Coexisting acromegaly and a unilateral cortisol-producing adrenal adenoma: a possible variant of multiple endocrine neoplasia type I.

An unusual case of coexisting acromegaly and Cushing's syndrome is reported in a 34-yr-old female. There was no biochemical or morphological evidence to suggest the presence of other endocrinopathies. She did not have any family history to suggest a hereditary tendency to endocrine disorders. Her acromegaly and Cushing's syndrome were proven to be due to a pituitary somatotroph adenoma and a cortisol-producing adenoma in the right adrenocortex, respectively. Surgical removal of both tumors led to a marked biochemical improvement of the two endocrinopathies. To account for the simultaneous occurrence of the two endocrine tumors, at least two endocrine syndromes may be considered. One of them is Carney's complex. However, Cushing's syndrome in this complex is unexceptionally due to primary pigmented nodular adrenocortical disease, differing from the adrenal pathology of our patient. In addition, a lack in this case of any other characteristic suggestive of this syndrome appears to speak against this possibility. A second possibility is multiple endocrine neoplasia type 1. The absence of a parathyroid or pancreatic islet cell tumor does not strongly support this possibility, but adrenocortical lesions are not rare in this syndrome although they are only rarely functional. However, existence of similar case reports, although very few, in the literature leaves the possibility that she represents another rare variant of sporadic multiple endocrine neoplasia type I syndrome.     

A decrease in the dose of pegvisomant was needed for the treatment of acromegaly after adrenalectomy in a patient with coexisting preclinical Cushing's syndrome

We herein describe the case of a 47-year-old woman with pre-clinical Cushing's syndrome caused by a left adrenal adenoma, which was diagnosed 6 years after trans-sphenoidal selective removal of a pituitary adenoma for acromegaly at age 35. The patient was started on bromocriptine and then somatostatin analogues after the surgery; however, since her serum insulin-like growth factor-1 (IGF-1) values remained above the age-adjusted normal range, the treatment for acromegaly was switched from somatostatin analogues to pegvisomant (10 mg daily), before a left laparoscopic adrenalectomy. After the subsequent adrenalectomy, the dose of pegvisomant could be reduced gradually to once every 4 days without any increase in the serum IGF-1 values. This is the first report describing the need for a different dose of pegvisomant for the treatment of acromegaly before and after adrenalectomy for pre-clinical Cushing's syndrome.     

The improvement of insulin resistance in patients with adrenal incidentaloma by surgical resection

OBJECTIVE: Several recent studies have indicated that patients with adrenal incidentaloma often have disturbed glucose tolerance or/and hypertension. It is unclear whether these metabolic conditions could be caused by adrenal incidentaloma. We investigated the prevalence of disturbed glucose tolerance, hypertension and insulin resistance in the patients with non-functioning adrenal incidentaloma and evaluated the changes of the parameters such as glucose tolerance, blood pressure and insulin sensitivity after adrenalectomy. PATIENTS AND METHODS: Among 15 patients with incidentally discovered adrenal tumours in our department from 1996 to 1999, 4 patients were diagnosed as having pre-clinical Cushing's syndrome and the other 11 as having non-functioning tumours based on detailed endocrinological examinations including dexamethasone suppression testing. Four tumours with pre-clinical Cushing's syndrome and 8 tumours out of 11 patients with non-functioning tumours were diagnosed histopathologically as adrenocortical adenomas and the other 3 as of non-adrenal origin including a myelolipoma, an adrenal vascular cyst and an endothelioma. The prevalence of disturbed glucose tolerance was determined with an oral glucose tolerance test, and insulin sensitivity was evaluated by the method of steady state of plasma glucose (SSPG). RESULTS: All 12 patients with adrenocortical adenoma exhibited insulin resistance based on the SSPG (6.9-13.2 mmol/l). Before surgical removal of the tumours, the SSPG titre was relatively higher in the patients with pre-clinical Cushing's syndrome than in those with non-functioning with adrenocortical adenoma (mean value 11.65 vs. 8.99 mmol/l), whereas 2 of the 3 patients with non-adrenocortical tumours did not have insulin resistance. Among the 12 patients with adrenocortical adenoma, 7 (58%) and 9 (75%) patients exhibited hypertension and disturbed glucose tolerance, respectively. After removal of the tumours, SSPG of the patients with adrenocortical adenoma, but not that of the other 3 patients with non-cortical tumours, was significantly decreased compared to pre-adrenalectomy values. There are no significant differences in the changes of SSPG titres between in pre-clinical Cushing's syndrome and in non-functioning adrenocortical adenoma. Systolic blood pressure, but not diastolic blood pressure, was also significantly decreased in the patients with adrenocortical adenoma. CONCLUSION: High prevalences of disturbed glucose tolerance, insulin resistance and hypertension were found among the patients with non-functioning adrenocortical tumours. Adrenocortical adenoma may be one of the risk factors for insulin resistance that is believed to induce disturbed glucose tolerance and/or hypertension. Therefore, it is useful to evaluate insulin resistance for the patients with adrenal incidentalomas since results are likely to be helpful in deciding whether to remove the tumour by surgery.     

