamin K1, content in lipid emulsions were measured throughout the period of HPN. RESULTS: All lipid emulsions, except for Eurolip 20% and Clinoleic 20% (Baxter SA, Maurepas, France) contained vitamin K1, with concentration ranges from 179 +/- 39 to 353 +/- 78 ng/L. Group I patients had an initial high plasma vitamin K1 concentration due to the vitamin K1 supplementation. After this supplementation was discontinued, plasma vitamin K1 decreased and remained in normal ranges with a normal PT. Throughout the HPN period after 1989, patients received 255 +/- 104 micrograms of vitamin K1 weekly through lipid emulsions. The PT and plasma vitamin K1 concentrations in group II patients were restored by lipid emulsions, which contained 418 +/- 143 micrograms/wk of vitamin K1. CONCLUSIONS: In patients receiving i.v. lipids (except for Eurolip and Clinoleic), a normal vitamin K1 status can be maintained during long-term HPN without vitamin K1 supplementation. However, vitamin K supplementation cannot be abandoned until the vitamin K content of emulsions is standardized by manufacturers. A weekly supply of 250 to 400 micrograms of vitamin K1 is enough to maintain and even restore a normal vitamin K1 status in HPN.

Adult↗