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PubMed1991

The modification and expression of 21-hydroxylase gene in normal human adrenal gland and adrenal cancer.

Genomic DNA and total RNA from three adrenal cancer tissues were analyzed by hybridization with human 21-hydroxylase gene. Southern blot analysis with restriction enzyme Eco RI revealed major fragments at 18, 13 and 9 kilobase (kb) in normal adrenal glands. In two of three adrenal cancers, however, the band at 18 kb was either absent or decreased and the 9 kb fragment showed an increase in its intensity. Normal liver, kidney and leucocytes has only 18 and 13 kb while lacking the 9 kb fragment. Using Taq I, Bam HI or Bgl II, we found no difference in restriction fragment patterns between adrenal cancer and normal tissues. Cleavage with Hpa II after digestion with Bgl II showed that significantly more DNA was digested into low-molecular weight fragments in adrenal cancer and the normal adrenal gland than those in other normal tissues. By Northern blot analysis, there was difference of signal intensity of hybridizing mRNA between the adrenal cancers and normal adrenal glands. These results suggest that the Eco RI site in the flanking region of the 21-hydroxylase gene may be modified in adrenal cancer tissue, and that inadequate 21-hydroxylase is present in some forms of adrenal cancers.

Adrenal Cortex Hormones↗
PubMed1975

Adrenal venography and ultrasound in the investigation of the adrenal gland: an analysis of 58 cases.

Adrenal venography has been carried out in 58 patients with the left adrenal vein being successfully catheterized in 91 per cent and the right in 77 per cent. Of the 30 patients with primary hyperaldosteronism, 11 adenomas (12-35 mm diameter) have been demonstrated at venography and two of 15 mm suspected, all of which were confirmed surgically. Aldosterone levels in the adrenal vein plasma were raised on the affected side. In the group of proved micronodular hyperplasia, two patients had surgically confirmed macronodules and venography demonstrated one of 12 mm diameter. Two adenomas of 11 mm and one macronodule of 15 mm have been demonstrated at venography in the remainder who have not had an operation. Ultrasound was carried out in 12 patients with primary hyperaldosteronism, ten of which had tumours at venography. Two adenomas measuring 30 and 31 mm were outlined by ultrasound and confirmed surgically. Seven adenomas, including one macronodule (10-25 mm in diameter) were not defined. Three intra-adrenal phaeochromocytomas (45-90 mm) and one extra-adrenal (80-85 mm) were demonstrated at arteriography, identified by ultrasound and confirmed surgically. Of the ten patients with Cushing's syndrome three had enlarged glands at venography, this was confirmed surgically. Cumulative experience from this analysis and published reports indicate that venography will demonstrate tumours of 10 mm or more in diameter and outline enlarged glands; aldosterone assays will lateralize tumours as small as 3 mm; ultrasound will outline tumours of 30 mm and selective adrenal arteriography will demonstrate tumours of 10 mm. One patient developed acute adrenal cortical insufficiency with intra-adrenal extravasation on one side and thrombosis of the central vein on the opposite side. A second case developed temporary adreno-cortical insufficiency. Published reports indicate that the risk of complication is about 1 per cent. The report includes an anatomical study of the efferent adrenal veins in 50 patients paying particular attention to the diameter, number of accessory hepatic veins, and the angle of entry and position of the right adrenal vein.

Adenoma↗
PubMed1981

Iodocholesterol adrenal scanning for the detection of adrenal metastases in lung cancer and its clinical significance.

Detection of adrenal metastases is difficult. Since metastatic growth fails to destroy sufficient adrenal tissue to produce clinical symptoms of adrenal insufficiency, and since adrenal metastases have been reported in 28--36% of autopsied patients with primary lung cancer, the authors studied 25 patients with lung cancer by using iodocholesterol adrenal scans. Six patients (24%) were found to have abnormal scans suggestive of adrenal metastases by this technique. Two of these patients were confirmed by biopsy to have adrenal metastases. Four of the six patients died within a mean of six weeks of the positive scan. Iodocholesterol adrenal scanning appears to be a promising noninvasive technique in the detection of adrenal metastases. The prognostic significance of adrenal metastases is discussed.

