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PubMed1993

[A case of adrenal mixed tumor of pheochromocytoma and adrenocortical adenoma presenting diabetes mellitus and hypertension].

A 61-year-old woman with hyper-catecholaminemia and hyper-glucocorticoidemia due to a mixed tumor of the right adrenal gland is described. The patient, who had been medicated for hypertension since 1977, complained of thirst and general malaise in 1986. Body weight loss was remarkable. There was neither absolute truncal obesity nor moon face. In September 1986, her blood pressure was 180/110 mmHg and blood glucose level was 400mg/dl. Noradrenaline levels in plasma and in urine were remarkably elevated (1659 pg/ml and 120 micrograms/day, respectively), and adrenaline levels were also high (397 pg/ml in plasma, 34 micrograms/day in urine). Plasma cortisol and urinary 17-OHCS were elevated (39.2 micrograms/dl and 11.9 mg/day, respectively). Plasma ACTH was in the normal range (42.6 pg/ml). Oral administration of neither 1mg nor 8 mg of dexamethasone suppressed plasma cortisol or ACTH levels. Both 131I-metaiodobenzylguanidine and 131I-adosterol accumulated in the right adrenal gland. In 1987 the adrenal tumor (3.0 x 3.5 cm, 30 g) was resected. After the operation, her blood pressure and blood glucose level returned to normal, so that the medication became unnecessary. Histologically it was revealed that the tumor was a mixed adenoma consisting of adreno-medullary and cortical cells (corticomedullary adenoma). The literature on 21 cases of pheochromocytoma associated with Cushing's syndrome was briefly reviewed. Mathison (1969) reported the first case of a mixed tumor of adreno-medullary and cortical cells. So far as we know the present case is the second.

Adenoma↗
PubMed1994

[Endocrinological and imaging analyses of adrenal incidentalomas with hypertension and/or diabetes mellitus].

Adrenal tumors showing no clinical manifestations (incidentaloma) are frequently encountered during imaging analysis upon routine examinations. These tumors are sometimes associated with hypertension and/or diabetes mellitus (DM). We have examined six cases of incidentalomas with these symptoms in this study. All patients underwent endocrinological evaluation by measuring plasma cortisol and aldosterone levels to assess adrenocortical function. The levels of urinary 17-hydroxysteroids, 17-ketosteroids and catecholamines were also measured. Imaging analysis were performed by using 131I-adosterol scintigraphy, computed tomography and magnetic resonance imaging. Whereas one case was diagnosed as having an adrenal adenoma without the examination of a surgical specimen, other cases underwent surgical removal of the tumor, and final diagnoses were made by pathohistological examination of the tumors. Three cases were diagnosed as having adrenocortical adenomas (one was functioning and others were non-functioning) and one case was diagnosed as having a functional adrenocortical carcinoma. Adenomas were found to produce either non-functional steroids or a small amount of functional steroid hormones. The adenoma patients all suffered hypertension, whereas one of the adenoma patients and the carcinoma patient showed signs of DM. By contrast, of the six cases, one case was diagnosed as having an adrenal cyst, and one case was diagnosed with myelolipoma. Although these two cases suffered DM and hypertension, respectively, it seemed to be unlikely that these clinical symptoms were caused by the adrenal disease. Thus, the present analysis of the six incidentaloma patients suggests that once an adrenal incidentaloma patient with hypertension and/or DM is found, both endocrinological and imaging examinations are necessary to determine the indication of surgical treatment. This analysis supports the present consensus that non-functional adenomas whose sizes are 3cm or less and whose sizes do not change at any reevaluation period, as well as adrenal cysts and myelolipoma should not be surgically removed.

17-Ketosteroids↗
PubMed1995

Possible pre-Cushing's syndrome due to an adrenal adenoma incidentally discovered.

