Haemorrhage from a canine adrenocortical tumour: a clinical emergency.
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Adrenal Cortex Diseases↗
Biomedical subjects
A Rijnberk
Publications and source records attributed to A Rijnberk.
Corticoid production by four dogs with hyperfunctioning adrenocortical tumours during treatment with mitotane (o,p'-DDD).
In two dogs with hyperadrenocorticism due to an adrenocortical tumour, treatment with o,p'-DDD was started. Their hormonal response was monitored by measurements of the urinary corticoid/creatinine ratio. In one dog, two courses of 10 days treatment with o,p'-DDD were ineffective, whereas in the other dog the urinary corticoids decreased to very low levels after only six days of treatment, and corticosteroid supplementation had to be started. Two other dogs received o,p'-DDD according to a protocol used for the treatment of pituitary-dependent hyperadrenocorticism which aims at the complete destruction of the adrenal cortices, with substitution for the induced hyperadrenocorticism. Both dogs made a good recovery and their urinary corticoid/creatinine ratio decreased to within the reference range. In one of them the tumour had decreased considerably in size by five weeks after the start of the treatment.
Adenoma↗
Corticoid:creatinine ratio.
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Adrenocortical Hyperfunction↗
In vivo studies on the effects of ovine corticotrophin-releasing hormone, arginine vasotocin, arginine vasopressin, and haloperidol on adrenocortical function in the racing pigeon (Columba livia domestica).
This study investigates the effects of in vivo administration of pituitary stimulants in racing pigeons (Columba livia domestica). Plasma corticosterone concentrations were measured following intravenous administration of ovine corticotrophin-releasing hormone (oCRH) (0.1, 1, 10, and 100 micrograms/kg), arginine vasopressin (AVP) (0.01, 0.1, 1, and 10 micrograms/kg), arginine vasotocin (AVT) (0.01, 0.1, 1, and 5 micrograms/kg), and haloperidol (0.05, 0.5, and 5 micrograms/kg). Compared with mammals the pituitary-adrenocortical system of the pigeon appeared to be less sensitive to stimulation with oCRH, although high doses were well tolerated and gave a clear response. Both AVP and AVT stimulated corticosterone secretion, AVT in a more pronounced dose-dependent manner than AVP. The natural neurohypophysial peptide in birds, AVT, was less well tolerated in high doses than AVP. The clear response to haloperidol indicates that the hypothalamo-pituitary-adrenocortical system is under dopaminergic inhibition. Of the pituitary stimulants tested AVP (10 micrograms/kg) and oCRH (100 micrograms/kg) are the most appropriate for testing the integrity of the pituitary-adrenocortical system in the pigeon.
Adrenal Cortex↗
Effect of the aquaretic vasopressin antagonists d(CH2)5[D-Tyr(Et)2-Val4]AVP and d(CH2)5[D-Phe2-Phe4]AVP on urine production in healthy dogs.
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Animals↗
Corticotropin-releasing hormone and adrenocorticotropic hormone concentrations in cerebrospinal fluid of dogs with pituitary-dependent hyperadrenocorticism.
There is still some controversy concerning the question of whether Cushing's disease in man is caused by a primary dysfunction of the pituitary or a hypothalamic disorder. In the latter option, excessive hypothalamic stimulation of pituitary corticotropes would cause or contribute to the genesis of POMC-secreting adenomas. In the present study cerebrospinal fluid (CSF) CRH levels and levels of ACTH and cortisol in CSF and plasma were measured in clinically healthy dogs, in dogs with pituitary-dependent hyperadrenocorticism (PDH), and in dogs with hyperadrenocorticism due to an adrenocortical tumor (ATH). In CSF from dogs with PDH, CRH concentrations (226.6 +/- 14.4 ng/liter) were significantly (P < 0.05) lower than those in control dogs (309.5 +/- 20.3 ng/liter). In the dogs with ATH, CSF CRH concentrations (211.0 +/- 40.3 ng/liter) were in the range of those in PDH dogs. In dogs with ATH, CSF ACTH levels (13.0 +/- 3.0 ng/liter) were significantly (P < 0.05) lower than those in control dogs (63.4 +/- 3.5 ng/liter), whereas in dogs with PDH, the levels (116.8 +/- 47.5 ng/liter) were not different from those in the control group. In control dogs, the concentrations of CSF CRH and plasma ACTH were significantly correlated (r = 0.635; P < 0.01). This functional dependency appeared to be disturbed in dogs with PDH, as in these dogs CSF CRH concentrations did not correlate with plasma ACTH concentrations. It is concluded that continuous hyperstimulation of pituitary corticotropes with hypothalamic CRH is probably not the cause of excessive ACTH secretion in dogs with pituitary-dependent hyperadrenocorticism.
