Bilateral Adrenocortical Adenomas Research Articles

Diagnostic and therapeutic approaches to a case of pregnancy complicated by bilateral adrenocortical adenomas with primary aldosteronism and Cushing's syndrome.

Aldosterone/cortisol co-secreting adenomas (A/CPA) are a rare type of primary aldosteronism(PA), and cases of aldosterone/cortisol co-secreting adenomas during pregnancy are extremely rare, with no reported cases to date. The unique physiological state of pregnancy increases cortisol secretion through the hypothalamic-pituitary-adrenal (HPA) axis and leads to elevated levels of all components of the renin-angiotensin-aldosterone system (RAAS). This can cause overlapping symptoms with abnormal cortisol and aldosterone secretion, making diagnosis very challenging. This case involves a 29-year-old woman who developed hypercortisolism at 33 weeks of pregnancy. Despite receiving treatment for her symptoms and having a successful delivery, she continued to experience hypertension and hypokalaemia after giving birth. Eventually, she was diagnosed with ACTH-independent Cushing's syndrome and primary aldosteronism due to independent cortisol and aldosterone secretion from bilateral adrenal adenomas. Following a thorough diagnosis, classification, treatment, and follow-up, the patient achieved a clinical cure while preserving normal adrenal function. Further investigation revealed that both diseases were caused by KCNJ5 and PRKACA mutations found in the bilateral adrenal adenomas.

Bilateral co-secretory lesions presenting with coexisting Cushing syndrome and primary aldosteronism: a case report

BackgroundThere is an increasing number of cases of aldosterone- and cortisol-producing adenomas (A/CPAs) reported in the context of primary aldosteronism (PA). Most of these patients have PA complicated with subclinical Cushing's syndrome; cases of apparent Cushing's syndrome (CS) complicated with aldosteronism are less reported. However, Co-secretory tumors were present in the right adrenal gland, a cortisol-secreting adenoma and an aldosterone-producing nodule (APN) were present in the left adrenal gland, and aldosterone-producing micronodules (APMs) were present in both adrenal glands, which has not been reported. Here, we report such a case, offering profound insight into the diversity of clinical and pathological features of this disease.Case presentationThe case was a 45-year-old female from the adrenal disease diagnosis and treatment centre in West China Hospital of Sichuan University. The patient presented with hypertension, moon-shaped face, central obesity, fat accumulation on the back of the neck, disappearance of cortisol circadian rhythm, ACTH < 5 ng/L, failed elevated cortisol inhibition by dexamethasone, orthostatic aldosterone/renin activity > 30 (ng/dL)/(ng/mL/h), and plasma aldosterone concentration > 10 ng/dL after saline infusion testing. Based on the above, she was diagnosed with non-ACTH-dependent CS complicated with PA. Adrenal vein sampling showed no lateralization for cortisol and aldosterone secretion in the bilateral adrenal glands. The left adrenocortical adenoma was removed by robot-assisted laparoscopic resection. However, hypertension, fatigue and weight gain were not alleviated after surgery; additionally, purple striae appeared in the lower abdomen, groin area and inner thigh, accompanied by systemic joint pain. One month later, the right adrenocortical adenoma was also removed. CYP11B1 were expressed in the bilateral adrenocortical adenomas, and CYP11B2 was also expressed in the right adrenocortical adenomas. APN existed in the left adrenal gland and APMs in the adrenal cortex adjacent to bilateral adrenocortical adenomas. After another surgery, her serum cortisol and plasma aldosterone returned to normal ranges, except for slightly higher ACTH.ConclusionsThis case suggests that it is necessary to assess the presence of PA, even in CS with apparent symptoms. As patients with CS and PA may have more complicated adrenal lesions, more data are required for diagnosis.

Different cell compositions and a novel somatic KCNJ5 variant found in a patient with bilateral adrenocortical adenomas secreting aldosterone and cortisol.

