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Cytokine response to infection in patients with acute myelogenous leukaemia following intensive chemotherapy
Author(s) -
Ostermann Helmut,
Rothenburger Markus,
Mesters Rolf M.,
Loo Jürgen,
Kienast Jochen
Publication year - 1994
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1994.tb05027.x
Subject(s) - septic shock , cytokine , sepsis , medicine , immunology , shock (circulatory) , chemotherapy , tumor necrosis factor alpha , gastroenterology
Summary. Septic shock is the major cause of treatmentrelated death in patients with acute myelogenous leukaemia (AML) undergoing intensive chemotheray. Interleukins (IL)‐1 β , −6, −8, and tumour nerosis factor α (TNF‐α) have been implicated as mediators of septic shock, with circulating leucocytes being considered a major source for their release. However, Plasma cytokine levels of leucocytopnic patients with evolving sepsis have not been studied. We have prospectively measured plasma cytokines during chemotherapy‐induced leucocytopenia (< 1 × 10 9 /1) in 50 patiens with AML. Cytokine levels in patients with severe sepsis (n=5) or septic shock (n=8) were cmpared to those measured in 13 matched patients with uncmplicated febrile infections. In evolving septic shock, IL‐6, IL‐8 and TNF‐α peaked within 48 h of fever onset at levels reported for nonleucocytopenic patients and distinctively higher than during uncomplicated febrile episodes (P < 0.05). Peak concentrations measured within 48 h after onset of fever were related to fatal outcome. IL‐1β was detected in less than 5% of all samples. Cytokine concentrations were unrelated to leucocyte counts and markers of neopterphil or monocyte activation (elastase and neeopterin levels, respectively). We conclude that cytokine release associated with evolving septic shock in patients with AML does not depend on circulating leucocytes.