title: Attainment and maintenance of platelet inhibition through standard dosing of abciximab in diabetic and nondiabetic patients undergoing percutaneous coronary intervention.
abstract: BACKGROUND
  Although the effectiveness of abciximab (c7E3 Fab; ReoPro) in large populations of patients undergoing a percutaneous coronary intervention has been consistently proved in clinical trials, it is unknown whether all patients achieve and maintain target inhibition during treatment. Diabetic patients in particular are a subgroup of patients with known underlying platelet abnormalities whose long-term response to abciximab has been shown to vary from that of nondiabetic patients.
  
  
  RESULTS
  Forty-nine diabetic and 51 nondiabetic patients who received adjunctive abciximab therapy during percutaneous coronary interventions were evaluated prospectively. The degree of platelet function inhibition was determined immediately after the abciximab bolus, 8 hours after the bolus (during the 12-hour abciximab infusion), and the next morning (13 to 26 hours after the bolus) with the use of a rapid platelet function assay (Accumetrics). After the abciximab bolus, platelet function was inhibited by 95+/-4% (mean+/-SD). By 8 hours, the average percent inhibition had decreased to 88+/-9%, with 13% of patients with <80% inhibition. The next morning (mean 19 hours after the bolus), mean inhibition was 71+/-14%. A difference was not found between diabetics and nondiabetics, nor was any physiological parameter found to be predictive of the response to abciximab.
  
  
  CONCLUSIONS
  Although the majority of patients achieve and maintain >/= 80% platelet inhibition during the 12-hour infusion with standard-dose abciximab, there is substantial variability among patients. Diabetic status does not appear to influence this variability.
authors.affiliation: Department of Cardiology, Wilford Hall Medical Center, Lackland AFB, TX 78236, USA. steinhubl@sprintmail.com
authors.forename: S R
authors.initials: SR
authors.lastname: Steinhubl
authors.forename: K
authors.initials: K
authors.lastname: Kottke-Marchant
authors.forename: D J
authors.initials: DJ
authors.lastname: Moliterno
authors.forename: M L
authors.initials: ML
authors.lastname: Rosenthal
authors.forename: N K
authors.initials: NK
authors.lastname: Godfrey
authors.forename: B S
authors.initials: BS
authors.lastname: Coller
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
authors.forename: A M
authors.initials: AM
authors.lastname: Lincoff
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D003920:Diabetes Mellitus / Q000097:blood*; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D008297:Male; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011446:Prospective Studies
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077284:Abciximab