Premature adrenarche in indentical twins.
Monozygotic female twins with premature adrenarche are reported. Endocrine work-up excluded the existence of an endocrinopathy or a tumor.
Adrenocortical Hyperfunction↗
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17-Hydroxyprogesterone in normal children and congenital adrenal hyperplasia. Measurement in serum by radioimmunoassay after thin-layer chromatography.
Serum 17alpha-hydroxyprogesterone (17 OH-P) was measured by a specific radioimmunoassay technique combined with thin-layer chromatography. Normal values for children are less than 1.1 microgram/1 (less than 3.3 nmol/l)--corresponding to values found in the literature. In congenital adrenal hyperplasia (CAH) values up to several hundred microgram/l are found. The values rise after ACTH stimulation and are suppressed by decadrone or cortisone treatment. The rise in 17 ketosteroids and pregnanetriol in untreated CAH is relatively smaller (15--25 fold). This clinical sensitivity of 17 OH-P is thus valuable for the diagnosis of CAH (21 hydroxylase deficiency). Furthermore it is easier to take a blood sample than to collect urine for 24 hours. The usefulness in therapeutic monitoring is being studied.
17-Ketosteroids↗
Hypoglycaemia and congenital adrenal hyperplasia.
We report the case history of a child with congenital adrenal hyperplasia which was complicated by recurrent hypoglycaemic episodes during common infections. There are few reports in literature on the association of hypoglycaemia and congenital adrenal hyperplasia. In accordance with others, we believe that hypoglycaemic attacks in adrenal hyperplasia are perhaps more frequent than recorded in literature.
Adrenal Hyperplasia, Congenital↗
Loperamide test: a simple and highly specific screening test for hypercortisolism in children and adolescents.
The overnight dexamethasone (DXM) test can give false-positive results in a few conditions (e.g. stress, strenuous exercise, depression, anorexia, anxiety, anticonvulsive therapy) in diagnosing simple obesity and hypercortisolism (HC). The loperamide (LP; a peripheral opioid agonist) test has proven useful in such conditions in adults. Thirty-one obese subjects (age 10.0-19.7 y) were studied by both overnight DXM test and LP test (8 mg orally, samples for cortisol at 0, 90, 150, 180 and 210 min) on 2 separate days. LP suppressed cortisol (< or = 138 nmol l-1) at a dose of 0.1 mg kg-1 bw (half the minimum recommended dose for the drug's antidiarrhoea effect) in 14 subjects who had normal urinary (< 4970 nmol l-1) and serum (< 552 nmol l-1) cortisol, in the absence of signs and symptoms of HC (group A). The DXM test failed to suppress cortisol in three subjects in group A, two of whom were on anticonvulsive treatment. The LP test suppressed cortisol in all of 13 subjects with elevated urinary and/or serum cortisol and/or with signs or symptoms of HC (but in whom HC was subsequently excluded on clinical grounds) (group B), while the DXM test failed to suppress cortisol in three subjects of this group. One of these was under anticonvulsive treatment and one suffered from anxiety and depression. In four patients with Cushing's syndrome (group C) neither DXM nor LP could suppress cortisol levels. Therefore, the sensitivity was 100% for both DXM and LP, while the specificity was 84% for DXM and 100% for LP. No side-effects were observed with either drug. In conclusion, LP is a useful alternative to DXM in those particular conditions that can affect its specificity in children.
Adolescent↗
Changes in ultrasonographic appearance of adrenal glands in dogs with pituitary-dependent hyperadrenocorticism treated with trilostane.
Trilostane, a 3beta-hydroxysteroid dehydrogenase inhibitor, has been used successfully over the last few years for the treatment of canine pituitary-dependent hyperadrenocorticism. In a prospective study of 19 dogs with pituitary-dependent hyperadrenocorticism, the adrenal glands were measured before and at least 6 months after initiation of trilostane therapy. Right adrenal gland length and caudal pole thickness and left adrenal gland caudal pole thickness increased significantly (p < or = 0.05); there was no significant change in left adrenal gland length. Enlargement of adrenal glands during trilostane therapy may occur as a result of suppression of the negative feedback mechanism affecting cortisol production.
