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To the Editor—In a recent paper, Chiwakata et al. [1] demonstrated a striking relationship between procalcitonin (PCT) levels and outcome in severe Plasmodium falciparum malaria. However, the authors did not discuss the possible role of PCT in the pathogenesis of severe P. falciparum malaria. In addition to being a marker of severity, PCT levels also might reflect pathomechanisms responsible for lethal complications. A similar observation has been made for plasma thrombomodulin levels, which are extremely elevated in fatal malaria cases and seem to reflect neutrophil-mediated endothelial damage [2]. The possible role of PCT in malarial pathology might be found by also looking at the calcitonin gene–related peptide (CGRP), which is an alternative splicing product derived from the same calcitonin gene transcript. In sepsis and septic shock, elevated serum levels of PCT and CGRP [3] correlate with severity and outcome. Both peptides reduce endotoxin-induced tumor necrosis factor–a (TNF-a) production by cells in human whole blood [4]. Reduced ex vivo TNF-a production capacity is seen before therapy, and a rapid recovery of TNF-a production capacity predicts rapid clearance of malarial parasites and clinical cure [5]. On the other hand, factors that inhibit TNF-a production may be associated with high parasitemia [6]. In addition, the serum levels of PCT correlate with those of granulocyte colony-stimulating factor in P. falciparum malaria [7]. Such a link also exists for CGRP, which enhances adhesion of neutrophils to the vascular endothelium [8]. Interaction between neutrophils and endothelial cells probably contributes to endothelial damage and organ failure in patients with P. falciparum malaria [2]. Thus, PCT might be involved in the pathogenesis of severe malaria.

Procalcitonin Levels in SeverePlasmodium falciparumMalaria: Predictor of Outcome or Reflection of Pathomechanisms?