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Decrease in arterial oxygen partial pressure within the first 24 h of rhGM–CSF administration in AML patients
Author(s) -
Zühlsdorf Michael,
Eiff Michael,
Thomas Michael,
Büchner Thomas
Publication year - 1997
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1997.tb01689.x
Subject(s) - medicine , dlco , anesthesia , dose , diffusing capacity , lung , lung function
GM–CSF may induce pulmonary complications, such as dyspnea with temporary decreases in oxygen saturation described as first dose effect for higher dosages of intravenous rhGM–CSF. This study investigated possible pulmonary disturbances in adult de novo AML patients receiving yeast rhGM–CSF 24 h prior to chemotherapy under phase II/III conditions. Eighteen patients were monitored for 22 treatment episodes. GM–CSF was given s.c. 1 q.d., 2 q.d. or continuously i.v. at 250 μg/m 2 /d 24 h prior to induction chemotherapy (TAD9, n = 18) and consolidation (TAD9, n = 4). Spirometry, bodyplethysmography, single breath‐diffusion capacity (DLCO) and arterial blood gas analyses were obtained prior to GM–CSF, and repeated after 24 h. Pulse oxymetric oxygen saturation (saO 2 ) was registered continuously for the first 16 h within day 1 of rhGM–CSF treatment. Patients were aged 21–75 years. The saO 2 monitoring did not reveal any first dose effect. PaO 2 values decreased from 78.9 mmHg before GM–CSF to 72.8 mmHg after 24 h ( p <0.01, maximum shift 15 mmHg). PaO 2 shifts occurred mainly with pre‐existing lowered paO 2 , but otherwise were independent of age, the route of GM–CSF administration, leukocyte levels, or increase of leukocytes with GM–CSF. Increases in AaDO 2 reflected the paO 2 shifts ( p <0.05). No dyspnea corresponded to these changes. DLCO values did not decrease significantly after 24 h. Summarily, contemporary dosage of yeast rhGM–CSF avoids short‐term oxygen desaturations, but leads to clinically benign impairment in oxygen tension, based on ventilation/perfusion mismatches. This should be taken into account for patients starting at subnormal paO 2 .