This study aimed to explore the possible pathogenesis of a rare case of co-existing Cushing's syndrome (CS) and primary aldosteronism (PA) caused by bilateral adrenocortical adenomas secreting aldosterone and cortisol, respectively. A 41-year-old Chinese woman with severe hypertension and hypokalemia for 5 and 2 years, respectively, was referred to our hospital. She had a Cushingoid appearance. Preoperative endocrinological examinations revealed autonomous cortisol and aldosterone secretion. Computed tomography revealed bilateral adrenal adenomas. Subsequently, adrenal vein sampling and sequential left and right partial adrenalectomy indicated the presence of a left aldosterone-producing tumor and a right cortisol-producing tumor. Pathological examination included immunohistochemical analysis of the resected specimens. Secretions of aldosterone and cortisol were observed both in vivo and in vitro. Further, whole-exome sequencing was performed for DNA that was extracted from peripheral blood leukocytes and bilateral adrenal adenomas in order to determine whether the patient had relevant variants associated with PA and CS. Immunohistochemical staining revealed that the left adenoma primarily comprised clear cells expressing CYP11B2, whereas the right adenoma comprised both eosinophilic compact and clear cells expressing CYP11B1. The mRNA levels of steroidogenic enzymes (including CYP11B1 and CYP17A1) were high in the right adenoma, whereas CYP11B2 was highly expressed in the left adenoma. A novel somatic heterozygous missense variant-KCNJ5 c.503T > G (p.L168R)-was detected in the left adrenal adenoma, but no other causative variants associated with PA and CS were detected in the peripheral blood or right adrenocortical adenoma. In the primary cell culture of the resected hyperplastic adrenal adenomas, verapamil and nifedipine, which are two calcium channel blockers, markedly inhibited the secretion of both aldosterone and cortisol. We present an extremely rare case of bilateral adrenocortical adenomas with distinct secretion of aldosterone and cortisol. The heterogeneity of the tumor cell compositions of aldosterone- and cortisol-producing adenoma (A/CPA) and somatic mutation of KCNJ5 may have led to different hormone secretions in the bilateral adrenal adenomas.

Aortic and iliac thrombosis in a dog with adrenal-dependent hypercortisolism due to bilateral adrenocortical adenoma

ABSTRACT: Hypercortisolism is a common endocrinopathy in dogs; however, in a few cases, bilateral functional adrenocortical adenomas cause spontaneous disease, and thrombotic events are considered uncommon complications. The aim of this report was to describe a case of bilateral adrenocortical adenoma in a dog with hyperadrenocorticism associated with distal aortic and iliac thrombosis, with emphasis on clinical and pathological aspects. A 15-year-old spayed female Dachshund with a previous clinical history of hyperadrenocorticism presented with acute bilateral hindlimb paraparesis. A vertebral thoracolumbar radiography was performed and did not present any evidence of intervertebral disk disease or vertebral abnormalities; however, abdominal ultrasound and vascular Doppler evaluation revealed bilateral adrenal enlargement in addition to an aortic and external iliac artery thrombus. The animal was euthanized. At necropsy, both adrenal glands were enlarged by well-demarcated neoplastic nodules in the parenchyma, and a thrombus caudal to the abdominal aorta bifurcation within the external iliac arteries that extended to the left external iliac artery was noted. Histological evaluation revealed a well-differentiated neoplastic proliferation of cortical epithelial cells, consistent with bilateral adenoma, and muscular necrosis in the pelvic limbs was also observed. Bilateral functional adrenocortical adenoma; although, very rare, should be considered as a cause of hypercortisolism, and aortic thrombosis in dogs should be considered as a possible consequence.

