Search

The TRH test has been used in psychiatry these last 20 years. One of the most promising results is that concerning the possibility to use it to identify the best moment to stop a treatment after clinical recovery of the depressive episode. For that it is necessary to demonstrate an absence of intrinsic action of antidepressants on the HPT axis physiology. This overt, randomized study has compared the actions on T3, T4, basal TSH and its response to the TRH test after 75 mg/day of maprotiline and 100 mg/day of fluvoxamine, both administrated in depressed patients during 28 days. Forty patients (20 men and 20 women) were studied, 20 patients per treatment. The inclusion criteria were those of DSM III-R for major depression and dysthymia as well a minimum score of 25 at MADRS scale. Blood samples for T3, T4 and basal TSH dosages were made before TRH intranasal administration (2 mg) at days 1 and 28 of the treatment. We haven't observed any difference before treatment between the 2 groups for clinical and biological studied parameters. After treatment both antidepressants produced equivalent improvement of depression evaluated by MADRS (fluvoxamine:dMADRS = 16.95 +/- 7.11; maprotiline: dMADRS = 17.10 +/- 6.84. t = 0.07, NS). T3 and T4 variations between the beginning and the end of the study weren't also significantly different between the 2 groups. Basal TSH was increased in the maprotiline group but decreased in the fluvoxamine group resulting in a significant difference (fluvoxamine: dTSH = 0.31 +/- 0.76 mUI/l. Maprotiline : dTSH = -0.23 +/- 0.66 mUI/l. t = 2.40, p < 0.02). The TSH response to TRH was decreased in the fluvoxamine group (ddTSH = 0.24 +/- 6.65 mUI/l. dAUC = 103.98 +/- 596.84 mUI/l) while it was increased in the maprotiline group (ddTSH = -3.59 +/- 5.88 mUI/l. dAUC = -355.80 +/- 505.67 mUI.min/l). The difference between the 2 treatments was not significant when evaluated by ddTSH (t = 1.53, NS) but it became significant if evaluated by dAUC (t = 2.63, p < 0.01). As we could demonstrate an absence of influence of the clinical evolution between both groups in the hormonal variations observed, we concluded to a intrinsic difference action on HPT axis between fluvoxamine and maprotiline. This difference could be linked to the different aminergic action of these 2 antidepressants.

This preliminary report compares the FT3, FT4, TSH basal levels and FT4/FT3 ration of depressed patients (DSM III-R criteria) with those of a healthy control group. Authors have also studied thyroid parameters in function of some clinical depression data (polarity, intensity and endogenous character) and other factors as age and sex. 81 depressed patients (31 men, 50 women), with mean age of 44.85 years were studied. 44 patients suffered of an endogenous depression and 37 of a non endogenous depression (Newcastle criteria). 60 patients had an unipolar depression while 21 patients had a bipolar depression. The control group was constituted of 36 healthy subjects (20 men, 16 women), with mean age of 40.94 years. There is no significant difference between the two groups for sex and age, besides the different size of the two groups. FT3 mean of depressed patients was 4.39 pmol/l. There was a significant difference between unipolar group FT3 mean (4.51 +/- 1.01 pmol/l) and bipolar FT3 mean (4.03 +/- 0.91 pmol/l; t = 2.02, p < 0.05). Depression intensity was correlated negatively to FT3 mean (r = -0.23; t = 2.10, p < 0.005). FT4 mean in the depressed group was 12.62 +/- 4.14 pmol/l. The only significative result for FT4 was its correlation to TSH levels (r = -0.36; t = 3.43, p < 0.001). TSH mean in depressed patients was 1.43 +/- 0.85 microIU/ml. When we have compared these results with those of control group we concluded that FT3 and TSH levels were significantly lower in the depressed group (FT3: t = 4.83, p < 0.0001; TSH; t = 2.44 p < 0.02) and that FT4 was slightly but not significantly increased in the depressed group. FT3 decrease and the slight FT4 increase in depression may be the consequence of a metabolic deviation of FT4 transformation into FT3. Its link with intensity and polarity of depression suggests that it can be considered as a biological marker of this disease.