• Critical care medicine · Aug 1997

    Effect of classic heatstroke on serum procalcitonin.

    • E S Nylén, A Al Arifi, K L Becker, R H Snider, and A Alzeer.
    • Department of Medicine, Veterans Affairs Medical Center and George Washington University, Washington, DC, USA.
    • Crit. Care Med. 1997 Aug 1; 25 (8): 1362-5.

    ObjectiveProcalcitonin, the precursor peptide of calcitonin, has been shown to be a serum marker of the severity and mortality of several systemic inflammatory response syndromes. This study addressed the correlation of serum procalcitonin with the course of classic (nonexertional) heatstroke.DesignSerum samples were collected prospectively every 6 hrs for 24 hrs.SettingHeatstroke treatment unit, Makkah, Saudi Arabia.PatientsA total of 25 patients were admitted during the annual Hajj pilgrimage in 1994. Ten patients evaluated in the same treatment center with minor illnesses and without pyrexia served as controls.InterventionsPatients were cooled according to an established evaporation method.Measurements And Main ResultsStandard critical care parameters including continuous rectal temperature. A rapid immunochemical assay for serum procalcitonin was utilized. The mean serum procalcitonin was elevated 20-fold on admission in patients with heatstroke compared with controls (p < .011). The procalcitonin concentration subsequently increased to a plateau by 6 hrs and remained increased at 24 hrs, compared with the admission level (p < .0001). In this study, 77% of the patients with heatstroke survived. A subgroup analysis demonstrated that the patients who survived had a significantly higher procalcitonin concentration than those patients who died of heatstroke; a procalcitonin concentration of >0.5 ng/mL (>0.15 nmol/L) at 6 hrs predicted survival (p = .02).ConclusionClassic heatstroke is associated with increased concentrations of serum procalcitonin, particularly among survivors. Further studies are required to elucidate the source and action(s) of procalcitonin as well as its relationship to cytokine activation.

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