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At least 55 records · Page 3Linked to original sources
PubMed2005

Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis.

OBJECTIVE: A serine protease from rat adrenal cortex was recently characterized and named adrenal secretory protease (AsP). AsP is expressed in the adrenal cortex and is capable of cleaving pro-gamma-melanocyte-stimulating hormone (1-76 N-terminus of pro-opiomelanocortin) into fragments that act as adrenal mitogens. AsP may therefore play a crucial role in adrenal growth and tumourigenesis. The aim of this study was to further characterize the human homologue of AsP and its possible role in adrenal tumourigenesis. METHODS AND RESULTS: Starting with the rat cDNA sequence of AsP we detected high homology to the catalytic C-terminus of the human airway trypsin-like protease (HAT). Further analysis revealed that the HAT gene is the human homologue of a long splice variant of AsP, which we recently described as rat airway trypsin-like serine protease 1. In contrast to rodents, no short isoform of HAT was found in humans due to a stop codon in exon 6 which prevents the expression of a short isoform. While high expression of HAT mRNA was found in the trachea and in the gastrointestinal tract, expression in the adrenal was only very weak. RT-PCR and real-time PCR analysis revealed a complex tissue expression pattern of HAT, indicating a role for this protease in multiple tissues. We further investigated HAT expression in five normal adrenal glands, 15 adrenocortical adenomas (five hormonally inactive adenomas, five aldosterone-producing adenomas and five cortisol-producing adenomas), nine adrenocortical carcinomas, five phaeochromocytomas and two adrenal hyperplasias. Weak HAT expression was detectable in only two out of five normal adrenal glands, in one out of twenty-four adrenocortical tumours and four out of five phaeochromocytomas. However, the expression in the adrenal tissue was several orders of magnitude lower than in the trachea. In addition, we could not detect any HAT transcripts in a sample of fetal adrenal. CONCLUSION: Gene structure and tissue distribution of HAT, the human homologue of the rat adrenal secretory protease AsP, reveal major interspecies differences. The observation of very low expression levels in normal adrenal tissue and adrenocortical tumours casts doubt about a role for HAT in the physiological and pathological growth of adrenocortical cells.

Adenoma↗
PubMed2001

Adrenal masses: quantification of fat content with double-echo chemical shift in-phase and opposed-phase FLASH MR images for differentiation of adrenal adenomas.

PURPOSE: To quantify fat content in adrenal lesions with double-echo chemical shift magnetic resonance (MR) imaging in a phantom study and to differentiate adrenal adenomas from other adrenal masses by assessing fat content in a clinical study. MATERIALS AND METHODS: The study consisted of two parts: a phantom study and a clinical study. To explore the effect of the T1 value on in- and opposed-phase MR images of fat-containing tissues, phantom models with various proportions of fat and gadopentetate dimeglumine concentrations were implemented. Signal intensity (SI) indexes ([SI in-phase - SI opposed-phase]/SI in-phase) were calculated with double-echo fast low-angle shot (FLASH) MR imaging. In the clinical study, 23 patients with 28 adrenal masses (16 adrenal adenomas, nine adrenal metastases, and three pheochromocytomas) underwent double-echo FLASH MR imaging, and SI indexes were calculated. RESULTS: SI index reached a maximum of 0.87 at 53% fat fraction for gadopentetate dimeglumine concentration at 0.5 mmol/L as the simulated T1 of the adrenal mass. The SI indexes of the adrenal adenomas, adrenal metastases, and pheochromocytomas, respectively, were 0.36, -0.15, and -0.07, and estimated fat fraction from the phantom study was 26.5%, 0%, and 0%. All adrenal adenomas contained fat on double-echo FLASH images. There was no overlap in SI index between adenomas and other tumors. CONCLUSION: Preliminary experience indicates that quantitative measurement of the fat fraction of adrenal masses is possible with the double-echo chemical shift FLASH technique and allows for differentiating adrenal adenomas from other adrenal masses.

Adenoma↗
PubMedDate not supplied

Adrenal insufficiency with enlarged adrenals.