19-Iodocholesterol↗
PubMed2000

Virilizing adrenal adenoma and primary amenorrhea in a girl with adrenal hyperplasia.

We report a 14-year-old girl with primary amenorrhea and virilization. The chromosomal analysis showed a normal 46,XX female karyotype and the hormonal assays disclosed high serum levels of testosterone (T): 450 ng/dL (normal 5-90), dehidroepiandrosterone-sulfate (DHEA-S): 690 microg/dL (normal 30-450) and 17-hydroxiprogesterone (17-OHP) >20 ng/mL (normal <2). A pelvic ultrasound disclosed a small uterus and bilateral enlargement of the ovaries, a computed axial tomographic scan of the abdomen identified a large right mass in the adrenal gland and a norcholesterol-I 131 adrenal gammagraphy revealed a functional adrenal tumor. The histological analysis of the surgical removed tumor revealed and adrenal adenoma. After surgery, a steep decline to normal serum levels of T and DHEA-S was observed, remaining an elevated level of 17-OHP: 5.4 ng/mL. During the first three months of follow up, the hirsutism declined sharply and spontaneous mammary development occurred, remaining elevated the 17-OHP serum level: 4.8 ng/mL. Prednisone 5 mg/day, was initiated decreasing the 17-OHP to normal level: 1.4 ng/mL, appearing the menarche followed by cyclical menses. One year after surgery, prednisone was withdrawn during one week, and an ACTH test and HLA typing were done, disclosing a 17-OHP response of an heterozygote for adrenal hyperplasia, and identifying B65 a subtype of B14, and DR1, that are frequently associated to adrenal hyperplasia. Previous reports have informed silent adrenal tumors associated to adrenal hyperplasia, but this is the first report of a functional adrenal tumor associated to adrenal hyperplasia.

Adenoma↗
PubMed1994

Evidence of a steroidogenic enzyme gene dose effect on adrenal gene expression in hereditary rabbit congenital adrenal hyperplasia.

We previously reported the gene deletion encoding cytochrome P-450 cholesterol side-chain cleavage enzyme (P-450SCC, resulting in complete elimination of the adrenal gene expression and causing congenital adrenal hyperplasia in the rabbit. Using the rabbit congenital adrenal hyperplasia model, we investigated the wild type (wt) P-450SCC gene dose effect on gene expression in three P-450SCC genotype animals [wt/wt, wt/mutant (mt), mt/mt] identified by Southern blot analysis. Northern blots using a rabbit P-450SCC cDNA probe revealed no detectable P-450SCC mRNA in individual adrenals of animals with congenital adrenal hyperplasia (mt/mt) and approximately half or slightly less than half the levels of the mRNA in the pooled adrenals of five heterozygous (wt/mt) newborn animals compared with the mRNA levels in the pooled adrenals of five homozygous normal (wt/wt) newborn animals. Identical P-450SCC mRNA levels were found individual adrenals of adult animals with regard to the P-450SCC genotype, although at a higher expression level than in the newborn animals of the same genotype. Control Northern blots using human CPY21-B cDNA and cytoplasmic actin cDNA probes confirmed the accuracy and integrity of RNA. Western immunoblotting using anti-ovine P-450SCC antibody revealed decreased P-450SCC protein in the adrenals of wt/mt animals at approximately half the level of the P-450SCC protein in the adrenals of the wt/wt animals. Baseline and ACTH-stimulated serum corticosterone (B) levels in vivo were similar between the age-matched wt/mt and wt/wt animals, whereas ACTH-stimulated B levels in adult animals were higher than those in the newborn animals irrespective of P-450SCC genotype.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1999

Testicular adrenal rest tissue in congenital adrenal hyperplasia: serial sonographic and clinical findings.

