Thyroid hormones, body temperature, and antidepressant treatment

Abstract

Depression is frequently observed in patients with primary thyroid disorders (Whybrow and Felrell 1974). Moreover, the importance of thyroid function in the regulation of mood and affective illness has been noted by several investigators in recent years (Joffe et al 1984; Loosen 1986; Bauer and Whybrow 1988). In particular, several abnormalities of thyroid function have been reported in patients with primary affective disorder (Gold et al 1981; Joffe et al 1985). For instance, Loosen and Prange (1982) found that approximately one-third of depressed patients exhibit a blunted thyrotropin (TSH) response to thyrotropin releasing hormone (TRH). Furthermore, it has been shown that there is a decrease of '13 and T4 and an increase of TSH after antidepressive treatment with carbamazepine (Roy-Byrne et al 1984), lithium (Benaim and Page 1984), the combination of carbamazepine and lithium (Kramlinger and Post 1990), and electroconvuisive treatment (Kirkegaard and Faber 1981). These results are consistent with animal studies indicating that tricyclic antidepressants decrease thyroid function (Fischetti 1962; Morley et al 1981). Nevertheless, there are reports that did not find any alterations in thyroid hormones with tricyclic antidepressant treatment (Gregoire et al 1977; Linnoila et al 1979; Nordgren and Sheele 1981). Recent studies also indicete that a significant reductio~ in total thyroxine (tT4) and free thyroxine (f14) might be associated with the antidepressant response to clomipramine and maprotiline (Baumgartner e, al 1988) and to desipramine (Joffe and Singer 1990). Recently, Wehr (1990) hypothesized that thermoregulation may provide a framework for understanding the pathophysiology of affective disorders. Higher nocturnal body temperature has been reported to be associated with lower levels of TSH in acutely depressed patients when compared with controls or with remitted cases (Souetre et al 1988). Based on existing knowledge, we attempted to further elicidate the effects of antidepressive medication on the hypothalamic-pituitary-thyroid axis (HPTA) and body temperature. We choose fluvoxamine, which is considered to be a selective serotonine reuptake inhibitor (Claasen 1983) and maprotiline, which is believed to exert its antidepressant effect predominantly via the noradrenergic (NA) system (Maitre et al 1971), to find out if these drugs induced chaages in HPTA or in body temperature.