Etiology and Natural History of Neutropenia in Human Immunodeficiency Virus Disease: A Prospective Study

Abstract

The objective of this prospective, observational study was to define the natural history of neutropenia in human immunodeficiency virus (HIV) disease. Eighty-seven consecutive patients developing neutropenia (absolute neutrophil count [ANC], <1000 cells/mm(3)) were recruited and closely followed for the duration of the episode. Episodes lasted a median of 13 days, with a mean ANC nadir of 660 cells/mm(3). Presumed or proven infection occurred in 12 (17%) of 71 evaluable subjects, and culture-proven infection occurred only in 6 (8%) of 71. Most of the episodes of neutropenia were brief, mild to moderate in nadir, and self-limiting without complications. Myelosuppressive therapies were implicated in almost all episodes. Serious infections occurred infrequently and were associated with low ANC nadirs but not with duration of the neutropenic episode. Low CD4(+) cell counts also increased the risk of infection complicating an episode of neutropenia.

Rituximab does not improve clinical outcome in a randomized phase 3 trial of CHOP with or without rituximab in patients with HIV-associated non-Hodgkin lymphoma: AIDS-Malignancies Consortium Trial 010

“…21 Seven of the 12 individuals who developed infectious complications had CD4 ϩ counts less than 50 cells/mm 3 . Borg et al 22 recently reported that a low pretreatment CD4 count (Ͻ 450/mm 3 ) was an independent risk factor for febrile-neutropenia and early death in patients receiving cytotoxic chemotherapy.…”

Normal hematopoiesis is maintained by activated bone marrow CD4+ T cells

“…Some authors argue that it could derive from the cytotoxic effects of antiviral drugs commonly used in AIDS treatment, but granulopenia also can be observed in the absence of an antiviral therapy. 45,46 Another proposed mechanism for HIV-associated granulopenia is direct infection of BM hematopoietic progenitors by HIV. Nonetheless, efforts to detect HIV infection in cultured hematopoietic progenitors either failed or were left inconclusive.…”

Interactions between Human Immunodeficiency Virus Type 1 and Polymorphonuclear Neutrophils

“…Several lines of evidence suggest that this can be attributed to a direct effect of protease inhibitors via calpaine inhibition [70,80]. Nevertheless, PMN defects are still observed in some patients who respond positively to HAART [81]. …”