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Am. J. Trop. Med. Hyg., 80(1), 2009, pp. 141-145
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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Hyponatremia in Severe Malaria: Evidence for an Appropriate Anti-diuretic Hormone Response to Hypovolemia

Josh Hanson*, Amir Hossain, Prakaykaew Charunwatthana, Mahtab Uddin Hassan, Timothy M. E. Davis, Sophia W. K. Lam, S. A. Paul Chubb, Richard J. Maude, Emran Bin Yunus, Gofranul Haque, Nicholas J. White, Nicholas P. J. Day, AND Arjen M. Dondorp
Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand; Chittagong Medical College Hospital, Chittagong, Bangladesh; School of Medicine and Pharmacology, Fremantle Hospital, Fremantle, Western Australia, Australia; Department of Clinical Biochemistry and School of Medicine and Pharmacology, Fremantle Hospital, Fremantle, Western Australia, Australia; Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom

Although hyponatremia occurs in most patients with severe malaria, its pathogenesis, prognostic significance, and optimal management have not been established. Clinical and biochemical data were prospectively collected from 171 consecutive Bangladeshi adults with severe malaria. On admission, 57% of patients were hyponatremic. Plasma sodium and Glasgow Coma Score were inversely related (rs = –0.36, P < 0.0001). Plasma antidiuretic hormone concentrations were similar in hyponatremic and normonatremic patients (median, range: 6.1, 2.3–85.3 versus 32.7, 3.0–56.4 pmol/L; P = 0.19). Mortality was lower in hyponatremic than normonatremic patients (31.6% versus 51.4%; odds ratio [95% confidence interval]: 0.44 [0.23–0.82]; P = 0.01 by univariate analysis). Plasma sodium normalized with crystalloid rehydration from (median, range) 127 (123–140) mmol/L on admission to 136 (128–149) mmol/L at 24 hours (P = 0.01). Hyponatremia in adults with severe malaria is common and associated with preserved consciousness and decreased mortality. It likely reflects continued oral hypotonic fluid intake in the setting of hypovolemia and requires no therapy beyond rehydration.


Received August 5, 2008. Accepted for publication September 25, 2008.

Acknowledgments: The authors thank KrisTan from the Biochemistry Department, Royal Prince Alfred Hospital, Sydney, Australia, for performing the ADH measurements.

* Address correspondence to Josh Hanson, Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, Bangkok 10400, Thailand. E-mail: joshinthailand{at}gmail.com

Authors’ addresses: Josh Hanson, Prakaykaew Charunwatthana, Sophia W. K. Lam, Richard J. Maude, Nicholas J. White, Nicholas P. J. Day, and Arjen M. Dondorp, Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, Bangkok, 10400 Thailand. Amir Hossain, Mahtab Uddin Hassan, Emran Bin Yunus, and Gofranul Haque, Chittagong Medical College Hospital, Chittgong, Bangladesh. Timothy M. E. Davis, School of Medicine and Pharmacology, Fremantle Hospital, PO Box 480, Fremantle, Western Australia 6959, Australia. S. A. Paul Chubb, Department of Clinical Biochemistry, and School of Medicine and Pharmacology, Fremantle Hospital, PO Box 480, Fremantle, Western Australia 6959, Australia. Richard J. Maude, Nicholas J. White, Nicholas P. J. Day, and Arjen M. Dondorp, Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.




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