The determination of steroids in plasma and urine, and the diagnosis of hyperplasia and tumour of the adrenal cortex.
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Severe generalized alopecia and marked vulvar enlargement were observed in a 5-year-old spayed ferret with high serum estradiol concentrations. A neoplastic left adrenal gland was removed. Staining of the neoplastic cells for estradiol was demonstrated by use of immunohistochemistry. Clinical findings in this ferret were typical of adrenal-associated endocrinopathy, a syndrome characterized by increased secretion of adrenocortical hormones by hyperplastic or neoplastic adrenal glands.
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OBJECTIVE: To determine plasma concentrations of steroid hormones in ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland, the effect of surgical removal of the affected adrenal gland on concentrations of these hormones, and whether any hormone concentrations could be used as a marker for the disease. DESIGN: Prospective case series. ANIMALS: 32 ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland. PROCEDURE: A blood sample was obtained from each ferret before adrenalectomy. In 26 of the 32 ferrets, a second blood sample was collected 24 to 48 hours after adrenalectomy. Plasma concentrations of 7 hormones were measured (cortisol, estradiol, testosterone, progesterone, 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate). RESULTS: Median plasma concentrations of 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate were significantly higher in ferrets with adrenal gland disease, compared with concentrations in clinically normal ferrets. After adrenalectomy, median concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione decreased significantly. Of 23 ferrets in which concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione all were measured, 22 (96%) had high concentrations of at least 1 of these 3 hormones, but only 5 (22%) ferrets had high concentrations of all 3 hormones. CLINICAL IMPLICATIONS: The condition that develops in ferrets with adrenal gland disease apparently is caused by excessive secretion of 1 or more steroids other than cortisol. Because concentration of a particular hormone was not high in all ferrets, we recommend determining plasma concentrations of several sex steroids, including androstenedione, 17-hydroxyprogesterone, and estradiol.
AN INTERESTING METHOD FOR PATIENTS AND PHYSICIANS: Measurement of salivary cortisol has not modified the investigation of hospitalized patients but offers very original possibilities for exploring outpatients. REPEAT MEASUREMENTS AND STIMULATION TESTS: As for serum cortisol levels, repeat measurements or stimulation tests are required for reliable evaluation of salivary cortisol. SEVERAL APPLICATIONS: Salivary cortisol level can be an appropriate tool in screening for adrenal insufficiency, using the short ACTH injection test, evaluating hypercorticism through the circadian cycle of cortisol and overnight dexamethasone suppression test either at the physician's office or in the patient's home. In addition, long-term follow-up is possible for outpatients investigated or treated for Cushing's syndrome.
Disturbed adrenal function may present in various ways. Here are outlined some of the functions of the adrenals and the clinical effects of adrenal disorder, followed by a more detailed consideration of the application of laboratory tests to the identification of adrenocortical hypo- and hyperfunction.
Histological and morphometric studies of large-cell and small-cell hypothalamic nuclei, adenohypophysis, and adrenal cortex of patients who died from acute coronary failure revealed signs of persistent hyperfunction of small-cell nuclei of the hypothalamus, bundle and retinal adrenocortical zones, and signs of short-term hyperfunction of pituitary adenocytes. These changes indicate disorders in the hypothalamic regulation of adrenal activity.
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Seven patients with Cushing's syndrome secondary to adrenocortical tumors were studied using 131I-19-iodocholesterol. The diagnosis of all cases were verified histologically. In three cases with adenoma the uptake of the tracer was in the tumor only, while the two patients with adrenocortical carcinoma failed to show adrenal accumulation of the labelled compound. In two patients there was a hyperplasia-like scintigraphic pattern, while the stimulation and suppression biochemical tests suggested adrenal tumor. One of these cases was verified as a mixed form (adenoma plus hyperplasia), and the tumor bearing gland was significantly larger on the scan which helped the preoperative localization. In the other case, verified as bilateral multiple adrenocortical adenomas, the autonomus function of both adrenals was proved by dexamethasone suppression scanning. It seens reasonable to use the latter as an adunctive diagnostic procedure in patients where there is a discrepancy between the standart scintiscan and the biochemical indexes of adrenal hyperfunction.