We demonstrated the functional evaluation of adrenal incidentaloma in 8 patients who had no abnormal finding associated with Cushing's syndrome. Adrenal tumors were incidentally discovered by abdominal echogram in 5 patients and by computed tomography (CT) in 3 patients. Serum cortisol levels and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were within normal limits in four of 8 patients. Urinary excretion of free cortisol was also within normal limits except for patient 8. Urinary excretion of 17-OHCS, however, was not suppressed by dexamethasone administration in five of 8 patients. Excretion of urinary 17-OHCS did not increase in response to metyrapone in 3 of 4 dexamethasone-insuppressible patients, but increased in 3 dexamethasone-suppressible ones. Serum cortisol increased in response to exogenous ACTH in all 6 patients examined. 131I-Adosterol accumulation was found in only the tumor side in 7 patients and bilaterally in one patient. Adrenalectomy was done in 7 patients, and microscopic findings showed adrenocortical adenoma. Serum cortisol was significantly suppressed in response to dexamethasone in the post-operative stage in all 7 patients examined. These results indicate that these adrenal incidentalomas seem to have a cortisol over-production which is dexamethasone-insuppressible and ACTH-dependent, and that they can be classified as "Pre-Cushing's Syndrome."

17-Hydroxycorticosteroids↗
PubMed2006

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.

Adrenal Cortex Neoplasms↗
PubMed1981

Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome.

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.

Adrenocorticotropic Hormone↗
PubMed1985

A case of Cushing's syndrome associated with possible adrenomedullary hyperplasia.

A 57-year-old male, who had been suffered from hypertension and diabetes mellitus for 10 years, was admitted to the hospital because of thirst, lassitude and muscle wasting. On admission, his urinary excretion of 17-OHCS and plasma cortisol levels were elevated without diurnal variations. Plasma ACTH levels were found to be very low with repeated determinations. Dexamethasone suppression test, 2 mg 4 times a day orally for 2 days, showed no changes in plasma cortisol levels and only a mild reduction in urinary 17-OHCS excretion. Estimation of urinary catecholamines showed an increase only in norepinephrine. Abdominal computerized tomography and radionuclide scanning of adrenal glands with 131I-adosterol demonstrated a well-defined adrenal mass in the left side without apparent changes in the right side. 131I-metaiodobenzylguanidine scintigraphy was negative. At surgery, his left adrenal medulla was found to be hypertrophic in addition to the cortical tumor. The left adrenal gland was also removed. After surgery, excretion of urinary catecholamines fell to nearly the normal range and he was discharged without insulin and antihypertensive drugs. Microscopically, the cortical tumor is an adenoma consisting of lipid laden cells and eosinophilic compact cells. Medullary cells were distinctly hyperplastic in appearance and many of the cells were extensively vacuolated, suggesting an active functional status. The present report describes a patient with Cushing's syndrome who showed increased urinary catecholamine excretion due to the possible coexistence of adrenal medullary hyperplasia. As far as we know, this is the first case of Cushing's syndrome with this abnormality.

Adrenal Medulla↗
PubMed1998

Cushing's syndrome due to unilateral adrenocortical hyperplasia.

A 49-year-old woman with Cushing's syndrome due to unilateral adrenal hyperplasia is presented. She had developed obesity and menopause for 2 years, but no hypertension or hypertrichosis was observed. Although plasma adrenocorticotropin and serum cortisol levels were within normal ranges, the circadian rhythm has completely disappeared. Free thyroxine and triiodothyronine levels were decreased. Adrenocorticotropin did not respond to corticotropin-releasing hormone, and urinary excretion of 17-hydroxycorticosteroids was not suppressed by dexamethasone. Abdominal computed tomography and 131I-Adosterol scintigraphy demonstrated a unilateral functioning mass in the left adrenal gland. The resected left adrenal mass was pathologically diagnosed as the rare condition of adrenocortical nodular hyperplasia.

17-Hydroxycorticosteroids↗
PubMed2003

Adrenal pseudocyst mimicking a pheochromocytoma found after a traffic accident.

