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PubMed1998

Etiological diagnosis of primary adrenal insufficiency using an original flowchart of immune and biochemical markers.

Approximately 70-80% of cases of primary adrenal insufficiency are classified as idiopathic. An effective protocol for the etiological diagnosis of primary adrenal insufficiency is needed to ensure correct patient management. With the aim of developing an algorithm for the etiological diagnosis of primary adrenal insufficiency, we studied 56 Italian patients with nonsurgical primary adrenal insufficiency and 24 French patients with X-linked adrenoleukodystrophy (ALD) for serum levels of adrenal cortex, steroid-21-hydroxylase (21OHAb), islet cell (ICA), glutamate decarboxylase (GAD65Ab), IA2/ICA512 (ICA512Ab), thyroid peroxidase (TPOAb) autoantibodies, and plasmatic concentrations of very long chain fatty acids (VLCFA). High levels of 21OH and adrenal cortex antibodies were found in 35/42 (83%) and 17/42 (40%) Italian patients with idiopathic adrenal insufficiency, respectively. Levels of adrenal autoantibodies correlated inversely with disease duration (P < 0.0001). Elevated VLCFA were found in 4/42 (10%) idiopathic patients. A total of 34/35 (97%) idiopathic patients with a disease duration of less than 20 yr was positive for either 21OHSAb or elevated levels of VLCFA. None of 14 patients with posttuberculosis adrenal insufficiency had elevated levels of either adrenal antibodies or VLCFA. ICA, GAD65Ab, ICA512Ab, and TPOAb were found in 6/56 (11%), 8/56 (14%), 4/56 (7%), and 23/56 (41%) patients, respectively. None of 24 French ALD patients with adrenal insufficiency was positive for organ-specific autoantibodies. The measuring of 21OH antibodies and plasma VLCFA levels enabled a correct diagnosis of autoimmune (89%) and ALD (8%) in 97% of patients with idiopathic primary adrenal insufficiency of less than 20 yr of duration. The results of our study have important therapeutic and prognostic implications.

Adolescent↗
PubMed1976

[Comparative study of diagnosis for location of adrenal adenoma in patients with primary aldosteronism (author's transl)].

Four methods; retroperitoneal air insufflation study, adrenal phlebography, adrenal scintiscan and estimation of plasma aldosterone in adrenal or renal veins, were compared to determine the diagnostic value for the location of adrenal adenoma in 27 patients with primary aldosteronism and one with idiopathic aldosteronism. The location of adrenal adenoma could be certainly determined, in 12 of 27 patients with primary aldosteronism by retroperitoneal air insufflation study, in 7 of 22 by adrenal phlebography, in 18 of 23 by estimation of aldosterone in adrenal or renal vein blood, and in 19 of 27 by adrenal scintiscan. From these results, it is concluded that firstly adrenal scintiscan with 131I-cholesterol and then adrenal phlebography and estimation of aldosterone in adrenal and renal vein blood combined with retroperitoneal air insufflation study should be performed for determination of location of adrenal adenoma in primary aldosteronism.

Adenoma↗
PubMed2003

Activin signal transduction in the fetal rat adrenal gland and in human H295R cells.

The presence of activin A and its effects have previously been documented in the adrenal gland, particularly in the human fetal adrenal gland and the rat adrenal gland. The primary signaling pathway of activin involves interactions between receptor and intracellular (Smad) proteins that have not been completely described in the adrenal gland. In this study, we demonstrate that the components of the activin signaling cascade are present in two complementary models, the fetal rat adrenal gland and the human adrenocortical cell line, H295R, by means of RT-PCR, western analysis, and immunoprecipitation techniques. Using the cell line, activin signaling was analyzed using an activin-responsive reporter gene, p3TP-luc, and luciferase assays to assess transcriptional activity with co-expression of the different activin receptors and Smads to demonstrate the functionality of the signaling cascade. In the fetal rat adrenal gland, the relative amounts of mRNA of the type II receptors, RII and RIIB, were regulated by gestational age, such that the RIIB levels increased after birth while RII levels fell. Using immunodetection techniques, the activin receptors and the different Smad proteins were detected in the rat fetal adrenal glands. Notably, the presence of Smad4 protein is significantly increased after birth in the rat adrenal gland. RT-PCR established a similar profile in the H295R cells. Using p3TP-luc, the H295R cells show transcriptional activation of this activin-responsive reporter in the presence of activin A. Co-expression of type I and type II receptors as well as Smads, results in ligand-independent transcriptional activity in addition to an activin-stimulated response. In determining activin's effects on adrenal function, adrenal steroid production was evaluated by incubation of the H295R cells with increasing doses of activin A and inhibin A, resulting in a detectable increase in P450c17 expression. Co-incubation of activin A with follistatin diminishes this response. These results are consistent with a role for activin A in the adrenal gland by demonstrating that the elements of the activin signaling pathway are present, intact, and functional. This suggests that in the adrenal gland the components of the activin receptor/Smad pathway are dynamically changing in the transition from fetal to neonatal life, and are important to the function of this organ.

