Abstract
It is known that approximately 20-50% of acquired immunodeficiency syndrome (AIDS) patients are neutropenic and the cause of the neutropenia has not been conclusively elucidated. From 1993 to 1994, a pharmacokinetic study of single-dose rhG-CSF at5μg/kg i. v. was carried out to investigate the correlation between neutrophil counts andserum rG-CSF level using enzyme immunoassay (ETA) in 6 human immunodeficiencyvirus (HIV) patients with the following:(A) chronic neutropenia (<1, 000/μl) for over 6 months in 5 patients(B) septicaemia accompanied with acute neutropenia in 1 patientIn Class A, the serum concentration of G-CSF was undetectably low, and less than themeasurement limit (30.0 pg/ml) in 4 out of 5 patients. In Class B, the serum G-CSF levelwas 5, 830 pg/ml. The neutrophil count reached the maximum level at 8 hours afteradministration of rhG-CSF and the neutrophil count remained higher than the preadministration level at 24 hours after the administration. A transient decrease in themonocyte count was observed 1 hour after the rhG-CSF administration in 5 out of 6patients. No effect was observed in the other WBC differentials. Pharmacokinetic profileof rhG-CSF obtained in this study (Class A/B) are summarized as follows ;*T1/2 (α) =1.66±0.47/1.14 (h)*T1/2 (β) = 3.32±0.66/3.85 (h)*Vc=38.66±6.48/26.38 (ml/kg)*AUC (0-24) = 1201.73±560.06/995.46 (pg⋅h/ml)*CL=10.78±3.61/11.4 (ml/h/kg)Further, the serum rG-CSF concentration decreased biphasically. In conclusion, it wasfound that excretion, transformation and inactivation of G-CSF was not enhanced inHIV-positive hemophiliacs who showed neutropenia. It was suspected that a productiondisorder of G-CSF might be a factor in neutropenia in patients with chronic neutropenia (Class A), because the serum G-CSF concentration was low in these patients.
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