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PubMedDate not supplied

[Recurrent hyperaldosteronism and hypertension post adrenalectomy (author's transl)].

Primary Aldosteronism may be due to adenoma or hyperplastic adrenals. Such a distinction can be obtained from biochemical studies. In our observation, a man with recurrent aldosteronism after right adrenalectomy was studied. Radiological and surgical data might indicate an adenoma. This opinion was modified by pathological studies. This absence of capsule and the presence of microadenomatous hyperplastic lesions indicated pseudo-adenomatous hyperplastic glands. On the other hand, high blood pressure remained after adrenalectomy. A treatment with beta-blocking substances corrected this hypertension.

Adenoma↗
PubMed2002

Experience with laparoscopic adrenalectomy in pediatric patients.

BACKGROUND: Laparoscopic adrenalectomy (LA) is now being recognized as the standard in the management of benign adrenal pathology in adult patients. Few reports have described the use of this technique in pediatric patients. This study combines experience from 2 institutions with lateral transperitoneal LA in children to analyze our results and the clinical and biochemical response to laparoscopic adrenalectomy in patients with hormonally active adrenal tumors. METHODS: A bi-institutional retrospective review of all patients undergoing LA between January 1997 and January 2001 was performed. Clinical and biochemical data were obtained during routine follow-up. RESULTS: Seventeen laparoscopic adrenalectomies were performed during this period. The average operating time was 120 minutes, mean estimated blood loss was 25 mL, the mean size of the adrenal lesion was 4.8 cm, and the mean length of hospitalization was 35 hours. Resolution of clinical and biochemical parameters of adrenal hyperfunction was accomplished in all patients with adrenocortical hyperplasia and pheochromocytoma in postoperative follow-up. CONCLUSIONS: Laparoscopic adrenalectomy can be performed safely and effectively with a short hospital stay, minimal blood loss, and excellent functional outcome in this age group. The authors believe laparoscopic adrenalectomy is an excellent approach for the management of benign pediatric adrenal pathology.

Adenoma↗
PubMed1998

Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates.

Hormonal and morphological data were investigated in 202 consecutive patients with adrenal incidentalomas (171 unilateral and 31 bilateral) in an attempt to assess subclinical hyperfunction or malignancy. In addition to the classical evaluation, scintiscan was carried out in a large number of these patients. In unilateral incidentalomas, 83% showed normal hormonal function, whereas 17% had biochemical signs of adrenal overactivity (hyperaldosteronism in 3, hypercortisolism in 17, medullary hyperfunction in 9). [75Se]Methylnorcholesterol scintigraphy depicted malignant, space-occupying lesions as decreased or absent radiotracer uptake by the mass, and cortical adenomas as increased or normal uptake. In cortical adenomas a relationship between radiocholesterol uptake and degree of functional autonomy was demonstrated. [123I]Metaiodobenzilguanidine scintiscan visualized 7 of 8 pheochromocytomas. In bilateral incidentalomas, abnormal adrenal function was more frequent, accounting for 29% of cases (hyperaldosteronism in 3, hypercortisolism in 3, adrenal insufficiency in 2, and congenital adrenal hyperplasia in 1). Malignant lesions were not scintigraphically visualized. [75Se]Methylnorcholesterol scan also provided functional information in the case of a cortisol-secreting adenoma and an aldosteronoma with a concomitant contralateral nonhypersecreting adenoma, showing the greatest uptake in the hyperfunctioning adenomas. In both unilateral and bilateral lesions, endocrine testing failed to differentiate benign from malignant tumors. Although hormonal assessment is mandatory to clarify the functional patterns, only morphofunctional examination by scintiscan seems to provide more data about the likelihood of malignancy.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Free urinary cortisol radioimmunoassay (application in the diagnosis of adrenal diseases).

