Calcifications in ovary and endometrium and their neoplasms.
In this study, we investigated the role of hormones in the pathogenesis of calcifications in ovary and in endometrium and their neoplasms of the gynecologic tract and assessed the anatomic location and incidence of these calcifications. The study consists of three parts designed to investigate the pathogenesis, the location, and the incidence of calcifications in ovary and endometrium and their neoplasms. In the first part, 79 female guinea pigs were divided into 10 groups, and different hormones, given weekly for 12 months, were administered to the guinea pigs by group. A control group of 7 guinea pigs received sterile water. Calcifications developed in 5 of 7 guinea pigs treated with prolactin, 10 of 20 treated with human chorionic gonadotropin, 5 of 11 treated with estradiol, 3 of 7 treated with estrone, 1 of 6 treated with growth hormone, and 1 of 10 treated with testosterone; in 20 of the guinea pigs, the calcifications developed in the stroma of the endometrium, and in 5 guinea pigs, they developed in the ovary. The second part of the study consisted of an evaluation of the specific location of calcifications in 43 consecutive human surgical ovaries and endometria. Calcifications were seen only in the stroma in 100% of the ovarian serous adenofibroma specimens; in ovarian serous borderline neoplasms, the stroma contained 70 to 100% of the calcifications, and the epithelium had 0 to 30% of the calcifications. In ovarian serous carcinoma specimens, the calcifications were seen in the stroma in 50 to 60% of the cases, in the epithelium in 40% of the cases, and in areas of necrosis in 10% of the cases. The third part of the study was directed to determine the frequency of calcifications in ovarian lesions. We found that all cases of endosalpingiosis and ovarian low-grade serous carcinoma had calcifications, whereas 80% of the cases of serous borderline tumor had calcifications, and only 50% of the cases of ovarian high-grade serous carcinoma contained calcifications. The results of this study indicate that the majority of the calcifications in the ovary and the endometrium and their neoplasms are present in the stroma. This is most probably secondary to metabolic changes, which could be related to hormones and not caused by degenerative changes in epithelial cells.
Silva
Elvio G
EG
Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. esilva@mdanderson.org.
Deavers
Michael T
MT
Parlow
A F
AF
Gershenson
David M
DM
Malpica
Anais
A
D000818:Animals; D002114:Calcinosis / Q000150:complications*; D006063:Chorionic Gonadotropin / Q000378:metabolism; D002996:Clomiphene / Q000378:metabolism; D013196:Dihydrotestosterone / Q000378:metabolism; D016889:Endometrial Neoplasms / Q000150:complications / Q000473:pathology*; D004717:Endometrium / Q000473:pathology*; D004958:Estradiol / Q000378:metabolism; D004970:Estrone / Q000378:metabolism; D005260:Female; D013006:Growth Hormone / Q000378:metabolism; D006168:Guinea Pigs; D006728:Hormones / Q000378:metabolism*; D019290:Megestrol Acetate / Q000378:metabolism; D010051:Ovarian Neoplasms / Q000150:complications / Q000473:pathology*; D010053:Ovary / Q000473:pathology*; D011388:Prolactin / Q000378:metabolism; D013629:Tamoxifen / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism
D006063:Chorionic Gonadotropin; D006728:Hormones; D013196:Dihydrotestosterone; D013629:Tamoxifen; D002996:Clomiphene; D004970:Estrone; D013739:Testosterone; D004958:Estradiol; D011388:Prolactin; D013006:Growth Hormone; D019290:Megestrol Acetate