Sweet's syndrome during therapy with granulocyte colony‐stimulating factor in a patient with aplastic anaemia

Abstract

A patient with aplastic anaemia developed Sweet's syndrome (a febrile neutrophilic dermatosis) during granulocyte colony-stimulating factor (G-CSF) therapy. Three repeated episodes of appearance and disappearance of erythematous nodules after administration and withdrawal of G-CSF confirmed that G-CSF induced Sweet's syndrome in the patient. Sweet's syndrome has been reported in patients with myelodysplastic syndrome and acute leukemia, but not in patients with aplastic anaemia. This is the first report of a patient with aplastic anaemia who developed G-CSF-induced Sweet's syndrome.

Granulomatous Dermatitis with Enlarged Histiocytes: A Characteristic Pattern of Granulocyte Colony-Stimulating Factor

“…Localized reactions at the site of injection are characterized by urticarial wheals with edema although lichenoid reactions have also been described [8,9,10]. Development of neutrophilic dermatoses such as Sweet’s syndrome [11,12,13], pyoderma gangrenosum [14, 15], neutrophilic eccrine hidradenitis [16], leukocytoclastic vasculitis [17,18,19] and folliculitis [20] have occasionally been reported. In some instances, exacerbation of certain diseases, such as acne [21] or psoriasis [22, 23], has also been noted.…”

Sweet's Syndrome and Erythema Nodosum

“…30 Griffin et al 39 also reported that AML-conditioned media containing IL-1 bioactivity induced human endothelial cells to express the G-CSF gene. Additional reports document the occurrence of SS after treatment with G-CSF, 40,41 and ReussBorst et al 42 described a patient during the acute phase of SS with markedly elevated serum levels of G-CSF and IL-6 (an endogenous pyrogen that also enhances the production of acute phase proteins). 43 Other authors, however, have failed to confirm these data.…”

Unusual adverse events following peripheral blood stem cell (PBSC) mobilisation using granulocyte colony stimulating factor (G-CSF) in healthy donors

“…17,18 Induction of secondary inflammatory cytokines by G-CSF has been discussed as being responsible for the occurrence of ARDS during G-CSF treatment for druginduced neutropenia. 27,28 However, the capacity of G-CSF to induce secondary cytokines and/or chemokines or chemoattractants that may be instrumental in orchestrating the progression of inflammation remains controversial. 29 Recently, anti-inflammatory properties of G-CSF by downregulation of TNF-␣, IL-12, and IFN-␣ release in response to LPS after a prolonged administration of G-CSF at dosages even lower than used for stem cell mobilisation have been reported.…”