Insights Into the Pathogenesis of Sweet's Syndrome

被引:103
作者
Heath, Michael S. [1 ]
Ortega-Loayza, Alex G. [1 ]
机构
[1] Oregon Hlth & Sci Univ, Dept Dermatol, Portland, OR 97201 USA
关键词
acute febrile neutrophilic dermatosis; neutrophilic dermatoses; malignancy; drug induced; autoinflammation; clonality; hematology; FEBRILE NEUTROPHILIC DERMATOSIS; COLONY-STIMULATING FACTOR; TRANS-RETINOIC ACID; NONTUBERCULOUS MYCOBACTERIAL INFECTION; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; HYDRALAZINE-INDUCED LUPUS; ACUTE MYELOID-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA;
D O I
10.3389/fimmu.2019.00414
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Sweet's syndrome, also known as Acute Febrile Neutrophilic Dermatosis, is a rare inflammatory condition. It is considered to be the prototype disease of neutrophilic dermatoses, and presents with acute onset dermal neutrophilic lesions, leukocytosis, and pyrexia. Several variants have been described both clinically and histopathologically. Classifications include classic Sweet's syndrome, malignancy associated, and drug induced. The cellular and molecular mechanisms involved in Sweet's syndrome have been difficult to elucidate due to the large variety of conditions leading to a common clinical presentation. The exact pathogenesis of Sweet's syndrome is unclear; however, new discoveries have shed light on the role of inflammatory signaling, disease induction, and relationship with malignancy. These findings include an improved understanding of inflammasome activation, malignant transformation into dermal infiltrating neutrophils, and genetic contributions. Continued investigations into effective treatments and targeted therapy will benefit patients and improve our molecular understanding of inflammatory diseases, including Sweet's syndrome.
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页数:22
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