Pathogenesis of insulin resistance in different endocrinopathies

Visceral obesity, insulin resistance and increased cardiovascular morbidity and mortality are strongly related. Development of visceral obesity and regulation of body fat distribution in general are influenced by many factors. This article is a summary of current knowledge about pathogenesis of insulin resistance in different endocrinopathies, particularly in the Cushing's syndrome and acromegaly, as they are both connected with the pathological conditions mentioned above.     

Preclinical Cushing's syndrome resulting from adrenal black adenoma diagnosed with diabetic ketoacidosis

A right adrenal tumor was incidentally discovered on abdominal computed tomography performed on a 53-year-old Japanese man, who had been hospitalized with diabetic ketoacidosis. Normal values were obtained for adrenal hormones in the morning after an overnight fast and urinary cortisol excretion after treatment of diabetic ketoacidosis with insulin. However, overnight dexamethasone administration with 1 mg or 8 mg did not completely suppress serum cortisol levels. There were no remarkable physical findings related to Cushing's syndrome. The patient was diagnosed as having preclinical Cushing's syndrome (PCS). Histological examination of the adrenalectomy specimen demonstrated adrenal black adenoma. Blood glucose levels subsequently improved after adrenalectomy, and the patient never developed adrenal insufficiency after hydrocortisone withdrawal. The patient was treated with diet therapy alone, and maintained good glycemic control. However, the patient still showed a diabetic pattern in an oral glucose tolerance test. It seems that the existence of PCS in addition to the underlying type 2 diabetes mellitus contributed to aggravation of blood glucose levels. Although there are many aspects of the natural course of PCS that have not been thoroughly elucidated, it is necessary to remain aware that a PCS patient with abnormal glucose metabolism may develop diabetic ketoacidosis by environmental agents.     

Exacerbations of Graves' disease after unilateral adrenalectomy for Cushing's syndrome

Cushing's syndrome is characterized by endogenously increased production of glucocorticoids. The activity of immune system is regulated mainly by two systems in the body. Glucocorticoids and NF-kappaB counteract the effects of each other on the immune system. It has been reported that immune response is exaggerated after the amelioration of Cushing's syndrome. We report a rare case of exacerbation of Graves' disease after unilateral adrenalectomy for Cusing's syndrome. A 50-yr-obese woman with hypertension, dyslipidemia, impaired glucose tolerance and insulin resistance wasadmitted to outpatients clinic of endocrinology. The results of evaluation of glucocorticoids metabolism and adrenal magnetic resonance imaging revealed the Cusing's syndrome. We also assessed thyroid function tests because of the diagnosis of goiter and thyroid hormone replacement in her medical history, and the presence of exophthalmia and tachycardia in examination. Althoug TSH level was detected at the lower border of normal range, free T4 and free T3 were in normal range and autoantibody of thyroidal peroxidase and thyroglobulin was higer than normal reference range. An operation was performed and a mass was removed from her left adrenal gland. The pathologic examination confirmed adrenal adenoma. She was re-admitted to the outpatient clinic 9 months after with complaints of palpitation, malaise and weight loss. Tests carried out to determine the thyroid function revealed Graves' disease. We prescribed propylthiouracil and beta-blocker treatment.     