OBJECTIVE: The purpose of this study was to describe the serial sonographic findings and clinical and laboratory data obtained during follow-up of patients with congenital adrenal hyperplasia in whom testicular adrenal rest tissue develops. MATERIALS AND METHODS: We retrospectively reviewed testicular sonography and laboratory data for 12 patients with congenital adrenal hyperplasia who also had intratesticular masses consistent with adrenal rest tissue. The studies were done during follow-up that ranged from 7 months to 10 years. RESULTS: During follow-up of 11 of the 12 patients after the initial sonographic diagnosis, the testicular adrenal rest tissue either remained stable in size (n = 1), grew larger or smaller (n = 9), disappeared (n = 4), or reappeared after disappearing (n = 3). In one patient, the testicular adrenal rest tissue grew very rapidly in a 1-month interval. Discordant changes in the testicular adrenal rest tissue were noted in 10 patients with bilateral masses. We found no relationship between the change in size of the masses and clinical control (based on 17-hydroxyprogesterone level) at the time of sonography. CONCLUSION: In patients with congenital adrenal hyperplasia who have testicular masses detected sonographically, testicular adrenal rest tissue is the most likely diagnosis. Testicular adrenal rest tissue may remain stable in size, grow larger or smaller, or disappear during sonographic follow-up. The change in size may be marked, may occur very rapidly, and, in our study cohort, was not related to short-term clinical control based on 17-hydroxyprogesterone level at the time of sonography.

Adrenal Hyperplasia, Congenital↗
PubMed1989

[Flow cytometric DNA analysis of normal adrenal tissues and adrenal tumors].

Flow cytometric DNA analysis (FCM) of adrenal tumors was studied to evaluate whether FCM will be a useful examination for differentiating between benign and malignant adrenal tumors. 10 specimens of surgically resected (for renal cell carcinoma confined within the middle or lower pole) normal adrenal glands and 20 specimens of surgically resected adrenal tumors were submitted for the study. Hyperplastic adrenal cortex as well as normal adrenal gland showed normal diploid pattern. On the other hand, some of the cortical adenomas showed tetraploid patterns, which has been known to be an index of malignancy in most of the flow cytometric intervention to other solid tumors. Conn adenomas were especially apt to show this tendency, in which as much as 86% showed tetraploid pattern. Proliferation Index (PI) (ratio of S + G2 +M cells for the whole population of analyzed cells) were as much as 9.45 +/- 6.97% in normal adrenal cells, whereas it was much higher in cortical adenomas (17.75 +/- 8.53%). As a matter of fact, PI of hyperplastic adrenal cortex was within the same range as that of the normal adrenal glands. In pheochromocytomas, aneuploid pattern, which has been believed to be a definite index of malignancy, was shown in 60% of the cases, tetraploid pattern in 20%, and normal diploid pattern in only 20%. As a matter of fact, a case of non functioning cortical adenocarcinoma and a case of malignant pheochromocytoma were judged to show typical aneuploid pattern. Thus, the application of the flow cytometric diagnosis for adrenal tumors was supposed to require some refinement in understanding the significance of aneuploidy or tetraploidy.

Adrenal Gland Neoplasms↗
PubMed1993

Congenital adrenal hyperplasia diagnosed in a man during workup for bilateral adrenal masses.

We studied an asymptomatic 55-year-old man who was found to have markedly enlarged adrenal glands on an abdominal computed tomographic scan and was scheduled to have adrenal biopsy because of suspicious findings on an adrenal magnetic resonance image. However, hormonal studies revealed congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Treatment with dexamethasone decreased the size of the adrenal glands. This is, we believe, the first report of congenital adrenal hyperplasia in an adult, diagnosed during the evaluation of an incidental adrenal lesion. Although congenital adrenal hyperplasia can present with varying severity and remain undiagnosed into adulthood, it is usually not considered in the evaluation of asymptomatic adult adrenal masses. We emphasize the need for proper hormonal studies in the evaluation of incidental adrenal lesions.

Adrenal Gland Diseases↗
PubMed1999

Clinical utility of adrenal ultrasonography in the diagnosis of congenital adrenal hyperplasia.