Hypercortisolism and primary aldosteronism caused by bilateral adrenocortical adenomas: a case report

BackgroundCo-existing Cushing’s syndrome and primary aldosteronism caused by bilateral adrenocortical adenomas, secreting cortisol and aldosterone, respectively, have rarely been reported. Precise diagnosis and management of this disorder constitute a challenge to clinicians due to its atypical clinical manifestations and laboratory findings.Case presentationWe here report a Chinese male patient with co-existing Cushing’s syndrome and primary aldosteronism caused by bilateral adrenocortical adenomas, who complained of intermittent muscle weakness for over 3 years. Computed tomography scans revealed bilateral adrenal masses. Undetectable ACTH and unsuppressed cortisol levels by dexamethasone suggested ACTH-independent Cushing’s syndrome. Elevated aldosterone to renin ratio and unsuppressed plasma aldosterone concentration after saline infusion test suggested primary aldosteronism. Adrenal venous sampling adjusted by plasma epinephrine revealed hypersecretion of cortisol from the left adrenal mass and of aldosterone from the right one. A sequential bilateral laparoscopic adrenalectomy was performed. The cortisol level was normalized after partial left adrenalectomy and the aldosterone level was normalized after subsequent partial right adrenalectomy. Histopathological evaluation of the resected surgical specimens, including immunohistochemical staining for steroidogenic enzymes, revealed a left cortisol-producing adenoma and a right aldosterone-producing adenoma. The patient’s symptoms and laboratory findings resolved after sequential adrenalectomy without any pharmacological treatment.ConclusionsAdrenal venous sampling is essential in diagnosing bilateral functional adrenocortical adenomas prior to surgery. Proper interpretation of the laboratory findings is particularly important in these patients. Immunohistochemistry may be a valuable tool to identify aldosterone/cortisol-producing lesions and to validate the clinical diagnosis.

Adrenal venous sampling is useful for a definitive diagnosis in Cushing's syndrome with bilateral adrenal tumors

We report three cases of Cushing's syndrome (CS) with bilateral adrenal tumors. When bilateral adrenal tumors are encountered, a differential diagnosis is difficult to make, especially in the case of functioning bilateral adrenocortical adenoma. Adrenal scintigraphy has become a standard technique to determine the laterality of excessive hormone secretion; however, this examination results in bilateral adrenal activity in the functioning bilateral adrenocortical adenoma. Our three patients were diagnosed with adrenocorticotropic hormone (ACTH)-independent CS based on biochemical testing, and an abdominal computed tomography (CT) scan detected bilateral adrenal tumors. Adrenal scintigraphy showed bilateral adrenal activity in all cases. However, adrenal venous sampling (AVS) demonstrated three different hormone-excess patterns (case 1: bilateral cortisol-excess secretions; case 2: unilateral cortisol-excess secretion and bilateral aldosterone-excess secretions; and case 3: bilateral cortisol-excess secretions and bilateral aldosterone-excess secretions). Based on these findings, we could select optimal treatment for each case. Therefore, AVS is useful to obtain a definitive diagnosis and adequate therapy for CS with bilateral adrenal tumors.

Bilateral Adrenocortical Masses Producing Aldosterone and Cortisol Independently.

A 31-year-old woman was referred to our hospital with symptoms of hypertension and bilateral adrenocortical masses with no feature of Cushing syndrome. The serum aldosterone/renin ratio was elevated and the saline loading test showed no suppression of the plasma aldosterone level, consistent with a diagnosis of primary hyperaldosteronism. Overnight and low-dose dexamethasone suppression tests showed no suppression of serum cortisol, indicating a secondary diagnosis of subclinical Cushing syndrome. Adrenal vein sampling during the low-dose dexamethasone suppression test demonstrated excess secretion of cortisol from the left adrenal mass. A partial right adrenalectomy was performed, resulting in normalization of blood pressure, hypokalemia, and high aldosterone level, implying that the right adrenal mass was the main cause of the hyperaldosteronism. A total adrenalectomy for the left adrenal mass was later performed, resulting in a normalization of cortisol level. The final diagnosis was bilateral adrenocortical adenomas, which were secreting aldosterone and cortisol independently. This case is the first report of a concurrent cortisol-producing left adrenal adenoma and an aldosterone-producing right adrenal adenoma in Korea, as demonstrated by adrenal vein sampling and sequential removal of adrenal masses.