Cushing's syndrome due to bilateral adrenocortical adenomas with unique histological features

Cushing's syndrome due to bilateral cortisol-secreting adenomas rarely occurs. We present a case of Cushing's syndrome due to bilateral adenomas. Both adenomas had distinct cell compositions, and were compared with emphasis on immunohistochemical and enzyme histochemical analysis for cytochrome P450(11beta) and 3beta-hydroxysteroid dehydrogenase (3betaHSD). A 37 year-old female was diagnosed with ACTH-independent Cushing's syndrome based on physical findings and hormonal evaluation. High-resolution CT scan showed bilateral adrenocortical adenomas and atrophied glands. 131I-methylnorcholesterol incorporation into both glands suggested both adenomas were functional. Clinical diagnosis prior to surgery was ACTH-independent Cushing's syndrome due to functioning bilateral adenomas. The left adrenal gland was totally resected, while the right one was partially resected by laparoscopic approach. Both adenomas were black on cut sections, and were comparatively evaluated by immunohistochemical and enzyme histochemical analysis for P450(11beta) and 3betaSD. The left adenoma was 1.6 cm in diameter and had a complex cellular composition and enzyme expression similar to that of primary pigmented nodular adrenocortical disease (PPNAD), while the right adenoma was 1.8 cm in diameter with compact cells typical of a solitary cortisol-producing adenoma. Adjacent bilateral adrenal cortex showed marked atrophy, but contained several micronodules. Serum cortisol levels, both at basal and after a low dodexamethasone, normalized thirteen months after surgery. In conclusion, the present case of Cushing's syndrome with bilateral adrenal adenomas demonstrated for the first time the simultaneous occurrence of two distinct adenomas, an ordinary cortisol-producing adenoma and a PPNAD-like adenoma. Further case reports of multiple adrenal adenomas should be well-analyzed to clarify whether the results from this case represent a new subgroup of ACTH-independent Cushing's syndrome.     

LONG-TERM RESULTS OF ADRENAL SURGERY IN PATIENTS WITH CUSHING''S SYNDROME DUE TO ADRENOCORTICAL ADENOMA

Fourteen of 16 patients with Cushing's syndrome due to adrenal adenoma who had undergone adrenal surgery in the period 1967-1981 participated in a follow-up study 1 to 15 (mean 4.5) years after the operation. There were 14 unilateral and two bilateral adenomas. Two patients have died: one from postoperative complications, the other by suicide 10 years after surgery. None of the patients relapsed and none showed clinical features of Cushing's syndrome. However, five patients remained obese and four hypertensive. Furthermore, in the female patients the bone mineral density was lower than in age-matched controls. The function of the pituitary-adrenal axis recovered slowly. Postoperative replacement therapy was withdrawn 3 to 28 (mean 11.8) months after surgery in all but one patient. The function of the remaining adrenal gland was completely normal in 10 patients. In two patients the plasma cortisol response to ACTH-stimulation was still blunted and associated with elevated plasma ACTH-levels. The plasma ACTH-level was low in the only patient having persistent hypocortisolism. In conclusion, the results show that most patients with Cushing's syndrome due to adrenal adenoma recover fully after surgery. In some patients, however, the suppressed pituitary and/or adrenal fail to resume normal function.     

Classic and Recent Etiologies of Cushing’s Syndrome

Endogenous Cushing's syndrome can result from excess adrenocorticotropic hormone (ACTH; corticotropin) production by a pituitary adenoma (Cushing's disease) or by ectopic tumors secreting ACTH or corticotro- pin-releasing hormone (CRH). ACTH-independent Cushing's syndrome is caused by adrenocortical tumors or hyperplasias. Initial diagnosis is performed using 24-hour urinary free cortisol, low-dose dexamethasone tests, salivary cortisol, or night-time plasma cortisol values. A dexamethasone CRH test can discriminate between Cushing's syndrome and pseudo-Cushing's syndrome. If ACTH is elevated, combinations of high-dose dexamethasone tests, CRH/desmopressin tests, and pituitary magnetic resonance imaging can indicate a pituitary source. Discrimination from an ectopic ACTH tumor often requires inferior petrosal sinus sampling to confirm the ACTH source. If ACTH is low, adrenal computed tomography scan will identify the adrenal lesion(s) implicated. Some cortisol-producing adrenal tumors or, more frequently, bilateral macronodular hyperplasias, are under the control of aberrant membrane hormone receptors, or altered activity of eutopic receptors. The initial therapy of choice for patients with Cushing's disease is the selective transsphenoidal removal of the corticotroph adenoma; this induces remission in approximately 80% of patients, but long-term relapse occurs in up to 30% of these cases. The choice of second-line therapy remains controversial. Repeat surgery can be successful when residual tumor is detectable on magnetic resonance imaging, but carries a high risk of hypopituitarism. Bilateral adrenalectomy may be a better choice in patients without visible residual tumors, particularly in women desiring fertility. Radiotherapy combined with ketoconazole or radiosurgery was recently found effective, but longer-term evaluation of hypopituitarism and brain function is required. Current studies do not support the systematic use of prophylactic radiotherapy after bilateral adrenalectomy to decrease the risk of Nelson's syndrome; however, as soon as the residual tumor progresses, surgery and radiotherapy should be initiated. Various drugs which inhibit steroid synthesis (ketoconazole, metyrapone, aminoglutethimide, mitotane) are often effective for rapidly controlling hypercortisolism either in preparation for surgery, after unsuccessful removal of the etiologic tumor, or while awaiting the full effect of radiotherapy or more definitive therapy. Surgery is usually the treatment of choice for removal of cortisol-secreting adrenal tumors or ectopic ACTH/CRH-secreting tumors. The identification of aberrant adrenal receptors has recently allowed normalization of cortisol secretion by specific ligand receptor antagonists in limited cases of Cushing's syndrome secondary to bilateral macronodular adrenal hyperplasia. The long-term follow-up of patients treated for Cushing's syndrome should include the adequate replacement of glucocorticoids and other hormones, treatment of osteoporosis, and detection of long-term relapse of Cushing's syndrome.     