Rapid, accurate diagnosis of congenital adrenal hyperplasia (CAH) is essential in the neonate with ambiguous genitalia, life-threatening salt loss, or both. We aimed to determine the accuracy of adrenal ultrasonography in the diagnosis of CAH in a retrospective analysis of 52 children with ambiguous genitalia or salt-losing crises. Adrenal ultrasounds were interpreted as follows: "normal" if the adrenals were normal in size (adrenal limb width <4 mm), had a smooth surface, and a central echogenic stripe with a hypoechoic rim, and "abnormal" if they were increased in size (limb width >4 mm), had a lobulated or cerebriform surface, or showed abnormal echogenicity. Group 1 consisted of 25 neonates and infants with CAH; group 2, 19 children with conditions other than CAH; and group 3, 8 with treated CAH: 7 receiving replacement therapy and 1 whose mother received glucocorticoids during pregnancy. In all children in groups 2 and 3, adrenal ultrasounds were read as normal. In group 1 adrenal ultrasonography was normal in 2 (8%) and abnormal in 23 (92%). Thus adrenal ultrasonography has a sensitivity of 92% and a specificity of 100% for diagnosing CAH. Adrenal ultrasonography is a highly sensitive and specific adjunct in the diagnosis of CAH. The presence of enlarged, lobulated adrenals with stippled echogenicity is invariably associated with CAH.

17-alpha-Hydroxyprogesterone↗
PubMed2005

Adrenal pheochromocytoma with contralateral cortisol-producing adrenal adenoma: diagnostic and therapeutic management.

There is evidence for a close interrelation between the adrenomedullary and adrenocortical tissues, and there are well-characterized models of their paracrine interaction. To contribute to the studies of systemic interactions between these tissues, we studied a 52-year-old female patient with a pheochromocytoma and a contralateral cortisol-producing adenoma. Due to a misunderstanding, she presented to her family doctor to have an inherited kidney disease ruled out. An adrenal mass was discovered incidentally by ultrasound. A computerized tomography of the abdomen revealed bilateral adrenal masses. Due to excess catecholamine secretion, bilateral pheochromocytomas based on multiple endocrine neoplasia syndrome were suspected. Laboratory work-up, selective adrenal venous sampling and magnetic resonance imaging studies established the diagnosis of a pheochromocytoma in the right-hand adrenal gland and a cortisol-producing adenoma on the left. Simultaneous bilateral laparoscopic subtotal adrenalectomy was performed. Immunohistochemistry showed positive staining against chromogranin A in a histological specimen obtained from the right-hand adrenal gland, while the left was negative; the left-hand adrenal gland stained positive against the ACTH receptor (MC2R) while the right was negative. Genetically, the patient was negative for MEN2, von Hippel-Lindau disease, and mutations in subunits B, C, and D of the succinate dehydrogenase gene. Although presence of bilateral adrenal adenomas or bilateral adrenal pheochromocytomas in certain inherited disorders are possible, this rare case of an adrenal pheochromocytoma combined with a contralateral cortisol-producing adrenal adenoma may further underline the wide range of complex interactions between the two endocrine systems.

Adrenal Cortex Neoplasms↗
PubMed1998

Unknown primary cancer presenting as an adrenal mass: frequency and implications for diagnostic evaluation of adrenal incidentalomas.

BACKGROUND: Fine-needle aspiration biopsy to identify adrenal metastasis from an occult primary malignancy has been recommended as part of the evaluation of the patient who presents with an incidentally discovered adrenal mass. This recommendation was assessed by examining the frequency of adrenal involvement in patients with suspected unknown primary cancer. METHODS: Data from 1715 patients referred for evaluation of suspected unknown primary cancer were retrospectively reviewed. RESULTS: Of 1639 patients found to have cancer, the adrenal gland was identified as a site of involvement at presentation in 95 (5.8%). Involvement was limited to the adrenal gland in 4 patients (0.2%). All 4 patients had large (> or = 6 cm) adrenal tumors, 3 of 4 had bilateral involvement, and all had symptoms that otherwise mandated evaluation for an occult malignancy; none had a true adrenal incidentaloma. CONCLUSIONS: Although cancer of an unknown primary site occasionally involves the adrenal gland, metastatic cancer presenting as a true adrenal incidentaloma is extremely rare. Therefore, in the absence of a history of prior malignancy or symptoms, physical examination findings, radiographic findings, or laboratory findings suggestive of an occult malignancy, we do not recommend fine-needle aspiration biopsy as part of the diagnostic evaluation of the patient who presents with a unilateral adrenal mass.