Adrenal Cortex Neoplasms↗
Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont terriers.
Adrenocortical function studies were performed in seven Dandie Dinmont terriers with pituitary-dependent hyperadrenocorticism. The ability of dexamethasone at a dose rate of 0.1 mg/kg body weight to suppress cortisol secretion was only moderate in four out of the six dogs tested. Concentrations of alpha-melanocyte-stimulating hormone in plasma were highly increased. Responses to stimulation with corticotrophin-releasing hormone and the dopamine-antagonist haloperidol, examined in three animals, were moderate or absent. These results indicate that adrenocortical stimulation, i.e. hyperadrenocorticotrophism, was caused by pituitary lesions which were functioning autonomously. In six of the seven animals there was a very close familial relationship and the coefficients of relationship and the coefficients of inbreeding were significantly higher than in a representative control population. It was concluded that these seven related terriers with hyperadrenocorticotrophism had the biochemical characteristics of de-novo neoplasms of proopiomelanocortin-producing cells, and there was evidence for a genetic involvement in tumorigenesis.
Adenocarcinoma↗
Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: a study in dogs with hyperadrenocorticism.
In 9 dogs with pituitary-dependent hyperadrenocorticism and in 6 dogs with hyperfunctioning adrenocortical tumours, the osmoregulation of arginine vasopressin (AVP) release was investigated by iv infusion of 20% NaCl for 2 h at a rate of 0.03 ml per kg body weight. The responses were analysed in terms of sensitivity and threshold of the osmoregulation of AVP secretion. The sensitivity was normal in 6 dogs and lowered in 9. In 4 of the latter dogs there was complete absence of a response to hypertonicity. The osmotic threshold of AVP release was raised in 9 dogs and normal in 2 dogs, whereas in the four dogs without any response the term threshold was not applicable. The results were not different for dogs with pituitary-dependent hyperadrenocorticism and dogs with hyperfunctioning adrenocortical tumour. It is concluded that corticosteroid excess per se induces a marked impairment of the osmoregulation of AVP secretion. The loss of reactivity of the osmoreceptor system may contribute to the corticosteroid-induced polyuria, which is also the result of resistance to AVP in the kidney.
Adrenal Cortex↗
Congenital hypothyroidism in two cats due to defective organification: data suggesting loosely anchored thyroperoxidase.
Two cats with congenital hypothyroidism are described. In vivo discharge of accumulated labelled iodide by perchlorate administration revealed defective organification of iodide, which was complete in one cat and partial in the other. In the cat with the partial organification defect, thyroid tissue was obtained for biochemical studies. No membrane-bound peroxidase activity could be demonstrated. The activity was found in the 100,000 x g supernatant. It is suggested that the loose enzyme anchoring caused decreased availability of peroxidase and as a consequence reduced capacity for organic binding of trapped iodide.
Animals↗
Aging and the hypothalamus-pituitary-adrenocortical axis, with special reference to the dog.
Aging affects the hypothalamus-pituitary-adrenocortical (HPA) system in various ways. It affects the receptors for glucocorticosteroids in the limbic system, the hypothalamus and the pituitary; the basal and stress-induced secretion of proopiomelanocortin-derived peptides and glucocorticoids; and the neuronal integrity, especially in the hippocampus. The homeostatic actions of glucocorticoids occur through the glucocorticoid and the mineralocorticoid receptors. It has been hypothesized that the balance between these two receptors, which are co-localized in the hippocampus, determines the basal HPA activity and the magnitude of the response to challenges. Feedback actions of glucocorticoids are mediated via glucocorticoid receptors in the hypothalamus and the pituitary. In aged rats many changes in the binding capacity of the mineralocorticoid receptor and glucocorticoid receptor and in the regulation of the HPA activity have been reported, but the findings often seem contradictory. The only consistent finding has been that the binding capacity of mineralocorticoid receptor in the hippocampus is reduced. The number of glucocorticoid receptors may be increased, reduced or unchanged in senescent rats. In old dogs the receptor changes were largely confined to mineralocorticoid receptor, there being a 60% reduction in the binding capacity in the limbic system, but glucocorticoid receptor was unchanged in all brain regions. Senescent dogs also had an increased basal secretion of ACTH, and of cortisol. The old dogs had exaggerated responses to stress and to administered corticotropin-releasing hormone, but the termination of the response by the feedback mechanism was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex↗
Progestins and growth hormone excess in the dog.
