A study of the aetiology of pseudopregnancy in the bitch and the effect of cabergoline therapy
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Thirty-two permanently pseudopregnant bitches were treated with the anti-prolactin drug cabergoline. They had all been ovariohysterectomised up to five months after their last season, in some cases over two years previously, when most were reported as showing no signs of the condition. The clinical signs were mainly behavioural, the majority being aggressive, and a small number were lactating. The efficiency of the cabergoline therapy was classified by the owners as 'excellent' or 'good' in 50 per cent of the cases, and fair in 36 per cent. The rate of success was markedly better than in similar cases treated with reproductive steroids. In all but one of the bitches, the plasma prolactin concentrations were basal.Keywords:
Cabergoline
Etiology
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Anorexia nervosa
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In order to determine the mechanism by which glucocorticosteroids decrease the serum concentration of thyrotropin (TSH), we studied eight normal subjects before and after they received 16 mg of dexamethasone daily for 2½ days. Serum levels of TSH and prolactin (PRL) were measured in the basal state and in response to the intravenous administration of 200 μg thyrotropinreleasing hormone (TRH); T4, free T4 (fT4), T3, and free T3 (fT3) were measured before TRH injection. Metabolic clearance rates of TSH corrected for body surface area (MCR-TSH/m2) were determined by the method of constant infusion to equilibrium; the production rates of TSH (PR-TSH/m2) were calculated. Dexamethasone produced a decrease in basal TSH from 2.2 to 0.8 μU/ml (P < 0.02), a statistically insignificant elevation in MCR-TSH/m2 from 25.8 to 34.1 ml/min/m2, and a decrease in PRTSH/m2 from 79 to 30 mU/day/m2 (P < 0.01). Peak TSH response to TRH decreased from 16.4 to 5.8 μU/ml (P < 0.005), as did TSH reserve from 1.58 to 0.54 mU · min/ml (P < 0.005). Repetitive TRH testing alone did not account for these changes. Basal PRL, peak PRL after TRH, and PRL reserve did not change significantly after dexamethasone administration. Although Basal T4 and fT4 did not change significantly, dexamethasone did decrease T3 from 106 to 61 ng/dl (P < 0.001) and fT3 from 174 to 76 pg/dl (P < 0.05). Dexamethasone produced similar changes in patients with various thyroid disorders. In addition, when plasma cortisol was lowered by metyrapone administration in 25 euthyroid patients, the serum TSH concentration rose from 1.6 to 3.1 μU/ml (P < 0.001). These data indicate that dexamethasone a) suppresses TSH secretion without increasing fT3 and fT4 and b) blunts the TSH, but not the PRL response, to TRH. Hence, one effect of the administration of dexamethasone in high dose is a direct suppression of pituitary TSH secretion. Furthermore, physiologic levels of circulating cortisol also have a suppressive effect on serum TSH.
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In the present study the influence of dexamethasone treatment of rats on the basal values of thyrotrophin (TSH) and prolactin (PRL) and the response of both hormones to thyrotrophin releasing hormone (TRH) has been investigated. Male rats were given 100 μg of dexamethasone/rat for 8 days at the same time of day. Four hours after the last administration of dexamethasone 200 ng or 100 μg of TRH/rat was injected ip. Blood was collected 10 min later by decapitation. TSH and PRL were estimated by radioimmunoassay (RIA) using the NIAMD kits. The basal and TRH stimulated values of PRL in plasma were significantly lower in dexamethasone treated rats than in controls (P < 0.01). The basal TSH levels in the treated animals were also lowered (P < 0.05). After 200 ng TRH/rat the increase in TSH was not as high in both groups than after the administration of 100 μg/rat. There was no significant difference between the response of TSH to TRH in the dexamethasone treated and the control rats. The different effects of dexamethasone on PRL and TSH release after TRH may give a further insight into the different regulating mechanisms of both hormones in rats.
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Reports of suppression of plasma prolactin (PRL) in humans by water loading led us to examine the effect of a 20 cc/kg water load on serum TSH in 21 normal volunteers. In addition, the effects of a water load on basal and TRH stimulated TSH and PRL levels were evaluated in seven patients with primary hypothyroidism. The water load had no effect on basal serum TSH levels in either normal or hypothyroid subjects, and did not alter the TSH response to TRH in hypothyroid subjects. Basal or TRH-stimulated plasma PRL was also unaffected by water loading in the hypothyroid subjects. These data suggest that a water load of 20 cc/kg does not significantly affect TSH release by the anterior pituitary, and also provide further evidence that water loading does not consistently suppress PRL secretion.