Adrenal Gland Neoplasms↗
PubMed2002

Adrenal splanchnic innervation modulates adrenal cortical responses to dehydration stress in rats.

Classically, the production of glucocorticoids by the adrenal gland is thought to be controlled exclusively by adrenocorticotropic hormone (ACTH). However, there are several examples in stressed humans and animals of increased plasma glucocorticoids in the absence of increased plasma ACTH, suggesting that an additional, non-ACTH mechanism(s) may contribute to the control of glucocorticoid production. The present studies were designed to determine the role of the thoracic splanchnic nerve in controlling plasma corticosterone levels in response to chronic water deprivation in rats, a model previously reported to demonstrate dissociations between plasma corticosterone and ACTH. Briefly, rats underwent right unilateral adrenalectomy and left thoracic splanchnic nerve transection or sham transection. After recovery, rats were water deprived for 48 h or given free access to water, and then sacrificed for collection of plasma and adrenal glands. Water deprivation resulted in consistent, robust increases in plasma corticosterone that were attenuated by splanchnic nerve transection, in the absence of changes in post-dehydration plasma ACTH. Adrenal content of steroidogenic acute regulatory factor (StAR) and cyclic AMP (cAMP) were increased after dehydration; splanchnic nerve transection decreased post-dehydration adrenal cAMP, but not StAR. Splanchnic nerve transection also attenuated plasma corticosterone responses to submaximal doses of ACTH in dexamethasone-blocked, dehydrated rats, suggesting a decreased adrenal sensitivity to ACTH. Collectively, the present results demonstrate that the thoracic splanchnic nerve normally augments the adrenal corticosterone response to dehydration stress by increasing adrenal sensitivity to ACTH, and this augmentation is associated with elevations in adrenal cAMP content. These data support the hypothesis that the splanchnic innervation of the adrenal gland represents an additional physiological mechanism to control stress-induced adrenal cortical responses in vivo.

Adrenal Glands↗
PubMed1981

Iodocholesterol adrenal tissue uptake and imaging adrenal neoplasms.

To correlate iodocholesterol tissue uptake with the ability to visualize adrenal cortical neoplasms, eight female patients with adrenal carcinoma had adrenal scintiscans after the injection of 19-[131I]iodocholesterol. Patients with cortisol-secreting carcinomas failed to image either the tumor or uninvolved adrenal tissue. In contrast, patients with androgen-secreting carcinomas (which do not suppress pituitary ACTH secretion), although still failing to image the tumor, had visible concentration of the radionuclide in the ipsilateral and contralateral adrenal glands. Slices of these tissues obtained at either surgery or postmortem examination were analyzed for iodocholesterol uptake. Results were compared with adrenal tissue obtained from patients with either cortisol- or aldosterone-secreting adenomas and patients on dexamethasone suppression. There was a strong correlation between the adrenal tissue concentration of iodocholesterol and the ability to form an image on scintiscanning. The concentration of iodocholesterol in an adenoma and a carcinoma determined in this manner was compared with their cortisol secretion during in vitro incubation. The concentration of 19-[131I]iodocholesterol and the in vitro secretion of cortisol were greater in the adenoma than in the carcinoma and corresponded with adrenal imaging in the former and lack of imaging in the latter. These data provide a quantitative assessment of the differences in radioactivity concentration required for imaging of adrenal tumors. It also demonstrates that differences in the concentration of radioactivity within adrenal carcinomas and adenomas corresponds to their ability to release cortisol in vitro.