Activin Receptors, Type II↗
PubMed1994

[Contribution of nuclear medicine to the diagnosis of silent adrenal masses].

The role of adrenal scintigraphy in the noninvasive characterization of silent adrenal masses was investigated in 40 patients. The mass had been detected by US or CT performed in the evaluation of non-malignant extra-adrenal diseases (25 cases) or during staging or follow-up of a malignant extra-adrenal neoplasm (15 cases). In all cases radio-cholesterol scintigraphy (74 MBq i.v. of 131I-6 beta-iodomethylnorcholesterol in 19 cases; 11 MBq i.v. of 75Se-6 beta-selenomethylnorcholesterol in 21 cases) was performed; in 7 cases also 131I-MIBG scan (18.5-37 MBq i.v.) was carried out. When compared with CT data, radiocholesterol scintigraphy (standard or after suppression with dexamethasone) showed: concordant uptake (increased uptake of radiocholesterol on the side of the adrenal mass) in 24/26 patients with adrenal cortical adenoma; discordant uptake (absent or decreased uptake on the side of the adrenal mass) in 12 patients: 5 with adrenal metastases and 7 with non-adenomatous benign space-occupying lesions (2 ganglioneuromas, 1 post-traumatic hemorrhagic lesion, 3 adrenal cysts, 1 myelolipoma); indeterminate uptake (symmetric bilateral uptake) in 4 patients: 2 with a small adenoma, 1 with adrenal metastasis and 1 with a "false incidentaloma" (hepatic regenerative nodule). The results confirm the utility of radiocholesterol scintigraphy in demonstrating the benignity of adrenal lesions (particularly in identifying adrenocortical adenomas) and assess its place among the procedures used to characterize silent adrenal masses. The possible use of MIBG scintigraphy is also discussed.

Adrenal Gland Diseases↗
PubMed1995

Adrenal gland volume in major depression. Increase during the depressive episode and decrease with successful treatment.

BACKGROUND: Hyperactivity of the pituitary-adrenocortical axis is the most prominent neuroendocrine abnormality in major depression. It is state-related, returning to normal with resolution of the depressive episode. Adrenal gland enlargement also has been reported in patients with major depression and has been hypothesized as an index of cumulative lifetime depression. However, whether or not adrenal enlargement decreases with successful treatment of depression has not yet been studied, to our knowledge. We, therefore, determined adrenal gland volume in patients with major depression before and after treatment and in matched normal controls, and compared adrenal size with functional indexes of pituitary-adrenocortical activity. METHODS: Adrenal volumes were measured by magnetic resonance imaging in nine adult and two adolescent patients with major depression during their illness and during full remission when medication had been stopped for at least 1 month, and in nine adult and two adolescent normal control subjects individually matched to the patients. Basal, 4 to 7 PM plasma corticotropin 1-39 and cortisol levels, and corticotropin 1-39 and cortisol responses to administration of ovine corticorelin and lowdose cosyntropin also were measured. RESULTS: Mean adrenal gland volume was significantly larger, by about 70% in the patients while depressed than after successful treatment, and it also was significantly larger, again by about 70%, than the mean adrenal gland volume of their matched controls. After treatment, the mean adrenal volume of the patients decreased and was no longer significantly different from that of their controls at baseline. The magnitude of the decrease was significantly positively correlated with the duration of the depressive episode. Basal, late-afternoon plasma corticotropin 1-39 levels were significantly lower in the patients while depressed than in their matched controls, but basal plasma cortisol levels did not differ significantly among the three groups, nor did the corticotropin 1-39 and cortisol responses to corticorelin or the cortisol response to cosyntropin. Correlations between adrenal gland volume and basal corticotropin and cortisol levels, and the corticotropin and cortisol responses to hormone challenge, were not consistently in the expected direction in any of the three groups of subjects. CONCLUSIONS: Adrenal gland enlargement occurring during an episode of major depression appears to be state-dependent, in that it reverts to the normal size range during remission after treatment. It thus does not appear to be an index of cumulative lifetime depression. The lack of a discernible relationship between adrenal volume and pituitary-adrenocortical activity remains to be explained and might be related to noncorticotropin influences on the adrenal gland, including other tropic hormones and/or neural mechanisms.

