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Lichenoid and psoriasiform drug induced rush during imatinib therapy: a clinical case

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Tyrosine kinase inhibitor imatinib is a standard agent for treatment of gastrointestinal stromal tumors (GIST). Treatment courses are quite long and are usually well tolerated. However, skin rash can occur on treatment, with a prevalence of 7 to 88.9%. We describe a clinical case of a patient with GIST, who has been on treatment with imatinib at daily dose of 400 mg for one year. Several weeks from the treatment initiation, she had facial edema, and 4 months thereafter psoriasiform rash appeared which was initially considered to be psoriatic. After 8 months, the patient had lichenoid rash on the inguinal skin and oral, tongue and vulvar mucosae. Clinically, the lichenoid rash was similar with lichen ruber planus. To confirm the diagnosis, we performed biopsy of psoriasiform and lichenoid foci. Histological examination verified the drug-induced rash. Topical treatment of psoriasiform rash with glucocorticosteroids resulted in regression of some plaques, although a proportion of them persisted. Inguinal and vulvar lichenoid rashes completely regressed and numbers of oral and tongue foci decreased after a 6-week daily application of the 0.1% tacrolimus cream. Treatment with imatinib 400 mg daily was not interrupted. The clinical observation illustrates the possibility of skin and mucosal lichenoid and psoriasiform rash simultaneously during treatment with imatinib and demonstrates the first successful experience in the treatment of lichenoid rashes with 0.1% tacrolimus cream.
Title: Lichenoid and psoriasiform drug induced rush during imatinib therapy: a clinical case
Description:
Tyrosine kinase inhibitor imatinib is a standard agent for treatment of gastrointestinal stromal tumors (GIST).
Treatment courses are quite long and are usually well tolerated.
However, skin rash can occur on treatment, with a prevalence of 7 to 88.
9%.
We describe a clinical case of a patient with GIST, who has been on treatment with imatinib at daily dose of 400 mg for one year.
Several weeks from the treatment initiation, she had facial edema, and 4 months thereafter psoriasiform rash appeared which was initially considered to be psoriatic.
After 8 months, the patient had lichenoid rash on the inguinal skin and oral, tongue and vulvar mucosae.
Clinically, the lichenoid rash was similar with lichen ruber planus.
To confirm the diagnosis, we performed biopsy of psoriasiform and lichenoid foci.
Histological examination verified the drug-induced rash.
Topical treatment of psoriasiform rash with glucocorticosteroids resulted in regression of some plaques, although a proportion of them persisted.
Inguinal and vulvar lichenoid rashes completely regressed and numbers of oral and tongue foci decreased after a 6-week daily application of the 0.
1% tacrolimus cream.
Treatment with imatinib 400 mg daily was not interrupted.
The clinical observation illustrates the possibility of skin and mucosal lichenoid and psoriasiform rash simultaneously during treatment with imatinib and demonstrates the first successful experience in the treatment of lichenoid rashes with 0.
1% tacrolimus cream.

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