Lamotrigine-induced Sweet syndrome: Possible new drug association

Neely, Gabriel; Fajre, Ximena; Cabrera, Raúl; Castro, Álex

doi:10.1016/j.jdcr.2020.07.043

Cited by 4 publications

(5 citation statements)

References 11 publications

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“…6,[12][13][14] In the cases documented with biological data, neutrophilia was present in 67.7% of cases and a high ESR in nine of the ten documented cases. The same biological abnormalities have been found in other case reports, 15,16 and by Walker and Cohen (38% neutrophilia; 3/3 patients with high ESR). 6 Neutrophilic leucocytosis and high ESR are the most common laboratory abnormalities in patients with Sweet's syndrome and should raise suspicion about its diagnosis.…”

Section: Discussionsupporting

confidence: 88%

“…The TTO of Sweet's syndrome among our cases was variable, ranging from a few days to several years, with a median TTO of 15 days (range 1-1095). This has also been observed in the literature, with some lesions appearing days, 6,17,29 months, 16,32 or even years after drug administration. 33 Thompson and Monterella 14 found a mean time from G-CSF initiation to lesion onset of 46 days, 17 days with ATRA and 4 h to 15 days with vaccines.…”

Section: Discussionsupporting

confidence: 77%

“…It is difficult to assess the temporal suggestiveness of the onset of symptoms as there may be a latency of months to years between the drug administration and the appearance of Sweet's lesions. 16,28,32 A reappearance of the lesions after rechallenge as well as a clinical improvement after stopping the drug involved support the hypothesis of an iatrogenic aetiology. 28 Another problem with the fourth and fifth criteria is that they are retrospective diagnostic criteria that cannot be used in prospective diagnosis.…”

Section: Discussionmentioning

confidence: 58%

“…The absence of leukocytoclastic vasculitis in the histopathological diagnostic criterion of Sweet's syndrome is controversial, due to the close relationship between these two pathologies in terms of clinical appearance, histopathology, triggers, evolution and response to treatment. 40 Although this criterion has been met in many publications, 1,16,29,32,38 others have reported leukocytoclastic vasculitis in a variable number of patients. [40][41][42] The hypothesis of a vasculitis secondary to noxious products released by the neutrophil infiltrate is postulated.…”

Section: Discussionmentioning

confidence: 99%

“…The fourth diagnostic criterion requires a ‘temporal relationship between drug ingestion and clinical presentation, or temporally‐related recurrence after oral challenge’. It is difficult to assess the temporal suggestiveness of the onset of symptoms as there may be a latency of months to years between the drug administration and the appearance of Sweet's lesions 16,28,32 . A reappearance of the lesions after rechallenge as well as a clinical improvement after stopping the drug involved support the hypothesis of an iatrogenic aetiology 28 .…”

Section: Discussionmentioning

confidence: 99%

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Drug‐induced Sweet's syndrome: A case/non‐case study in the French pharmacovigilance database

Martin¹,

Trenque²,

Herlem³

et al. 2023

Brit J Clinical Pharma

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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.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Drug‐induced Sweet's syndrome: A case/non‐case study in the French pharmacovigilance database

Martin¹,

Trenque²,

Herlem³

et al. 2023

Brit J Clinical Pharma

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New Practical Aspects of Sweet Syndrome

et al. 2022

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Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, is an inflammatory, non-infectious skin reaction characterized clinically by tender, erythematous papules/plaques/pustules/nodules commonly appearing on the upper limbs, trunk, and head and neck; histologically, SS is characterized by dense neutrophilic infiltrate in the dermis. SS is accompanied by fever; an elevation of inflammatory markers (e.g., erythrocyte sedimentation rate, C reactive protein) in serum may also be observed. Although most cases of SS are idiopathic, SS also occurs in the setting of malignancy or following administration of an associated drug. SS has also been reported in association with pregnancy and a burgeoning list of infectious (most commonly upper respiratory tract infections) and inflammatory diseases; likewise, the litany of possible iatrogenic triggers has also grown. Over the past several years, a wider spectrum of SS presentation has been realized, with several reports highlighting novel clinical and histological variants. Corticosteroids continue to be efficacious first-line therapy for the majority of patients with SS, although novel steroid-sparing agents have been recently added to the therapeutic armamentarium against refractory SS. New mechanisms of SS induction have also been recognized, although the precise etiology of SS still remains elusive. Here, we catalogue the various clinical and histological presentations of SS, summarize recently reported disease associations and iatrogenic triggers, and review treatment options. We also attempt to frame the findings of this review in the context of established and emerging paradigms of SS pathogenesis.

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Lamotrigine

2020

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Lamotrigine-induced Sweet syndrome: Possible new drug association

Cited by 4 publications

References 11 publications

Drug‐induced Sweet's syndrome: A case/non‐case study in the French pharmacovigilance database

Drug‐induced Sweet's syndrome: A case/non‐case study in the French pharmacovigilance database

New Practical Aspects of Sweet Syndrome

Lamotrigine

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