3-Hydroxysteroid Dehydrogenases↗
Three cases of alopecia in the dog related to adrenocortical dysfunction.
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Adenoma↗
Efficacy of daily amitraz on generalised demodicosis in dogs.
Fifty dogs with generalised demodicosis were treated with daily applications of 0.125 per cent amitraz solution over half the body. This was applied once a day, alternating the body half treated. Nine dogs were lost to follow-up; the remaining dogs were classified as either a success (25 dogs, 61 per cent) or a failure (16 dogs, 39 per cent) according to their response to treatment. Eight of the failures were due to persistent demodicosis and eight relapsed within one year after treatment. All eight of the relapsed dogs were cured after a second course of daily amitraz treatment. For the 25 dogs considered treatment successes, the median duration of treatment was 6.5 weeks (range, three weeks to nine months), and the median interval from completion of treatment to last post treatment evaluation was 3.4 years (range, two to four-and-a-half-years). Including the eight dogs that were cured after retreatment, the daily amitraz applications were curative in 33 of 41 dogs (80 per cent) with generalised demodicosis.
Administration, Topical↗
Mitotane (o,p'-DDD) treatment in a cat with hyperadrenocorticism.
An 11-year-old male castrated Persian cat with spontaneous hyperadrenocorticism was presented. Both adrenals were grossly enlarged and calcified. A diagnosis of pituitary-dependent hyperadrenocorticism was made. Signs of hyperadrenocorticism resolved with long-term mitotane treatment. Concurrent diabetes mellitus resolved after 220 days of therapy. No severe adverse drug reactions were noted.
Adrenal Cortex↗
Evaluation of the urinary cortisol: creatinine ratio in the diagnosis of hyperadrenocorticism in dogs.
The diagnostic accuracy of the urinary cortisol:creatinine ratio (CCR), with the cortisol being measured by ELISA, was evaluated by subjecting data from 18 dogs with and 20 dogs without hyperadrenocorticism to receiver operating characteristic (ROC) curve analysis. The area under the ROC curve (W 0.93, SE(w) 0.044) was much higher than 0.5, indicating that the CCR did distinguish between dogs with and without hyperadrenocorticism. A cutoff value of about 60 x 10(-6) was associated with the highest sensitivity (1.0) and specificity (0.85). At the disease prevalence rate of the present study (0.47), the positive and negative predictive values were 0.87 and 1.0, respectively. These numbers indicate that canine hyperadrenocorticism may be safely excluded when the CCR is below 60 x 10(-6) but that a test of higher specificity (eg, the ACTH stimulation test) should be used to confirm the diagnosis of canine hyperadrenocorticism when the CCR is above 60 x 10(-6).
Adrenocortical Hyperfunction↗
Hyperadrenocorticism in six cats.
The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had diabetes mellitus on presentation. Abdominal radiographs revealed an adrenal mass in one case, obesity in all cases but no hepatomegaly. The adrenal glands were identified ultrasonographically in three out of six cases. Clinicopathological findings were non-specific. The diabetic cats had a significantly lower serum potassium concentration than the non-diabetic cats (P < 0.05). Results of adrenocorticotrophic hormone (ACTH) stimulation tests were supportive of a diagnosis of hyperadrenocorticism in the five cats in which they were performed. Five cats had pituitary-dependent hyperadrenocorticism (PDH) and one had an adrenal tumour. Differentiation between the two forms of hyperadrenocorticism was possible preoperatively in five out of six cats. Adrenal histopathology confirmed hyperplasia in four cats and adenocarcinoma in one cat. Three cats with PDH underwent bilateral adrenalectomy and two of these cats had low, flat ACTH stimulation tests postoperatively and survived for significant periods. The cat with an adrenal tumour underwent partial unilateral adrenalectomy, maintained a positive ACTH stimulation test postoperatively and was euthanased one week after surgery.
Adrenal Cortex Function Tests↗
Aortic and iliac thrombosis in six dogs.