Adolescent↗
PubMed2006

Prevalence of adrenal incidentaloma in a contemporary computerized tomography series.

Adrenal incidentalomas, defined as masses discovered incidentally during imaging investigation of non-adrenal disorders, have become a rather common finding in clinical practice. The prevalence is not well characterized and varies among studies. The aim of the present study was to perform a prospective evaluation of the prevalence of adrenal incidentalomas among subjects undergoing computerized tomography (CT) scan of the chest in a screening program of lung cancer (Tic TAC study) in Piedmont, a region of Northwestern Italy. This evaluation included 520 subjects (382 males and 138 females, aged between 55-82 yr), referred to our hospital from April to December 2001. Twenty-three patients with adrenal masses were identified: 21 adrenal adenomas, 1 myelolipoma, and 1 metastasis of lung cancer. Therefore, the overall prevalence of adrenal lesions was 4.4%, and that of benign adrenal masses was 4.2%. This prevalence is higher than those found in previous CT scan series reported in the literature, probably because of the use of high-resolution CT scanning technology. Another factor that influenced our results is that subject age is skewed towards the decades characterized by a greater occurrence of adrenal masses. The outcome of this study confirms that we are presently able to identify incidentally discovered adrenal masses more often than in early years and that the prevalence of adrenal incidentalomas on CT images is approaching that of autopsy series. The present study provides a reliable estimate of the prevalence of adrenal incidentaloma with currently used CT scanners. Notwithstanding that our subjects were at increased risk of lung cancer, the rate of adrenal metastases was low. We think that the present results can be generalized even if we may disclose the lack of histological diagnosis.

Adrenal Gland Neoplasms↗
PubMed1996

Immobilization-induced stress activates neuronal nitric oxide synthase (nNOS) mRNA and protein in hypothalamic-pituitary-adrenal axis in rats.

The purpose of this study was to determine whether immobilization stress can cause changes in the enzyme activity and gene expression of neuronal nitric oxide synthase (nNOS) in the hypothalamus, pituitary, and adrenal gland in rats. NOS enzyme activity was measured as the rate of [3H]arginine conversion to citrulline, and the level of nNOS mRNA signal was determined using in situ hybridization and image analysis. NOS-positive cells were also visualized using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase) histochemistry and by immunohistochemistry using an anti-nNOS antibody. A significant increase of NOS enzyme activity in the anterior pituitary, adrenal cortex, and adrenal medulla (1.5-, 3.5-, and 2.5-fold) was observed in the stressed animals (immobilization of 6 h) as compared to non-stressed control rats. Up-regulation of nNOS mRNA expression in anterior pituitary and adrenal cortex was already detectable after stress for 2 h with 1.5- and 2-fold increase, respectively. The nNOS mRNA signals in hypothalamic paraventricular nucleus (PVN) significantly increased after the stress for 6 h. This increase in NOS enzyme activity was confirmed using NADPH-diaphorase staining and immunostaining in the PVN and adrenal cortex. An increase of NOS enzyme activity in adrenal medulla after immobilization for 6 h posited by far longer than in the adrenal cortex and anterior pituitary. The present findings suggest that psychological and/or physiological stress causes NO release in hypothalamic-pituitary-adrenal (HPA) axis and in sympatho-adrenal system. It is suggested that NO may modulate a stress-induced activation of the HPA axis and the sympatho-adrenal medullary system. The different duration of stress-induced NOS activity in HPA axis and the adrenal medulla may suggest NO synthesis is controlled by separate mechanism in the two HPA and the sympatho-adrenal systems.