A case of preclinical Cushing's syndrome associated with diurnal rhythms of ACTH and cortisol in blood: correlation with histological findings

We describe a case of adrenocortical adenoma with preclinical Cushing's syndrome demonstrating diurnal rhythms of ACTH and cortisol in blood. A 50-year-old man was admitted to the hospital for the evaluation of incidental right adrenal mass with hyperglycemia and hypertension. On admission, there were no signs of clinical manifestation of hypercortisolism. The basal levels of cortisol (9.3 microg/dl) and ACTH (9.4 pg/ml) at 0800 h were not elevated and these diurnal rhythms were maintained. One or 8 mg of dexamethasone given orally overnight suppressed the plasma ACTH but not serum cortisol. Ultrasonogram, CT and scintiscan of (131)I adosterol all demonstrated an enlarged adrenal mass in the right adrenal gland. The right adrenal gland was subsequently resected by laparoscopic surgery. Histopathological findings of resected adrenal tumor were consistent with adrenocortical adenoma. Adjacent non-neoplastic adrenal tissue demonstrated adrenocortical atrophy but DHEA-sulfotransferase immunoreactivity in the zona reticularis was detected.     

Cushing's syndrome during pregnancy

Two cases of Cushing's syndrome during pregnancy are reported, both due to an adrenal adenoma. The association of pregnancy and Cushing's syndrome has up to now been described in 48 patients (including our two cases); Cushing's syndrome was ACTH-independent in 59%, ACTH-dependent in 33%, and of unknown cause in 8%. The obvious preponderance of ACTH-independent Cushing's syndrome in pregnancy--in contrast to the higher prevalence of ACTH-dependent Cushing's syndrome in the nonpregnant state--is unexplained, but might be related to less severe hypercortisolism in patients with adrenal adenoma. Active treatment of Cushing's syndrome in pregnancy is associated with a slightly but not significantly better outcome of pregnancy.     

Normal final height and apparent cure after pituitary irradiation for Cushing's disease in childhood: long-term follow-up of anterior pituitary function

Pituitary-dependent Cushing's syndrome is rare in childhood. Two patients are reported who had unsuccessful transsphenoidal microadenomectomy and therefore underwent pituitary radiotherapy. In both patients there was progressive normalization of hypothalamo–pituitary–adrenal function and at 8 and 10 years after radiotherapy their Cushing's syndrome remained in remission clinically and biochemically. Most importantly, they have both achieved adult heights within their respective expected ranges with close clinical observation and replacement growth hormone therapy. Thyroid and gonadal function is normal and neither patient requires any other hormone replacement therapy. Pituitary radiotherapy is thus a safe, effective and well tolerated second-line therapy for paediatric Cushing's disease. Collaboration between the paediatric and adult departments and an experienced radiotherapist contributed to the successful outcome of these two patients.     