We report a case of adrenal pseudocyst difficult to differentiate from pheochromocytoma. A right adrenal mass was found in a 41-year-old man after a traffic accident. Plasma level of renin was low, plasma level of aldosterone, and urine levels of aldosterone and catecholamines were high. Dynamic tests for primary aldosteronism and pheochromocytoma were negative. No abnormal uptake was shown in 131I-adosterol or 131I-MIBG scintigram. Adrenal venous sampling presented high levels of catecholamines. Laparoscopic adrenalectomy was performed. Histological examination revealed a pseudocyst with a thick fibrocollagenous wall. We discuss the mechanism of high catecholamine levels in the right adrenal vein.

Accidents, Traffic↗
PubMed1990

[A case report of Cushing syndrome due to three distinct adenomas of the right adrenal].

A case is presented of a 40 y.o. female with Cushing's syndrome. Her plasma glucocorticoid values were elevated (11-deoxy-cortisol: 3.46 ng/ml, cortisol: 25.6 micrograms/dl and cortisone: 35.7 ng/ml) with loss of diurnal variation. Urine 17-OHCS value failed to b suppressed by high dose dexamethasone and was unchanged after metyrapone administration. Her plasma mineral corticoids and androgens were within normal limits. There were 3 separate tumors in the right adrenal on CT and the left adrenal had no uptake on 131I-adosterol scintigram. We, therefore, diagnosed her illness as Cushing's syndrome due to unilateral multiple adenomas. Gross and histological examination of the right adrenal revealed one compact cell dominant adenoma and two clear cell dominant adenomas. This is the 4th case of Cushing syndrome due to unilateral multiple adrenal adenomas in Japan.

Adenoma↗
PubMed1997

[Clinical evaluation of scintigraphy and tumor biopsy for incidentally detected adrenal masses].

PURPOSE: A decision tree in diagnosis of incidentally detected adrenal masses (incidentaloma) was made on the basis of these results. METHODS: The clinical usefulness of adrenal scintigraphy with 131I-adosterol and ultrasonically guided tumor biopsy was investigated in 44 patients. RESULTS: Adrenal scintigraphy was performed in 32 patients, of whom 21 were found to have an increased uptake in the tumor, including 19 cases of cortical adenoma and 2 of hematoma. No abnormal uptake was found in the remaining 11 patients, including 2 of cortical adenoma, 1 of adrenocortical oncocytoma and 8 of non-cortical tumors. Adrenal scintigraphy was thus thought to be useful in the differentiation of cortical tumor from non-cortical tumor, showing the sensitivity of 86%, the specificity of 80% and the diagnostic accuracy of 84%. Cytological or histological study on specimens obtained by percutaneous adrenal tumor biopsy was performed in 19 patients, of whom 18 (95%) were correctly diagnosed in terms of the malignancy of incidentaloma. CONCLUSIONS: Taken together, the differential diagnosis and the surgical indication of adrenal incidentaloma could be made successfully based on adrenal scintigraphy and tumor biopsy.

Adenoma↗
PubMed1999

[ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH): a case report].

We report a case of adrenocorticotropic hormone (ACTH)-independent macronodular adrenocortical hyperplasia (AIMAH). A 54-year-old Japanese man was admitted to our hospital for further examination of obesity and hypertension. Endocrinological studies showed that plasma cortisol was high (22.5 micrograms/dl) without diurnal rhythm, and plasma ACTH was low. Two or 8 mg of dexamethasone did not suppress the plasma cortisol levels. Abdominal computed tomography revealed nodular hyperplasia of bilateral adrenal glands. Adrenal scintigraphy showed the positive uptake of 131I-adosterol to bilateral adrenal glands. Brain magnetic resonance imaging revealed no abnormalities. He was diagnosed as having Cushing's syndrome with bilateral adrenal hyperplasia, and bilateral adrenalectomy was performed. Left and right adrenal glands were 52 g and 35 g, respectively, and were occupied by yellow nodular lesions. Histologically, hyperplastic lesions were composed of clear cells. Finally he was diagnosed with AIMAH.

Adrenal Cortex↗
PubMed2000

[Nuclear medicine for general radiologists: endocrinological examinations].

