Systemic sclerosis & Raynaud's
Drug‐Induced Raynaud's Phenomenon and Underlying Mechanism: A Disproportionality Analysis From the World Health Organization Pharmacovigilance Database
Authors' conclusion
This study allowed us to identify robust safety signals (such as solriamfetol, tyrosine kinase inhibitors, and calcitonin gene-related peptide inhibitors) for drugs associated with RP and potential implicated pathophysiologic mechanisms.
Study context
- Population
- Individual Case Safety Reports (ICSRs) of Raynaud's phenomenon (RP) (MedDRA Preferred Term "Raynaud's phenomenon") in the World Health Organization (WHO) pharmacovigilance database, excluding ICSRs with at least one drug used in RP treatmentICSRs of RP
- Participants
- 4,430 icsrs
- Outcome
- Signals of disproportionate reporting
Methodological detailsWHO pharmacovigilance database, information component (ICLB >0 deemed significant), sensitivity analyses, clustering analysis, DrugBank drug target extraction
- WHO pharmacovigilance database
- Information component (ICLB >0 deemed significant)
- Sensitivity analyses
- Clustering analysis
- DrugBank drug target extraction
Main finding
As reported in the abstract
Significant signals of disproportionate reporting (SDRs) in primary analysis
124
SDRs consistent across all sensitivity analyses
52
SDRs considered probable after signal evaluation and prioritization (incl. amphetamine-like, antimigraine drugs, antineoplastics, dopaminergic agonists)
16
Observational data: associations, not effects.
Further findings
Drug targets involved
- Most targets: 5-HT1A receptors, sodium-dependent noradrenaline transporters, beta-1 and beta-2 adrenergic receptors
Cluster analyses
- Inconsistent results according to the method used
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
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