Animals↗
PubMed1995

Adrenal insufficiency occurring during septic shock: incidence, outcome, and relationship to peripheral cytokine levels.

PURPOSE: In patients with septic shock, to (1) determine the incidence of adrenal insufficiency (AI), (2) observe the effects of glucocorticoid therapy on outcome in those with impaired adrenal function, and (3) investigate a possible correlation between adrenal function and peripheral cytokine levels. PATIENTS AND METHODS: Twenty-one patients admitted to the medical and surgical intensive care unit with septic shock and 11 healthy volunteers were studied. Cortisol, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) levels were measured before and after infusion of low (1 microgram) and standard doses (250 micrograms) of adrenocorticotropic hormone (ACTH) within 24 hours of the diagnosis of septic shock. Patients with subnormal adrenal responses to ACTH were treated with stress doses of steroids. Hormone, cytokine, and survival data in patients with normal response were compared to those with subnormal adrenal function. RESULTS: Five patients (23.8%) exhibited AI by ACTH stimulation testing. Three of them received steroid supplementation with rapid improvement in hemodynamic parameters. Autopsies of 2 patients with AI revealed intact adrenal cortices. Sixteen patients had adequate adrenal responses (AAR) to the standard-dose ACTH infusion. TNF-alpha levels were inversely correlated with mean arterial pressure (MAP) (r = -.52, P = 0.038) in AAR but not AI. There was no difference in mean peripheral TNF-alpha levels between AAR and AI. There was no correlation between TNF-alpha levels and mortality or adrenal function in those with septic shock. A trend toward lower IL-6 levels in AI suggests a link between reduced IL-6 levels and understimulation of the pituitary-adrenal axis in this group. Mortality in patients with AI was 80% at 4 weeks as compared with 43.8% in the group with normal adrenal response. CONCLUSIONS: Adrenal hyporesponsiveness is a feature of septic shock in some patients. Its etiology is probably complex. Steroid supplementation appeared to improve short-term survival when AI occurred, although these patients' overall mortality was worse than that of patients with septic shock and AAR. The standard-dose (250 micrograms) rapid ACTH infusion test was adequate for detecting AI. Adrenal insufficiency should be suspected in patients with septic shock who do not respond to conventional treatment. Performing the ACTH infusion test and initiating a trial of stress doses of glucocorticoids pending the results is a reasonable strategy in this situation.

Adrenal Insufficiency↗
PubMed2002

Inhibition of 3beta-hydroxysteroid dehydrogenase-isomerase in mouse adrenal cells: a direct effect of testosterone.

Gonadal steroids modulate adrenal gland size and function in a variety of species, and our previous studies demonstrate that circulating androgens suppress 3beta-hydroxysteroid dehydrogenase-isomerase (3betaHSD) activity in the adrenal cortex of male mice. The present study tests the hypothesis that androgens have a direct, receptor-mediated inhibitory effect on adrenal 3betaHSD. Treatment of cultured adrenal cells from C57BL/6J and C3H/HeJ mice with 0.02-2.0 microM testosterone for 7 days significantly reduces 3betaHSD activity in cells from both strains. However, treatment for 3 days reduces 3betaHSD activity in the adrenal cells from C3H/HeJ, but not C57BL/6J mice. The decreases in 3betaHSD activity in response to testosterone treatment is reflected in decreases in the amount of 3betaHSD immunoreactive protein, such that extended treatment decreases 3betaHSD immunoreactive protein in adrenal cells from both strains, but short-term treatment only decreases 3betaHSD immunoreactive protein in adrenal cells from C3H/HeJ mice. Thus, there appears to be a temporal difference between strains in the effect of the testosterone on 3betaHSD activity and immunoreactive protein. Treatment of the adrenal cells with androgen agonists and an antagonist indicate that the effect of testosterone is androgen receptor mediated. The effect of testosterone appears to be specific for 3betaHSD, since none of the treatments alter P450(scc) in cells from either strain. Testosterone treatment also causes a decrease in the amount of 3betaHSD mRNA. However, in contrast to the effect on activity and immunoreactive protein, there is no strain-related temporal difference because testosterone decreases 3betaHSD mRNA within 24h in adrenal cells from both strains. These results indicate that testosterone can act directly on the adrenal gland to decrease 3betaHSD activity, immunoreactive protein, and mRNA content in mouse adrenal glands, and thus contribute to the sex difference in adrenal function observed in many species.

