Invasive fungal infections are associated with severe depletion of circulating RANTES.
Serum RANTES (regulated on activation, normal T-cell expressed and secreted) concentrations were measured in 14 patients who had haematological malignancies and developed invasive fungal infections (three of them definite, eight probable and three possible). RANTES levels fell substantially from pre-chemotherapy values at the start of and throughout the fungal infection, and recovered in patients who survived the fungal infection. However, in patients who died from the invasive fungal infection, RANTES levels did not recover. For survivors the mean +/- sd levels for RANTES were 7656 +/- 877 pg ml(-1) on the day prior to chemotherapy, 3723 +/- 2443 pg ml(-1) on the first day of fungal infection diagnosis (significantly different from baseline; P = 0.001) and 9078 +/- 2256 pg ml(-1) at recovery from the fungal infection (significantly different from lowest value; P < 0.0001). Platelet counts were closely correlated with the RANTES levels (r = 0.63, P < 0.001). The RANTES concentrations for the three patients who died were similar to those who survived at all equivalent timepoints, but were significantly lower at the time of death (792 +/- 877) compared to the values at recovery for survivors (P = 0.005). The finding that patients who died from an invasive fungal infection had very low platelet counts and RANTES concentrations suggests that these could play a role in host response to such infections.
Ellis
Michael
M
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
Al-Ramadi
Basel
B
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
Hedström
Ulla
U
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
Alizadeh
Hussain
H
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
Shammas
Victor
V
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
Kristensen
Jörgen
J
Department of Medicine1 and Department of Medical Microbiology2, Faculty of Medicine and Health Sciences, UAE University Medical School, PO Box 17666, Al-Ain, United Arab Emirates 3Department of Haematology and Oncology, Tawam Hospital, PO Box 15555, Al-Ain, United Arab Emirates.
D018946:Chemokine CCL5 / Q000097:blood*; D006801:Humans; D007945:Leukemia, Lymphoid / Q000150:complications*; D007951:Leukemia, Myeloid / Q000150:complications*; D007958:Leukocyte Count; D009181:Mycoses / Q000097:blood* / Q000150:complications; D010976:Platelet Count
D018946:Chemokine CCL5