Five patients with adrenal insufficiency and large adrenal glands at presentation are reported. Addison's disease was due to adrenal tuberculosis in three patients, with important changes in adrenal configuration on CT reflecting the natural history of the disease. Adrenal infiltration by non-Hodgkin lymphoma and metastatic carcinoma of the lung was the cause of the disease in the fourth and fifth patients, respectively, who developed signs of adrenal insufficiency before the diagnosis of the primary lesion became apparent. Histologic confirmation was established after unilateral adrenalectomy in three patients. In two patients with adrenal tuberculosis, long clinical and laboratory follow-up confirmed the diagnosis. This report indicates that Addison's disease is not infrequently associated with adrenal enlargement. Adrenal size is related to the cause and duration of the various disease states leading to adrenal insufficiency. Moreover, adrenal insufficiency associated with enlarged adrenal glands can be the presenting manifestation of lymphoma or metastasis.

Adrenal Gland Diseases↗
PubMed1999

Regulation of adrenal angiotensin receptor subtypes: a possible mechanism for sympathectomy-induced adrenal hypertrophy.

OBJECTIVE: Previous studies indicate that the adrenal gland plays a compensatory role in the maintenance of blood pressure in chemically sympathectomized rats. However, the mechanisms responsible for compensatory adrenal responses are poorly understood. This study examined the regulation of adrenal growth and type 1 A, 1 B, and type 2 angiotensin II (Ang II) receptor (AT1A, AT1B and AT2) expression in the adrenal gland induced by sympathectomy. METHODS: Five-week-old male Sprague-Dawley rats were treated with either guanethidine (50 mg/kg per day, intraperitoneally) or vehicle for 5 weeks. Norepinephrine and epinephrine levels in the atrium of the heart were measured by high-pressure liquid chromatography. Plasma renin activity was determined by radioimmunoassay. Adrenal AT1 and AT2 receptor density was determined by radioligand binding assay. Adrenal AT1A, AT1B and AT2 mRNA levels were determined by Northern blot analysis. RESULTS: Norepinephrine and epinephrine levels in the atrium of the heart were decreased 86% (P < 0.0001) and 58% (P < 0.05) by guanethidine treatment, respectively. Plasma renin activity was decreased 71% (P< 0.001) in guanethidine-treated rats compared with vehicle. In contrast, the ratio of adrenal to body weight was increased 38% in guanethidine-treated rats compared with vehicle (P< 0.001). Adrenal AT1 and AT2 receptor density was increased by guanethidine treatment (P< 0.05). Adrenal mRNA levels for AT2 (P< 0.001) and AT1A (P< 0.01), but not AT1B (P>0.05), were increased in guanethidine-treated rats compared with vehicle (P< 0.01). There were positive correlations between adrenal weight and AT2 (r = 0.9, P< 0.001) and AT1A (r = 0.6, P< 0.05) but not AT1B (r = - 0.01, P > 0.05) expression. CONCLUSIONS: Impairment of the sympathetic nervous system with guanethidine withdraws the normal stimulation of this system on the circulating renin-angiotensin system, but upregulates the expression of adrenal Ang II receptors. Increased expression of adrenal AT2 and AT1A receptors may play an important role in adaptive adrenal hypertrophy and hormonal responses to sympathectomy.

Adrenal Glands↗
PubMed2006

Impact of periconceptional undernutrition on adrenal growth and adrenal insulin-like growth factor and steroidogenic enzyme expression in the sheep fetus during early pregnancy.

Periconceptional undernutrition (PCUN) results in an earlier prepartum activation of the pituitary-adrenal axis in twin compared with singleton fetuses. We have tested the hypotheses that the functional development of the fetal sheep adrenal is delayed in twins compared with singletons in early gestation and that PCUN accelerates adrenal growth and increases the expression of intraadrenal IGF-I and -II and cytochrome P450 17-hydroxylase (CYP17) as early as 55 d gestation. We have investigated the effect of PCUN in the ewe (restricted at 70% of control allowance, n=21; control, n=24) from at least 45 d before mating until d 7 after mating on maternal cortisol and progesterone concentrations, fetal adrenal weight, adrenal IGF-I, IGF-I receptor (IGF-IR), IGF-II, IGF-IIR, and CYP17 mRNA expression and placental 11beta-hydroxysteroid dehydrogenase-1 and -2 mRNA and protein expression at d 53-56 pregnancy. The relative weight of the fetal adrenal and adrenal IGF-I, IGF-IR, IGF-II, IGF-IIR, and CYP17 mRNA expression were lower in twin compared with singleton fetuses. In singleton fetuses of PCUN ewes, there was a loss of the relationship between adrenal IGF-II/IGF-IIR expression and either adrenal weight or CYP17 mRNA, which was present in controls. Similarly in twin fetuses, PCUN resulted in the loss of the relationships between adrenal weight and IGF-I expression and between adrenal CYP17 and IGF-II expression, which were present in controls. Our findings suggest that differences in the timing of the prepartum activation of the fetal adrenal in twins and singletons have their origins in early gestation and highlight the importance of the interaction between the periconceptional environment and embryo number in setting the growth trajectory of the fetal adrenal.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2003

