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Sweet syndrome (Introduction, Types, Pathophysiology)

 

Acute Febrile Neutrophilic Dermatosis (Sweet Syndrome)

Introduction

Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, was first described by Robert Douglas Sweet in 1964. It is a reactive process characterized by the sudden onset of tender, red-to-purple papules and nodules that often merge to form plaques, usually occurring on the upper extremities, face, or neck. This dermatologic condition is often associated with fever and elevated neutrophil levels in the blood (peripheral neutrophilia).


Sweet syndrome


Sweet syndrome is categorized into three types based on the underlying cause:

1. Classic or Idiopathic Sweet Syndrome

This is the most common form, predominantly affecting young women and often following a mild respiratory illness. It may also be associated with pregnancy, inflammatory bowel disease (IBD), vaccinations, other inflammatory conditions, and infections.

2. Malignancy-Associated Sweet Syndrome

This form occurs alongside an underlying malignancy, sometimes being the first indication of a hidden cancer. It can also present as a paraneoplastic syndrome or as part of an established cancer, most commonly linked with acute myelogenous leukemia and myelodysplastic syndrome.

3. Iatrogenic Sweet Syndrome

 This variant is triggered by certain medications, most notably granulocyte colony-stimulating factor (G-CSF). Other implicated agents include trimethoprim/sulfamethoxazole, minocycline, contraceptives like levonorgestrel/ethinyl estradiol, and all-trans retinoic acid (ATRA). Antineoplastic agents, biologics, and radiotherapy have also been linked to iatrogenic Sweet syndrome.


sweet syndrome


Pathophysiology of Sweet Syndrome

Sweet syndrome is a “neutrophil-mediated hypersensitivity reaction” triggered by factors such as infections, malignancies, drugs, or inflammation. Its hallmark is an abnormal activation of neutrophils, supported by the presence of neutrophilia and the condition’s response to treatments targeting neutrophil function.

Granulocyte colony-stimulating factor (G-CSF) plays a key role by prolonging neutrophil survival and increasing their activity. Elevated G-CSF levels correlate with disease severity, and even in cases with low neutrophil counts, lesions can develop due to heightened neutrophil function. All-trans retinoic acid (ATRA), used in acute promyelocytic leukemia, has also been linked to neutrophil dysfunction in drug-induced cases.

Cytokines, such as IL-1, IL-2, and IFN-γ, contribute to the disease, particularly in malignancy-related forms. Elevated IL-6 levels also track with disease activity, decreasing with corticosteroid treatment.

Genetically, HLA-B54 (in Japanese populations) and chromosome 3q abnormalities are associated with the condition. Mutations in FLT3 have also been linked to Sweet syndrome-like skin disease, and familial cases suggest a genetic predisposition.

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