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First Posted July 26, 2010
Jul 26, 2010

Granulosa-Theca Cell Tumors in the Mare

Winter 2003 Newsletter
Granulosa-Theca Cell Tumors in the Mare

Granulosa-theca cell tumors (GCT's) represent the most common group of tumors that develop in the equine ovary and probably comprise 2.5% of all equine tumors. These tumors have been reported in all ages and breeds, even in pregnant mares, but are most common in five- to ten-year-old mares. They arise from sex cord- stromal tissue within the ovary; most are benign and unilateral, but hormonally active. The opposite ovary is usually inactive, probably because inhibin produced by granulosa-theca cell tumors suppresses the pituitary follicle stimulating hormone (FSH) secretion.

Mares with GC's usually exhibit one of three types of behavior depending upon the type and amount of hormones produced by their tumor. These are 1) prolonged anestrus, 2) persistent or intermittent estrus behavior (nymphomania), or 3) stallion-like behavior. Mares exhibiting the latter may also have a crested neck and enlarged clitoris.

Serum inhibin and testosterone are elevated in 87% and 54%, respectively, of mares with granulosa cell tumors. A serum testosterone concentration of >100 pg/ml is considered diagnostic for a GCT in a mare. Mares with elevated serum testosterone are those that usually exhibit stallion-like behavior. Other hormone levels, such as estrogen and progesterone, do not correlate to clinical signs.

The diagnosis of GCT's in mares is based on clinical history, including changes in behavior, rectal palpation, ultrasonography, and serum hormone analysis. By rectal palpation, the affected ovary is enlarged; it may be cystic and/or abnormally firm; an ovulation fossa is typically absent. Palpation of both ovaries is important because ovarian enlargement may be associated with other conditions, e.g. hematoma. If the contralateral ovary is active, the enlarged ovary probably does not have a GCT. A transitional ovary with multiple anovulatory follicles can be mistaken for an ovarian tumor. Sequential examination usually distinguishes between neoplastic and non-neoplastic conditions of the ovary, since tumors continue to enlarge.

Ultrasonography can provide additional diagnostic information, but may not provide a definitive diagnosis. Sonographic features of a GCT depend on the size and number of cysts within the tumor. Consequently, GCT's can be multilocular and honeycombed to dense, knobby or smooth. Some GCT's may appear with a single, fluid-filled cyst or as a solid ovarian mass. Ultrasonography of the contralateral ovary can demonstrate the presence or absence of follicle development and/or substantiate findings obtained by rectal palpation.

Grossly, GCT's are quite characteristic. The enlarged ovary is usually 10-20 cm in diameter, but may be 40 cm or larger. Loss of the ovulation fossa is due to the growth of the tumor, and usually occurs before the ovary enlarges. On cut surface, GC's are polycystic, solid, or a combination of both. Cyst fluid is sanguinous or serous. Solid areas are white and grayish to yellow and orange, depending on the degree of hemorrhage that has occurred within the tumor. Larger tumors usually have areas of hemorrhage and/or necrosis. Histopathology generally provides a definitive diagnosis. Neoplastic granulosa-theca cells are generally oval to cuboidal and arranged in cords, trabeculae, sheets or tubules. In some tumors, neoplastic cells are arranged in rosettes resembling rudimentary follicles, so-called Call-Exner bodies, that may contain proteinaceous fluid.

Treatment for granulosa-theca cell tumors is surgical removal of the affected ovary. Most mares return to normal estrous cycles within 6-8 months following the ovariectomy, with a range of 2-16 months. Fertility usually returns to presurgical status after estrous cycles have been re-established.

-by Kristen Abderhalden-Telfer, Class of 2002
-edited by Evan Janovitz, ADDL Pathologist

References:

1. Colahan, Patrick T., et al, eds: 1999. Equine Medicine and Surgery, 5th ed.
2. Jones, Thomas, Ronald Hunt and Norval King: 1997. Veterinary Pathology, 6th ed.
3. Jubb, K., P. Kennedy and N. Palmer, eds.: 1993. Pathology of Domestic Animals.
4. McKinnon, Angus and James Voss, eds.: 1993. Equine Reproduction.
5. Robinson, N., Edward, ed.: 1997. Current Therapy in Equine Medicine.
6. Smith, Bradford, ed.: 2002. Large Animal Internal Medicine, 3rd ed.

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