19-Iodocholesterol↗
PubMed2005

Expression of urocortin 3/stresscopin in human adrenal glands and adrenal tumors.

Urocortin 3 (Ucn 3)/stresscopin (SCP) is a novel peptide of the corticotropin-releasing factor (CRF) family and is a specific ligand for the CRF type 2 receptor. In the present study, we studied expression of Ucn3/SCP in the normal adrenal and adrenal tumors by radioimmunoassay and reverse transcriptase-polymerase chain reaction (RT-PCR). High concentrations of immunoreactive (IR)-Ucn3 were present in the normal portions of adrenal glands (4.2+/-0.51 pmol/g wet weight, mean+/-S.E.M., n = 14), and the levels were higher than those in the brain. IR-Ucn3 was also detected in the tumor tissues of aldosterone-secreting adenomas (6.2+/-0.6 pmol/g wet weight, n = 10), cortisol-secreting adenomas (5.0+/-1.2 pmol/g wet weight, n = 4), and pheochromocytomas (1.9+/-0.4 pmol/g wet weight, n = 7). Reverse phase high performance liquid chromatography showed that IR-Ucn3 in normal portions of adrenal glands and aldosterone-secreting adenomas was eluted mainly in the positions of Ucn3 and SCP with several minor peaks eluting earlier. The RT-PCR showed expression of Ucn3 mRNA in normal portions of adrenal gland (positive ratio; 4/4), aldosterone-secreting adenomas (3/4), cortisol-secreting adenomas (1/3) and pheochromocytomas (6/7). These findings indicate that Ucn3 is produced in normal adrenal and adrenal tumors (both adrenocortical tumors and pheochromocytomas), and suggest that Ucn3 acts as an autocrine or paracrine regulator in normal adrenal and adrenal tumors.

Adenoma↗
PubMed1999

Detection of Ob-receptor in human adrenal neoplasms and effect of leptin on adrenal cell proliferation.

Leptin, a hormone mainly secreted from adipose tissue, communicates a metabolic signal to the adrenal gland. Ob-Receptor (Ob-R) expression was reported in rat, mice and human adrenal glands. This study intended to investigate possible differences in the Ob-R expression and distribution of Ob-R protein in human adrenal tumors as compared to normal adrenal tissue. Proliferative effects of leptin were analyzed in the human adrenocortical carcinoma cell line (NCI-H295). The full length Ob-R mRNA and the isoforms B219.1 and B219.3 could be demonstrated by RT-PCR in all adrenal tumors (n=8), the tumor cell line (NCI-H295) and normal tissue. In contrast the Ob-R isoform B219.2 was absent in the carcinoma cell line and in most of the adrenal tumors (n=5), whereas it was present in normal adrenals. The Ob-R protein could be demonstrated in benign and malignant adrenocortical tumors. Pheochromocytomas showed only a weak immunostaining with the human Ob-R antibody. Human leptin did not affect the proliferation or variability of adrenal tumor cells as demonstrated by [3H]-thymidine assay and WST-1 test. In conclusion, although functional leptin receptors are expressed in human adrenal tumors, leptin does not regulate tumor cell proliferation.

Adenoma↗
PubMed1987

Prospective evaluation of adrenal insufficiency in patients with adrenal metastasis.

Fifteen consecutive patients with metastatic carcinoma who demonstrated bilateral adrenal metastasis on abdominal computed tomography (CT) were evaluated by the cosyntropin challenge test. Primary sites of tumors included lung, ten; colon, two; gastric, one; ovarian, one; and unknown primary, one. Bilateral adrenal enlargement was defined as greater than 1 cm on CT scan. Adrenal insufficiency was defined as a failure to increase serum cortisol by at least 5 micrograms/100 ml to a minimum of 15 micrograms/100 ml at either 30 or 60 minutes postcosyntropin. No patient had previously been on corticosteroids. All patients were questioned and examined for symptoms/signs of adrenal insufficiency. Five patients (33%) were found to have adrenal insufficiency based on the cosyntropin test. Of the clinical parameters evaluated, all five patients had nausea, anorexia, and orthostatic hypotension. The clinical onset of adrenal insufficiency was insidious; no patient experienced acute adrenal crisis. We conclude that adrenal insufficiency is not a rare occurrence in patients with metastatic cancer and bilateral adrenal involvement on CT scan.

