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Annals of African Medicine
Annals of African Medicine Society
ISSN: 1596-3519
Vol. 6, Num. 4, 2007, pp. 207–208
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Annals of African Medicine, Vol. 6, No. 4, 2007, pp. 207 – 208
Hyponatraemia
during Low-Dose Carbamazepine Therapy
F.Salawu1 and A.Danburam2
1Department of Medicine, State Specialist Hospital, Maiduguri 600001. Nigeria
2Department of Medicine, Federal Medical Centre, Yola
640001. Nigeria
Reprint
requests to: Dr. F. K. Salawu, P. O. Box 246, Maiduguri 600001, Nigeria. E-mail: dr_abdulsalawu@yahoo.com
Code Number: am07047
Abstract
We report the syndrome of inappropriate
antidiuresis as a much earlier side-effect of carbamazepine administration in a
29-year Nigerian female patient with generalized tonic-clonic seizures.
Although asymptomatic, the biochemical abnormality improved after
discontinuation of carbamazepine. Hyponatraemia developed after rechallenge
with controlled release carbamazepine. The authors suggest that serum sodium
levels be carried out before commencement of carbamazepine and caution be used
in prescribing carbamazepine to patients with low or borderline low sodium
values.
Key words: Carbamazepine, hyponatraemia
Résumé
Nous rapportons le syndrome de lantidicirose inappropriée comme beaucoup
plus tôt aux effets secondaires de ladministration carbamazepine chez une
malade nigériane âgée de 29 ans avec de la convulsion toniques clonique
généralisée. Bien que asymptomatique, lanomalie biochimique avait amélioré après
larrêt de la carbamazepine. Lhyponatemie avait développé après ré
administration de la carbamazepine contrôlée. Les auteurs suggèrent que les
niveaux de sérum de sodium devront être effectués avant le début de la
carbamazephine et de prudence être utilisée dans lordonnance de la
carbamazepine pour des patients atteints de la faible ou basse limite des
valeurs de sodium.
Mots clés: Carbamazepine, hypenatrémie
Introduction
Carbamazepine
is widely used in Nigeria in the treatment of seizure disorders and of
trigeminal and other neuralgias. It has found a role in the prophylaxis of
affective disorders.1 It is used in adults and
children in the prophylaxis management of partial seizures, generalized
tonic-clonic seizures and mixed seizure patterns. It has been used in the
symptomatic management of the acute phase of schizophrenia as an adjunct to
therapy with an antipsychotic agent in patients who fail to respond to an
adequate trial of the antipsychotic alone.2 Although hyponatraemia is a well-recognized side-effect of carbamazepine
therapy, it has previously been reported only at moderate or high doses and
usually after weeks or months of treatment.3-9 This paper reports a case of carbamazepine-induced hyponatraemia in a young
Nigerian woman being treated for generalized tonic-clonic seizures.
Case report
A
29-year-old Nigerian female presents with a 3-month
history of generalized tonic-clonic seizures. Her first seizure occurred when
she was 17 years, and her second seizure occurred 2 years after that. She chose
not to start antiepileptic drugs at that time because the seizures were rare,
but she has now had five seizures over the past 6 months. After seven days of
treatment with carbamazepine 200mg twice daily increasing to 400mg twice daily,
a routine estimation of plasma electrolytes gave sodium of 121 mmol/l with
chloride of 89 mmol/l; other results were within normal limits. She had a
normal plasma sodium level of 135mmol/l before commencement of carbamazepine
therapy. She did not use other medications such as diuretics and antipsychotics
that could cause hyponatraemia. Carbamazepine was discontinued, leading to a
rise in plasma sodium to reach a normal value after two weeks without any
medication. Physical examination and investigations, including chest and skull
radiographs, showed no alternative explanation for the hyponatraemia such as
meningitis, encephalitis or pulmonary tuberculosis.
The
suspected role of carbamazepine in producing this effect was confirmed by a
period of rechallenge with the drug, during which plasma electrolyte levels were
monitored daily. Although plasma carbamazepine levels could not be monitored,
the dose given was 200mg on the first day and 200mg twice daily thereafter. On
day 3, after a total dose of 600mg, the sodium level was 132 mmol/L, just below
the laboratorys normal range 135-145 mmol/L. The following day it was 128
mmol/L with a plasma osmolality of 255 mmol/L and urine osmolality of 325
mmol/L. On stopping carbamazepine, the electrolyte returned to normal in four
days. At no time during the period of hyponatraemia did the patient show
symptoms. Her medication was changed to phenytoin capsule 300mg nocte.
Discussion
The goal
of treatment with antiepileptic drugs (AEDs) is complete control of seizures
without side effects. The choice of initial therapy is perhaps the most
critical juncture in the care of epilepsy patients, as many patients will
remain on this therapy for years, if not a lifetime. There is no such thing as
an ideal AED that would be the first choice in patients with epilepsy or even
all patients with a given epilepsy syndrome. This case demonstrates the
potentially profound disturbance of water balance, which can occur as result of
carbamazepine monotherapy. We attributed the acute hyponatraemia to
carbamazepine since there was no concomitant use of medications associated with
hyponatraemia. Carbamazepine has led to hyponatraemia in patients with
epilepsy, neuralgia, mental retardation, and psychiatric disorders with a frequency
varying from 4.8 to 40%.10 It shows that this
side-effect can occur at lower doses and after much shorter periods than has
previously been recognized.
Possible
mechanisms for the antidiuretic effects of carbamazepine have been proposed.
Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors
appear likely, but an increased sensitivity of the renal tubules to circulating
antidiuretic hormone cannot be explained. It suggests the need to estimate
plasma electrolytes in patients complaining of side-effect such as nausea,
headache and dizziness-all symptoms of hyponatraemia-in the first few days of
carbamazepine therapy. Several risk factors have been reported to increase the
risk of hyponatraemia including age greater than 40 years, concomitant use of
medications associated with hyponatraemia, menstruation, psychiatric conditions, surgery,
psychogenic polydipsia and female gender.11 Most patients with carbamazepine-induced hyponatraemia are asymptomatic. In
rare cases, water intoxication has been reported,10 necessitating treatment discontinuation. We therefore suggest that caution be
used in prescribing carbamazepine to patients with low or borderline sodium
values.
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Copyright 2007 - Annals of African Medicine
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