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Biomedical subjects

R V Blanke

Publications and source records attributed to R V Blanke.

40 records · Page 3Linked to original sources
PubMedDate not supplied

Subacute chlordane poisoning.

A 30 year old female was exposed to chlordane through careless and excessive domestic use over a 1 to 4 week period. Early symptoms included circumoral numbness, anorexia, nausea, and fatigue. Myoclonic jerks occurred after a delay of one month. Malaise and anorexia became the dominant symptoms leading to referral at six months. Dysfunctional bleeding was attributed to hepatic enzyme induction by the chlordane and increased metabolism of contraceptive medication. Cholestyramine increased the stool elimination of chlordane.

Adipose Tissue↗
PubMedDate not supplied

Assessment of laboratory quality in urine drug testing. A proficiency testing pilot study.

As part of a program to develop accreditation guidelines for urine drug testing laboratories, a pilot study for proficiency testing was conducted. Fifty civilian, commercial laboratories were included on a voluntary basis. Drug-free urine specimens were collected and either fortified with commonly abused drugs at concentrations comparable to casual use or submitted unfortified to participating laboratories as blanks. Samples were submitted on both an open and blind basis to the laboratories. Laboratory performance on open proficiency testing was comparable with that reported in existing proficiency testing programs. Blind proficiency testing produced less accurate results in terms of apparent false-negatives, but significant difficulties were evident in carrying out blind testing and in comparing its results with those of open testing. Specific problems have been identified to guide future programs.

False Negative Reactions↗
PubMedDate not supplied

Demonstration of major metabolic pathways for chlordecone (kepone) in humans.

The hypothesis that liver is the site of the previously demonstrated chlordecone alcohol formation in man was tested. Human bile obtained from chlordecone-poisoned factory workers contained substantial amounts of free chlordecone, but little free chlordecone alcohol. However, when the same bile specimens were pretreated with beta-glucuronidase before analysis by gas-liquid chromatography, large amounts of chlordecone alcohol appeared, accounting for 75% of total organochlorine compounds. Confirmation of the identity of chlordecone and chlordecone alcohol was made by using gas liquid chromatography-mass spectrometry. Whereas biliary chlordecone alcohol was present predominantly as its glucuronide conjugate (93%), chlordecone was excreted primarily as the unaltered compound (72%) with only a small portion conjugated with glucuronic acid (9%). The remaining fraction of the total chlordecone measured in bile appeared to be a stable polar metabolite resistant to beta-glucuronidase. This unidentified metabolite could be converted to free chlordecone only by acid hydrolysis under harsh conditions. In contrast to human bile, rat bile contained only trace amounts of chlordecone alcohol (less than 0.5% of total chlordecone), thus indicating that hepatic metabolism of chlordecone is species-specific. We conclude that in man, the major metabolic route for chlordecone is its reduction in the liver followed by glucuronidation.

Animals↗