17-Hydroxysteroid Dehydrogenases↗
PubMed2002

Ipsilateral adrenal involvement from renal cell carcinoma: retrospective study of the predictive value of computed tomography.

OBJECTIVES: To compare the radiologic evidence of adrenal involvement on computed tomography (CT) with pathologic reports and to assess the accuracy of CT in the diagnosis of adrenal involvement with renal cell carcinoma. METHODS: Between January 1992 and June 2000, we treated 229 patients with renal cell carcinoma. In this study, we retrospectively analyzed 73 patients who had been examined by CT before surgery and had undergone radical nephrectomy, including removal of the ipsilateral adrenal gland. The abnormal integrity of the adrenal glands on CT and the pathologic adrenal involvement of renal cell carcinoma were demonstrated by a radiologist and pathologist, respectively. RESULTS: The blinded review by a radiologist of the CT results of 73 patients with renal cell carcinoma identified a normal appearance of the ipsilateral adrenal gland in 54 patients (74%), none of whom had pathologic evidence of malignant involvement. The adrenal gland was diagnosed as abnormal on CT in 19 patients (26%), including enlargement in 7 patients, nodule formation in 7, and an irregular surface in 8. Two of these 19 patients had adrenal involvement. Both were staged at T3M1, and their primary tumors were large, measuring more than 10 cm. In this study, CT demonstrated 100% sensitivity, 76% specificity, 11% positive predictive value, and 100% negative predictive value for ipsilateral adrenal involvement of renal cell carcinoma. CONCLUSIONS: Normal adrenal images on CT could exclude adrenal involvement by renal cell carcinoma. However, radical nephrectomy, including removal of the ipsilateral adrenal gland, should be performed in patients with large tumors.

Adrenal Gland Neoplasms↗
PubMed1999

Endothelin regulation of adrenal function.

1. The goal of the present review is to recount the evidence that endothelin (ET) has a significant influence on the peripheral sympathetic nervous system by regulating the function of the adrenal medulla. 2. The presence of an active ET system in the adrenal medulla has been clearly demonstrated. Endothelin protein, mRNA, binding sites and ET-converting enzyme have been identified in adrenal tissue and medullary chromaffin cells, suggesting that this peptide may contribute to the regulation of adrenal medullary function. 3. Studies investigating the function of ET in the adrenal gland have demonstrated that ET has a stimulatory effect on the adrenal medulla. Endothelin elicits an increase in catecholamine release from perfused intact adrenal glands as well as from cultured chromaffin cells. This effect has been shown to be mediated by ETA and ETB receptors. 4. The mechanism by which ET causes an increase in catecholamine release from the adrenal medulla appears to be independent of cholinergic activation of chromaffin cells. Endothelin has been shown to act directly at chromaffin cells to increase intracellular calcium, which results in catecholamine release. 5. Endothelin can indirectly affect catecholamine release by its effect on adrenal blood flow. Studies indicate that ET has both vasoconstrictor and vasodilator effects in the adrenal gland, which suggests a role for ET in the regulation of adrenal blood flow. Endothelin has also been proposed to participate in the selective contraction of the adrenomedullary veins, which enhances the discharge of catecholamines from the adrenal gland during activation.

Adrenal Medulla↗
PubMed1987

[Sonographic imaging of normal adrenal glands in children and adolescents. An analysis of forms and reflex properties].

