Disease relevance of Dindevan

• The oral anticoagulant phenindione [2-phenyl-1H-indene-1,3(2H)-dione] is associated with hypersensitivity reactions in 1.5 to 3% of patients, the pathogenesis of which is unclear [1].
• The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning [2].
• Reports on phenindione toxicity have limited its use as an oral anticoagulant [3].

High impact information on Dindevan

• In a multi-centre (n = 12), observational, prospective study we compared 666 pregnant women exposed to phenprocoumon (n = 280), acenocoumarol (n = 226), fluindione (n = 99), warfarin (n = 63) and phenindione (n = 2) to a non-exposed control group (n = 1,094) [4].
• Phenindione was presented to T-cells via two pathways: first, bound directly to major histocompatibility complex and second, bound to a processed peptide [1].
• A lymphocyte transformation test showed proliferation of T-cells from the hypersensitive patient, but not from four controls on exposure to phenindione in vitro [1].
• 1. The ionization kinetics of phenindione were determined at an ionic strength of 0.1 and 25 degrees using stopped-flow spectrophotometry and a pH jump technique [5].
• The effect of batch and column process, complexation time, temperature, and pH on ciprofloxacin loading on Indion 234 is reported [6].

Biological context of Dindevan

• Ionization kinetics of the carbon acid phenindione [5].
• Pharmacokinetics of 2-phenyl-1,3-indandione in the rat after i.v. and oral administration [7].

Analytical, diagnostic and therapeutic context of Dindevan

• Bleeding from self-administration of phenindione: a detailed case study [8].
• The pharmacokinetics of the anticoagulant drug, 2-phenyl-1,3-indandione, after i.v and oral administration in the rat might be best described as a non-linear open two-compartment model with elimination fromthe peripheral compartment [7].

References