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We read with interest the recently published paper by Lorente and colleagues reporting that levels of soluble CD40 ligand (CD40L) are increased in septic patients compared with healthy controls and that increased circulating CD40L levels may be an independent predic tor of mortality in patients with sepsis [1]. Th e relation ship between platelets and soluble CD40L seen in this study is consistent with previous data showing that soluble CD40L is mainly released from activated platelets and mediates neutrophil-induced lung injury in sepsis [2]. We believe that the functional role of soluble CD40L is complex, however, and not solely related to the presence of sepsis or its severity. Th is is indicated in the study by Lorente and colleagues, in which no associations were found between soluble levels of CD40L and Acute Physiology and Chronic Health Evaluation scores, Sequential Organ Failure Assessment scores, and TNF and IL-10 levels [1], which is in agreement with previous fi ndings [3,4]. Further, although the study was conducted in patients with sepsis, we suggest that soluble CD40L is a common denominator for patients with shock, rather than with sepsis per se. Th us, in a study of critically ill patients admitted to the intensive care unit with shock due to diff erent aetiologies, we found no diff erences in the levels of soluble CD40L between septic and nonseptic shock patients [4]. Th e relevance of soluble CD40L as a potential therapeutic target for sepsis therefore remains to be explored. We suggest that targeting CD40L in order to ameliorate pathological infl ammatory responses is not limited to septic patients but also includes nonseptic shock patients.

Soluble CD40 ligand is not solely related to the presence and severity of sepsis