A Case of Ovarian Dysplasia and a Vaginal Fibroleiomyoma in a Young Golden Retriever

This case demonstrates a unique ovarian congenital anomaly that likely contributed to the development of a rare fibroleiomyoma in the cranial vagina of a young bitch. A 13 month old intact female Golden Retriever presented to the veterinary teaching hospital for urinary incontinence, hematuria, and persistent vaginal discharge. Physical examination revealed a mucopurulent serosanguinous malodorous vulvar discharge, and after further diagnostics was reclassified as persistent estrus. Abdominal palpation and ultrasound revealed uterine thickening and poorly visualized ovaries. The reproductive tract was removed during an ovariohysterectomy, revealing small ovaries and a white anterior vaginal mass. Histopathology revealed dysplastic ovaries with hyperplastic granulosa cells and a benign vaginal fibroleiomyoma. These morphologic changes are consistent with elevated estrogen levels. It was thus concluded that her persistent estrus and the fibroleiomyoma were both secondary to persistent estrogen production by the hyperplastic granulosa cells.

Canine ovarian dysgerminoma

ABSTRACT: This research aimed to describe a clinical case of ovarian dysgerminoma in a bitch, by showing clinical, ultrasound, surgical and pathological findings. The research also sought to emphasize the importance of establishing an early and definitive diagnosis through histopathology, establishing appropriate protocols for each patient. Ovarian tumors have a low incidence in dogs and cats. Dysgerminomas are a type of ovarian germ cell tumor. They develop in dogs of variable age, that may present clinical signs of hormonal imbalance such as persistent estrus, or pyometra. Prognosis is good in animals that undergo surgery and show no evidence of metastasis. This article presents a clinical case of a 6-year-old English Bulldog with persistent estrus for 2 months, and slightly depressed mental state. Ultrasound revealed the presence of a mass on the left ovary and uterine content. Ovariohysterectomy was performed and the mass was submitted to histopathological exam, which diagnosed an ovarian dysgerminoma.

Chronic estrus disrupts uterine gland development and homeostasis

Female mice homozygous for an engineered Gnrhr E90K mutation have reduced gonadotropin-releasing hormone signaling, leading to infertility. Their ovaries have numerous antral follicles but no corpora lutea, indicating a block to ovulation. These mutants have high levels of circulating estradiol and low progesterone, indicating a state of persistent estrus. This mouse model provided a unique opportunity to examine the lack of cyclic levels of ovarian hormones on uterine gland biology. Although uterine gland development appeared similar to controls during prepubertal development, it was compromised during adolescence in the mutants. By 20 weeks of age, uterine gland development was comparable to controls, but pathologies, including squamous neoplasia, tubal neoplasia, and cribriform glandular structures, were observed. Induction of ovulations by periodic human chorionic gonadotropin treatment did not rescue post-pubertal uterine gland development. Interestingly, progesterone receptor knockout mice, which lack progesterone signaling, also have defects in post-pubertal uterine gland development. However, progesterone treatment did not rescue post-pubertal uterine gland development. These studies indicate that chronically elevated levels of estradiol with low progesterone and therefore an absence of cyclic ovarian hormone secretion disrupts post-pubertal uterine gland development and homeostasis.

Comparative Study of Tamoxifen and Raloxifene on Endometrial Cell Proliferation of Female Rats in Persistent Estrus

ObjectiveThe objective of the study was to compare the effect of tamoxifen and raloxifene on the endometrium of female rats in persistent estrus, by Ki-67 protein expression.MethodsThe study comprised 60 Wistar-Hannover female rats in persistent estrus, induced by a single subcutaneous dose of 1.25 mg of testosterone propionate on the second day of age. At 90 days of life, the animals were randomly divided into 3 groups of 20 animals each. Group 1 (control), received only placebo; group 2, the animals were treated with tamoxifen, 250 μg/d; and group 3, the rats were treated with 750 μg/d of raloxifene by gavage during 30 days. Then, the animals were killed, and the endometrium was removed for immunohistochemical analysis of Ki-67 antigen expression. Statistical analysis was performed by β regression model (P < 0.05).ResultsMean percentages of Ki-67 protein expression in the endometrium of rats in persistent estrus were 43.21% ± 3.39%, 7.36% ± 0.95%, and 7.20% ± 0.76% in groups 1, 2 and 3, respectively (P < 0.001). There was no statistical difference between groups 2 and 3 (P = 0.7159).ConclusionsThe present results indicate that, at the doses and during the time of treatment used, both tamoxifen and raloxifene induce atrophy in a similar way of endometrial epithelium of rats in persistent estrus.