Abstract
Polydipsia is not uncommon among psychiatric patients, with a prevalence of about 6–17% [1]. Some anticonvulsant drugs, like Carbamazepine can induce hyponatremia with or without polydipsia [2]. To our knowledge, this is the ?rst case report of polydipsia with Sodium Valproate (VPA).
BG, a 50-year-old white male patient with schizoaffective disorder, was admitted in our unit for a manic relapse. The patient had been treated with VPA at the dose of 1000 mg day−1, for about 18 months. Concomitant medication on admission was Flupenthixol 5 mg daily, which was started after VPA. BG reported polydipsia on admission, with a daily water intake of about 8–10 L. This patient reported that the increased water intake was caused by excessive thirst. He told us that he had been taking this amount of water since he was started on VPA 18 months earlier. Sodium levels on admission were normal (141 mMol L−1). Thyroid and liver function tests were unremarkable. The patient did not have any known physical problem. Past sodium levels, done 8 and 6 months before admission, were also normal (142 and 141 mMol L−1, respectively). We also have VPA serum levels on admission, which were within normal range as well (487 μmol L−1; normal range 347–692 μmol L−1). Polydipsia continued 8 days after the admission, when Risperidone 2 mg daily was introduced and Flupenthixol was stopped. On the eighth day of his stay in hospital, we measured serum sodium levels, which were again within the normal range (141 mMol L−1), in spite of the excessive amount of water drunk. We decided to stop VPA and replace it with Lithium on the ninth day. On the day VPA was interrupted, the polydipsia ceased as well. BG started drinking about 1–2 L of water a day and did not develop it during his stay at the hospital. The patient gave informed consent for the data to published anonymously.
The mechanism by which VPA caused polydipsia is unclear. We can exclude Syndrome of Inappropriate Secretion of antidiuretic hormone, because the levels of serum sodium were normal all throughout the time the patient had polydipsia. It may as well be possible that VPA induced a compulsive need for water, but our patient did not report the compulsion to drink. Some authors propose that polydipsia with anticonvulsants can be a primary phenomenon [3]. Proposed mechanisms for primary polydipsia among psychiatric patients include: dry mouth, direct stimulation of thirst centres in the hypothalamus, delusional ideation or dopamine supersensitivity [1]. Sodium Valproate can increase prefrontal dopamine release by activating 5-HT1A receptors [4]. There is evidence showing that the dopamine system can be involved in polydipsia [5]. It is possible that VPA could have caused excessive thirst by increasing the effect of dopamine. Our patient did not take any antipsychotic medication while on VPA. Although suggestive, this remains just a speculative hypothesis.