Six dogs had signs of pelvic limb weakness, pain and collapse as a result of occlusion of the distal aorta and/or the iliac arteries by a thrombus. Antemortem diagnosis was made on the basis of clinical signs, angiography and ultrasonography. Five dogs had concurrent disease that probably predisposed to thrombosis, including hyperadrenocorticism (three dogs), neoplasia and cardiac disease. Two dogs died shortly after the episode of thrombosis. Dogs that survived the acute episode received aspirin in an attempt to prevent thrombosis occurring again and all regained pelvic limb function. For dogs that survived longer than one month after the acute episode, repeat thrombosis was uncommon; hence the prognosis was related to the underlying disease. Aortic and iliac thrombosis in dogs is an uncommon condition that usually arises secondarily to a predisposing disease process; it carries a more favourable prognosis than feline aortic thromboembolism.
Adrenocortical Hyperfunction↗
Cortisol concentrations following stimulation of healthy and adrenopathic dogs with two doses of tetracosactrin.
A prospective study was undertaken to compare intravenous tetracosactrin at doses of 5 microg/kg and 250 microg for diagnosing hyperadrenocorticism in dogs. Both healthy dogs and dogs with pituitary-dependent hyperadrenocorticism were evaluated with the two doses of the drug, and serum cortisol concentrations were compared at 60 minutes post-stimulation. Some of the dogs had additional samples taken at 90 and 120 minutes. For four dogs with hyperadrenocorticism, timed samples were also obtained at 150, 180 and 240 minutes post-injection. Cortisol concentrations 60 minutes after stimulation with either 5 microg/kg or 250 microg intravenous tetracosactrin were similar for both healthy dogs and dogs with hyperadrenocorticism. The lower dose can therefore be used for diagnosing hyperadrenocorticism in dogs.
Adrenocortical Hyperfunction↗
Osteopenia and other radiographic signs in canine hyperadrenocorticism.
The specificity of conventional radiography in assessing canine hyperadrenocorticism was evaluated by comparing the Incidence of related radiographic findings in 24 hyperadrenocorticoid, 15 diabetic and 20 hypothyroid dogs. Hyperadrenocorticoid dogs showed significantly more perihilar bronchial mineralisation than other groups. There was no significant variation between the disease groups with respect to obesity, hepatomegaly, contour of the caudoventral hepatic margin, peripheral bronchial mineralisation or osteopenia. Adrenal mineralisation and calcinosis cutis were rare findings observed only in hyperadrenocorticoid dogs. The effect of obesity on the radiographic appearance of bone was studied using a dissected lumbar spine from a canine cadaver. An osteopenic effect could be demonstrated by superimposition of a 10 cm-thick fat block. The low specificity of almost all common signs in canine hyperadrenocorticism and the low incidence of characteristic findings demonstrate the limited potential of radiography in assessing this condition. Radiographic assessment of bone density is unreliable because of artefactual osteopenic effects of high kVp settings necessary in obese dogs.
Adrenocortical Hyperfunction↗
Use of endogenous ACTH concentration and adrenal ultrasonography to distinguish the cause of canine hyperadrenocorticism.
Twenty-nine dogs were diagnosed with hyperadrenocorticism (HAC). A single determination of endogenous plasma adrenocorticotropic hormone (ACTH) and adrenal ultrasonography were used in a prospective study to differentiate between pituitary-dependent HAC (PDH) and adrenal-dependent HAC (ADH). In 27 out of the 29 dogs (93 per cent), both endogenous plasma ACTH concentrations and adrenal ultrasonography indicated the same cause of HAC. Twenty-one of the 29 cases (72 per cent) were shown to be pituitary-dependent; all had plasma ACTH concentrations of greater than 28 pg/ml (reference range 13 to 46 pg/ml) and both adrenal glands were ultrasonographically of similar size and of normal shape. All 21 cases responded well to mitotane therapy. Six cases (21 per cent) were shown to be adrenal-dependent; all had plasma ACTH concentrations below the limit of the assay (<5 pg/ml) and the presence of an adrenal mass on ultrasonography. The sensitivity and specificity of adrenal ultrasonography and endogenous ACTH determinations to identify the cause of HAC were demonstrated to be 100 per cent and 95 per cent, respectively, for ADH. These discriminatory tests are more accurate than published figures for dexamethasone suppression testing.