168 sonographic examinations were performed in 156 children and adolescents for evaluation of the adrenal glands. For the ventrolateral approach, real-time sonography was used resulting in 99% visualisation of the adrenal glands on the right and 91% on the left side. In prone position, static scanning provided acceptable imaging of the right adrenal gland in 85% and the left in 95% of examinations. The "success rate" of transverse scanning was relatively low (67%) as compared to longitudinal sections. The reflective property of the adrenal glands was compared with the reflex intensity pattern of the adjacent parenchyma of the normal kidney. In 71% of examinations no distinction could be made between the adrenal glands and the upper pole of the kidney on the basis of echointensity. In 29% the adrenal gland was echolucent in comparison to the kidney's parenchyma. In no instance was the echointensity of the normal adrenal gland greater. Although the shape of the adrenal glands was found to vary according to the angle and position of the transducer, the most common appearance in children of one year or older was that of a triangle, helmet or cap. This caplike appearance and the similarity in echointensity often make it difficult or even impossible to distinguish the adrenal glands from the upper pole of the kidney. It is therefore advisable to examine the adrenal glands in children from both laterally and dorsally to allow for optimum visualization. In contrast to some reports in adults, increased echointensity of the adrenal gland (adrenal cortex) in children should be considered as an abnormal finding.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Management of contralateral adrenal metastasis from renal cell carcinoma: possibility of inferior vena cava tumour thrombus.

OBJECTIVE: The contralateral adrenal gland is a rare metastatic site in renal cell carcinoma (RCC). We describe our experiences with this metastasis in a cohort of 610 radical nephrectomy patients analysed. To our knowledge this study is the first to demonstrate an inferior vena cava tumour thrombus from metachronous contralateral adrenal metastasis. PATIENTS AND METHODS: After radical nephrectomy for RCC, 610 patients treated at our institution from 1985-99 were retrospectively investigated for the incidence of contralateral adrenal metastasis, additional clinical findings, treatment modalities and survival after treatment for contralateral adrenal gland metastasis. RESULTS: The incidence of contralateral adrenal metastasis was 1.1% (7/610 patients), while the incidence of ipsilateral metastasis was 3.4% (21/610). In 3 of 7 cases the contralateral adrenal metastasis occurred simultaneously with primary RCC in the kidney. The contralateral adrenal gland was affected by distant tumour spread metachronously in 4 of 7 cases (3/4 bilateral adrenal involvement, 1/4 unilateral disease). In 1 case a metachronous contralateral adrenal metastasis caused vena cava tumour thrombus by propagation via the suprarenal venous route. After a mean follow-up of 20 months (range 1-54 months), 4 of 6 patients showed no evidence of disease after contralateral adrenalectomy. CONCLUSIONS: The probability of contralateral adrenal metastasis from RCC is 1.1%. Adrenalectomy in these cases offers a good chance of cure. In 71% of cases contralateral adrenal metastasis occurs in conjunction with ipsilateral disease, which provides a strong argument for routine ipsilateral adrenalectomy during radical nephrectomy. Care must be taken in preoperative diagnostics, as metachronous adrenal metastasis is capable of causing vena cava tumour thrombus.

Adrenal Gland Neoplasms↗
PubMed2005

Adrenal metastasis in renal cell carcinoma: a recommendation for adjustment of the TNM staging system.

OBJECTIVES: To study the incidence of adrenal metastasis in patients with renal cell carcinoma (RCC) of all stages, its correlation with clinicopathological variables and its impact on survival. Furthermore, the need for adrenalectomy as part of the routine radical nephrectomy was assessed. MATERIAL AND METHODS: The medical records of 321 patients with RCC of all stages who were operated on with the aim of performing adrenalectomy combined with radical nephrectomy between 1982 and 2000 were reviewed. The accuracy of the available preoperative radiological examinations was evaluated and any adrenal involvement was compared with other clinical and histopathological findings. RESULTS: Ipsilateral adrenal tumour involvement was detected in 17/321 patients (5.3%). In four of these patients, the adrenal gland was the only preoperatively found metastatic site. Factors predicting the presence of ipsilateral adrenal metastases were male gender, tumour size, vein invasion, renal capsule and perirenal fat invasion. Tumour location within the kidney and tumour side had no predictive value for the presence of adrenal metastasis. The presence of ipsilateral adrenal involvement was a significant adverse prognostic variable, indicating a short survival time (p<0.001). CONCLUSIONS: Ipsilateral adrenal metastasis is a highly adverse prognostic factor. In the TNM staging system, adrenal gland involvement should be staged as M1a. Ipsilateral adrenalectomy in conjunction with radical nephrectomy should be performed if an adrenal lesion cannot be cleared of suspicion after preoperative radiological imaging, as in locally advanced tumours. The adrenal gland can be left in situ if the ipsilateral adrenal gland is assessed as normal at the preoperative investigation and perioperatively by the surgeon.

