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1.
Summary

In a 10‐year‐old ovariohysterectomized standard Schnauzer, the finding of dexamethasone‐resistant hypersecretion of cortisol, the results of computed tomography, and elevated plasma concentrations of ACTH suggested the presence of both adrenocortical tumour and pituitary‐dependent hyperadrenocorticism. The dog made an uneventful recovery after bilateral adrenalectomy and remained in good health for 31/2 years with substitution for the induced hypoadrenocorticism. Then the enlarged pituitary caused neurological signs and eventually euthanasia was performed. The surgically excised right adrenal contained a well‐circumscribed tumour of differentiated adrenocortical tissue and in the left adrenal there were two adrenocortical tumours and a pheochromocytoma. The unaffected parts of the adrenal cortices were well developed and without regressive transformation. At necropsy there were no metastatic lesions. The cells of the pituitary tumour were immunopositive for ACTH and had characteristics of malignancy.

The present combination of corticotrophic tumour, adrenocortical tumours, and pheochromocytoma may be called ‘multiple endocrine neoplasia’ (MEN), but does not correspond to the inherited combinations of diseases known in humans as the MEN‐1 and the MEN‐2 syndromes. It is suggested that the co‐existence of hyperadrenocorticism and pheochromocytoma may be related to the vascular supply of the adrenals. Some chromaffin cells of the adrenal medulla are directly exposed to cortical venous blood, and intra‐adrenal cortisol is known to stimulate catecholamine synthesis and may promote adrenal medullary hyperplasia or neoplasia.  相似文献   

2.
In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess.Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased.The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects.Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.  相似文献   

3.
Summary

A total of 38 adrenocortical tumours were removed from 36 dogs with hyperadrenocorticism. The surgical approach was by way of a unilateral flank laparotomy (32 dogs; 14 left and 18 right), a bilateral flank laparotomy (3 dogs) or a midline celiotomy (1 dog).

Two dogs were euthanized during surgery because their tumours could not be resected. Eight dogs died from post‐operative complications. Pancreatic necrosis with peritonitis was the most common cause of death. Eight of the 26 dogs that survived had signs of recurrence of hyperadrenocorticism. Unsuppressible hyperadrenocorticism was found in four dogs; one dog had probably pre‐existent pituitary‐dependent hyperadrenocorticism, and adrenocortical function could not be re‐examined in the remaining three dogs.

Among the 37 tumours examined microscopically expansion of neoplastic tissue into blood vessels was found in 22 of them. Four adrenal glands with adrenocortical tumours also contained phaeochromocytomas. Necropsy was performed in eight dogs. Metastases were found in the lungs of two dogs and in the lungs and liver in one dog.

In combination with the data of previous reports, it is suggested that histological findings in surgery specimens are not good predictors for the clinical outcome.  相似文献   

4.
Congenital central hypothyroidism was diagnosed in a one-year-old boxer dog. The dog was presented for investigation of lameness, lethargy and obesity. Survey skeletal radiographs revealed delayed bone maturation and epiphyseal dysgenesis. A diagnosis of hypothyroidism was confirmed on the basis of a low basal serum thyroxine (T4) concentration that failed to increase following bovine thyroid stimulating hormone (TSH) administration. However, repeated administration of TSH resulted in reactivation of the thyroid gland suggesting a central rather than a primary problem. Consistently low basal plasma Cortisol concentrations were suggestive of a concurrent secondary or tertiary hypoadrenocorticism. Surprisingly, plasma growth hormone concentrations were elevated before treatment but decreased once thyroid replacement therapy had commenced.  相似文献   