Adrenal Gland Neoplasms↗
PubMed2003

High diagnostic accuracy of adrenal core biopsy: results of the German and Austrian adrenal network multicenter trial in 220 consecutive patients.

Incidentally detected adrenal tumors are a common finding during abdominal ultrasonography, computed tomography, and magnetic resonance imaging. Although most of these lesions are benign adenomas, adrenocortical carcinomas and metastases constitute 5% to 10% of all tumors. Adrenal biopsy may be helpful, but its diagnostic value is controversial and disputed, and prospective studies have not yet been performed. Therefore, the diagnostic accuracy of adrenal core biopsy was evaluated in a prospective multicenter study involving 8 surgical centers in Germany and Austria. A total of 220 biopsies from surgical specimens of the adrenal gland were punctured in an ex vivo approach and processed for pathohistologic diagnosis using paraffin sections, routine staining, and immunohistochemistry (keratin KL1, vimentin, S100 protein, chromogranin A, synaptophysin, neuron-specific enolase, D11, MiB-1, and p53 protein). The evaluating pathologist was blinded for clinical data from the patients. A total of 89 adrenal adenomas (40.5%), 22 adrenal carcinomas (10.0%), 55 pheochromocytomas (25.0%), 15 metastases (6.8%), 16 adrenal hyperplasias (7.2%), and 23 other tumors (10.5%) were studied. Nine cases were excluded due to incomplete data (n = 2) or insufficient biopsy specimen (n = 7). In the remaining 211 tumors, compared with the final diagnoses of the surgical specimen, bioptic diagnoses were absolutely correct in 76.8% of the cases, nearly correct in 13.2% of the cases, and incorrect in 10% of the cases. Pheochromocytomas were correctly diagnosed in 96% of the cases, cortical adenomas were correctly or nearly correctly reported in 91% of the cases, cortical carcinomas were correctly or nearly correctly reported in 76% of the cases, and metastases were correctly or nearly correctly reported in 77% of the cases. Of the 39 malignant lesions, only 4 were misclassified, 2 as benign and 2 as possibly malignant. This resulted in an overall sensitivity for malignancy of 94.6% and specificity of 95.3%. Our findings suggest that adrenal core biopsy is a useful method for identifying and classifying adrenal tumorous lesions if sufficient biopsy specimens can be obtained. However, in clinical practice it remains to be shown whether the benefits of biopsy outweigh the risks of the procedure.

Adenoma↗
PubMed2004

Adrenal insufficiency due to primary bilateral adrenal non-Hodgkin's lymphoma.

A case of primary adrenal insufficiency, secondary to primary bilateral adrenal lymphoma is reported. A 50-year-old woman presented with features of primary adrenal insufficiency (darkening of skin, asthenia, anorexia, constipation) for at least 8 months. Clinical examination was unremarkable except for low body mass index and generalized skin and buccal mucosal pigmentation. Routine investigations including complete hemogram, serum chemistry, urine analysis, chest radiograph and electrocardiogram were normal; serum lactate dehydrogenase was moderately elevated. Primary adrenal insufficiency was confirmed on cortisol dynamics (very low basal and peak cortisol) after insulin-induced hypoglycemia. Routinely detected adrenal masses on ultrasonography were confirmed by contrast enhanced CT abdomen. A diagnosis of primary adrenal non- Hodgkin's lymphoma (B-cell) was made after exploratory laprotomy and further staging. The patient was put on combination chemotherapy (CHOP) protocol, but was lost to follow-up after receiving two cycles of treatment. Primary adrenal lymphoma, although a rare entity, needs to be suspected in patients with features of primary adrenal insufficiency who have evidence of bilateral adrenal masses on imaging.

Adrenal Gland Neoplasms↗