[Significance of the Thorn test in internal diseases. I].
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Seventeen dogs with hyperadrenocorticism were studied. Three dogs had functioning adrenocortical tumors and 14 had pituitary-dependent hyperadrenocorticism. Each dog was evaluated by determining the endogenous plasma ACTH concentration and by performing 4 tests: ACTH stimulation, dexamethasone screening, dexamethasone suppression, and a 6-hour combined dexamethasone suppression/ACTH stimulation test. The combined test was less reliable as a screening test in diagnosing hyperadrenocorticism than was the dexamethasone screening test or the ACTH stimulation test. Compared with the endogenous plasma ACTH concentration, results of the dexamethasone suppression portion of the combined test were less reliable in distinguishing dogs with adrenocortical tumors from those with pituitary-dependent hyperadrenocorticism. It was concluded that the combined test cannot be recommended for use.
The following examinations, including the estimation of urinary neutral steroid metabolites, plasma cortisol, the percentage of unbound-cortisol, cortisol production rate, plasma adrenocorticotrophin (ACTH), dexamethasone suppression test, ACTH stimulation test, metopirone test, lysine-vasopressin (LVP) test and insulin tolerance test, were conducted in 16 patients with Cushing's syndrome for the presence of hypercoticism and for identifying the cause of this syndrome. Of these tests, the measurements of plasma cortisol late in the day and single dose dexamethasone suppression test were most useful for the diagnosis of hypercorticism because of their reliability and simplicity. Urinary 17-KGS, THF/THE ratio, cortisol production rate and low dose dexamethasone suppression test were also useful, whereas insulin test and LVP test were less valuable for this purpose. For the identification of the causes of this syndrome, lysine vasopressin test and metopirone test were most reliable, and plasma ACTH was also useful for this purpose, whereas insulin test and ACTH stimulation test were less valuable.
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OBJECTIVE: Tuberculosis of the adrenal glands is a common cause of Addison's disease in developing countries. We conducted a study to determine if treatment of such patients with modern anti-tuberculous chemotherapy would lead to an improvement in plasma cortisol and aldosterone levels. DESIGN: Prospective study. PATIENTS: 5 patients with Addison's disease secondary to tuberculosis. MEASUREMENTS: Basal and ACTH stimulated plasma cortisol and aldosterone levels were measured prior to instituting anti-tuberculous chemotherapy, as well as one month after its conclusion. Four patients were again studied over the next 2-5 years. RESULTS: Peak plasma cortisol levels prior to treatment were markedly reduced (range, < 14-110 mumol/l). There was no improvement one month (< 14-143 mumol/l) or 2-5 years (< 14-69 mumol/l) after completing anti-tuberculous chemotherapy. Peak plasma aldosterone at diagnosis was < 56-210 pmol/l; it was undetectable in 4 patients. No improvement was observed one month (< 56-210 pmol/l), or 2-5 years (< 56-389 pmol/l) after stopping anti-tuberculous chemotherapy. Plasma aldosterone levels at both these time points were far lower than those in control subjects (median 736 pmol/l, 560-1512 pmol/l; p < 0.01). One patient had an increase in peak aldosterone from < 56 pmol/l to 389 pmol/l, though peak cortisol actually declined in this subject (from 110 mumol/l to 69 mumol/l). CONCLUSIONS: Treatment of tuberculous Addison's disease with anti-tuberculous chemotherapy does not lead to normalization of ACTH stimulated plasma cortisol or aldosterone levels during the 2-5 year period of study. However, prolonged follow up with regular adrenal function tests is warranted in all such patients.
A generation ago, the determination of urinary 17-hydroxycorticoids was the best available laboratory procedure for assessing adrenocortical function. Today, the plasma cortisol concentration, measured by radioimmunoassay, is a much more specific and reliable parameter, particularly in combination with simple functional tests, which are also suitable for ambulatory patients. The most appropriate tests of adrenocortical function for the diagnosis or exclusion of Cushing's syndrome or of primary and secondary adrenocortical failure are briefly described. Substitution therapy in patients with adrenocortical insufficiency must be evaluated by clinical criteria and not by steroid analysis.
A patient with preserved adrenocortical function despite densely calcified adrenals is described. Similar cases have demonstrated a discrepancy between the apparent destruction of the glands, as judged by the extent of calcification radiographically, and their functional integrity. This case provided a unique opportunity to compare the results of adrenal function testing, adrenal appearance by computed tomograms, and adrenal histology with an actual clinical response to a variety of stresses capable of precipitating acute adrenal insufficiency.
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