Adrenal Gland Neoplasms↗
PubMed1983

Increased free plasma corticosterone and adrenal hyperactivity associated with graft-versus-host disease.

This study profiles adrenal function in 14-day-old neonatal and adult rats with graft-versus-host disease (GVHD). Measurements of adrenal function included total serum corticosterone, the relative percentage of free corticosterone (a measure of biologically active hormone), adrenal cholesterol content, adrenal weights, and adrenal histology. Diseased animals in both age groups displayed a shift from the protein-bound to the free corticosterone fraction, with, surprisingly, no change in total serum corticosterone titers. We discuss the possibility that such a shift toward the biologically active, free-hormone pool results in a physiologic hyperglucocorticoidism that might contribute to the progress of GVHD. Compared with littermate controls, diseased adults had enlarged adrenals. In neonates with GVHD, no adrenal hypertrophy was evident, yet decreased adrenal cholesterol content and associated depletion of adrenal lipid droplets--evidence of adrenal hyperactivity--were identified. The GVHD must be responsible for the observed alterations in adrenal function because treatment of affected animals with alloantiserum directed against donor cells halted the disease and elevated the cholesterol content toward control levels. The possible contribution of adrenal dysfunction to the pathogenesis of secondary manifestations of GVHD is discussed.

Adrenal Glands↗
PubMed2005

Absolute and relative adrenal insufficiency in children with septic shock.

OBJECTIVE: Corticosteroid replacement improves outcome in adults with relative adrenal insufficiency and catecholamine-resistant septic shock. We evaluated the relationship of absolute and relative adrenal insufficiency to catecholamine-resistant septic shock in children. DESIGN: Prospective cohort study. SETTING: University hospital pediatric intensive care unit in Brazil. PATIENTS: Fifty-seven children with septic shock. Children with HIV infection, those with a history of adrenal insufficiency, and those submitted to any steroid therapy or etomidate within the week before diagnosis of septic shock were excluded. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: A short corticotropin test (250 microg) was performed, and cortisol levels were measured at baseline and 30 and 60 mins posttest. Adrenal insufficiency was defined by a response < or =9 microg/dL. Absolute adrenal insufficiency was further defined by a baseline cortisol <20 microg/dL and relative adrenal insufficiency by a baseline cortisol >20 microg/dL. Absolute adrenal insufficiency was observed in 18% of children, all of whom had catecholamine-resistant shock. Relative adrenal insufficiency was observed in 26% of children, of whom 80% had catecholamine-resistant and 20% had dopamine/dobutamine-responsive shock. All children with fluid-responsive shock had a cortisol response >9 microg/dL. Children with adrenal insufficiency had an increased risk of catecholamine-resistant shock (relative risk, 1.88; 95% confidence interval, 1.26-2.79). However, mortality was independently predicted by chronic illness or multiple organ failure (p < .05), not adrenal insufficiency. CONCLUSIONS: Absolute and relative adrenal insufficiency is common in children with catecholamine-resistant shock and absent in children with fluid-responsive shock. Studies are warranted to determine whether corticosteroid therapy has a survival benefit in children with relative adrenal insufficiency and catecholamine-resistant septic shock.

Adolescent↗
PubMed2005

Traumatic adrenal injuries.

