Division of Dermatology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Department of Dermatology, Stanford University School of Medicine, Palo Alto, California, USA.
Dermatol Ther. 2021 Jan;34(1):e14461. doi: 10.1111/dth.14461. Epub 2020 Nov 5.
Tyrosine kinase inhibitors are a class of targeted anticancer drugs that inhibit cancer cell proliferation by inactivating proteins involved in signal transduction cascades. Various cutaneous adverse events have been observed after tyrosine kinase inhibitor administration, including Sweet syndrome. We queried the PubMed database to identify 14 cases of Sweet syndrome thought to be secondary to tyrosine kinase inhibitors. Tyrosine kinase inhibitor-induced Sweet syndrome had a median of 2 months latency following drug administration. All cases but one had morphologic features classic for Sweet syndrome (erythematous and tender papules, plaques, or nodules). All cases also had classic histopathologic findings (dermal neutrophilic infiltrate without vasculitis or necrosis). Using diagnostic criteria for drug-induced Sweet syndrome and the Naranjo Drug Reaction Probability Scale for a drug-induced cutaneous eruption, we found that six cases favored a drug-induced etiology over malignancy, two cases favored a malignancy-associated Sweet syndrome, and the remaining eight met drug-induced Sweet syndrome criteria but had low Naranjo scores. Nine cases resulted in medication discontinuation, while five cases continued anticancer therapy and were treated only with corticosteroids with quick resolution of skin lesions. Dermatologists should be aware of this adverse cutaneous reaction to tyrosine kinase inhibitors and should treat on a case-by-case basis, though limited evidence in this review suggests that oncologic therapy may safely be continued with prompt corticosteroid treatment.
酪氨酸激酶抑制剂是一类靶向抗癌药物,通过使参与信号转导级联的蛋白质失活来抑制癌细胞增殖。在使用酪氨酸激酶抑制剂后,观察到各种皮肤不良事件,包括 Sweet 综合征。我们查询了 PubMed 数据库,以确定 14 例被认为是由酪氨酸激酶抑制剂引起的 Sweet 综合征病例。酪氨酸激酶抑制剂诱导的 Sweet 综合征在药物给药后中位潜伏期为 2 个月。除 1 例外,所有病例均具有 Sweet 综合征的形态学特征(红斑性和压痛性丘疹、斑块或结节)。所有病例均具有经典的组织病理学发现(无血管炎或坏死的真皮中性粒细胞浸润)。使用药物诱导的 Sweet 综合征的诊断标准和 Naranjo 药物反应概率量表对药物引起的皮肤发作进行评估,我们发现 6 例更倾向于药物引起的病因而不是恶性肿瘤,2 例更倾向于与恶性肿瘤相关的 Sweet 综合征,其余 8 例符合药物诱导的 Sweet 综合征标准,但 Naranjo 评分较低。9 例导致停药,而 5 例继续接受抗癌治疗,仅用皮质类固醇治疗,皮肤病变迅速消退。皮肤科医生应该意识到这种酪氨酸激酶抑制剂的不良皮肤反应,并应根据具体情况进行治疗,尽管本综述中的有限证据表明,在迅速给予皮质类固醇治疗的情况下,肿瘤学治疗可能可以安全地继续进行。