We reviewed nuclear endocrinological examinations of the thyroid, parathyroid, and adrenal glands that are clinically performed in Japan as well as somatostatin receptor imaging, which is widely used in Europe, the United States, and other countries. 123I thyroid scintigraphy is especially useful in detecting ectopic goiters and differentiating between Basedow's disease and subacute thyroiditis or Plummer's disease, all of which exhibit thyrotoxicosis. 201Tl is useful to detect foci metastasized from well differentiated thyroid cancer and to differentiate malignant from benign tumors. 67Ga-citrate is an agent used for patients suspected of having malignant lymphoma or undifferentiated carcinoma of the thyroid. Radioiodinated MIBG is a specific agent for medullary thyroid carcinoma. 99mTc-MIBI is a good agent for locating hyperfunctioning parathyroid tissues. 131I-adosterol is useful to locate the lesions of primary aldosteronism, Cushing's syndrome, adrenogenital syndrome, and select adenomas among incidental tumors. Radioiodinated MIBG scintigraphy has high diagnostic accuracy in locating pheochromocytomas and neuroblastomas. 111In-labeled octreotide is useful in locating, hormone-producing gastrointestinal and pancreatic tumors including carcinoids, gastrinomas, and insulinomas. Radiolabeled somatostatin receptor analogs are used not only to locate but also to treat malignant somatostatin receptor-positive tumors. We hope that Octreoscan will be available in Japan in the near future.

Endocrine Glands↗
PubMed2001

Clinical and endocrinological features of adrenocorticotropic hormone- independent bilateral macronodular adrenocortical hyperplasia.

PURPOSE: We report clinical findings in 5 patients with adrenocorticotropic hormone independent bilateral macronodular adrenocortical hyperplasia. MATERIALS AND METHODS: In 4 males and 1 female 32 to 61 years old (median age 50) we evaluated clinical symptoms, endocrinological and radiological characteristics, treatment modality and postoperative clinical course. RESULTS: All cases presented with some features of Cushing's syndrome. Endocrinological examination revealed autonomous adrenal cortisol production with suppressed adrenocorticotropic hormone and a loss in the diurnal circadian rhythm of plasma cortisol. Abdominal computerized tomography showed bilateral enlargement of the adrenal glands with multiple nodules. 131Iodine labeled adosterol scintigraphy demonstrated remarkable bilateral uptake by the adrenal glands. The pituitary gland appeared normal on magnetic resonance imaging. Open unilateral complete adrenalectomy and contralateral partial adrenalectomy were performed in patient 1, open bilateral complete adrenalectomy was done in patients 2 and 3, and 2 and 1-stage laparoscopic bilateral complete adrenalectomy was performed in patients 4 and 5. Single removed adrenal glands weighed 32 to 108 gm. (median 60). The histological diagnosis was macronodular adrenocortical hyperplasia in all cases. Postoperative followup was 3 to 90 months. Clinical symptoms of Cushing's syndrome disappeared or improved after surgery in all cases. CONCLUSIONS: Although adrenocorticotropic hormone independent bilateral macronodular adrenocortical hyperplasia is a rare form of Cushing's syndrome, physicians are advised to consider it when diagnosing and treating cases of Cushing's syndrome with enlarged bilateral adrenal glands. Bilateral complete adrenalectomy is currently recommended as the treatment of choice.

Adrenal Glands↗
PubMed2003

[A case of non-functioning adrenocortical adenoma associated with renal cell carcinoma].

Left renal and left adrenal masses were incidentally found by computerized tomography (CT) in a 56-year-old man who was admitted to our hospital for treatment of upper digestive tract hemorrhage. Apparently no clinical signs suggestive of Cushing's syndrome existed. The renal tumor was diagnosed as renal cell carcinoma based on the findings on enhanced CT. 131I-adosterol uptake in the examination of adrenal scintigraphy under dexamethasone suppression was definitely increased in the left adrenal gland, although hormonal examinations of serum and urine for adrenal functions were within the normal range. Plasma adrenocorticotropic hormone (ACTH) and serum cortisol were suppressed by administration of 2 mg dexamethasone for 2 days. The left kidney was radically removed by surgery together with the left adrenal gland. Histological diagnoses were left renal cell carcinoma and adrenocortical adenoma.

