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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Malaria Journal 1/2012

Hyponatraemia in imported malaria: the pathophysiological role of vasopressin

Zeitschrift:
Malaria Journal > Ausgabe 1/2012
Autoren:
Ewout J Hoorn, Marlies E van Wolfswinkel, Dennis A Hesselink, Yolanda B de Rijke, Rob Koelewijn, Jaap J van Hellemond, Perry JJ van Genderen
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2875-11-26) contains supplementary material, which is available to authorized users.
Ewout J Hoorn, Marlies E van Wolfswinkel contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

EJH contributed to the data analysis and writing of the manuscript. MEvW, DAH and JvH participated in the data analysis and revising of the manuscript. YdeR carried out the copeptin measurements and contributed to the data analysis. RK is responsible for collection of patient materials and database management. PJvG participated in the data acquisition and analysis and in writing and revising the manuscript. All authors have seen and approved the final version.

Abstract

Background

In the pathophysiology of hyponatraemia in malaria, the relative contribution of appropriate and inappropriate arginine vasopressin (AVP) release is unknown; the trigger for inappropriate AVP release is also unknown.

Methods

Serum copeptin, a stable and sensitive marker for AVP release, was analysed in a large cohort of patients with imported malaria (204 patients) and in a small prospective substudy (23 patients) in which urine sodium and osmolality were also available. Hyponatraemia was classified as mild (serum sodium 131-134 mmol/l) and moderate-to-severe (< 131 mmol/l).

Results

Serum copeptin on admission was higher in patients with moderate-to-severe hyponatraemia (median 18.5 pmol/L) compared with normonatraemic patients (12.7 pmol/L, p < 0.05). Despite prompt fluid resuscitation, the time to normalization of serum sodium was longer in patients with moderate-to-severe hyponatraemia (median 2.9 days) than in patients with mild hyponatraemia (median 1.7 days, p < 0.001). A poor correlation was found between serum sodium and copeptin levels on admission (rs = -0.17, p = 0.017). Stronger correlations were identified between serum C-reactive protein and copeptin (rs = -0.36, p < 0.0001) and between serum C-reactive protein and sodium (rs = 0.33, p < 0.0001). Data from the sub-study suggested inappropriate AVP release in seven of 13 hyponatraemic malaria patients; these patients had significantly higher body temperatures on admission.

Conclusions

In hyponatraemic patients with imported malaria, AVP release was uniformly increased and was either appropriate or inappropriate. Although the exact trigger for inappropriate AVP release remains unknown, the higher body temperatures, correlations with C-reactive protein and long normalization times of serum sodium, suggest an important role of the host inflammatory response to the invading malaria parasite.
Zusatzmaterial
Additional file 1: Dot plot of relationship between serum C-reactive protein and serum Copeptin on admission as a function of sodium level on admission. A significant correlation between C-reactive protein and serum Copeptin was present (rS = 0.33, p < 0.0001). Patients with moderate or severe hyponatraemia were grouped (labelled as "severe"). (JPEG 1 MB)
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Additional file 2: Dot plot of relationship between serum C-reactive protein and serum sodium on admission as a function of copeptin on admission. Copeptin levels above and below the 97.5th percentile of normal are separately given. A significant inverse correlation was present between C-reactive protein and sodium on admission (rS = -0.36, p < 0.0001). (JPEG 171 KB)
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Authors’ original file for figure 1
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Authors’ original file for figure 2
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Authors’ original file for figure 3
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