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  1. Pubblicazioni

Oral lichenoid eruption secondary to imatinib(Glivec)

Articolo
Data di Pubblicazione:
2004
Citazione:
Oral lichenoid eruption secondary to imatinib(Glivec) / Ena, Pasquale; Chiarolini, F; Siddi, Gm; Cossu, A.. - In: THE JOURNAL OF DERMATOLOGICAL TREATMENT. - ISSN 0954-6634. - 15:(2004), pp. 253-255.
Abstract:
Abstract
BACKGROUND:
Oral lichenoid drug eruption (OLE) is a self-restricted inflammatory condition usually secondary to a variety of drugs and dental materials (mercury, gold), and rarely to immunomodulators and new antineoplastic agents such as imatinib mesylate (Glivec). OLE clinical features are reminiscent of lichen planus and include symmetric and asymptomatic, erythematous, reticulated and painful ulcerated plaques. Histological examination reveals perivascular lymphocytic infiltrate and the presence of eosinophils that obscures the dermal-epidermal junction, with acanthosis and mild hyperkeratosis.
METHODS:
A 62-year-old man was treated with Glivec for metastatic gastrointestinal stromal tumour (GIST).
RESULTS:
The patient presented with grey-violaceous plaques on both cheek mucosal surfaces and the lateral sides of the tongue and labial mucosa, with a reticular pattern resembling oral lichen planus. These lesions appeared approximately 1 year after therapy and partially subsided in about 10 weeks, to clear after topical corticosteroids and oral omeprazole. The diagnosis of OLE induced by imatinib was confirmed by histological biopsy evaluation; immunohistochemical analysis revealed intense immunoreactivity with only cytokeratins 5/6 and 14 in the epithelium of affected mucosa. All laboratory investigations proved asiderotic anaemia but excluded infectious causes.
CONCLUSION:
It is believed that this patient developed imatinib-induced OLE; this relationship with therapy rather than the underlying disease rules out a paraneoplastic reaction, and negative immunofluorescence excluded autoimmune dermatosis. In addition, we propose that these lesions are correlated with abnormal expression of some cytokeratins directly caused by this drug.
Tipologia CRIS:
1.1 Articolo in rivista
Elenco autori:
Ena, Pasquale; Chiarolini, F; Siddi, Gm; Cossu, A.
Autori di Ateneo:
COSSU Antonio Giuseppe Maria
Link alla scheda completa:
https://iris.uniss.it/handle/11388/146730
Pubblicato in:
THE JOURNAL OF DERMATOLOGICAL TREATMENT
Journal
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