Sweet's syndrome: a review of current treatment options.
Sweet's syndrome: a review of current treatment options.
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DOI：
10.2165/00128071-200203020-00005
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发表时间：
2002-01-01
影响因子：
7.3
通讯作者：
Kurzrock, Razelle
中科院分区：
文献类型：
--
作者：
Cohen, Philip R;Kurzrock, Razelle
斯威特综合征最初是在1964年被罗伯特·道格拉斯·斯威特医生描述为“急性发热性中性粒细胞皮肤病”。该综合征的特征是发热、中性粒细胞计数升高、疼痛的红色丘疹、结节、斑块(可能是复发的)和主要由弥漫在真皮上部的成熟中性粒细胞组成的浸润物。除皮肤和粘膜损害外，Sweet‘s综合征还可出现皮肤外症状。Sweet综合征可根据其发生的临床环境进行分类：经典型或特发性Sweet综合征、恶性肿瘤相关的Sweet综合征和药物诱导的Sweet综合征。全身性皮质类固醇被认为是治疗Sweet综合征患者的‘金标准’；此外，局部和/或皮内皮质类固醇治疗可能与单一疗法或辅助疗法一样有效。然而，在一些没有启动疾病特异性治疗干预的Sweet综合征患者中，以及在停用引起皮肤病的药物后，一些药物引起的Sweet综合征患者的症状和皮损自发消失。口服碘化钾或秋水仙碱通常能迅速缓解Sweet综合征的症状和皮损；因此，对于有潜在全身感染或皮质类固醇禁忌症的Sweet综合征患者，将这些药物作为一线治疗开始治疗是合理的。消炎痛、氯法齐明、氨苯砜和环孢菌素也是治疗Sweet综合征的有效药物。然而，吲哚美辛和氯法齐明似乎不如皮质类固醇、碘化钾和秋水仙碱有效。在使用氨苯松钠或环孢菌素治疗时，有必要进行适当的初始和后续实验室监测，因为可能会产生严重的药物相关不良反应。具有抗金黄色葡萄球菌活性的全身性抗菌药物在脓疱病或继发性感染时，往往会导致Sweet综合征皮损的部分改善。在一些皮肤病相关细菌感染的患者中，机体敏感的特定系统抗菌药物对他们的Sweet‘s综合征的治疗很有帮助。尽管血液系统恶性肿瘤相关的Sweet综合征患者经常接受细胞毒性化疗药物和抗代谢药物来治疗他们潜在的疾病，但这些药物很少单独用于治疗Sweet综合征的症状和皮损。曾有报道称，使用依维甲酸酯或α-干扰素治疗Sweet‘s综合征的患者是单一病例；这两名患者不仅其Sweet’s综合征的皮损得到改善，而且其相关的血液系统疾病也得到改善。
Sweet's syndrome was originally described in 1964 by Dr Robert Douglas Sweet as an 'acute febrile neutrophilic dermatosis'. The syndrome is characterized by pyrexia, elevated neutrophil count, painful red papules, nodules, plaques (which may be recurrent) and an infiltrate consisting predominantly of mature neutrophils that are diffusely distributed in the upper dermis. In addition to skin and mucosal lesions, Sweet's syndrome can also present with extra-cutaneous manifestations. Sweet's syndrome can be classified based upon the clinical setting in which it occurs: classical or idiopathic Sweet's syndrome, malignancy-associated Sweet's syndrome and drug-induced Sweet's syndrome. Systemic corticosteroids have been considered the 'gold standard' for the treatment of patients with Sweet's syndrome; in addition, treatment with topical and/or intralesional corticosteroids may be effective as either monotherapy or adjuvant therapy. However, spontaneous resolution of the symptoms and lesions has occurred in several patients with Sweet's syndrome for whom disease-specific therapeutic intervention was not initiated and in some of the patients with drug-induced Sweet's syndrome after withdrawal of the dermatosis-causing medication. Oral therapy with either potassium iodide or colchicine typically results in rapid resolution of Sweet's syndrome symptoms and lesions; therefore, in patients with Sweet's syndrome who have a potential systemic infection or in whom corticosteroids are contraindicated, it is reasonable to initiate treatment with these agents as a first-line therapy. Indomethacin, clofazimine, dapsone, and cyclosporine have also been effective therapeutic agents for managing Sweet's syndrome. However, indomethacin and clofazimine appear less effective than corticosteroids, potassium iodide, and colchicine. Appropriate initial and follow-up laboratory monitoring is necessary when treating with either dapsone or cyclosporine because of the potential for severe adverse drug-associated effects. Systemic antibacterials with activity against Staphylococcus aureus frequently result in partial improvement of Sweet's syndrome lesions when they are impetiginized or secondarily infected. In some patients with dermatosis-associated bacterial infections, organism-sensitive specific systemic antibacterials have been helpful in the management of their Sweet's syndrome. Although patients with hematologic malignancy-associated Sweet's syndrome often receive cytotoxic chemotherapy agents and antimetabolic drugs for the treatment of their underlying disorder, these agents are seldom used solely for the management of the symptoms and lesions of Sweet's syndrome. The treatment of patients with Sweet's syndrome with either etretinate or interferon-alpha have been reported as single case reports; both patients had improvement of not only their Sweet's syndrome lesions, but also their associated hematologic disorder.