A Case of Bilateral ACTH-independent Adrenal Adenomas with Cushing's Syndrome Treated by Ipsilateral Total and Contralateral Partial Laparoscopic Adrenalectomy

ACTH-independent Cushing syndrome, which is mainly caused by a unilateral adrenal adenoma or adrenal carcinoma, account for 15~20% of Cushing’s syndrome. Cushing’s syndrome caused by bilateral adrenal masses is rare, including bilateral adrenal adenomas or carcinomas (AIMAH and PPNAD). Adrenal adenoma is commonly treated by Laparoscopic total adrenalectomy. However, bilateral total adrenalectomy causes acute adrenal insufficiency (Addisonian crisis), requiring lifelong steroid replacement. We present a young female patient with bilateral adrenocortical adenoma causing Cushing’s syndrome who was completely cured by successful laparoscopic total & partial adrenalectomy. Primarily we decided to remove the right adrenal gland to preserve the residual function of the left adrenal gland. However, after right total adrenalectomy, the patient manifested symptoms of subclinical Cushing syndrome including hypertension, truncal obesity, diabetes, low HDL cholesterol, and elevated triglycerides. Subsequently the patient underwent partial left adrenal mass excision, preserving the normal portion of the adrenal gland. The patient thereafter achieved biochemical resolution and significant improvement of hypertension, obesity, and diabetes without the need of any medication.

Cardiac Myxosarcoma With Adrenal Adenoma and Pituitary Hyperplasia Resembling Carney Complex in a Dog

A 9-year-old female Golden Retriever was presented with an acute onset of progressive respiratory distress. Echocardiography revealed a left atrial mass that limited blood flow from the pulmonary veins. The pathological evaluation revealed a left atrial ossifying myxosarcoma, bilateral adrenocortical adenomas, multifocal pituitary hyperplasia with expression of adrenocorticotrophic hormone, and multiple pituitary Rathke's cleft cysts. These pathologic findings are similar to those described in Carney complex, a familial human syndrome characterized by cardiac myxoma and extracardiac tumors associated with mutations in the protein kinase A regulator gene PRKAR1A. Mutations were not detected in PRKAR1A exons in the present case.

Biallelic APC Inactivation Was Responsible for Functional Adrenocortical Adenoma in Familial Adenomatous Polyposis with Novel Germline Mutation of the APC Gene: Report of a Case

Familial adenomatous polyposis (FAP) patients develop various extracolonic lesions, among which functional adrenocortical neoplasms are infrequent. A 44-year-old woman was hospitalized because of pseudo-Meigs' syndrome, caused by bilateral ovarian metastases from an advanced ascending colon cancer due to FAP of intermediate type. Furthermore, bilateral adrenocortical adenomas were detected, and functional analyses showed a hormonal secretion pattern consistent with Cushing's syndrome. She underwent a right hemicolectomy with extirpation of bilateral ovaries. At 10 months post-operative with no detectable metastatic lesions, the residual colorectum and the larger, left adrenal gland were resected, and the hormonal hypersecretion was normalized. Direct sequencing of the adenomatous polyposis coli (APC) gene revealed a nonsense germline mutation at codon 1577 and an additional nonsense somatic mutation at codon 554 in cancer tissues. Biallelic APC inactivation due to loss of the normal allele was evident in the adrenocortical adenoma. There were no hypermethylated CpG islands detected in APC promoter regions. Immunostaining for beta-catenin revealed diffuse cytoplasmic expression in resected tissues including adrenocortical adenoma. Biallelic APC inactivation may play a role in developing cortisol-secreting adrenocortical adenoma in FAP patients. It is noteworthy that biallelic APC inactivation was caused in different ways in different tumors from the same individual.