Unilateral adrenalectomy improves insulin resistance and diabetes mellitus in a patient with ACTH-independent macronodular adrenal hyperplasia

ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a rare cause of Cushing's syndrome. Bilateral adrenalectomy is considered to be a standard therapy for AIMAH, although lifetime replacement of glucocorticoids is necessary after the procedure. This paper describes a subject with AIMAH who underwent unilateral adrenalectomy of the predominantly enlarged gland and subsequently displayed an improvement in insulin resistance and diabetes mellitus, the cardinal symptoms before the operation, concomitant with alleviation of abnormal cortisol secretion. The patient was a 61-year-old man with a body mass index of 25.6 kg/m2. He was diagnosed as having diabetes mellitus, hypertension, and hyperlipidemia at 50 years of age. Eight years after diagnosis, bilateral enlargement of the adrenal glands was revealed by chance upon computed tomography of the abdomen. Typical manifestations of Cushing's syndrome were not demonstrated. Basal levels of serum and urinary cortisol had not increased, although the serum cortisol level displayed no circadian rhythm and no response to the administration of dexamethasone. Despite sulfonylurea treatment, the patient's HbA1C level was as high as 7.6% (normal range 4.3-5.8%). Fasting insulin concentration was increased to 42.6 microU/ml, and the homeostasis model insulin resistance index (HOMA-R) was calculated to be 15.5 (with a normal range of less than 2.5), indicating severe insulin resistance. Unilateral adrenalectomy of the predominantly enlarged gland revealed that the resected gland consisted of multiple nodules of various sizes. Based on endocrinological, radiological, and pathological findings, a diagnosis of AIMAH was made. Ten months after the unilateral adrenalectomy, cortisol circadian rhythms were restored, and serum cortisol concentration was suppressed in response to the administration of low doses of dexamethasone, suggesting an improvement in the cortisol secretory pattern. Levels of HbA1C, fasting insulin, and HOMA-R decreased to 5.7%, 12.7 microU/ml, and 2.2, respectively. An improvement in hyperlipidemia was also observed. Insulin resistance and glucose intolerance are recognized as features of mild hypercortisolism. In the present case, unilateral adrenalectomy was effective in ameliorating insulin resistance and improving glycemic control. Unilateral adrenalectomy might be an alternative therapy for improvement of glucose and lipid metabolism in subjects with AIMAH.     

Cushing's syndrome presenting the coexistence of a pituitary corticotrophic cell hyperplasia and a unilateral functional adrenal adenoma

A very unusual case of Cushing's syndrome is presented. Most of the preoperative biochemical and radiological examinations were compatible with Cushing's syndrome owing to a right adrenal adenoma. Exceptional findings include normal concentrations of adrenocorticotrophin (ACTH) in plasma as well as a disturbance of its circadian rhythmicity and a significant adrenocortical responsiveness to exogenous ACTH. Secretory patterns of ACTH did not change even after right adrenalectomy. Studies in vitro revealed that the adenoma itself, but not the surrounding normal adrenal, was the source of cortisol secreted in response to ACTH. Post mortem examinations disclosed unexpectedly a hormonally inactive left adrenal adenoma and a focal hyperplastic lesion of the anterior pituitary with an ACTH concentration 53 times higher than that of the remaining tissue of the gland. It is a possibility that this case may have represented a transition between pituitary-dependent adrenocortical hyperplasia and adrenal adenoma to this date reported in only one similar case.     

Plasma testosterone profiles in Cushing's syndrome.

Elevated plasma testosterone levels were found in 8 women with Cushing's disease and oligo-or amenorrhea and/or hirsutism. In 4 men with Cushing's syndrome either due to adrenal hyperplasia or adenoma, plasma testosterone levels were lowered. Three of these 4 men complained of impotence or loss of libodo. Evidence for a major adrenal origin of the elevated testosterone values in the women with Cushing's disease was derived from the parallel suppression of cortisol and testosterone during dexamethasone administration, the testosterone responsiveness to ACTH and its dramatic fall after adrenalectomy. In the men with Cushing's syndrome the lowered plasma testosterone values were further suppressed by high doses of dexamethasone irrespective of concomitant cortisol suppression. Adrenalectomy or adenotomy restored the decreased plasma testosterone levels to normal. In women with Cushing's syndrome adrenal hyperandrogenism may account for the sexual and gonadal disturbances, in men glucocorticoid induced suppression of Leydig cell function may be responsible.     

