Eosinophilia resulting from administration of recombinant granulocyte‐macrophage colony‐stimulating factor (rhGM‐CSF) in a patient with T‐γ lymphoproliferative disease

Gonzales‐Chambers, Rowena; Rosenfeld, Craig S.; Winkelstein, Alan; Dameshek, L

doi:10.1002/ajh.2830360219

Cited by 23 publications

References 11 publications

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Immunologic Aspects of Lung Diseases and Cystic Fibrosis

Greenberger¹

1997

JAMA

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Immunologic lung disorders are accompanied by an array of laboratory abnormalities, some of which contribute to disease pathogenesis. Allergic bronchopulmonary aspergillosis, which complicates asthma and cystic fibrosis, causes mucous plugging of airways, eosinophilic pneumonia, and bronchiolitis obliterans. Aspergillus fumigatus, growing saprophytically in bronchial mucus, is responsible for most cases, and prednisone, not antifungal agents, is the drug of choice because it controls the immunologic responses of the lung. In cystic fibrosis, epithelial surface fluid from the lung does not kill Pseudomonas aeruginosa, in part because antibodies to P aeruginosa are plentiful but ineffective in opsonizing bacteria. Neutrophil-derived elastase cleaves immunoglobulins and digests the C3b receptor on neutrophils, which limits phagocytosis of pathogens. In helminth infections and infestations, pulmonary and peripheral blood eosinophilia can be accompanied by increases in total and antiparasite IgE concentrations and generate T(H)2 CD4+ T-lymphocyte responses. Understanding the immunologic abnormalities of lung disorders may lead to more effective therapies.

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Immunologic Aspects of Lung Diseases and Cystic Fibrosis

Greenberger¹

1997

JAMA

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Pulmonary Eosinophilias

Leitch¹

2000

Crofton and Douglas's Respiratory Diseases

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Successful treatment of T‐γ lymphoproliferative disease with human‐recombinant granulocyte colony stimulating factor

Lang¹,

Rosenfeld²,

Diamond³

et al. 1992

American J Hematol

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A trial of recombinant human granulocyte colony-stimulating factor (rhG-CSF) was attempted in a male with agranulocytosis, infection, and T-gamma lymphoproliferative disease (T-gamma-LPD). During five days of rhG-CSF (960 micrograms/day), the absolute neutrophil count (ANC) increased from 0.0 to 4.5 K/microliters. There were no changes in eosinophil or lymphocyte counts. In addition, there was no toxicity. Bone marrow cytotoxic/suppressor cells (CD57+/CD8+) were elevated (21.9%) before and decreased to 10.6% (normal less than 12%) following rhG-CSF. By contrast, there was no change in activated T cells (CD3+DR+) or T cell gene rearrangements. These findings suggest rhG-CSF can improve granulopoiesis in T-gamma-LPD, possibly by altering T-cell mediated marrow suppression.

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Eosinophilia resulting from administration of recombinant granulocyte‐macrophage colony‐stimulating factor (rhGM‐CSF) in a patient with T‐γ lymphoproliferative disease

Cited by 23 publications

References 11 publications

Immunologic Aspects of Lung Diseases and Cystic Fibrosis

Immunologic Aspects of Lung Diseases and Cystic Fibrosis

Pulmonary Eosinophilias

Successful treatment of T‐γ lymphoproliferative disease with human‐recombinant granulocyte colony stimulating factor

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