PubMed · 8384669
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S Fukuchi. 1993. [Hypoaldosteronism].. https://pubmed.ncbi.nlm.nih.gov/8384669/
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A 7-year-old 7-kg (16-lb) neutered male Himalayan cat had nonpruritic progressive alopecia of 9 months' duration. The cat had hyperglycemia and glucosuria. Physical examination revealed complete alopecia along the abdomen, inguinal area, medial and caudal areas of the thighs, ventral area of the thorax, and axilla. Clinical signs were consistent with endocrine-induced alopecia and hyperadrenocorticism, however, results of diagnostic tests (ACTH stimulation and low-dose dexamethasone suppression) were not supportive of hyperadrenocorticism. Abdominal ultrasonography revealed a mass cranial to the left kidney. Blood samples were obtained before and after ACTH stimulation to measure sex hormone concentrations. Analysis revealed markedly high blood progesterone concentrations before and after ACTH stimulation. An adrenalectomy was performed and histologic examination of the mass revealed a well-differentiated adrenocortical carcinoma. The right adrenal gland could not be viewed during surgery and was assumed to be atrophic. Following surgery, the hyperglycemia and glucosuria resolved. Within 4 months of surgery, the hyperprogesteronemia had resolved, and at 12 months the cat's coat quality appeared normal. Findings suggest that cats with signs of hyperadrenocorticism should be evaluated not only for abnormal cortisol concentrations, but also for sex hormone abnormalities.
BACKGROUND: POEMS syndrome is a multisystem disorder. It usually presents as severe polyneuropathy and monoclonal gammapathy associated with endocrinopathies, organomegaly, skin hyperpigmentation. CASE REPORT: A patient with POEMS syndrome developed primary adrenocortical deficiency revelated by asthenia and hyperpigmentation. Hydrocortisone replacement therapy produced a rapidly beneficial effect on asthenia and hyperpigmentation. DISCUSSION: Although asthenia and skin pigmentation are common in POEMS syndrome, adrenocortical deficiency is seldom reported. This endocrinopathy might be underestimated in POEMS patients. We suggest systematic screening with a rapid ACTH test in all POEMS patients in order to detect underlying adrenal deficiency.
OBJECTIVE: Increasing evidence favours subtle glucocorticoid excess in many patients with adrenal incidentalomas. However, existing evidence is based mainly on the overnight dexamethasone suppression test, a test that is commonly abnormal even among clinically euadrenal subjects. The aim of the present study was to evaluate patients with adrenal incidentalomas for subtle glucocorticoid excess by the more specific low-dose dexamethasone test (LDDST). Moreover, since the criteria of what constitutes an abnormal cortisol response following this test have been largely anecdotal, we report our results in comparison with those obtained in clinically euadrenal subjects, and patients with Cushing's syndrome. DESIGN: A prospective study of 57 patients with adrenal incidentalomas with CT characteristics highly suggestive of benign adrenocortical adenomas and 85 clinically euadrenal subjects consisting of 54 obese women with BMI > 30 kg/m2 (range 30-54.7), 13 women with BMI < 30 kg/m2 (range 20.3-29.6) and 18 healthy volunteers (10 women and eight men) over 40 years of age (mean age 51.7 +/- 9.9, range 40-74; mean BMI 30 +/- 6.6, range 20.3-47.5 kg/m2). A retrospective analysis was performed on 60 patients with a confirmed diagnosis of Cushing's syndrome. MEASUREMENTS: All subjects were admitted to the endocrine ward and underwent a standard LDDST, as follows: after a 48-h stabilization period, a 24-h urine collection for basal urinary free cortisol was performed. Basal serum cortisol and plasma ACTH were measured at 0800 h the following day, and subjects were started on dexamethasone 0.5 mg 6-hourly for 2 days. Post-dexamethasone cortisol and ACTH levels were measured at 0800 h, 6 h after the last dose of dexamethasone. RESULTS: Following dexamethasone suppression serum cortisol concentrations became undetectable (< 28 nmol/l) in all clinically euadrenal subjects. In patients with incidentally discovered adrenal masses, post-LDDST cortisol concentrations were undetectable in 12 (21%), between 28-140 nmol/l in 38 (67%), and 140-216 nmol/l in seven (12%) patients; post-LDDST cortisol values correlated positively with the size of the adenoma (r = +0.482, P < 0.001). Post-LDDST cortisol concentrations in patients with Cushing's syndrome ranged from 85 to 1786 nmol/l; in 3/42 (7%) patients with ACTH-dependent Cushing's syndrome cortisol concentrations were < 140 nmol/l. CONCLUSIONS: On the basis of our data in a large group of clinically euadrenal subjects, we suggest that following LDDST cortisol concentrations should become undetectable with the currently used radioimmunoassays. In patients with adrenal incidentalomas, application of the LDDST confirmed the presence of incomplete suppression of cortisol in the majority of patients. We suggest that the LDDST is a sensitive index of autonomous cortisol production in patients with adrenal incidentalomas; following this test a grading of subtle glucocorticoid excess may be obtained but future studies correlating biochemical, clinical and epidemiological data are required, in order to develop widely agreed cut-off levels of clinically significant glucocorticoid excess in these patients.