Background: The metabolic syndrome (MS) is associated with insulin resistance (IR), a systemic low-grade inflammatory state and endothelial dysfunction. These disorders may arise at a very early age in obese children. This study aimed to investigate the relationship between endothelial dysfunction and both IR and inflammation in prepubertal obese children. Methods and results: Von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were measured in 46 obese prepubertal children aged 6–9, and in 46 non-obese, age-and sex-matched controls; the possible association of these levels with MS, various inflammatory biomarkers and plasminogen activator inhibitor-1 (PAI-1) was analyzed. Obese children displayed significantly elevated values for sICAM-1 (P = 0.008), vWF (P = 0.034), insulin (P = 0.006), homeostasis model assessment for IR (HOMA-IR; P = 0.003), C-reactive protein (CRP) (P < 0.001), PAI-1 (P = 0.002) and leptin (P < 0.001). Nonsignificant differences were found in interleukin 6 (IL-6) levels. In the obese group, sICAM-1 showed a positive correlation with insulin (P = 0.013), HOMA-IR (P = 0.015), CRP (P = 0.020), IL-6 (P = 0.023) and PAI-1 (P = 0.015). Corrected for age and sex, insulin, HOMA-IR, IL-6 and CPR were found to be independent predictive factors for sICAM-1. Conclusions: Prepubertal obese children displayed alterations indicative of endothelial dysfunction as well as disorders typical of MS. An association was established between endothelial dysfunction, IR, inflammation and inappropriate fibrinolysis in the children studied.

Eosinophils in peripheral blood account for 0.3–5% of leukocytes, which is equivalent to 0.05–0.5 × 10⁹/L. A count above 0.5 × 10⁹/L is considered to indicate eosinophilia, while a count equal to or above 1.5 × 10⁹/L is defined as hypereosinophilia. In bone marrow aspirate, eosinophilia is considered when eosinophils make up more than 6% of the total nuclear cells. In daily clinical practice, the most common causes of reactive eosinophilia are non-hematologic, whether they are non-neoplastic (allergic diseases, drugs, infections, or immunological diseases) or neoplastic (solid tumors). Eosinophilia that is associated with a hematological malignancy may be reactive or secondary to the production of eosinophilopoietic cytokines, and this is mainly seen in lymphoid neoplasms (Hodgkin lymphoma, mature T-cell neoplasms, lymphocytic variant of hypereosinophilic syndrome, and B-acute lymphoblastic leukemia/lymphoma). Eosinophilia that is associated with a hematological malignancy may also be neoplastic or primary, derived from the malignant clone, usually in myeloid neoplasms or with its origin in stem cells (myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions, acute myeloid leukemia with core binding factor translocations, mastocytosis, myeloproliferative neoplasms, myelodysplastic/myeloproliferative neoplasms, and myelodysplastic neoplasms). There are no concrete data in standardized cytological and cytometric procedures that could predict whether eosinophilia is reactive or clonal. The verification is usually indirect, based on the categorization of the accompanying hematologic malignancy. This review focuses on the broad differential diagnosis of hematological malignancies with eosinophilia.