123I]Iodometomidate for Molecular Imaging of Adrenocortical Cytochrome P450 Family 11B Enzymes

Due to advances in conventional imaging, adrenal tumors are detected with increasing frequency. However, conventional imaging provides only limited information on the origin of these lesions, which represent a wide range of different pathological entities. New specific imaging methods would therefore be of great clinical value. We, therefore, studied the potential of iodometomidate (IMTO) as tracer for molecular imaging of cytochrome P450 family 11B (Cyp11B) enzymes. Inhibition of Cyp11B1 and Cyp11B2 by IMTO, etomidate, metomidate, and fluoroetomidate was investigated in NCI-h295 cells and in Y1 cells stably expressing hsCyp11B1 or hsCyp11B2. Pharmacokinetics and biodistribution after iv injection of [(123/125)I]IMTO were analyzed in mice in biodistribution experiments and by small-animal single-photon emission computed tomography (SPECT). Furthermore, four patients with known adrenal tumors (two metastatic adrenal adenocarcinomas, one bilateral adrenocortical adenoma, and one melanoma metastasis) were investigated with [(123)I]iodometomidate-SPECT. In cell culture experiments, all compounds potently inhibited both Cyp11B1 and Cyp11B2. Adrenals showed high and specific uptake of [(123/125)I]IMTO and were excellently visualized in mice. In patients, adrenocortical tissue showed high and specific tracer uptake in both primary tumor and metastases with short investigation time and low radiation exposure, whereas the non-adrenocortical tumor did not exhibit any tracer uptake. We have successfully completed the development of an in vivo detection system of adrenal Cyp11B enzymes by [(123)I]IMTO scintigraphy in both experimental animals and humans. Our findings suggest that [(123)I]IMTO is a highly specific radiotracer for imaging of adrenocortical tissue. Due to the general availability of SPECT technology, we anticipate that [(123)I]IMTO scintigraphy may become a widely used tool to characterize adrenal lesions.

Laparoscopic Bilateral Partial Adrenalectomy for Adrenocortical Adenomas Causing Cushing's Syndrome: Report of a Case

Laparoscopic total adrenalectomy has become a standard technique for small adrenal tumors; however, bilateral adrenalectomy results in postoperative adrenal insufficiency, necessitating lifelong steroid replacement. To preserve adrenocortical function in a 41-year-old woman with bilateral adrenocortical adenoma (BAA) causing Cushing's syndrome, we performed laparoscopic bilateral partial adrenalectomy. We based our preoperative diagnosis of bilateral adrenocortical tumors causing Cushing's syndrome on the results of endocrinological investigations and imaging findings. Thus, we performed lateral transperitoneal laparoscopic bilateral partial adrenalectomy, preserving the adrenal glands, which were normal. Pathological examination of both tumors confirmed the diagnosis of adrenocortical adenoma. The patient had no postoperative complications, and her adrenocortical function was normal without steroid replacement at her 10-month follow-up. This report shows that Cushing's syndrome resulting from bilateral adenomas can be effectively treated by laparoscopic bilateral partial adrenalectomy as a minimally invasive, adrenocortical-preserving operation.

両側副腎腺腫による原発性アルドステロン症に腎細胞癌を合併した稀な一例

We report a rare case of bilateral primary aldosteronism with renal cell carcinoma. A 55-year-old woman developed symptoms of hypertension and hypokalemia. The cause of these symptoms was suspected to be primary aldosteronism, based on the high levels of plasma aldosterone concentrations (PAC) and low levels of plasma rennin activity (PRA), resulting in a high PAC/PRA ratio. Abdominal CT and MRI revealed tumor masses in both adrenal glands, and a large left renal mass. The preoperative diagnosis was primary aldosteronism due to bilateral functioning adrenocortical adenomas and left renal cell carcinoma. The patient underwent left radical nephrectomy and right partial adrenalectomy. The Pathological diagnosis was left renal cell carcinoma and bilateral functioning adrenocortical adenomas. Primary aldosteronism due to bilateral functioning adrenocortical adenomas is relatively rare and its complication with renal cell carcinoma is an extremely rare case.

Bilateral asynchronous adrenocortical adenoma in a girl with beckwith-wiedemann syndrome.