5.
The objectives of this study were first to show adrenocortical response to a long‐acting adrenocorticotropic hormone preparation (tetracosactide acetate zinc suspension) (ACTH‐Z) and its effect on adrenocortical function in beef cows ( Experiment 1 ) and second to apply the ACTH‐Z challenge in dairy cows based on cortisol concentrations in milk collected at routine milking ( Experiment 2 ). In Experiment 1 , four beef cows in luteal phase were challenged with ACTH‐Z, and plasma cortisol concentrations were determined for 48 h after the injection at 30‐min to 2‐h intervals. A rapid ACTH test was conducted 3 days before and 2 h after the completion of ACTH‐Z injection for 48 h to investigate the effect on adrenocortical function. Plasma cortisol concentrations increased significantly 30 min after ACTH‐Z injection (p < 0.001), and the high cortisol levels were maintained for approximately 10 h after the injection. In Experiment 2 , eight dairy cows were subjected to ACTH‐Z challenge 1–2 weeks and 4–5 weeks post‐partum. Blood and milk samples were taken at morning and afternoon milking. All the cows showed a significant increase in cortisol concentrations in plasma as well as in skim milk 8 h after ACTH‐Z injection 1–2 weeks and 4–5 weeks post‐partum (p < 0.001). There was a significant correlation between plasma and skim milk cortisol concentrations 8 h after ACTH‐Z challenge (r = 0.74, p < 0.001). The results obtained in this study suggest that elevated levels of plasma cortisol are maintained for approximately 10 h after ACTH‐Z treatment without adverse effect on adrenocortical function and a long‐acting ACTH‐Z challenge based on cortisol concentrations in milk, which were collected at the morning and the afternoon milking, can be a useful tool to monitor adrenocortical function in cows.  相似文献   

6.
A four-year-old Labrador retriever was presented with lethargy and exercise intolerance. Clinical examination was unremarkable. A subnormal Cortisol response to adrenocorticotrophin hormone (ACTH) was demonstrated (plasma Cortisol concentrations before and after administration of ACTH were both below the detection limit of the assay) but plasma aldosterone concentrations were within the normal range. Endogenous plasma ACTH concentrations were high, indicating primary adrenocortical disease. Following glucocorticoid supplementation at a replacement dose (prednisolone 0.1 mg/kg) the dog made a full clinical recovery.  相似文献   

7.
We evaluated the effect of ovine corticotropin-releasing hormone (CRH) on plasma immunoreactive (IR) concentrations of ACTH, alpha-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma IR-ACTH concentrations, which failed to increase after administration of CRH. Basal plasma alpha-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by CRH administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of CRH. Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma IR-ACTH concentrations and exaggerated responses to CRH, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of IR-ACTH that did not increase after stimulation with CRH.  相似文献   

8.
Summary

Water balance studies were performed in 7 experimental dogs before and during a period of cortisol‐induced polyuria and in one dog with spontaneous hyperadrenocorticism before and after removal of an adrenocortical carcinoma. Measurements of urine and plasma osmolality and plasma arginine vasopressin concentration were made at regular intervals during the water deprivation studies. The results indicate that cortisol does not block the release of vasopressin but interferes with its action in the kidney.  相似文献   

9.
Summary

A review is given of the available literature concerning the relationship between the bovine pituitary‐adrenocortical axis and milk yield in dairy cattle. A severe drop in milk yield (more than 50%) can be induced by a single or repeated intramuscular injection of at least 200 IU ACTH or by a single intramuscular injection of 14.6 mg dexamethasone. Sixty minutes after an intravenous injection, both 200 IU ACTH and 100 mg cortisol are equivalent to a plasma cortisol concentration of at least 31 ng/ml. Thus the decrease in milk yield after an intramuscular injection of more than 200 IU ACTH can hardly be induced by cortisol only. The fact that bovine plasma hardly binds any dexamethasone, in sharp contrast with bovine mammary epithelial tissue, is a possible explanation of the special part which dexamethasone plays in milk yield.  相似文献   

10.

Background

Thyrotropin (TSH) can be increased in humans with primary hypoadrenocorticism (HA) before glucocorticoid treatment. Increase in TSH is a typical finding of primary hypothyroidism and both diseases can occur concurrently (Schmidt's syndrome); therefore, care must be taken in assessing thyroid function in untreated human patients with HA.

Objective

Evaluate whether alterations in cTSH can be observed in dogs with HA in absence of primary hypothyroidism.