Adrenal Glands↗
Investigation of the role of aldosterone in hypertension associated with spontaneous pituitary-dependent hyperadrenocorticism in dogs.
The aim of this study was to evaluate the role of aldosterone as an initiating and/or perpetuating factor in hypertension associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Thirteen dogs with PDH and 11 healthy control dogs were used. In all dogs, arterial blood pressure and plasma sodium, potassium, basal aldosterone, post-ACTH aldosterone, basal cortisol and post-ACTH cortisol concentrations were measured. The tests were repeated 10 days and three months after the beginning of o,p'-DDD treatment in PDH dogs. In untreated PDH dogs, plasma aldosterone was significantly decreased, whereas cortisol, sodium and arterial blood pressure were significantly increased compared to healthy dogs. Hypertension remained in most treated PDH dogs despite normalisation of cortisol and persistently low aldosterone levels. These results did not demonstrate that aldosterone is involved in the development and perpetuation of hypertension in PDH. However, glucocorticoids seemed to play a major role as an initiating and perpetuating factor in PDH in dogs.
Adrenocortical Hyperfunction↗
Use of aminoglutethimide in the treatment of pituitary-dependent hyperadrenocorticism in the dog.
The aim of this study was to evaluate the efficacy and safety of aminoglutethimide in the treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). Ten dogs were diagnosed with PDH based on clinical and laboratory data, adrenal function tests (adrenocorticotropic hormone [ACTH] stimulation test and urinary cortisol/creatinine ratio [UCCR] combined with a high dose oral dexamethasone suppression test) and ultrasonographic evaluation of the adrenal glands. Aminoglutethimide was administered daily at a dose of 15 mg/kg bodyweight for one month. Median basal cortisol concentration and post-ACTH cortisol concentration one month after treatment were significantly lower than pretreatment values. Complete response was achieved in one dog, and partial response was obtained in three dogs. Severe side effects of anorexia, vomiting and weakness occurred in one dog and medication was withdrawn. Two further dogs developed decompensations of concurrent diseases and medication was stopped in these animals as well. Mild toxicity occurred in four dogs. Moderate to severe elevations in liver enzymes occurred in all dogs. The efficacy of this drug is lower than that observed using mitotane and ketoconazole, and adverse effects limit its use. Aminoglutethimide, using the protocol described, cannot be recommended for long-term management of PDH in the dog.
Adrenal Glands↗
Trilostane treatment of a dog with functional adrenocortical neoplasia.
A 13-year-old, crossbreed dog presented with a history of recent onset polydipsia, progressive lethargy, weakness and reduced appetite. Blood tests showed raised concentrations of alkaline phosphatase and alanine aminotransferase with marginally low serum potassium. There was a leucocytosis with a mature neutrophilia and no eosinophils. Endocrine tests showed a normal aldosterone concentration and an exaggerated adrenocorticotropic hormone (ACTH) stimulation test, consistent with a diagnosis of hyperadrenocorticism (HAC). A diagnosis of adrenal-dependent HAC was made, based on the presence of a calcified mass involving the left adrenal gland, and hepatomegaly, on radiography and ultrasonography. The owners declined surgical adrenalectomy. Medical management with trilostane rapidly improved the clinical signs and normalised the serum chemistry. ACTH stimulation tests showed an improvement in post-ACTH cortisol concentrations and were used to make dose adjustments where necessary. At the time of writing, no adverse side effects had been seen and the dog remained well after 80 weeks of treatment.
3-Hydroxysteroid Dehydrogenases↗
Use of trilostane for the treatment of pituitary-dependent hyperadrenocorticism in a cat.
Hyperadrenocorticism occurs much less frequently in cats than in dogs and, at present, is more difficult to manage successfully. This report documents the use of the steroid synthesis inhibitor trilostane for the treatment of hyperadrenocorticism in a domestic shorthaired cat with pituitary-dependent disease. Although trilostane was able to alleviate the severity of the clinical signs and was well tolerated, the cat subsequently died of renal failure secondary to a fungal infection of the urinary tract.
3-Hydroxysteroid Dehydrogenases↗