PURPOSE: We determined the prevalence, management and general prognosis of blunt isolated and nonisolated adrenal injuries in a pediatric population. MATERIAL AND METHODS: We analyzed trauma data from a pediatric institution for the period 1991 to 1998 to identify patients with blunt traumatic adrenal injuries diagnosed by computerized tomography. We then performed a detailed chart review to obtain data on the presence of concomitant intra-abdominal and extra-abdominal injuries, transfusion requirements, intensive care unit monitoring requirements, hospital course and the presence of followup studies. RESULTS: Among 9,199 pediatric trauma cases we identified 20 adrenal injuries (0.22%), of which 15 (75%) were nonisolated and 5 (25%) were isolated. The right adrenal gland was injured in 17 (85%) of the 20 patients. In the 15 nonisolated adrenal injuries concomitant injury to the liver (13 cases, 87%) and ipsilateral kidney (8 cases, 53%) were most common. Three (60%) of the 5 patients with isolated adrenal injury required transfusion for adrenal hemorrhage. No patient required intensive care unit monitoring or operative intervention. Only 2 (10%) of the 20 patients underwent followup computerized tomography, both of whom had resolution of the adrenal injury. CONCLUSIONS: In the pediatric population blunt adrenal injuries are rare and typically present as part of a multiorgan trauma. The right adrenal gland is more likely to be injured, with liver trauma as the most commonly associated injury, followed by ipsilateral renal injury. Although there is a possibility of significant adrenal hemorrhage requiring transfusion, adrenal trauma is typically self-limited and does not require intensive care monitoring or operative intervention.

Abdominal Injuries↗
PubMed2006

Surgical treatment of adrenal metastasis from renal cell carcinoma: a single-centre experience of 45 patients.

OBJECTIVE: To report, in a retrospective study, the diagnostic problems and oncological results of surgery in patients with either synchronous or metachronous adrenal metastasis, which are uncommon in renal cancer, at 2-10% of patients. PATIENTS AND METHODS: Of 1179 patients treated for renal cancer between 1987 and 2003, 914 had renal surgery with concomitant ipsilateral adrenalectomy (routinely in 875 and for abnormal findings on computed tomography, CT, in 39) and 15 contralateral adrenalectomy (all after suspicious findings on CT). During the follow-up after renal surgery, another 14 patients had adrenalectomy for CT evidence of an abnormal adrenal gland, contralateral to the previous renal tumour in 12 and bilaterally in two. RESULTS: Of 914 ipsilateral adrenal glands removed during renal surgery, 854 (93.5%) were normal on pathological examination, 28 (3%) had a benign pathology, six (0.8%) were directly infiltrated by the tumour and 26 (2.7%) were metastatic. For both benign and metastatic ipsilateral adrenal pathology, CT had sensitivity, specificity and positive/negative predictive values of 47%, 99%, 73% and 96%, respectively. Of 29 contralateral glands removed because of suspicious CT findings (15 at diagnosis of renal cancer, 14 during the follow-up) there was no abnormality in one (3.4%), a benign pathology in seven (24%) and a metastasis in 21 (72%). Thus there were 32 synchronous (incidence 2.7%; ipsilateral to the renal tumour in 24, contralateral in six and bilateral in two), and 13 metachronous adrenal metastases (incidence 1.0%; contralateral in 11 and bilateral in two). The metachronous metastases were diagnosed at a mean (range) interval of 30.6 (8-73) months after renal surgery. No ipsilateral adrenal metastases were discovered at diagnosis or during the follow-up in the 382 patients with an organ-confined renal tumour of <4 cm in diameter. Twenty-seven patients with an isolated adrenal metastasis (synchronous in 14, metachronous in 13) had statistically significantly (P < 0.001) better survival than the 18 (all synchronous) with multiple sites of metastatic disease. In particular, there was long-term survival (mean 83 months) in 10 patients with an isolated adrenal metastasis. CONCLUSION: Sparing the ipsilateral adrenal is advisable only for organ-confined renal tumours of <4 cm in diameter; clinical local staging of renal cancer is the best predictor of the risk of adrenal metastasis. Conversely, CT had good diagnostic ability for the contralateral adrenal gland, especially during the follow-up. Some patients with isolated adrenal metastasis could be treated by metastasectomy, with long-term survival free of disease and confirming that, even if in a few and unselectable patients, removing all the neoplastic bulk can be curative. Nevertheless, the high rate of relapse underlines the need for an effective systemic therapy, and more so for widespread metastatic disease that currently cannot be cured.

Adrenal Gland Neoplasms↗