The Effect of Fluvoxamine on Serum Prolactin and Serum Sodium Concentrations

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Abstract
Hyperprolactinemia and hyponatremia are adverse drug reactions regularly reported for selective serotonin reuptake inhibitors. Results from animal studies suggest that serotonin receptors of different subtypes are involved in the mediation of these effects. We have investigated to what extent fluvoxamine alters serum prolactin and serum sodium levels and whether these effects are related to platelet 5-hydroxytryptamine 2A (5-HT2A) receptor status, as studied by [3H]lysergic acid diethylamide ([3H]LSD) binding. Eight healthy subjects were given fluvoxamine in increasing dosage from 25 mg/day to 200 mg/day during 4 weeks, and serum sodium and serum prolactin concentrations were obtained weekly. All subjects had normal prolactin and sodium levels before start of treatment. Two subjects had substantial increases in serum prolactin levels (up to 35 microg/L) during fluvoxamine treatment, and these two subjects had higher Bmax for platelet [3H]LSD binding before fluvoxamine treatment than the six other subjects (32.7 vs. 23.1 fmol/mg protein). There was a small, nonsignificant decrease (mean 1.0 mmol/L) in serum sodium levels after institution of fluvoxamine but a significant increase (mean 1.9 mmol/L) in serum sodium levels after discontinuation of the drug (p = 0.02). Bmax for [3H]LSD binding and change in serum sodium concentration after institution of fluvoxamine showed a significant positive correlation (r = 0.85;p = 0.007). The results indicate that fluvoxamine affects serum prolactin as well as serum sodium concentrations and lend indirect support to the suggestion that 5-HT2A receptors might be involved in the mediation of these effects.