Adrenal enucleation in MSG-damaged hyperleptinemic male rats transiently restores adrenal sensitivity to leptin.

It is known that the neonatal treatment of rats with monosodium L-glutamate (MSG) induces several metabolic abnormalities, resulting in enhanced adiposity and hyperleptinemia. Our study was designed to explore the consequences of MSG-induced chronic hyperleptinemia on adrenal sensitivity to the inhibitory effect of exogenous leptin. Neonatal male rats treated with MSG or vehicle (controls, CTR) were followed during 150 days in order to study changes observed over development in body weight, food consumption as well as in vivo hypothalamo-pituitary-adrenal (HPA) axis and adipocyte functions. During adulthood, adrenal response to adrenocorticotropin (ACTH) was evaluated both in vitro and in vivo in order to determine the adrenal sensitivity to the inhibitory effect of leptin. For this purpose, sham-operated as well as CTR and MSG rats with bilateral adrenal enucleation (AE) were used. Our results indicate that: (1) between 30 and 150 days of age, MSG animals developed hypophagia, accompanied by arrest in body weight gain, and concomitant enhanced basal levels of all HPA axis components and of leptin; (2) adrenals from of 150-day- old MSG rats displayed an in vitro adrenocortical hyperresponse to ACTH stimulation as well as an adrenal refractoriness to the physiological inhibitory effect of leptin on ACTH-stimulated glucocorticoid output, and (3) bilateral AE in adult MSG-treated rats transiently reversed the MSG-induced hyperleptinemia, restoring normal leptin levels as well as a normal adrenal sensitivity to the inhibitory effect of leptin. Our data indicate that adrenal exposure to the chronically high plasma leptin levels observed in MSG rats is involved in the loss of the inhibitory regulatory effect of leptin at the adrenal level, being therefore, at least in part, responsible for the increased total and free glucocorticoid production measured in MSG adult rats. Furthermore, this study strongly suggests that the adrenal overfunction, frequently associated with different phenotypes of obesity, could be due to an adrenal resistance to the leptin-negative regulation.

Adipocytes↗
PubMed1990

Immunoreactive corticotropin-releasing hormone, growth hormone-releasing hormone, somatostatin, and peptide histidine methionine are present in adrenal pheochromocytomas, but not in extra-adrenal pheochromocytoma.

CRH, GH-releasing hormone (GHRH), somatostatin (SRIH), and peptide histidine methionine (PHM) were measured by RIA in extracts of normal adrenal glands and in extracts from adrenal and extraadrenal pheochromocytomas. In normal adrenal glands, immunoreactive (IR) CRH, IR-SRIH, and IR-PHM were detectable, while IR-GHRH was undetectable. In all 11 cases of adrenal pheochromocytomas, the tumors contained 2 or more of these four IR-peptides. In particular, IR-CRH was found in 73% (n = 8) of adrenal pheochromocytomas, IR-GHRH in 91% (n = 10), IR-SRIH in 91% (n = 10), and IR-PHM in 82% (n = 9) of adrenal pheochromocytomas. There was no significant correlation among the concentration of these peptides in each tumor, i.e. the concentrations of the IR-peptides were independent of each other. In contrast to the adrenal pheochromocytomas, none of these 4 IR-peptides was detectable in 5 extraadrenal pheochromocytomas. Gel filtration of pooled extracts from adrenal pheochromocytomas showed that the major component of the IR-CRH, IR-GHRH, IR-SRIH, and IR-PHM eluted in the position of their synthetic counterparts. Our results suggest that 1) the normal adrenal gland contains IR-CRH, IR-SRIH, and IR-PHM, but not IR-GHRH; 2) all of the adrenal pheochromocytomas we examined contained a number of hypothalamic releasing or inhibiting hormones; 3) their tissue concentrations were independent of each other; and 4) all of the extraadrenal pheochromocytomas we examined contained no such IR-peptides. The presence of hypothalamic hormones in adrenal pheochromocytomas and their absence in extraadrenal pheochromocytomas may be due to the differences in the chromaffin cells of their origin. Our data may be helpful in the differential diagnosis between adrenal and extraadrenal pheochromocytomas.