Animals

Thirty dogs with newly diagnosed HA, and 30 dogs in which HA was suspected but excluded based on a normal ACTH stimulation test (controls) were prospectively enrolled.

Methods

cTSH and T4 concentrations were determined in all dogs and at selected time points during treatment (prednisolone, fludrocortisone, or DOCP) in dogs with HA.

Results

cTSH concentrations ranged from 0.01 to 2.6 ng/mL (median 0.29) and were increased in 11/30 dogs with HA; values in controls were all within the reference interval (range: 0.01–0.2 ng/dL; median 0.06). There was no difference in T4 between dogs with increased cTSH (T4 range 1.0‐2.1; median 1.3 μg/dL) compared to those with normal cTSH (T4 range 0.5‐3.4, median 1.4 μg/dL; P=0.69) and controls (T4 range 0.3‐3.8, median 1.8 μg/dL; P=0.35). After starting treatment, cTSH normalized after 2–4 weeks in 9 dogs and after 3 and 4 months in 2 without thyroxine supplementation.

Conclusions and Clinical Relevance

Evaluation of thyroid function in untreated dogs with HA can lead to misdiagnosis of hypothyroidism; treatment with glucocorticoids for up to 4 months can be necessary to normalize cTSH.  相似文献   

11.
The plasma cortisol response to exogenous ACTH (ACTH stimulation test) was evaluated in 22 dogs with hyperadrenocorticism caused by adrenocortical neoplasia. The mean basal cortisol concentration (6.3 microgram/dl) was high, but 7 dogs had basal cortisol concentrations that were within normal range. Administration of exogenous ACTH increased the plasma cortisol concentrations in each dog. Normal post-ACTH cortisol concentrations were found in 9 (41%) of the 22 dogs; 13 (59%) had an exaggerated increase in cortisol concentrations after ACTH administration. In 9 of 13 dogs with carcinoma and in 4 of 9 with adenoma, the cortisol response was exaggerated. The mean post-ACTH cortisol concentration in the dogs with carcinoma was approximately 4 times that of the dogs with adenoma; the 7 dogs with the highest concentrations had carcinoma. Repeat studies were performed in 6 dogs 2 to 8 weeks after initial testing. In 5 of the 6 dogs, repeat testing yielded data of similar diagnostic significance. One dog, however, had an abnormally high post-ACTH cortisol concentration at initial evaluation, but had only a minimal response to ACTH administration, with a normal post-ACTH cortisol concentration, at time of resting. Although ACTH stimulation testing is useful in diagnosing hyperadrenocorticism, it can not reliably separate dogs with hyperfunction adrenocortical tumors from clinically normal dogs or from dogs with pituitary-dependent hyperadrenocorticism (bilateral adrenocortical hyperplasia).  相似文献   

12.
The utility of a low dose (1 microgram/kg) synthetic ACTH challenge test in detecting moderate reductions in adrenocortical sensitivity in dogs was examined. First, the adrenocortical responses to an intravenous bolus of either 1 microgram/kg or 0.25 mg per dog of synthetic ACTH were compared in two groups of normal dogs. While plasma cortisol concentrations were similar in both groups 60 minutes after ACTH injection, dogs given 0.25 mg ACTH showed continued elevations in plasma cortisol concentrations at 90 and 120 minutes after ACTH injection. Later, the dogs previously tested with the 1 microgram/kg ACTH challenge were given a single intramuscular dose of prednisone (2.2 mg/kg) and retested with 1 microgram/kg of ACTH one week later. Plasma cortisol levels were significantly reduced after ACTH injection in dogs previously given prednisone demonstrating that a single intramuscular prednisone dose causes detectable adrenocortical suppression one week after administration. The 1 microgram/kg synthetic ACTH challenge test provides a sensitive means for evaluating adrenocortical suppression in dogs.  相似文献   

13.
Summary

ACTH (μg kg ‐1 i.v.) and prednisolone (1 μg‐1 i.v.) caused a moderate but statistically significant inhibition of rumen contractions, whereas no effects on heart rate and body temperature were observed. Both hormones induced hyperglycaemia and leucocytosis, characterised by moderate lymphopenia and a profound increase in the number of circulating neutrophils. A significant decrease in plasma iron and increase in plasma zinc concentrations were observed.

