Imatinib-induced diffuse hyperpigmentation of the oral mucosa, the skin, and the nails in a patient affected by chronic myeloid leukemia: report of a case and review of the literature.

BACKGROUND: Imatinib mesylate is a tyrosine-kinase inhibitor used as the first-line treatment in chronic myeloid leukemia patients, but it is also indicated for other hematological diseases and solid tumors. Imatinib treatment is often associated with hypopigmentation, but only a few cases of hyperpigmentation are described in literature. METHODS: We are reporting the first case of imatinib-related hyperpigmentation involving the oral mucosa, skin, and nails in a patient affected by chronic myeloid leukemia and treated with imatinib since 2002. A review of all the available literature regarding the imatinib-related hyperpigmentation was performed, and one additional case was analyzed. Due to the possibility of a post-inflammatory hyperpigmentation, all cases of pigmentary changes previously characterized by a rash and/or pruritus in the same body areas were excluded. RESULTS: Thirty cases of well-documented imatinib-related hyperpigmentation were described in literature. In our case, imatinib therapy was well tolerated for several years, and it led to an excellent hematological and cytogenetic response. However, the patient gradually developed a blue-gray pigmentation that involved the nose, fingernails, toenails, pretibial regions, posterior axillary folds, and hard palate. Other causes of pigmentary changes were excluded, and histopathological examination confirmed the clinical suspicion of imatinib-related hyperpigmentation. CONCLUSIONS: Hyperpigmentation induced by imatinib is an adverse reaction rarely described in literature. The underlying pathogenetic mechanisms are not yet completely clear, and further studies are necessary to elucidate them. Currently, no treatment is required for this condition, and there is no indication to discontinue imatinib treatment.

Monoclonal gammopathy of undetermined significance in patients with psoriasis: is it really a side effect of biological therapy?

Moderate-to-severe psoriasis is treated using biological drugs targeting cytokines involved in the pathogenesis of the disease, such as tumor necrosis factor alpha (TNF-α) (adalimumab, infliximab, etanercept) and interleukin 12/23 (IL 12/23) (ustekinumab). There is a slight risk of developing hematological malignancies, such as monoclonal gammopathy of undetermined significance (MGUS) with anti TNF-α agents. There are no data available on anti-IL12/23 drugs. This retrospective study of data from 191 patients describes the appearance and follow-up of MGUS in three patients with psoriasis receiving long-term biological therapy. Since the appearance of MGUS occurred after about 6 years of anti-TNFα treatment in only three subjects, it was deemed unlikely to be due to the biological treatment. The decision not to suspend biological therapy after the appearance of MGUS was taken after careful assessment of the possible risks and benefits.

Cutaneous lesions as initial signs of interferon alpha-induced sarcoidosis: report of three new cases and review of the literature.

Sarcoid reactions are well-recognized adverse events during interferon (IFN) therapy. They are frequently underdiagnosed because misinterpreted as IFN-induced side effects. Sarcoid cutaneous lesions may therefore represent useful hints to an early diagnosis, but their incidence is unknown. We report three new cases of mono-localized, purely cutaneous IFNalpha-induced sarcoidosis. In addition, an extensive review of the literature, with special attention to skin involvement, was performed through a PubMed search. The analysis of the retrieved articles showed that cutaneous lesions are frequent signs of IFN-induced sarcoidosis. Skin involvement is documented in 56% of the reports and it appears among the presenting and diagnostic signs of a sarcoid reaction in 51%. Special attention to dermatologic signs is imperative in the course of IFN therapy because even minimal skin involvement may offer a clue to an early diagnosis of IFN-induced sarcoidosis.