ABSTRACT
Background
Stevens-Johnson syndrome is a rare but serious skin condition, which can lead to death. Stevens-Johnson syndrome is usually attributed to drug-induced reactions, thus making it vital for clinicians to prevent its occurrence by knowing the trigger drugs. The objective of this study was to comprehensively and systematically excavate the drugs that cause SJS to provide references for clinician.
Research design and methods
This is an observational, retrospective study, conducting a disproportionality analysis. Where the Information Component (IC) method and Reporting odds ratio (ROR) are used to mine the drugs that cause SJS.
Results
A total of 17,787,905 reports were extracted from VigiBase database, of which 25,051 reports were related to SJS. The 18–44 age group had the largest number of cases (N=7,973, 31.83%). A total of 295 drugs was detected as signals. Allopurinol (IC025/ROR025=5.86/69.84), phenytoin (IC025/ROR025=5.60/57.65) and carbamazepine (IC025/ROR025=5.25/43.88) were the top 3 strongest signals. Our study only considered the possibility of SJS caused by a single drug.
Conclusions
Allopurinol, phenytoin and carbamazepine were three strongest signals. Garenoxaci, carbocisteine and dimetindene were strong signals, but there are no relevant cases reported on PubMed or specific SJS in labels, which need further study to verify.
Article highlights
Stevens-Johnson Syndrome is a rare but serious skin condition, which can lead to death.
Stevens-Johnson Syndrome is usually attributed to drug-induced reactions.
The target drugs that may trigger Stevens-Johnson syndrome were analyzed based on the WHO database.
Majorly Stevens-Johnson Syndrome were reported from 18-64-yearage group.
Carbamazepine and allopurinol were two strongest drug signals in different age groups and gender groups.
Acknowledgments
The data provided by VigiBase comes from a variety of sources. In all reports, the likelihood of causality is different. This information does not represent the opinion of the WHO. At the same time, the authors would like to thank the research department of Uppsala Monitoring Center (Uppsala, Sweden) for their help in data extraction.
Declaration of interests
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/14740338.2022.2045946