After 3 daily i.m. injections of ACTH (10 μg ‐1 day ‐1) decreases were seen in both serum Alkaline phosphatase (ALP) activity and plasma trace metal concentrations; heart rate was significantly higher. Intraveneous injection of E. coli endotoxin (0.1 μg kg ‐1) caused shivering, fever, inhibition of rumen contractions, changes in heart rate, lymphopenia, neutropenia followed by neutrophilic leucocytosis, hypoferraemia, hypozincaemia, hypoglycaemia and a decline in serum ALP activity. ACTH, given for 3 days, reduced the febrile responses to E. coli endotoxin, modified the changes in heart rate, intensified the inhibition of rumen contractions, and induced a more marked decrease in the number of circulating neutrophils. ACTH pretreatment did not affect the endotoxin‐induced decrease in blood glucose concentrations nor the drop in plasma zinc and iron values.

These results suggest that (1) glucocorticosteroids are not primarily involved in the fall in plasma iron and zinc concentrations during E. coli endotoxin‐induced fever, (2) the effects of endotoxin released glucocorticosteroids on white blood cells and blood glucose are masked by some other effect(s) of endotoxin, and (3) in dwarf goats, ACTH has antipyretic properties without influencing normal body temperature. This effect is probably not dependent on adrenal cortical activity.  相似文献   

14.
The adrenocortical (plasma corticosteroid) responses in female dogs given porcine ACTH in gelatin (1-39 amino acid sequence) and synthetic ACTH (1-24 amino acid sequence) were compared. Sixteen dogs were used. Each dog underwent 4 different ACTH stimulation studies, these being done with a 4- to 8-week interval. The studies in each dog included injections of 2 doses of porcine ACTH--2.2 IU and 4.4 IU/kg of body weight--and of 2 doses of synthetic ACTH--0.25 mg/dog and 0.50 mg/dog. The dogs were arbitrarily allotted to 4 groups, each group being subjected to a given sequence of stimulation studies. The purpose in this project was to determine whether the established methods for synthetic and porcine ACTH stimulation tests had similar results. Statistical analysis of the 4 stimulation methods revealed no significance (P greater than 0.05) in the resting or poststimulation plasma corticosteroid concentrations. Thus, it was concluded that either recommended method using ACTH (porcine ACTH at 2.2 IU/kg or synthetic ACTH at 0.25 mg/dog) causes maximal secretion of adrenocortical reserve. Either ACTH preparation, using the established method, can be used interchangeably.  相似文献   

15.
BACKGROUND: Differentiation between hypothyroidism and nonthyroidal illness in dogs poses specific problems, because plasma total thyroxine (TT4) concentrations are often low in nonthyroidal illness, and plasma thyroid stimulating hormone (TSH) concentrations are frequently not high in primary hypothyroidism. HYPOTHESIS: The serum concentrations of the common basal biochemical variables (TT4, freeT4 [fT4], and TSH) overlap between dogs with hypothyroidism and dogs with nonthyroidal illness, but, with stimulation tests and quantitative measurement of thyroidal 99mTcO4(-) uptake, differentiation will be possible. ANIMALS: In 30 dogs with low plasma TT4 concentration, the final diagnosis was based upon histopathologic examination of thyroid tissue obtained by biopsy. Fourteen dogs had primary hypothyroidism, and 13 dogs had nonthyroidal illness. Two dogs had secondary hypothyroidism, and 1 dog had metastatic thyroid cancer. METHODS: The diagnostic value was assessed for (1) plasma concentrations of TT4, fT4, and TSH; (2) TSH-stimulation test; (3) plasma TSH concentration after stimulation with TSH-releasing hormone (TRH); (4) occurrence of thyroglobulin antibodies (TgAbs); and (5) thyroidal 99mTcO4(-) uptake. RESULTS: Plasma concentrations of TT4, fT4, TSH, and the hormone pairs TT4/TSH and fT4/TSH overlapped in the 2 groups, whereas, with TgAbs, there was 1 false-negative result. Results of the TSH- and TRH-stimulation tests did not meet earlier established diagnostic criteria, overlapped, or both. With a quantitative measurement of thyroidal 99mTcO4(-) uptake, there was no overlap between dogs with primary hypothyroidism and dogs with nonthyroidal illness. CONCLUSIONS AND CLINICAL IMPORTANCE: The results of this study confirm earlier observations that, in dogs, accurate biochemical diagnosis of primary hypothyroidism poses specific problems. Previous studies, in which the TSH-stimulation test was used as the "gold standard" for the diagnosis of hypothyroidism may have suffered from misclassification. Quantitative measurement of thyroidal 99mTcO- uptake has the highest discriminatory power with regard to the differentiation between primary hypothyroidism and nonthyroidal illness.  相似文献   

