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PubMed1998

Juxta-adrenal cortical cell nests or nodular formation in the younger generation: what does it mean?

The number and size of juxta-adrenal cortical cell nests or nodular formation (JACN) and their histology were examined in autopsy material from 255 successive subjects of various ages (from fetuses to elderly patients). The study of number and size showed that JACN occurred significantly more frequently among subjects aged 0-year-old (0Y0) to 10Y0 (p < 0.01) than among other age groups. The study of numbers within each nodular size range (large nodular formations [LNF; nodules with a minor axis measuring 0.25 mm or more] and small nodular formations [SNF; smaller than LNF]) showed that the number of SNF and the SNF to LNF ratio decreased according to age, while the number of LNF remained relatively constant. Immunohistochemical examination of proliferating adrenal cortical cells using the mouse anti-human antibody MIB-1 demonstrated many positive cells in subjects with many JACN. No nodular proliferation of adrenocorticotrophic hormone positive cells occurred in the adenohypophysis. Fibrous thickening of the adrenal capsule increased gradually with age or medication. JACN was very frequently observed among subjects with conditions such as asplenic syndrome, acute lymphocytic leukemia and Down's syndrome. These data suggest that JACN might be an anatomic variant but that certain factors could increase the size and number of JACN after birth.

Adenoma↗
PubMed1992

Endocrine emergencies in pregnancy.

A number of endocrine conditions and emergencies have unique characteristics when present in the pregnant woman. Often the abnormal endocrine state affects both mother and fetus and the various diagnostic and therapeutic approaches have to be altered to avoid harming the fetus. Furthermore, the pregnant state itself may alter the natural course of the underlying endocrine condition. Prolactinomas may enlarge due to the hormonal milieu of pregnancy, causing mass effects and even apoplexy. Anticipation of this possibility and prompt recognition may prevent disastrous consequences. This stimulatory state may extend to the normal pituitary, resulting in Sheehan's syndrome. An acute form of Sheehan's may go unrecognized, leading to unnecessary maternal deaths. Autoimmune endocrine disorders may sometimes be exacerbated and at other times be ameliorated during pregnancy. Witness the development of lymphocytic hypophysitis during pregnancy, a condition best left alone if it can be diagnosed without surgery. Graves's disease usually improves during pregnancy but it may occasionally flare, resulting in potentially lethal thyroid storm. The various therapeutic alternatives for hyperthyroidism are very much affected by effects on the fetus. Cushing's syndrome has very bad consequences for the fetus and must be diagnosed and treated urgently, if not emergently. Phaeochromocytomas are always endocrine emergencies requiring urgent and sometimes emergent treatment. Hyperparathyroidism is usually mild, but severe hypercalcaemia can be a true endocrine emergency. Recognition of the interactions of these endocrine conditions and their specific treatments with the complicated maternal-fetal unit makes their diagnosis and treatment simultaneously both difficult and extremely rewarding.

Acute Disease↗
PubMed1999

Reproducibility of the cortisol response to stimulation with the low dose (1 microg) of ACTH.

OBJECTIVE: Previous studies have shown that the rapid ACTH stimulation test using a low dose of 1 microg is more sensitive than that using 250 microg ACTH for detecting subtle cases of adrenal insufficiency. However, there are controversies for the reproducibility of the 1 microg-test. To evaluate the reproducibility of the 1 microg-test, we assessed both day-to-day and diurnal variations of cortisol responses to 1 microg ACTH injection. In addition, optimum sampling time for the 1 microg-test was also determined. SUBJECTS: AND DESIGN Eight healthy volunteers and five patients with secondary adrenal insufficiency were recruited. Healthy subjects were given 1 microg ACTH 3 times in the morning (0800 h) and 2 times in the afternoon (1600 h). Patients with adrenal insufficiency had 2-tests in the morning and 2 in the afternoon. Serum cortisol levels were measured every 10 minutes for 1 h after the injection. RESULTS: In healthy subjects, basal and peak serum cortisol levels were significantly higher in the morning (P < 0.05), whereas maximum cortisol increments were higher in the afternoon (P < 0.001). In patients with adrenal insufficiency, basal and peak serum cortisol levels in the morning were not different from corresponding values in the afternoon. Intra-individual coefficient of variation (CV) of peak serum cortisol response to 1 microg ACTH ranged from 3.0 to 16.4% in healthy subjects and 10.0-34. 4% in patients. Also, there was a significant correlation between peak morning or afternoon cortisol levels after 1 microg ACTH injection given in different days in both healthy subjects and patients. Twenty-six of the 40 studies in healthy subjects showed peak response at 20 minutes, while nine showed it at 30 minutes Using the data acquired at 20 and 30 minutes, all 40 studies in healthy subjects showed normal results while none of 20 studies in patients was normal. CONCLUSIONS: We conclude that the cortisol response to 1 microg ACTH stimulation was reproducible in both healthy subjects and patients with secondary adrenal insufficiency. In order to assess adrenal function more accurately with the 1 microg ACTH stimulation test, serum cortisol should be measured before and 20 and 30 minutes after ACTH injection.

Adrenal Cortex Diseases↗
PubMed2002

Unique cases of unilateral hyperaldosteronemia due to multiple adrenocortical micronodules, which can only be detected by selective adrenal venous sampling.

