Feline mammary hyperplasia (also called fibroadenomatous hyperplasia, mammary hypertrophy, mammary dysplasia, mammary fibroadenomatosis, fibroadenoma complex, fibroepithelial hyperplasia, fibroglandular mammary hypertrophy and feline mammary hypertrophy/fibroadenoma complex) was described for the first time in 1973 as a condition characterized by a benign fibroglandular proliferation of one or more of the mammary glands in the young queen. Subsequently a similar condition was described in both male and female cats of any age following treatment with progestins. Some cases have also been found in dogs. Feline mammary hyperplasia is a breast disorder characterized by a rapid, widespread and large increase in the volume of the mammary gland, although it can also present as localised masses of various sizes which are not distinguishable from mammary gland neoplasms.
EPIDEMIOLOGY AND AETIOPATHOGENESIS
Feline mammary hyperplasia predominantly affects young, sexually intact queens between the age of 13 weeks and 2 years, gravid or not, and is caused by the effect of progesterone. Since this condition is caused by hormonal stimulation from the ovary, and in particular by progesterone, it is commonly found during pregnancy, when the circulating levels of progesterone are higher or, less frequently, during a pseudo-pregnancy. Given the hormonal aetiology of the disorder, there is also an iatrogenic form that can affect any animal, independently of gender and possible gonadectomy, which is provoked by the administration of progestins such as medroxyprogesterone acetate or megestrol acetate. These drugs were used, particularly in the past, to control oestrus in queens and for the treatment of some behavioural and dermatological problems in cats of both genders. Nowadays progestin-based treatments are rarely used because of their proven side effects, including the risk of mammary neoplasms. There are also reports of cases of feline mammary hyperplasia that have been attributed to the intake of some plants or contaminated water or to endocrine disorders with hyperprogesteronaemia.
SIGNS AND DIAGNOSIS
In most cases the condition is characterized by a rapid (2-5 weeks) and substantial increase in the volume and consistency of one or more mammary glands during pregnancy or pseudo-pregnancy. Pain and systemic effects are not normally present and haematological and blood-chemistry tests do not show abnormalities. However, in some cases, the mammary glands can develop infectious complications or ulcerations, with both local and systemic repercussions of variable importance (Fig. 1).
The diagnosis of feline mammary hyperplasia must be made by differentiating it from mastitis and mammary gland neoplasms. The diagnostic suspicion is based on signalment and the history, on the findings of the general and specific clinical examinations and on haematological and blood-chemistry tests. In young queens with a diffuse increase in the volume of the mammary glands it is considered that signalment, history and clinical examination can be sufficient to make the diagnosis without the aid of a biopsy. However, the biopsy finding of a benign fibroglandular hyperplasia, not usually accompanied by signs of inflammation or necrosis, or by lactation, provides confirmation of the differential diagnosis in all cases in which the signalment, history and clinical investigation have not be been sufficient to exclude neoplastic disease of the mammary glands, which in this species is often very malignant. In subjects with hyperplasia induced by progestin treatment, histological examination shows the presence of intraductal papillary growth. Animals with mammary hyperplasia, whether spontaneous or progestin-induced, have been found to have progesterone, but not oestrogen, receptors in the cytoplasm or nuclei of the cells of mammary gland tissue, providing further support for the proposed endocrine aetiology of the condition.
TREATMENT AND PROGNOSIS
In cases of spontaneous mammary hyperplasia, in which the fall in plasma progesterone levels at the end of gestation (delivery or abortion) or following luteolysis in a pseudo-pregnancy leads to spontaneous regression, mastectomy is not usually indicated. Gonadectomy, with removal of the ovaries, also leads to a rapid drop in the plasma levels of progesterone and regression of the mammary hyperplasia. In some cases, the application of an Elysabethan collar, to prevent or limit licking and/or sucking, can be useful, as may be antibiotic treatment during infections. Sometimes the infectious complications or the development of ulcerative lesions make complete resolution of the mammary gland disorder unlikely if not highly improbable, thereby indicating the need for mastectomy, which is also necessary in cases in which complete remission of the signs does not occur despite a decrease in progesterone levels.
Excellent results have recently been obtained with pharmacological treatment based on aglepristone, a progesterone receptor antagonist; different protocols have been used, including subcutaneous administration at a dose of 20 mg/kg once or week or 10 mg/kg/day for 2 consecutive days for 1-4 weeks. The side effects seem to be limited to local reactions at the injection site and abortion in pregnant queens. In cases of iatrogenic hyperplasia, even though suspension of progestin treatment can, in some cases, lead to remission of the signs, mastectomy is advisable both to achieve definitive resolution of the condition and to obtain histological confirmation of the diagnosis.
Suggested readings
- SD Johnston, MV, R Kustritz, PNS Olson. Canine and Feline Theriogenology. Saunders edition, 2001.
- Görlinger et al. Treatment of fibroadenomatous hyperplasia in cats with aglipristone. J Vet Intern Med, 2002;16:710-713.
- Ettinger Feldman. Textbook of veterinary internal medicine, Quinta edizione, 2000, Saunders.
- Allen HL. Feline mammary hypertrophy. Vet Pathol 1963;10:501-508.
- Hayden DW et al. Ultrastructure of feline mammary hypertrophy. Vet Pathol 1983;20:254-264.