The Association of Eosinophilia with Lymphoblastic Leukaemia or Lymphoma: a Study of Seven Patients

Abstract

Seven patients with hypereosinophilia in association with a lymphoblastic malignancy are described. The eosinophilia preceded or was present at diagnosis in all patients. Eosinophil counts fell during complete remission but rose significantly before or during relapses in five patients. Hypogranular and sometimes Pelger-eosinophils were seen in five cases. Surface and enzyme markers defined the malignancy in six cases as common-ALL (three), T-ALL (two) and T-lymphoblastic lymphoma (one). Although a diagnosis of eosinophilic leukaemia or acute myeloid leukaemia with eosinophil differentiation was considered in three patients, cytochemical and ultrastructural studies failed to show any evidence of myeloid differentiation in the blast cells. The bone marrow karyotype was normal in the four patients studied. All seven patients had one or more relapses and six died 6-62 months from diagnosis. Severe complications of the hypereosinophilic syndrome developed in one patient. As T-lymphocytes have been shown to be involved in the induction of eosinophilia in rodents, it is suggested that the hypereosinophilia in these patients was induced by eosinopoietic stimuli produced by lymphoblasts.

Spontaneous interleukin-5 production in cutaneous T-cell lymphoma lines is mediated by constitutively activated Stat3

“…Moreover, secretion of IL-5 and IL-13 could be involved in the complications that often follow CTCL such as eosinophilia, erythroderma, and elevated titers of IgE, since it is well known that IL-5 is one of the main controlling cytokines for eosinophilia and IL-13 induces IgE synthesis in B cells. Catovsky et al 11 found that eosinophil counts fell during remission and rose during relapse in patients with T-lymphoblastic lymphomas, supporting the idea that eosinophilia could be induced by cytokines produced by the malignant cells.…”

“…9 In CTCL patients, as well as many other lymphoma patients, concomitant eosinophilia, elevated levels of immunoglobulin (Ig)-E and IgA, and decreased cell-mediated immunity are often observed. 10,11 These complications could be caused by a shift in the cytokine pattern from a T H 1-like to a T H 2-like profile that accompanies progression of CTCL. In this regard, interleukin-5 (IL-5) is the predominant regulator of eosinophilia 12 and has been shown to play an important role in the development of eosinophilia in Hodgkin disease.…”

The FIP1L1-PDGFRα fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management

“…Eosinophilia is thought to result from the production of cytokines (eg, IL-3, IL-5, and granulocyte-macrophage colony-stimulating factor [GM-CSF]) from malignant cells in T-cell lymphomas, 98 Hodgkin disease, 99 and acute lymphoblastic leukemias. 100,101 In some cases, isolated eosinophilia may herald the initial diagnosis or relapse of these conditions. Over the last 3 decades, the list of chromosomal abnormalities in cases reported as HES or CEL has grown (reviewed by Bain 102 ).…”

Acute lymphocytic leukemia with eosinophilia and unusual karyotype

“…The disease can affect both children and adults with a median age of 14 years [2]. Most case reports in the literature suggest a male preponderance [3,4]. The majority of ALL cases with eosinophilia are of B-cell type; however, few cases of T-cell ALL with eosinophilia have been reported [4,5].…”

“…Most case reports in the literature suggest a male preponderance [3,4]. The majority of ALL cases with eosinophilia are of B-cell type; however, few cases of T-cell ALL with eosinophilia have been reported [4,5]. Eosinophilia usually precedes the diagnosis of ALL; however, it can also occur concomitantly or after the diagnosis of the leukemia [2,6].…”