Idiopathic Hypereosinophilic Syndrome Progressing to Acute Myelomonocytic Leukemia With Chloromas

Hypereosinophilic Syndrome and Clonal Eosinophilia: Point-of-Care Diagnostic Algorithm and Treatment Update

“…For example, eosinophil monoclonality has been demonstrated in some cases of HES 10,11 and progression into WHO-defined myeloid neoplasm in other cases. [12][13][14][15] Additionally, patients with FIP1L1-PDGFRA-positive clonal eosinophilia were often diagnosed as having HES before the mutation was discovered in 2003. 16 …”

Eosinophilia: secondary, clonal and idiopathic

“…HES is a subset of idiopathic eosinophilia that fulfils the traditional criteria of a persistent (>6 months) increase in AEC (>1·5 × 10 9 /l) associated with target organ damage (Chusid et al , 1975). However, evidence from both X‐linked clonality studies (Chang et al , 1999; Malcovati et al , 2004) and long‐term follow up of affected patients suggest that at least some patients with HES harbour an underlying clonal myeloid malignancy that could progress into frank acute leukaemia or MPD (Owen & Scott, 1979; Yoo et al , 1984; Brown & Stein, 1989; Needleman et al , 1990). On the other hand, the demonstration of a clonal (Simon et al , 1999) or phenotypically abnormal (Simon et al , 1999) T‐cell population in other patients with HES suggests the alternative possibility of a true secondary process with some of these patients progressing into clinically overt lymphoma (Butterfield, 2001).…”

Hypereosinophilic Syndrome Terminating in Acute Myelogenous Leukemia

“…In the majority of patients with HES the proliferation of eosinophils is thought to be due to a reaction to an unknown agent rather than to a clo nal expansion, although this syndrome often results in marked morbidity and mortality due to eosinophilic infil tration into various organs, especially the heart. Only a few cases of HES have been reported to terminate in acute myeloid leukemia (AML) [2][3][4][5][6][7], although the diagnosis of acute lymphoid leukemia has recently been noted to be preceded or masked by HES in some patients [8]. In this paper we describe a patient with typical HES who suffered from cardiac symptoms due to hypereosinophilia and thromboembolic complications for nearly 5 years; the dis ease terminated in AML.…”