16.
Effects of etomidate on adrenocortical function in canine surgical patients   总被引：1，自引：0，他引：1  
Adrenocortical function in canine surgical patients given etomidate at 1 of 2 dosages (1.5 mg/kg of body weight or 3 mg/kg, IV) was evaluated and compared with that of dogs given thiopental (12 mg/kg, IV). The adrenocortical function was evaluated by use of adrenocorticotropic hormone (ACTH) stimulation tests and determination of plasma cortisol concentrations at 0 minute (base line) and 60 minutes after ACTH administration. At 24 hours before administration of either drug (ie, induction of anesthesia), each dog had an increase in plasma cortisol concentration when given ACTH. The ACTH stimulation tests were repeated 2 hours after induction of anesthesia. Dogs given thiopental had base-line plasma cortisol concentrations greater than preinduction base-line values, but did not increase plasma cortisol in response to ACTH stimulation. Postinduction ACTH stimulation tests in dogs given etomidate at either dose indicated base-line and 60-minute plasma cortisol concentrations that were not different from preinduction base-line values. Therefore, adrenocortical function was suppressed 2 and 3 hours after the administration of etomidate in canine surgical patients.  相似文献   

17.
Objective : To assess the value of thyroid scintigraphy to determine thyroid status in dogs with hypothyroidism and various non‐thyroidal illnesses. Methods : Thyroid hormone concentrations were measured and quantitative thyroid scintigraphy performed in 21 dogs with clinical and/or clinicopathological features consistent with hypothyroidism. Results : In 14 dogs with technetium thyroidal uptake values consistent with euthyroidism, further investigations supported non‐thyroidal illness. In five dogs with technetium thyroidal uptake values within the hypothyroid range, primary hypothyroidism was confirmed as the only disease in four. The remaining dog had pituitary‐dependent hyperadrenocorticism. Two dogs had technetium thyroidal uptake values in the non‐diagnostic range. One dog had iodothyronine concentrations indicative of euthyroidism. In the other, a dog receiving glucocorticoid therapy, all iodothyronine concentrations were decreased. Markedly asymmetric technetium thyroidal uptake was present in two dogs. All iodothyronine concentrations were within reference interval but canine thyroid stimulating hormone concentration was elevated in one. Non‐thyroidal illness was identified in both cases. Clinical Significance : In dogs, technetium thyroidal uptake is a useful test to determine thyroid function. However, values may be non‐diagnostic, asymmetric uptake can occur and excess glucocorticoids may variably suppress technetium thyroidal uptake and/or thyroid hormone concentrations. Further studies are necessary to evaluate quantitative thyroid scintigraphy as a gold standard method for determining canine thyroid function.  相似文献   

