Purpose: To evaluate the clinical literature supporting reduced doses of dexamethasone to prevent taxane hypersensitivity reactions (HSRs), and edema/skin toxicities in respect to docetaxel, when taxanes are given weekly, as opposed to every 3 weeks.
Data Source: Clinical literature of human-controlled clinical trials, accessed through MEDLINE and meeting abstract databases (from 1990 to 2010).
Data Extraction: The retrieved literature was reviewed to include all human clinical trials that recorded adverse effect information with weekly taxanes utilizing reduced-dose or tapering dexamethasone schemas, either prospectively or retrospectively.
Data Synthesis: Prophylaxis for paclitaxel-related HSRs generally includes one or more 20 mg doses of dexamethasone, with histamine-1 and -2 receptor antagonists prior to infusion of paclitaxel. Prophylaxis for docetaxel-related HSRs generally includes dexamethasone beginning 1 day before docetaxel, and continuing twice daily for a total of 3 days. These schedules were designed for taxanes given every 3 weeks, but may lead to steroid-related adverse effects when given weekly with weekly taxane administration. Treatment strategies designed to reduce corticosteroid exposure in patients receiving weekly taxanes have been investigated.
Conclusions: Several predication strategies utilizing reduced doses of dexamethasone with weekly taxanes appear to be feasible and safe, and can be considered for patients experiencing, or at high risk for steroid-induced side effects. However, the optimal schedule is not yet determined; larger prospective clinical trials are needed.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1177/1078155211409473 | DOI Listing |
J Thorac Oncol
January 2025
Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
Introduction: Amivantamab, an EGFR-MET bispecific antibody, is approved for multiple indications in EGFR-mutated advanced non-small cell lung cancer (NSCLC) as monotherapy or combined with other agents. Intravenous amivantamab is associated with a 67% infusion-related reactions (IRR) rate.
Methods: The phase 2 SKIPPirr study (NCT05663866) enrolled patients with EGFR-mutated (Ex19del/L858R) advanced NSCLC after progression on osimertinib and platinum-based chemotherapy who received intravenous amivantamab plus oral lazertinib (amivantamab-lazertinib), a third-generation tyrosine kinase inhibitor.
Pharmaceutics
January 2025
CDL Research, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
Background/objectives: Glioblastoma is the most common and lethal primary brain tumor. Patients often suffer from tumor- and treatment induced vasogenic edema, with devastating neurological consequences. Intracranial edema is effectively treated with dexamethasone.
View Article and Find Full Text PDFDrug Test Anal
January 2025
Catalonian Antidoping Laboratory, Doping Control Research Group, Hospital del Mar Research Institute, Barcelona, Spain.
The detection of endogenous anabolic androgenic steroids (EAAS) is performed with the Steroidal Module of the Athlete Biological Passport (ABP). Glucocorticoids (GC) could be a confounding factor to the ABP Steroidal Module because they inhibit the hypothalamic-pituitary-adrenal axis, and ABP metabolites have partial adrenal origin. In previous studies, single-dose systemic GC administrations have been shown to reduce the urinary ratios A/T and 5αdiol/E.
View Article and Find Full Text PDFFront Cell Infect Microbiol
January 2025
Department of Critical Care Medicine, Xinxiang Medical University, Henan Provincial People's Hospital, Zhengzhou, China.
Objective: Severe community-acquired pneumonia (sCAP) is one of the major diseases within the ICU. We hypothesize that subtyping sCAP based on simple inflammatory markers, organ dysfunction, and clinical metagenomics results is feasible.
Method: In this study, we retrospectively enrolled immunocompetent sCAP patients requiring invasive mechanical ventilation, who underwent clinical metagenomics from 17 medical centers.
Unlabelled: Stress affects gastrointestinal (GI) function causing dysmotility, especially in patients. GI motility is regulated by the enteric nervous system (ENS), suggesting that stress alters ENS biology to cause dysmotility. While stress increases glucocorticoid levels through the hypothalamus-pituitary-adrenal axis, how glucocorticoids affect GI motility is not known.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!