Depression in Woman

Depression In Woman

Paz Toren, Jehoshua Dor, Roberto Mester, Tamar Mozes, Rachel Blumensohn, Moshe Rehavi, Abraham Weizman,

Depression in women treated with a gonadotropinreleasing hormone agonist,

Biological Psychiatry, Volume 39, pp 378-382, 1996

 דיכאון בנשים שטופלו באגוניסטים ל-GnRH

פז תורן, יהושוע דור, רוברטו מסטר, תמר מוזס, רחל בלומנזון, משה רכבי, אברהם ויצמן

Discussion

The major finding of the study is that pretreatment with GnRH-a, as part of an IVF protocol, is associated with a substantial increase in depression level in euthymic subjects. A rise in anxiety level was also demonstrated, but was not manifested on the subjective scales. The anxiety symptoms may have been mainly an expression of the known overlap between depression and anxiety symptomatology (Snaith and Turpin 1990). The hypogonadism caused by decapeptyl at the hypogonadal phase coincided with the increase in depression and anxiety levels. Previous reports have demonstrated an upregulatory effect of estradiol on the serotonin transporter (Weizman et al 1988), known to play a major role in the pathogenesis of depression (Van Praag 1984). Thus, the hypoestrogenism caused by GnRH-a might be associated with dysregulated serotonergic neurotransmission leading to depression. The depression, however, persisted at the peak follicular phase of the decapeptyl group, despite the marked increase in estradiol levels caused by hMG administration. Thus, hypoestrogenism might have induced the depression, which then took its own course irrespective of the subsequent changes in estradiol levels. Alternatively, GnRH-a might also affect depression or anxiety through its central activity–directly or by mediators other than the pituitary or ovarian hormones (Bancroft et al 1987). Previous studies have demonstrated a bidirectional saturable transport of GnRH across the blood-brain barrier (Barrera et al 1991); thus, the possibility of a central depressogenic effect of GnRH-a, unrelated to hypoestrogenism, cannot be disregarded. GnRH-a can sometimes diminish mood symptoms related to menstrual cycle (premenstrual syndrome), probably by abolishing ovarian cyclicity (Bancroft et al 1987; West and Hillier 1994). The factor of abolishing ovarian cyclicity may, in this specific syndrome, counteract the dysphoric changes of the GnRH-a treatment. The present study assessed the impact of GnRH-a treatment on mood for a short-term protocol involving GnRH-a for IVF patients. The results, however, may have broader implications because of the longer-term use of this medication in the treatment of endometriosis, uterine fibroids, and other conditions. It would be interesting to investigate how enduring the dysphoric effect is in chronic use of GnRH-a. The present preliminary study raised the possibility that GnRH-a may induce depression in euthymic subjects; however, despite the marked increase in depression and anxiety levels, the maximal scores on the Hamilton scales were quite modest, and none of the women developed full-blown major depression. Nevertheless, the possible deleterious effect of GnRH-a on mood should not be ignored and merits further investigation in a double blind, placebo-controlled design. In order to isolate the directneural from the hormonal factors as the possible mechanism of GnRH-a-induced depression, the effect of estrogen-replacement therapy during the hypogonadal phase on the emergence of depression and anxiety should be evaluated.

המאמר דיכאון בנשים שטופלו באגוניסטים ל-GnRH

שנכתב על ידי פז תורן, יהושוע דור, רוברטו מסטר, תמר מוזס, רחל בלומנזון, משה רכבי, אברהם ויצמן

Biological Psychiatryפורסם בעיתון

לקריאת המאמר של פז תורן, יהושוע דור, רוברטו מסטר, תמר מוזס, רחל בלומנזון, משה רכבי, אברהם ויצמן   לחץ כאן


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