[Hypereosinophilic syndrome as paraneoplastic presentation in an adolescent].

Rev Alerg Mex

Servicio de Alergia e Inmunología Clínica, Unidad Médica de Alta Especialidad, Hospital de Especialidades Antonio Fraga Mouret, Centro Médico Nacional La Raza, Instituto Mexicano de Seguro Social, México, DF.

Published: July 2014

AI Article Synopsis

  • Hypereosinophilic syndrome (HS) involves high eosinophil counts and organ damage, diagnosed after excluding other causes, and can present uniquely, as in a case of a 13-year-old girl previously treated for B cell lymphoblastic leukemia.
  • After two years in remission, she developed various symptoms like rash, hair loss, and respiratory issues, but early tests indicated only hypereosinophilia and no cancerous cells.
  • Despite treatment and investigations revealing complications like eosinophilic pneumonitis and leucocytoclastic vasculitis, her condition deteriorated, leading to a reemergence of leukemia, and unfortunately, she passed away.

Article Abstract

Hypereosinophilic syndrome is characterized by peripheral eosinophilia over 1,500 cell/mm3 and/or tissue eosinophilia, with dysfunction or damage to organ, once other causes were ruled out. This paper presents a case of hypereosinophilic syndrome (HS) which presented as lymphoblastic leukemia in a teenager. This is a 13 year old female, with B cell lymphoblastic leukemia at 9 years old, who received chemotherapy for 2 years achieving remission. One year after remission she presented malar rash, hair loss, arthralgias, conjuntival redness, dyspnea and thoracic oppression. The initial blood count only showed hypereosinophilia, and a bone marrow biopsy did not show blasts and had a negative immunophenotyping. Autoantibodies were negative, except for ANA (1:1,280 in one determination after one negative), complement was normal, lupic band in skin was negative for complement and immunoglobulins; serum IgG 2,195 mg/dL, IgA 231, IgM 327, IgE 109 U/mL; skin testing for aeroallergens and food allergens were negative. Prednisone was started at 1 mg/kg. Abdominal ultrasound only reported biliary sludge flow and hepatosplenomegaly; chest tomography showed centrolobullar interstitial pattern, suggesting eosinophilic pneumonitis. The patient started with a generalized dermatosis, and a biopsy reported leucocytoclastic vasculitis. Six months after the onset of symptomatology there were generalized malaise, uncontrolled fever, gingival haemorrhage, asthenia and adynamia; a blood cell count reported blasts, and bone marrow smear confirmed the diagnosis of cell B lymphoblastic leukemia. The patient deteriorated rapidly showing signs of respiratory difficulty and acute pulmonary edema, therefore chemotherapy was started without response, and finally the patient died. There are several causes of HS, yet one of the least frequent presentations in childhood is the association with neoplasms.

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