Adrenal Gland Neoplasms↗
PubMed2003

Risk factors for adrenal crisis in patients with adrenal insufficiency.

Patients with adrenal insufficiency have a life-threatening risk of adrenal crisis, thus preventing adrenal crisis is an important clinical issue. In order to clarify the risk factors for adrenal crisis, the medical records of 137 patients with established adrenal insufficiency were retrospectively investigated. The explanatory variables analyzed were gender, etiology of hypoadrenalism, class of adrenocortical hormone replaced, duration of steroid replacement, age at time of survey, age at time of diagnosis of hypoadrenalism, state of other hormone deficiencies (growth hormone and sex steroids), diabetes insipidus, and mental disorder. Diagnosis of adrenal crisis was based on physical and laboratory findings. Forty (29%) of the 137 patients had at least one episode of adrenal crisis. Based on the Akaike Information Criterion (AIC), steroid replacement therapy of more than 4 yrs' duration was the largest single contributor to the occurrence of an adrenal crisis, followed by mental disorder and sex steroid deficiency. In the subclass of patients with secondary adrenal insufficiency (N = 115), sex steroid deficiency was the greatest risk factor. Patients with untreated hypogonadism had a significantly higher relative risk of 3.70 (95% confidential interval: 1.71-7.98) compared to those without hypogonadism or with treated hypogonadism. Furthermore, among patients with hypogonadism aged younger than 50 yrs, those treated with sex hormone (5/51: 10%) suffered less frequently from adrenal crisis than those untreated (7/11: 64%, p = 0.0004). In conclusion, the present study has, for the first time, clarified the risk factors of adrenal crisis. Among them, sex hormone deficiency has an especially important implication because it can be treated by hormone replacement therapy with the hope of reducing the risk of adrenal crisis.

Adolescent↗
PubMed1990

[Clinical experience of adrenal incidentaloma with particular reference to adrenal cortical function].

The adrenal function mainly cortical one, was evaluated in 16 patients with incidentally discovered adrenal masses. Pathological examination was possible in 15 cases. The finding consisted of adrenocortical adenoma in 9, adrenocortical nodular hyperplasia in 1, adrenal medullary hyperplasia in 1, metastatic tumor in 2 and adrenal cyst in 2. Another case of adrenal cyst was diagnosed by percutaneous puncture. In all cases peripheral levels of plasma cortisol, plasma aldosterone concentration and plasma renin activity were normal. Plasma catecholamine levels were also normal except in a case of adrenal medullary hyperplasia. On the other hand, the cases of adrenocortical adenoma displayed elevation of urinary 17-hydroxycorticosteroids in 6/9 (67%), a loss of plasma cortisol circadian rhythm in 3/7 (43%) and insufficient suppression on dexamethasone (DXM) suppression test in 6/9 (67%). Their adrenal scintigraphy (with 131I-6 beta-iodomethyl-9-nor-cholest-5 (10)-en-3 beta-ol) revealed an increased ipsilateral up-take and insufficient suppression after DXM in all, while a diminished contralateral up-take in 4/9 (44%). These data suggested that a considerable number of adrenal incidentalomas may not be truly "non-functioning". Two patients with cortical adenoma experienced post operative adrenal insufficiency (25%). It was suggested that a pre-operative loss of plasma cortisol circadian rhythm was the most prognosticating of the post operative adrenal insufficiency, rather than insufficient DXM suppression or scintigraphic absence of contralateral up-take. Among the patients with malignancy, differentiation of incidental adrenal adenoma from metastasis by size alone may not be reliable.

Adenoma↗