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.

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.

Glycogen storage disease type I (GSD‐I) is an inherited disorder that is due to a glucose‐6‐phosphatase (G6Pase) deficiency. There have been recent reports of hepatocellular tumors in adults with this disease. Hepatic adenoma is the most common tumor described but others, including hepatocellular carcinomas, hepatoblastomas, and focal nodular hyperplasia (FNH) have been reported. FNH of the liver is a rare benign lesion that has been reported in eight patients with GSD‐I. Three of these eight patients, in addition to the patient in our study, had been treated with portacaval shunts. When these patients were compared with patients who had not received such treatment, it appeared that the portacaval shunts may have induced the development of FNH and may have been associated with earlier complications. FNH is a benign tumor that may coexist with adjacent fibrolamillar carcinomas and/or adenomas and requires careful follow‐up.

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The main purpose of the present study was to determine the response rate to immunosuppressive therapy combined with recombinant human granulocyte‐colony stimulating factor (rhG‐CSF) and its efficacy for preventing infections in patients with severe aplastic anemia. The treatments included one course of antithymocyte globulin, cyclosporin A, methylprednisolone, danazole and rhG‐CSF. Three patients had very severe aplastic anemia and two had moderate aplastic anemia. One patient relapsed 13 months following the first course of therapy and received a second course. Five patients received six courses of treatment and the response rate at 6 months was 83.3%. All patients achieved an absolute neutrophil count of greater than 1.0 × 109/L within 40 days. All patients with a complete response are transfusion‐free and doing well. All five patients are currently alive and have not had any episode of infection for 17–53 months. The results of the study indicate that this therapy may improve the poor prognosis of young patients with severe aplastic anemia. It has a good response rate and induces a rather rapid increase in the neutrophil count, which protects against life‐threatening bacterial and fungal infections.