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  • Title: Grwoth hormone, prolactin, and cortisol in dogs developing mammary nodules and an acromegaly-like appearance during treatment with medroxyprogesterone acetate.
    Author: Concannon P, Altszuler N, Hampshire J, Butler WR, Hansel W.
    Journal: Endocrinology; 1980 Apr; 106(4):1173-7. PubMed ID: 6444575.
    Abstract:
    Concentrations of (GH) growth hormone, (PRI) prolactin, cortisol, progesterone, and (MPA) medroxyprogesterone acetate were determined by RIA in blood sera collected from beagle bitches 17 months after initiating treatment with MPA (75 mg/kg.3 months; n = 12) MPA vehicle (controls; n = 12), or progesterone implants which produced physiological levels of progesterone (13.8 + or - 2.1 ng/ml; n = 12). In the MPA-treated bitches, mean MPA levels were 104 + or - 6 ng/ml, mean GH levels were elevated (9.5 + or - 3.0 vs. 0.4 + or - 0.1 ng/ml; P 0.01); mean PRL levels were unchanged (13.7 + or - 2.8 vs. 12.6 + or - 1.2 ng/ml); and mean cortisol levels were suppressed (1.7 + or - 0.2 vs. 13.7 + or - 1.4 ng/ml; P 0.01) in comparison to those in control animals. None of these parameters was significantly affected by progesterone treatment. External signs of an acromegaly-like condition and large mammary gland nodules (diameters, 5 mm) were noted in, and limited to, 9 bitches with elevated ( 2.5 ng/ml) GH levels (12.8 + or - 3.0 ng/ml). These were 8 MPA-treated bitches which developed the acromegal-like condition during treatment and 1 progesterone-treated bitch which appeared acromegalic before treatment and in which the condition was considered to have developed spontaneously. The data suggest that the acromegaly-like changes and large mammary nodules in dogs administered the contraceptive progestin MPA occurred as a result of MPA-induced elevations in GH. The results do not preclude the possibility that the MPA-induced suppression of cortisol and/or the direct action of MPA on the mammary glands also contributed to mammary nodule formation. MPA-treated dogs may also provide a unique experimental model for studying chronic elevations in endogenous GH levels and for testing compounds for their ability to suppress GH levels.
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