Chronic overproduction of growth hormone in man and the cat is most often caused by a GH-producing tumour of the pituitary gland. In dogs the usual cause is quite different. In this species endogenous progestins (during metestrus) and exogenous progestins (used to prevent estrus) cause excessive GH secretion that is reversible. For a better understanding of the mechanism of progestin-induced GH synthesis and secretion, studies were carried out in healthy dogs and in dogs presented with GH excess. The effectiveness of stimulation of GH secretion by hGHRH, and clonidine and of the inhibition with the somatostatin analogue SMS 201-995 were evaluated in healthy male dogs. SMS 201-995 had no influence on basal plasma GH levels, but significantly inhibited the hGHRH and clonidine-evoked GH release. In healthy female dogs the basal concentrations of plasma GH were significantly higher during metestrus than during anestrus. The elevated basal plasma GH levels were associated with a diminished responsiveness to stimulation with clonidine. In female dogs with experimental or spontaneous progestin-induced chronic overproduction of GH (and IGF-I), plasma GH levels were completely unresponsive to stimulation with hGHRH and clonidine and to inhibition with SMS 201-995. It is concluded that in the female dog the progestin-induced GH excess has characteristics of autonomous secretion.
Acromegaly↗
[Vaccination during corticosteroid therapy?].
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Animals↗
Assessment of survey radiography and comparison with x-ray computed tomography for detection of hyperfunctioning adrenocortical tumors in dogs.
Results of abdominal survey radiography and x-ray computed tomography (CT) were compared in 13 dogs with hyperadrenocorticism histologically attributed to adrenocortical tumors. X-ray computed tomography enabled accurate localization of the tumor in all 13 dogs. Apart from 2 poorly demarcated irregular-shaped and mineralized carcinomas, there were no differences between adenoma (n = 3) and carcinoma (n = 10) on CT images. In 1 dog, invasion of the caudal vena cava by the tumor was suggested on CT images and was confirmed during surgery. Suspicion of adhesions between tumors of the right adrenal gland and the caudal vena cava on the basis of CT images was confirmed during surgery in only 2 of 6 dogs. Survey radiography allowed accurate localization of the tumor in 7 dogs (4 on the right side and 3 on the left). In 6 of these dogs, the tumor was visible as a well-demarcated soft tissue mass and, in the other dog, as a poorly demarcated mineralized mass. The smallest tumor visualized on survey radiographs had a diameter of 20 mm on CT images. Six tumors with diameter less than or equal to 20 mm were not visualized on survey radiographs. In 1 of these dogs, a mineralized nodule was found in the left adrenal region, without evidence of a mass. In a considerable number of cases, survey radiography can provide presurgical localization of adrenocortical tumors in dogs with hyperadrenocorticism; CT is redundant in these instances. In the absence of positive radiographic findings, CT is valuable for localization of adrenocortical tumors.
Adenoma↗
Binding characteristics of mineralocorticoid and glucocorticoid receptors in dog brain and pituitary.
A series of studies was started to gain insight into the functioning of the canine hypothalamo-pituitary-adrenocortical axis during normo- and hypercortisolemic states. In this first study, we have focused on the binding characteristics of the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR) in the brain and pituitary of the adrenalectomized dog. In hippocampal cytosol at 0 C, corticosterone had the highest association rate, followed by cortisol and aldosterone. Cortisol had the most rapid rate of dissociation from MR at 0 C (t1/2 = 45.5 h), followed by aldosterone (70.4 h) and corticosterone (102 h). The selective glucocorticoid RU 28362 associated rapidly with hippocampal GR, attaining maximum binding within 4 h, and dissociated with a t1/2 of 34.8 h. Saturation binding of [3H]cortisol in adrenalectomized dog hippocampal cytosol produced a curvilinear Scatchard plot. After inclusion of RU 28362, [3H]cortisol bound solely to MR [dissociation constant (Kd) = 0.34 nM, Bmax = 72.8 fmol/mg]. GR capacity was determined with [3H]RU 28362 (Kd = 0.39 nM, Bmax = 120 fmol/mg). Competition binding analyses of various steroids for MR and GR revealed markedly different patterns of steroid binding specificity for these receptors. The rank order for displacement of [3H]aldosterone binding of MR was: corticosterone greater than aldosterone = cortisol greater than dexamethasone greater than ZK 91587 greater than RU 26752 greater than spironolactone much greater than RU 38486, and for displacement of [3H]RU 28362 binding of GR: RU 28362 much greater than corticosterone = cortisol greater than dexamethasone greater than aldosterone greater than ZK 91587 greater than RU 26752 = RU 38486 much greater than spironolactone. MR was located in all brain regions examined, with highest levels in the septo-hippocampal complex, whereas GR was rather evenly distributed. Substantial amounts of MR and GR were present in the anterior part of the pituitary as well as in the neurointermediate lobe. Our findings show that the ligand binding specificity of canine MR and GR is remarkably different from that of rodent MR and GR, but is similar to that of recombinant-derived human receptors. Spironolactone and RU 38486 are selective antagonists for MR and GR, respectively. In contrast to other species, the dog has relatively large quantities of MR widely distributed in the brain and pituitary, which makes this species an interesting animal model to study the role of corticosteroid receptor diversity in control of homeostasis.
