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The paediatric cytarabine syndrome can be viewed as a drug‐induced cytokine release syndrome

Chng (2003) indicated fever as an important part of the cytarabine syndrome and suggests cytokines as mediators. In an attempt to investigate the mechanisms behind cytarabine-induced fever, we evaluated 16 children (1AE5– 14AE8 years old) in clinical remission during high–dose cytarabine treatment (six infusions of 2 g/m 2 every 12 h). Fever (median 38AE5� C, range 38AE0–39AE7� C) occurred in 13 of 16 patients at a median of 28 h (20–47 h) after the start of the first infusion. The fever declined spontaneously in 10 of 13 patients despite continued infusions. The series of infusions was not interrupted in any case. Some patients showed signs of malaise, abdominal pain, myalgias and self-limiting rash, but none was severely ill. Blood cultures were negative and no antibiotics were administered. C-reactive protein was low at the beginning of treatment, but increased at 36 h to 21AE 5+6 AE6 mg/l [mean + standard error of the mean (SEM); P <0 AE001 compared with pretreatment levels] and at 60 h to 29AE 7+6 AE4 mg/l (P <0 AE001 compared with pretreatment levels). The plasma cytokine patterns are shown in Fig 1. We found a significant elevation of tumour necrosis factor-a (TNF-a )a t 12 h, which preceded the onset of fever in all 13 febrile patients. The levels of interleukin-6 (IL-6) and interferon-c (IFN-c) were highest at the onset of fever. An elevation of the anti-inflammatory cytokines IL-1ra and IL-10 was noted at the end of treatment (data not shown). Four children received steroids for symptomatic reasons after the onset of fever and they had significantly lower IL-6 and IL-1ra levels afterwards (Ek et al, 2001). Our data demonstrated an association between febrile reactions during high-dose cytarabine treatment and release of proinflammatory cytokines in a pattern resembling that of systemic inflammatory response syndrome (SIRS), with early release of TNF-a that induces a cascade of other pro- and antiinflammatory cytokines. The symptoms and the cytokine levels abated spontaneously in most cases. We are aware that the reaction can be much more pronounced in adults and even induce adult respiratory distress syndrome (Andersson et al, 1990). The absolute levels of TNF-a and IL-6 are often 5–10 times higher in SIRS than we detected.