ABSTRACT
PURPOSE: This article discusses key considerations regarding ticagrelor's reported effect on heparin-induced thrombocytopenia functional assays, such as literature gaps and possible management strategies. SUMMARY: Limited data indicate that ticagrelor may induce false-negative results in functional assays used in the diagnosis of heparin-induced thrombocytopenia. False-negative functional assays for heparin-induced thrombocytopenia could have catastrophic consequences. The manufacturer labeling of ticagrelor now includes a warning for this potential drug-laboratory interaction. This article suggests areas that would benefit from further research and strategies in navigating this possible interaction. CONCLUSION: Clinicians should exercise caution when evaluating functional assays for heparin-induced thrombocytopenia in patients receiving ticagrelor. This article offers suggestions for future areas of research and potential management strategies.
Subject(s)
Heparin , Thrombocytopenia , Ticagrelor , Ticagrelor/adverse effects , Heparin/adverse effects , Humans , Thrombocytopenia/chemically induced , Thrombocytopenia/diagnosis , Anticoagulants/adverse effects , False Negative Reactions , Platelet Function Tests/methods , Platelet Aggregation Inhibitors/adverse effects , Purinergic P2Y Receptor Antagonists/adverse effects , Adenosine/analogs & derivatives , Adenosine/adverse effects , Adenosine/administration & dosageABSTRACT
The objectives of this study were to investigate the effects of group housing (three calves per group) on bovine respiratory disease (BRD), diarrhea and antimicrobial resistance (AMR) to fecal commensal Escherichia coli (EC) and enterococci/streptococci (ES). Our study comprised two arms, one experimental and one observational. In the experimental arm, preweaned calves on a California dairy were randomized to either individual (IND; n = 21) or group (GRP; n = 21) housing, using a modified California-style wooden hutch. The study period lasted from birth to 56 days of age, during which calves were health scored daily. Cumulative incidence and hazard ratios were estimated for disease. Antimicrobial resistance outcomes were assessed using a prospective cohort design; feces were collected from each calf three times per week and EC and ES were evaluated for AMR using the broth microdilution method against a panel of 19 antimicrobial drugs (AMD). Analysis of treatment records was used to select calves that had been exposed (EXP) to an AMD-treated calf. In GRP, exposure occurred when a calf was a hutchmate with an AMD-treated calf. In IND, exposure occurred when a calf was a neighbor with an AMD-treated calf (TRT). Age-matched unexposed calves (UNEXP) were then selected for comparison. Proportions of AMR in fecal commensals among EXP, UNEXP, and TRT calves were compared between GRP and IND. Accelerated failure time survival regression models were specified to compare differences in minimum inhibitory concentration (MIC) of fecal commensals between EXP and UNEXP calves within each of GRP and IND calves separately. Group calves had a BRD hazard 1.94 times greater that of IND calves (p = 0.03), using BRD treatment records as the outcome. For AMR in EC isolates, higher resistance to enrofloxacin was detected in enrofloxacin-EXP GRP isolates compared with enrofloxacin-EXP IND isolates, and UNEXP GRP calves had lower resistance to ceftiofur compared with enrofloxacin-EXP and enrofloxacin-TRT calves. A significant housing-by-time interaction was detected for EC ceftiofur MIC in EXP GRP calves at 4-14 days post exposure to enrofloxacin (MIC EXP-UNEXP: µg/mL (95% CI): 10.62 (1.17, 20.07)), compared with UNEXP calves. The findings of this study show an increase in BRD hazard for group-housed calves and an increase in ceftiofur resistance in group-housed calves exposed to an enrofloxacin-treated calf.