Atrial natriuretic polypeptide inhibits cortisol secretion as well as aldosterone secretion in vitro from human adrenal tissue

The effect of alpha-human atrial natriuretic polypeptide (ANP) on adrenal steroidogenesis was studied in human adrenal tissues obtained surgically from four patients with Cushing's syndrome due to an adrenal adenoma and five patients with an aldosterone-producing adenoma (APA). ANP significantly inhibited basal and ACTH (3.4 X 10(-8) M)-stimulated cortisol and aldosterone secretion in both the adenomas and adjacent adrenocortical tissues from patients with Cushing's syndrome. ANP inhibited ACTH-stimulated, but not basal, secretion of cortisol and aldosterone in the adjacent tissues from patients with APA. In addition, ANP significantly inhibited both basal and ACTH-, angiotensin II (10(-6) M)-, and potassium chloride (10 mM)-stimulated secretion of aldosterone from the adenomas of patients with APA. ANP-induced changes in cortisol and aldosterone secretion were accompanied by a decrease in cAMP and an increase in cGMP secretion. These results suggest that ANP may be a possible regulator of cortisol as well as aldosterone secretion in humans, and these effects might be due to concomitant alteration in cyclic nucleotide metabolism.     

Myelolipomatous foci in an adrenal adenoma causing Cushing's syndrome?

We present a case of Cushing's syndrome in a 60-year old man. Abdominal imaging revealed a right adrenal mass. After confirmation of the diagnosis, the right adrenal gland was resected and revealed a tumor containing a combined myelolipoma and adenoma of the adrenal gland. After surgical removal of the adrenal mass, the symptoms and clinical signs of Cushing's syndrome resolved gradually. Immunohistochemical analysis of the adrenal adenoma specimens showed a high lymphocyte population, particularly within the myelolipoma, and an unusually marked intermingling of myelolipomatous and adrenocortical tumor cells. Adrenocortical clear cells were found in direct contact with T and B lymphocytes. Immune-endocrine mechanisms may have triggered the corticotropin-independent adrenal Cushing's syndrome in this patient.     

HUMAN PANCREATIC GROWTH HORMONE RELEASING HORMONE FAILS TO STIMULATE HUMAN GROWTH HORMONE BOTH IN CUSHING''S DISEASE AND IN CUSHING''S SYNDROME DUE TO ADRENOCORTICAL ADENOMA

An absent or severely blunted hGH response to an i.v. bolus injection (100 micrograms) of human pancreatic growth hormone releasing hormone (hpGRF 1-44) was found in seven female patients with Cushing's syndrome (five with pituitary dependent Cushing's disease and two due to an adrenal adenoma) and four men with pituitary dependent Cushing's disease. Three of the female and three of the male patients had an adequate hypoglycaemia after insulin administration. All these patients showed an absent or blunted hGH response after insulin induced hypoglycaemia. The GHRH data in these patients are in agreement with those in older literature on hGH responsiveness to stimuli such as L-dopa, arginine and insulin induced hypoglycaemia. It is concluded that hypercortisolism inhibits hGH release to various stimuli at the pituitary level.     

Image diagnosis of adrenal disorders--II. Cushing's syndrome

Comparative study of image diagnosis of ultrasonography (US) by linear electronic scanner, computed tomography (CT), and adrenal scintigraphy was performed in 14 patients with Cushing's syndrome. Adrenal imaging by scintigraphy was performed at the 5th and 6th day or further 7th day following the injection of 1 mCi of Adosterol. Cushing's disease (11 cases) US failed to detect the adrenals in 4 cases examined. Measurement of the adrenals on CT film demonstrated the enlargement of adrenals (greater than mean + 2SD) in 6 of 7 cases (85.7%). Scintiscanning showed the increased uptake of bilateral adrenals in 4 of 10 cases (40%). Adrenal scintigraphy with dexamethasone pretreatment (DP) still demonstrated the isotope uptake of bilateral adrenals in all of those 4 cases tested, although the other 6 cases were not studied with DP. From these findings, it was suggested that the measurement of adrenal size by CT was useful for the additional image diagnosis of Cushing's disease, and the adrenal scintigraphy with DP was also available for complementary study of Cushing's disease. Cushing's syndrome due to adrenocortical adenoma (3 cases) In one case examined by US, which had the smallest adenoma (0.6 X 1.0 X 2.0 cm) in this syndrome, the adenoma was not detected. All of 3 adrenal adenomas (2.6 X 2.6 X 2.2 cm to 0.6 X 1.0 X 2.0 cm) were detected by CT. Adrenal scintigraphy demonstrated good uptake by adrenal adenoma but no visualization of the contralateral adrenal in every case.