Aldosterone↗
Effects of a [Met]-enkephalin analogue ( [D-Ala2,N-Me-Phe4,Met-(O)5-ol]-enkephalin) on canine pituitary function.
In adult healthy beagle dogs, plasma concentrations of ACTH, cortisol, alpha-MSH, GH, prolactin and arginine vasopressin (AVP) were measured after i.v. administration of [D-Ala2,N-Me-Phe4,Met-(O)5-ol]-enkephalin (DAMME) at doses of 0.1, 0.5, 1, 5 and 10 micrograms/kg body weight. Significant dose-dependent increases occurred for ACTH, cortisol and GH at dose rates of 0.5, 1, 5 and 10 micrograms/kg body weight. Increments in plasma concentrations of prolactin were significant only at 5 and 10 micrograms DAMME/kg, and there was no significant effect on plasma concentrations of alpha-MSH and AVP. Prior i.v. administration of the opiate antagonist naloxone (0.1 mg/kg) attenuated the DAMME (10 micrograms/kg)-stimulated release of ACTH and cortisol. The results demonstrate that the [Met]-enkephalin analogue DAMME stimulates the release of ACTH, cortisol, GH and prolactin in dogs, and that this stimulation is, at least in part, mediated by mu-opioid receptors. The observations for ACTH and cortisol are different from those in man, where DAMME lowers their basal concentrations.
Adrenocorticotropic Hormone↗
Heterogeneity in Cushing's disease.
Some patients with Cushing's disease respond to neuropharmacological treatment, whereas others do not. This apparent heterogeneity has been attributed to the existence of a separate form of Cushing's disease of putative neurointermediate lobe origin as opposed to Cushing's disease of anterior pituitary origin. The present review summarizes recent observations in human and canine Cushing's disease which mitigate against this view. We propose that heterogeneity in Cushing's disease is related to heterogeneity of the normal anterior pituitary corticotroph. However, the most fundamental questions concerning the pathogenesis of Cushing's disease remain unanswered.
Cushing Syndrome↗
Nephrotomography and ultrasonography for the localization of hyperfunctioning adrenocortical tumors in dogs.
Nephrotomography and ultrasonography were used in 11 dogs with hyperadrenocroticism to assess the value of these techniques for the localization of biochemically diagnosed hyperfunctioning adrenocortical tumors. Both techniques enabled accurate localization of a unilateral adrenal mass in each of the dogs. Cross-sectional diameters of the masses ranged from 1 to 4 cm. In 1 dog, expansion of tumor into the caudal vena cava was revealed by caudal venacavography and ultrasonography. Mineralization in the tumor mass in 2 dogs was easily recognized by nephrotomography, but not by ultrasonography. Paracostal laparotomy confirmed the presence of an adrenocortical tumor in each dog, and expansion of tumor into the caudal vena cava in 1 dog. Cross-sectional diameters of the tumors ranged from 1.2 to 4.5 cm and corresponded well with cross-sectional measurements by nephrotomography and ultrasonography. It was concluded that nephrotomography and ultrasonography have similar diagnostic accuracies for the detection and localization of hyperfunctioning adrenocortical tumors.
Adrenal Cortex Neoplasms↗
Corticosteroid-induced alkaline phosphatase isoenzyme in the diagnosis of canine hypercorticism.
Corticosteroid-induced isoenzyme of alkaline phosphatase (AP) can easily be demonstrated in canine plasma as a routine procedure because of its greater heat stability at 65 degrees C in comparison with that of other AP-isoenzymes. In this study the accuracy of this test for the diagnosis of hypercorticism was investigated. The AP-65 degrees C test had its highest efficiency when applied to plasma AP levels exceeding 150 units/litre. In a group of 146 dogs, clinically suspected of having hyperadrenocorticism, the test had a sensitivity of 0.92 and a positive predictive value for a positive test result of 0.89. Its lack of specificity (0.44) makes it unsuitable as a diagnostic test. The main application of AP-65 degrees C is in detecting hypercorticism in dogs by routine laboratory measurements, as was demonstrated in 711 dogs, in which a positive predictive value for the presence of hypercorticism of 0.89 was found.
Adrenocortical Hyperfunction↗