Semin Reprod Med 2004; 22(1): 51-60
DOI: 10.1055/s-2004-823027
Copyright © 2004 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Aromatase and Leiomyoma of the Uterus

Makio Shozu1 , Kouich Murakami1 , Masaki Inoue1
  • 1Department of Obstetrics and Gynecology, Kanazawa University School of Medicine, Kanazawa, Japan
Further Information

Publication History

Publication Date:
13 April 2004 (online)

In leiomyoma of the uterus, both aromatase and 17β-hydroxysteroid dehydrogenase (17β-HSD) type I are overexpressed compared with myometrium. This suggests that leiomyoma cells convert circulating androstenedione into estrone (via aromatase), then into the active form of estrogen, estradiol (via 17β-HSD type I). In vitro experiments and several clinical findings support the notion that in situ estrogen plays a role in leiomyoma growth under hypoestrogenemic conditions, such as natural menopause and therapy with gonadotropin-releasing hormone (GnRH) agonists. GnRH agonists abolish estrogen production both in situ in leiomyoma and in the ovary, leading to quick and profound regression of the leiomyoma. Aromatase inhibitors also inhibit estrogen synthesis in both leiomyoma and the ovary and may be used therapeutically. Certain doses of competitive aromatase inhibitors would completely inhibit estrogen production in leiomyoma, whereas ovarian production of estrogen would continue at reduced levels. This may lead to advantageous therapeutic conditions in which leiomyoma regresses without adverse symptoms related to estrogen depletion because levels of ovarian estrogen would be insufficient to support leiomyoma growth but sufficient to prevent symptoms associated with deficiency. This article discusses the potential uses of aromatase inhibitors.

REFERENCES

Makio Shozu, M.D. 

Department of Obstetrics and Gynecology, Kanazawa University School of Medicine

13-1 Takara-machi, Kanazawa 920-0934, Japan