AimSweet’s syndrome is an acute febrile neutrophilic dermatosis first described in 1964 by Robert Douglas Sweet. The pathophysiological mechanism is not fully established, however several cases of Sweet’s syndrome have been reported following drug administration.MethodsTo investigate the existence of pharmacovigilance signals between drugs and the occurrence of Sweet’s syndrome, we performed a case/non‐case study on reports of “acute febrile neutrophilic dermatosis” registered in the French pharmacovigilance database. Reporting Odds Ratio (ROR) with its 95% confidence interval were calculated.ResultsAmong the 994,789 reports recorded in the database, 136 were Sweet’s syndrome. 50.7% of patients were men; median age was 59 years (range 15‐91). 224 drugs were mentioned as suspects: 21.0% were antibacterials, 19.2% were antineoplastics, 12.1% were immunosuppressants. Median time to onset from drug initiation to the development of Sweet’s syndrome was 15 days (range 1‐1095). Highest ROR were observed with bortezomib (74.04 [40.8‐134.2]), azacitidine (72.14 [29.4‐176.9]), perfilgrastim (67.05 [21.2‐211.6]), azathioprine (55.46 [34.8‐88.4]) and bendamustine (35.84 [11.4‐112.8]).ConclusionPharmacovigilance signals have been observed between the occurrence of Sweet’s syndrome and colony‐stimulating factors, immunosuppressants, antineoplastics and antibiotics. Clinicians should be aware of the potential associations with these drugs and encourage reporting any case of drug‐induced Sweet’s syndrome.