We report a case of asynchronous occurrence of bilateral adrenocortical adenoma in a 13-yr-old girl with Beckwith-Wiedemann syndrome. A right virilizing adrenal adenoma was surgically removed at age 6, following clinical manifestation of virilization such as acne, voice change, clitoris hypertrophy and overgrowth. Histopathological examination of the resected specimen revealed an adrenocortical adenoma predominantly composed of eosinophilic tumor cells expressing all the steroidogenic enzymes. High serum levels of DHEA-S (6,380 ng/ml) and testosterone (547 ng/dl) were noted prior to the operation. Postoperative course was unremarkable. Menstruation started at age 11, with a regular interval. At the age of 13 yr old, a high serum level of DHEA-S (8,250 ng/ml) was detected. In contrast to the episode of virilization at age 6, however, the serum testosterone level was not so high (122 ng/dl), and no clinical symptoms of virilization were apparent. Abdominal ultrasonography demonstrated the presence of a left adrenocortical adenoma. Pathological examination of the resected specimen revealed a circumscribed and well encapsulated tumor with essentially the same histological features as the tumor previously removed, except that the tumor cells showed a more prominent morphological similarity to the fetal adrenal cortex and did not express 3β HSD. The absence of virilization at the second episode was due to the relatively low serum level of testosterone compared with that of DHEA-S.

Adrenal-preserving laparoscopic surgery in selected patients with bilateral adrenal tumors

Background There have been few reports of laparoscopic adrenal-sparing surgery for bilateral adrenal tumors. We review our experience with this type of surgery with the aim of evaluating its feasibility and safety. Methods Over a 4-year period, we treated 9 patients with bilateral benign adrenal tumors. Seven patients had bilateral pheochromocytomas (MEN 2: 5, VHL: 1, sporadic: 1), and 2 patients had Cushing's syndrome caused by bilateral adrenocortical adenomas. Laparoscopic procedures were performed by a flank approach. The mean diameter of the tumors was 3.7 cm (range, 2.0-8.5 cm). Results All the tumors were removed laparoscopically. Four patients with hereditary pheochromocytomas underwent bilateral total adrenalectomy because of the large tumor size and multiplicity. The other 5 patients were treated successfully with preservation of adrenocortical function. In 4 of these 5 patients, the adrenal tumors were 3 cm or less in diameter. None of the patients experienced surgical complications. At a mean follow-up of 16 months (range, 4-40 months), none of the 5 patients who were treated by adrenal-sparing surgery required corticosteroid replacement. Conclusion Laparoscopic surgery is feasible for the treatment of bilateral adrenal tumors. Adrenal-preserving laparoscopic surgery may be practicable for the removal of these tumors, if the tumor on either side is 3 cm or less in diameter; however, our follow up is short (mean, 16 months).

Hyperadrenocorticism caused by bilateral adrenocortical neoplasia in dogs: Four cases (1983-1988)

Summary: Hyperadrenocorticism caused by bilateral adrenocortical neoplasia was diagnosed in 4 dogs. Three dogs had bilateral adrenocortical adenomas, and 1 dog had bilateral adrenocortical carcinomas. The history, physical findings, clinicopathologic abnormalities, and results of acth stimulation and low-dose dexamethasone suppression tests were compatible with diagnosis of hyperadrenocorticism. Adrenocortical neoplasia was differentiated from pituitary-dependent hyperadrenocorticism on the basis of a combination of test results, including lack of suppression of plasma cortisol after being given a high dose dexamethasone (n = 4), undetectable (&lt; 20 pg/ml) plasma endogenous acth concentration (n = 4), identification of a single mineralized adrenal mass by abdominal radiography (n = 2) and abdominal ultrasonography (n = 1), and identification of bilateral nonmineralized adrenal masses by ultrasonography (n = 1). A left adrenal mass was excised from 1 dog. Clinical signs persisted and administration of mitotane was initiated. One dog was treated only with mitotane. Treatment with ketoconazole was attempted in 2 dogs. All dogs died or were euthanatized because of persistent hyperadrenocorticism. Necropsy and histologic evaluation of the pituitary and adrenal tissue confirmed bilateral adrenocortical neoplasia in all dogs. Bilateral adrenocortical neoplasia should be considered as an uncommon, but possible, cause of bilaterally large adrenal glands in dogs with hyperadrenocorticism.