Primary aldosteronism is classified as aldosterone-producing adenoma (APA), idiopathic hyperaldosteronism (IHA), unilateral adrenal hyperplasia (UAH), primary adrenal hyperplasia (PAH), adrenal cancer, and glucocorticoid-remediable aldosteronism. We describe here 4 cases of primary aldosteronism due to unilateral hyperaldosteronemia, demonstrating unique histopathologic findings, such as unilateral multiple adrenocortical micronodules in the affected adrenals. Thirty-three patients with primary aldosteronism were consecutively admitted; 27 of them were treated by unilateral adrenalectomy. Four of them also had unilateral adrenal hypersecretion of aldosterone by selective adrenal venous sampling and adrenocortical multiple micronodules without an adenoma. These patients had hyporeninemic hyperaldosteronism with normokalemic hypertension. In these patients, furosemide plus upright test failed to increase plasma renin activity (PRA); the ratio of plasma aldosterone concentration (PAC) to PRA at 90 minutes after captopril administration was similar to that in patients with IHA and APA. Aldosterone concentrations were increased in each unilateral adrenal vein, and poorly encapsulated multiple adrenocortical micronodules from 2 to 3 mm in diameter were microscopically detected in the resected adrenal glands. Immunohistochemical analysis of steroidogenic enzymes, including cholesterol side chain cleavage, 3beta-hydroxysteroid dehydrogenase, 21-hydroxylase, 17alpha-hydroxylase, and 11beta-hydroxylase, indicated that the cortical cells within these micronodules were active in aldosterone production, while the non-nodular zona glomerulosa cells were inactive. We conclude that the clinical and pathologic characteristics of our 4 cases with unilateral multiple adrenocortical micronodules (UMN) are distinct from those of APA, IHA, UAH, and PAH. Furthermore, unilateral hyperaldosteronemia induced by UMN may be frequently misdiagnosed, because standard imaging tests, which cannot always detect tiny abnormalities of adrenals, showed "normal adrenal glands" in these patients. Thus, primary aldosteronism due to UMN should be carefully examined for differential diagnosis of each form of hyperaldosteronemia.

Adenoma↗
PubMed1986

Regulation of prolactin secretion in canine pituitary-dependent hyperadrenocorticism.

In 15 dogs with pituitary-dependent hyperadrenocorticism (PDH) the basal prolactin concentrations (means of 6 determinations; range 2.8-24.7 micrograms/l) were significantly higher than those of 23 healthy control dogs (0.9-10.5 micrograms/l). In five dogs with hyperadrenocorticism due to adrenocortical tumour (ATH) the prolactin concentrations were also significantly elevated, but still significantly lower than the values of the dogs with PDH. The prolactin concentrations of the dogs with PDH responded supranormally to TRH-stimulation, whereas in the dogs with ATH the response was not significantly different from the results in the control dogs. Following bromocriptine administration the plasma prolactin concentrations of the dogs with PDH decreased considerably but remained higher than the values obtained in the control dogs and the dogs with ATH. It is concluded that PDH in the dog is associated with a disturbance in the regulation of prolactin secretion, that is not secondary to hypercortisolism per se.

Adrenal Cortex Diseases↗
PubMed2004

Paradoxical inhibitory effect of serotonin on cortisol production from adrenocortical lesions causing Cushing's syndrome.

In the human adrenal gland, serotonin (5-HT) stimulates cortisol production through a paracrine mechanism involving 5-HT4 receptors positively-coupled to adenylyl cyclase. A hyperresponsiveness of adrenocortical tissue to 5-HT has also been described in several cases of ACTH-independent bilateral macronodular adrenal hyperplasias (AIMAHs) and adenomas causing Cushing's syndrome. In the present study, we report two cases of cortisol-producing adrenocortical lesions, i.e., one AIMAH (case 1) and one adenoma (case 2), whose secretory activity was inhibited in vitro by 5-HT. The potencies (pIC50) and efficacies (Emax) of 5-HT to inhibit cortisol secretion were 8.2 +/- 0.4 and -64.1% +/- 7.5% in case 1, and 9.2 +/- 0.5 and -32.3% +/- 3.8% in case 2. The specific 5-HT4 antagonist GR 113808 failed to influence the 5-HT-induced decrease in cortisol production by the two tissues, indicating that the paradoxical inhibitory effect of 5-HT could not be accounted for by activation of eutopic 5-HT4 receptors. These results suggest that the tissues expressed aberrant 5-HT receptors. In conclusion, the present study provides the first evidence for an inhibitory effect of 5-HT on cortisol secretion in adrenocortical lesions causing Cushing's syndrome. Our data also suggest that expression of illegitimate membrane receptors by cortisol-producing adrenal hyperplasias and/or adenomas may convert a paracrine stimulatory factor into an inhibitory signal.

Adenoma↗
PubMed1997

Adrenocortical disorders.

Preoperative preparation for the patient with adrenal disorders is directed toward restoring the intravascular volume and the electrolyte concentrations to normal. Hypertension and hypokalemia may be controlled by restricting sodium intake and administration of the aldosterone antagonist spironolactone. Patients taking steroids preoperatively must be adequately replaced throughout the perioperative phase at times of maximum stress.

Adrenal Cortex Diseases↗
PubMed1985

Adrenal scintigraphy with 75Se selenonorcholestenol: a review.

We have reviewed 58 patients on whom adrenal scintigraphy has been performed using 75Se selenonorcholestenol. For 15 patients whose adrenal function was biochemically normal, the upper limit of normal of the 7 day adrenal uptake test was 0.45%, considerably higher than the generally accepted value of 0.3%. There is evidence from this group of patients that stress and obesity might account for uptakes in the range 0.3-0.45%. The sensitivity of the uptake test is poor, with 7 out of 23 patients with Cushing's syndrome having uptakes within the normal range. Scintigraphy of such patients may still be useful in differentiating between unilateral and bilateral adrenal involvement.

Adrenal Cortex↗