Hemophagocytic syndrome and hepatosplenic gammadelta T-cell lymphoma with isochromosome 7q and 8 trisomy.

The authors describe a 15-year-old boy with hepatosplenic gammadelta T-cell lymphoma associated with hemophagocytic syndrome (HPS) along with isochromosome 7q and trisomy 8. He presented with prolonged fever, mild anemia, thrombocytopenia, and hepatosplenomegaly. Physical examination, radiography, and ultrasound tomography revealed no lymphoadenopathy. He had elevated levels of serum ferritin, interferon-gamma, soluble interleukin-2 receptor, and interleukin-6. Bone marrow aspirate showed hypercellularity with 50% lymphoblasts and erythrophagocytosis of macrophage. A cytogenetic study of bone marrow revealed an abnormal karyotype, 47,XY,I(7q),+8, in 5/30 cells. Clonal rearrangement of the genes for T-cell receptor gamma and delta chains was elucidated by polymerase chain reaction. He achieved a complete remission after intensive chemotherapy and underwent splenectomy 18 months after diagnosis. Although the patient was clinically in remission, minimal residual disease (MRD) was detected in the removed spleen by polymerase chain reaction. This might mean that this type of lymphoma is refractory, as reported previously, and might indicate that marrow ablative therapy is needed to achieve a cure. The present case illustrates the usefulness of MRD analysis, and MRD studies in this group of disorders may be helpful in the decision of whether to continue a more aggressive therapeutic approach.

Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood.

Respiratory viral infection is known to be a significant cause of asthma exacerbation. Eosinophils have been considered to play an important role in the pathogenesis of virus-induced asthma exacerbations. To determine how often asthma exacerbation is caused by virus infections and to examine the relationship between eosinophilia and asthma episode, we investigated 64 children who experienced asthma attacks between October 1999 and March 2000. We used rapid enzyme immunoassays to detect antigens of respiratory syncytial virus (RSV), influenza A virus, and adenovirus in nasopharyngeal secretions (NPS) of these children, and enumerated eosinophils in the blood and NPS. We detected RSV in 27% and influenza A virus in 17% of the patients. No adenovirus infection or RSV/influenza A co-infection was detected. RSV-infected children were younger (3.85 +/- 0.83 years old) than influenza A virus-infected patients (5.23 +/- 1.34 years old). Eighty-two per cent of patients in the RSV group and 36% of patients in the influenza A virus group had moderate-to-severe asthma episodes (p < 0.05). In RSV-infected children, the eosinophil counts in NPS were higher in the 'severe' group, and younger patients had a greater number of eosinophils in their NPS than older patients (p < 0.05). These trends were not found in influenza A virus patients. In conclusion, our results indicate that, compared with influenza A virus-induced asthma attacks, RSV infection had a higher probability of being associated with asthma exacerbation in infants and younger children and induced attacks of greater severity. The increase in the number of eosinophils in the NPS of RSV-infected children may be responsible, in part, for these differences.