18.
Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350 x 10(-6); reference range < 10 x 10(-6)). The UCCR remained elevated (226 x 10(-6)) after three oral doses of dexamethasone (0.1 mg/kg body weight) at 8-h intervals. Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia. Plasma ACTH concentration was clearly elevated (159 and 188 ng/l; reference range 5-85 ng/l). Computed tomography (CT) revealed that the pituitary was not enlarged. These findings were interpreted as indicating dexamethasone-resistant pituitary-dependent hyperadrenocorticism. Transsphenoidal hypophysectomy was performed but within 2 weeks after surgery, there was exacerbation of the clinical signs of hyperadrenocorticism. Plasma ACTH concentration (281 ng/l) and UCCRs (1518 and 2176 x 10(-6)) were even higher than before surgery. Histological examination of the pituitary gland revealed no neoplasia. Stimulation of the pituitary with corticotropin-releasing hormone did not affect plasma ACTH and cortisol concentrations. Treatment with trilostane was started and restored normocorticism. CT of the pituitary fossa, 10 months after hypophysectomy, revealed an empty sella. Hence, it was presumed that there was ectopic secretion of ACTH. CT of the abdomen revealed a mass in the region of the pancreas and a few nodules in the liver. Partial pancreatectomy with adjacent lymph node extirpation was performed and the liver nodules were biopsied. Histological examination revealed a metastasized neuroendocrine tumor. Abdominal surgery was not curative and medical treatment with trilostane was continued. At 18 months after the abdominal surgery, the dog is still in good condition. In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.  相似文献   

19.
A 11‐year‐old male neutered Shih Tzu was referred to a tertiary facility with a history of weight loss, decreased appetite, polydipsia, and lethargy. The dog had a 10‐year history of nonspecific allergic dermatitis and was being treated with 16 mg/kg of ketoconazole q12h for Malassezia dermatitis. Vague gastrointestinal signs, hypocholesterolemia, and lack of a stress leukogram increased suspicion for hypoadrenocorticism (HA). An adrenocorticotropic hormone (ACTH) stimulation test identified hypocortisolemia on pre‐ and post‐ACTH samples and ketoconazole was discontinued. After a short course of corticosteroid treatment, an ACTH stimulation test was repeated and pre‐ACTH cortisol concentration was within the reference range, and the post‐ACTH cortisol concentration was mildly increased. The temporal association between return of adequate adrenocortical cortisol production and discontinuation of ketoconazole led to the conclusion that the dog had developed iatrogenic HA secondary to ketoconazole treatment.  相似文献   

20.
Abstract

Administration of progestins in the dog may result in overproduction of growth hormone, suppression of the hypothalamic‐pituitary‐adrenocortical axis, and insulin resistance. In this paper we present a comparison of the histological findings in control dogs and dogs treated with either medroxyprogesterone acetate (MPA) or proligestone (PROL).

Depot preparations of MPA or PROL were administered (SC) at 3‐week intervals in two groups of seven ovariohysterectomized beagle dogs, after which three dogs of each group were killed. After a 6‐month period without hormone treatment during which recovery was studied, the remaining dogs received five additional injections at the same interval and were subsequently killed. Tissue samples of four intact female beagle dogs served as controls.

Progestin treatment resulted in atrophy of the adrenal cortex. In both MPA‐ and PROL‐treated dogs, the thickness of the combined zona fasciculata and reticularis was significantly smaller than in control animals. In the mammary glands of progestin‐treated dogs there were well developed alveoli and normal ducts adjacent to foci of hyperplastic ductular epithelium. Five dogs in each treatment group had developed benign mammary tumours which varied from simple tubular and papillary adenomas to benign complex and mixed tumours, whereas no mammary tumours were observed in the control animals. In each treatment group, steroid‐induced hepatopathy was observed in the liver of three dogs. Vacuolation of the cells of the islets of Langerhans and the epithelium of the intercalated ducts was present in two dogs of each treatment group and was only observed after the second series of progestin administrations. Incidental findings included chronic pyelonephritis, aspecific dermatitis, and mucinous dysplasia of the gall bladder. No abnormalities were found in sections of spleen, lung, brain, or pituitary gland.

There were no significant differences in the frequencies of the various abnormalities between MPA‐ and PROL‐treated dogs. Our findings correspond with the clinical and biochemical results after treatment of dogs with MPA and PROL. The high incidence of mammary tumours might be associated with our recent finding that in the dog progestins induce ectopic production of growth hormone in the mammary gland. The dog might be a good model for further studies on hormonally induced breast cancers.  相似文献   

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