Adrenal Cortex Neoplasms↗
PubMed1989

[A case of the benign adrenal adenoma with remarkably high concentrations of deoxycorticosterone and 11-deoxycortisol].

The case was a 33-year-old woman with hypertension and hypokalemia, who presented depression of renin activity and the abnormal elevation of plasma deoxycorticosterone (DOC) and 11-deoxycortisol on laboratory tests. After admission, abdominal CT scan, 131I-adosterol scintigram and adrenal venogram revealed a tumor in the left adrenal, which histologically seemed to be benign. When the tumor was resected, blood pressure and all the biochemical data returned to normal range. DOC and 11-deoxycortisol levels in the tumor were abnormally elevated as compared with those in the normal adrenal tissue. These findings suggested that the abnormal elevation of hormone levels resulted from depression of 11 beta-hydroxylase. Though numerous adrenal tumors have been documented, we rarely encounter an apparently benign adrenal tumor that produces 2 kinds of hormones. This seemed to be the first case of benign adrenal tumor in which both DOC and 11-deoxycortisol were elevated.

17-Hydroxycorticosteroids↗
PubMed1980

[Androgen-producing hilus cell tumor (Leydig cell tumor) of the ovary: case contribution to the differential diagnosis of virilization in the adult woman].

Severe hirsutism, deepening of the voice and enlargement of the clitoris developed in the course of two years in a 55-year old hysterectomized woman. Laboratory examinations showed markedly elevated plasma concentrations of testosterone and androstenedione and a moderately increased urinary excretion of 17-ketosteroids. Gaschromatographic analysis of the urinary steroids, revealed that she mainly excreted etiocholanolone, androsterone and pregnanetriol. Plasma androgens and urinary 17-ketosteroids were not suppressed by dexamethasone treatment. During catheterization of the vena cava blood samples were selectively taken from the ovarian veins. Androgen concentrations were the highest in the plasma from the right ovarian vein. However, phlebography as well as adrenal scanning with 131I-adosterol indicated a tumor of the right adrenal gland. During laparoscopy the right ovary was found to be enlarged, and it was subsequently removed. It contained a tumor 2.5 cm in diameter which had the histological features of a hilus cell tumor (Leydig cell adenoma). Two years later, the patient underwent surgery for suspected tumor of the left kidney. A functionless atrophic left kidney was removed. There was a complete thrombosis of the left renal and ovarian veins. Possibly, this severe lesion of the two vessels had been caused by their previous catheterization.

Androgens↗
PubMed1997

[A case of concurrent bilateral adrenocortical adenoma causing Cushing's syndrome].

A 43-year-old woman presented with obesity and lumbago. Endocrinological examinations revealed normal plasma cortisol levels and a suppressed serum adrenocorticotropic hormone (ACTH) level. On venous sampling, markedly elevated plasma cortisol levels were observed for bilateral adrenal veins (243 and 62.3 micrograms/dl on the right and left sides, respectively). Although the computed tomogram revealed bilaterally enlarged adrenal glands, 131I-adosterol scintigram showed a strong uptake only on the right side. Right adrenalectomy successfully relieved Cushing's syndrome. Pathological diagnosis was adrenocortical adenoma, 3.5 cm in diameter. Cushing's syndrome recurred in 9 years. At that time, she underwent left subtotal adrenalectomy including a 3-cm adrenocortical adenoma. Postoperative convalescence has been uneventful with oral steroid supplementation. All 14 previously reported cases of bilateral adrenocortical adenoma (BAA) causing Cushing's syndrome as well as the present case were concurrent and dominant in females of reproductive age. This suggests that some cofactors other than ACTH, such as estrogen, contribute to the pathogenesis of BAA.

Adenoma↗