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Microgram
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Plasma PRL fell in nine healthy subjects and four patients with hyperprolactinemia after iv administration of salmon calcitonin (CT). The maximum fall was observed 30–60 min after theinfusion. There was no change in the plasma concentrations of the other anterior pituitary hormones tested (GH, FSH, LH, and TSH). In five healthy subjects, TRH was injected 60 min after the CT infusion. This protocol was repeated in the same subjects at 3-day intervals, except CT was not administered. Plasma PRL before TRH injection was clearly lower when CT had been administered. Plasma concentrations of the other anterior pituitary hormones did not change. PRL and TSH responses to TRH were markedly inhibited when CT had been previously infused. These observations are in agreement with preceding studies showing a similar effect of CT on the plasma concentration of various other polypeptide hormones. This general effect of CT could be attributed to a change in intracellular calcium of the secreting cells. (J Clin Endocrinol Metab50: 1011, 1980)
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Thirty-six male patients with idiopathic haemochromatosis were subjected to measurements of basal plasma values of testosterone, LH and FSH and to an LRH test. Nineteen were also subjected to basal plasma determinations of T3, T4, cortisol, TSH and prolactin and to a TRH test. In 11 cases GH values were measured before, during and after an arginine infusion. Seventeen patients were found to hae low levels of testosterone, LH and FSH, and no gonadotrophin responses to LRH. Seventeen others had normal levels of these three hormones, with normal responses to LRH. The two remaining patients had normal testosterone values but very increased gonadotrophin values: a fact which remains unexplained. Basal levels of prolactin, GH, T3, T4, and TSH were normal: cortisol levels were either normal or increased in cases of poorly controlled diabetes. Prolactin responses to TRH were always normal. TSH responses to TRH were impaired in 2 cases, and GH responses to arginine in 3 cases. Considering that other factors may be involved in the few impairments found in TSH and GH stimulations, it is concluded that the only indisputable pituitary insufficiency in about half of the cases of idiopathic haemochromatosis is gonadotrophic.
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Abstract. Growth hormone (GH), prolactin (Prl) and cortisol secretion was studied in 5 ovariohysterectomized dogs before and after oestradiol implantation and medroxy-progesterone acetate (MPA) administration. MPA was given at regular intervals during a period of 10 months in a total of 12 injections. Short-term effects of oestradiol were restricted to significantly enhanced Prl responses to thyrotropin-releasing hormone (TRH). MPA treatment after oestradiol implantation resulted in significanly elevated basal GH levels in all dogs, with a continuing increase in one dog. Only in the latter dog was a significant decrease in basal Prl levels seen. MPA administration did not significantly change Prl responses to TRH. The GH responses to clonidine were significantly reduced at 9 and 16 weeks of oestradiol and MPA treatment. In the one dog which exhibited the greatest rise in basal GH levels, GH responses were completely abolished at 9, 16 and 43 weeks of oestradiol and MPA treatment. TRH never evoked significant GH responses. Both basal and lysine-vasopressin (LVP)-stimulated cortisol levels were significantly suppressed during combined oestradiol-MPA treatment. These findings denote that in the dog. 1) Oestradiol rapidly induces an enhanced Prl response to TRH. 2) The oestradiol-MPA induced GH overproduction is associated with a reduced responsiveness of GH to clonidine and is not accompanied by GH responsiveness to TRH. 3) Oestradiol-MPA treatment suppresses both basal and LVP-stimulated cortisol secretion.
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Beagle
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Basal plasma prolactin (hPRL) concentration is low, but the response to thyrotropin-releasing hormone (TRH) is within the normal range, in children with protein-carlorie malnutrition (PCM) before treatment. Treatment results in increased basal hPRL concentration and an increased response to TRH. The above findings contrast with normal or high basal TSH and the normal or exaggerated response to TRH provocation in untreated PCM. The reason for this divergence is obscure.
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Protein-calorie malnutrition
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SUMMARY Plasma prolactin and thyrotrophin (TSH) were measured by radioimmunoassay before, at 20 min and 60 min after the intravenous administration of 200 μg thyrotrophin‐releasing hormone (TRH) in thirty‐two patients with untreated primary hypothyroidism and in sixteen normal volunteers. Whereas basal plasma TSH was markedly elevated in all the patients with hypothyroidism, a slight, but significant increase ( P <0.05) in basal plasma prolactin in primary hypothyroidism could only be demonstrated by matching for age, sex and circulating gonadotrophin levels, ten patients with hypothyroidism with ten normal volunteers. There was, however, no significant difference between the two groups, matched or unmatched, in the plasma prolactin levels, in contrast to the plasma TSH levels, following TRH administration. No apparent relationship was found between basal prolactin and follicle‐stimulating hormone (FSH), luteinizing hormone (LH) or TSH. Assuming the release of prolactin by TRH to be of physiological significance, the results suggest that TRH secretion by the hypothalamus may be increased in untreated hypothyroidism and that low levels of circulating thyroid hormone increase the sensitivity of the pituitary thyrotrophs, but not the prolactin secreting cells, to TRH. Markedly elevated plasma prolactin levels associated with galactorrhoea were not seen in primary hypothyroidism in the absence of the puerperium or oestrogen therapy.
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Thyrotropic cell
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The role of the serotoninergic system in the control of LH, FSH and prolactin secretion was analyzed in control and neonatally estrogenized male rats. Animals injected s.c. with 500 µg of estradiol benzoate (EB) on day 1 of life, or their corresponding sham-treated controls, were divided on day 75 into the following groups: (1) orchidectomized; (2) injected intraventricularly with 5,7-dihydroxytryptamine (5,7-DHT); (3) orchidectomized and treated with 5,7-DHT, and (4) sham operated. 15 days later, the animals were decapitated and their FHS, LH and prolactin plasma values measured by specific RIA systems. After the treatment with 5,7-DHT, control animals showed a decline in basal prolactin levels but no modification in basal LH and FSH values. After castration, 5,7-DHT-treated animals showed a reduced LH increase and a more marked prolactin decrease. In neonatal estrogen-treated animals, the 5,7-DHT injection did not change FSH, LH or prolactin levels but did partially or completely abolish the post-castration rise in FSH and LH levels, respectively. These data seem to indicate that neonatal estrogenization induced a modification of the serotoninergic role in the control of LH, FSH and prolactin.
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5,7-Dihydroxytryptamine
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