Abstract | BACKGROUND:
Sweet's syndrome in the setting of hematologic dyscrasias can be categorized into paraneoplastic-associated SS, drug-induced SS, and SS with leukemia cutis. Apart from those cases demonstrating concomitant leukemic infiltrates, it has been surmised that SS is a reactive phenomenon induced by a specific cytokine milieu. METHODS: RESULTS: Routine light microscopic examination revealed differentiated myeloid precursors including myelocytes and metamyelocytes within the subcutis; myeloblasts were not identified. In addition, in the overlying skin, features typical of SS were observed. The neutrophils demonstrated dysplastic features including hypolobation compatible with a Pseudo Pelger-Huet anomaly. X inactivation studies showed clonality both within her post-treatment marrow and skin biopsy specimen. CONCLUSIONS:
Sweet's syndrome developing in CD34+ AML patients following GCSF therapy likely reflects therapy induced differentiation of sequestered leukemic cells, hence indicative of a clonal neutrophilic dermatosis.
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Authors | C M Magro, E De Moraes, F Burns |
Journal | Journal of cutaneous pathology
(J Cutan Pathol)
Vol. 28
Issue 2
Pg. 90-6
(Feb 2001)
ISSN: 0303-6987 [Print] United States |
PMID | 11168757
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- Antigens, CD34
- Granulocyte Colony-Stimulating Factor
- DNA
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Topics |
- Acute Disease
- Adult
- Antigens, CD34
(blood)
- Bone Marrow Cells
(pathology)
- Clone Cells
- DNA
(analysis)
- Female
- Flow Cytometry
- Granulocyte Colony-Stimulating Factor
(therapeutic use)
- Humans
- Leukemia, Myeloid
(complications, drug therapy, immunology, pathology)
- Neutrophils
(pathology)
- Polymerase Chain Reaction
- Skin
(pathology)
- Sweet Syndrome
(etiology, genetics, pathology)
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