The clinical response to treatment in adult Cushing's syndrome following remission of hypercortisolaemia

The clinical response of 57 adult patients with Cushing's syndrome due to bilateral adrenocortical hyperplasia or adrenocortical adenoma is documented following resolution of hypercortisolaemia by various forms of treatment. Despite satisfactory biochemical remission of the disease the clinical result was far less satisfactory when assessed by persistence of obesity (55%), menstrual irregularity (41%), hypertension (29%) and insulin-dependent diabetes (22%). Myopathy, hirsuitism and psychological abnormalities persisted to a lesser extent. The mortality rate of the series over a 30 year follow-up period was 4 times that of a general population matched for sex, age and year of entry into the series. Cardiovascular disease was the cause of death in 85%. Irreparable cardiovascular disease is produced early in the course of hypercortisolaemia, emphasizing the vital importance of the earliest possible recognition and treatment of this disease.

Renovascular hypertension associated with bilateral aldosteronoma

The authors present a 35-year-old male patient with renovascular hypertension caused by the stenosis of both renal arteries of the right kidney. Two years after the diagnosis of hypertension was made, an endarterectomy was performed but a successful correction of the upper stenotic artery was not achieved. During the next 2 years the hypertensive disease was uncontrollable with antihypertensive medications and gradually entered into a malignant phase. In addition to the atrophy of the right kidney, an adenoma of the left adrenal gland was revealed (19.75 g) which was operated on. Left adrenalectomy had only a transitory benefit on blood pressure level. Five months later an adenoma of the right adrenal gland was diagnosed and together with the ischaemic right kidney was operated on (right adrenalectomy and nephrectomy) which definitely cured the hypertension. The chronological sequence of events and the course of the disease in the patient point to the possibility that long-standing hyper-reninaemia, due to renal ischaemia, may cause the development of multiple bilateral adrenocortical adenomas and that secondary aldosteronism may transform into primary.

Adrenal scintigraphy with 131I-19-iodochlesterol in the diagnosis of Cushing's syndrome associated with adrenal tumor.

Seven patients with Cushing's syndrome secondary to adrenocortical tumors were studied using 131I-19-iodocholesterol. The diagnosis of all cases were verified histologically. In three cases with adenoma the uptake of the tracer was in the tumor only, while the two patients with adrenocortical carcinoma failed to show adrenal accumulation of the labelled compound. In two patients there was a hyperplasia-like scintigraphic pattern, while the stimulation and suppression biochemical tests suggested adrenal tumor. One of these cases was verified as a mixed form (adenoma plus hyperplasia), and the tumor bearing gland was significantly larger on the scan which helped the preoperative localization. In the other case, verified as bilateral multiple adrenocortical adenomas, the autonomus function of both adrenals was proved by dexamethasone suppression scanning. It seens reasonable to use the latter as an adunctive diagnostic procedure in patients where there is a discrepancy between the standart scintiscan and the biochemical indexes of adrenal hyperfunction.

Hypertension, Bilateral Renal Artery Stenosis, Adrenocortical Adenomas, and Normal Serum Electrolyte Levels

Aortography revealed bilateral renal artery stenosis in a patient with hypertension, diabetes mellitus, normal serum electrolyte levels, normal excretion of hydroxycorticosteroids, and increased excretion of aldosterone. Following an attempt at surgical correction of the stenosis, the patient died of a myocardial infarction. The autopsy revealed two adrenal adenomas which were morphologically indistinguishable from aldosterone-producing tumors. Therefore, the patient's hypertension would most likely not have been cured by correction of the renovascular lesions alone. Because concurrence of primary aldosteronism and renal artery stenosis is probably not rare, it is suggested that patients with renal artery stenosis be explored for adrenal adenomas prior to correction of the stenosis.