The availability of a specific antiserum has made it possible to develop in our laboratory a radioimmunoassay for free urinary cortisol which is quite simple and rapid to perform. No preliminary procedures of chromatographic purification are necessary, and no correction for losses is required. Precision and accuracy tests are satisfactory. Seventeen normal subjects, 10 obese subjects, 18 patients with Cushing's syndrome, 4 hypopituitaric patients and 4 with Addison's disease were studied. The values of free urinary cortisol were compared with those of urinary 17-OHCS, plasma cortisol and, in some cases, the cortisol secretion rate. In normal subjects, the mean free urinary cortisol was 77.22 +/- 7.74 microgram/24 h, in obese subjects it was 112.05 +/- 13.64 microgram/24 h, and in patients with Cushing's syndrome it was at significantly higher levels with a mean value of 488.06 +/- 64.39 microgram/24 h. There was no overlap between the values obtained in the first two groups and those of subjects with adrenal hyperfunction, and the results were similar to those shown by the cortisol secretion rate. The same was not true for urinary 17-OHCS and plasma cortisol. Thus, the assay of free urinary cortisol, that is the free biologically active circulating fraction, may provide a relatively simple alternative to measurement of the cortisol secretion rate, as a single differential test for the diagnosis of conditions with adrenal hyperfunction. Less satisfactory were the results obtained in patients with primary and secondary adrenal hypofunction. Another limitation of the method is its relative non-specificity, since the results of 16 urinary samples measured without preliminary chromatography were 29.6% higher than those after previous chromatographic purification. However, in our experience, this overestimation does not affect the value of the method as a screening test for the diagnosis of Cushing's syndrome.

Addison Disease↗
PubMed1984

Stages of hyperadrenocorticism: response of hyperadrenocorticoid dogs to the combined dexamethasone suppression/ACTH stimulation test.

A study was designed to evaluate the response of blood cortisol content in dogs tentatively diagnosed as having hyperadrenocorticism by using the combined dexamethasone suppression/ACTH stimulation test procedure. Four groups of abnormal responses were identified in 54 dogs. In group I (14.8% of the dogs with abnormal responses), the only abnormality was partial suppression with dexamethasone (clinically normal dogs suppressed to less than 10 ng/ml). In group II (29.6%), 2 abnormalities were found: partial suppression with dexamethasone and hyperreactivity to the ACTH stimulation test. In group III (typical pituitary-dependent hypercortisolism, 48.1%), 3 abnormalities were found: base-line hypercortisolemia, partial suppression with dexamethasone, and hyperreactivity to the ACTH stimulation test. In group IV (7.4%), 2 abnormalities were found: base-line hypercortisolemia and partial suppression with dexamethasone. Base-line blood cortisol content was normal in 44.4% of the adrenopathic dogs. A normal response to ACTH stimulation was seen in 25.9% of the dogs, and 74.1% of the dogs hyperreacted to the ACTH stimulation test. All of the adrenopathic dogs were found to suppress partially with dexamethasone. Failure to suppress the adrenal gland completely (less than 10 ng/ml) with dexamethasone was the most consistent finding in adrenopathic dogs when using the combined dexamethasone suppression/ACTH stimulation test procedure. It was concluded that the test procedure is feasible, flexible, and convenient for clinical situations. Also, these results suggested that there may be several stages in the negative feedback failure associated with hyperadrenocorticism in dogs.

Adrenal Cortex Function Tests↗
PubMed1998

Adrenal cystic lesions: report of 12 surgically treated cases and review of the literature.

Adrenal cysts are rare (0,064%-0,18% in autopsy series) and less than 500 cases have been reported in the western literature. Incidental diagnosis of adrenal cysts, however, is reported with increasing rates. We observed 12 patients with adrenal cyst. Each of them had a careful laboratory and instrumental evaluation; all the patients were operated. In our series about 67% of the patients were symptomatic (6 patients with abdominal pain, 1 with palpable mass, 1 with hemorrhagic shock). No biochemical alteration was observed. Conversely we observed an unusual subclinically hyperfunctioning cystic adenoma, potentially progressive to a clinically recognizable endocrine syndrome. US, CT and MRI had a sensitivity of 66,7%, 80% and 100% respectively. Adrenalectomy was performed in all patients. The pathological findings were: 1 epithelial cyst (cystic adenoma), 2 endothelial cysts (vascular cystic ectasia with adenomatous adrenocortical hyperplasia and 1 vascular cyst) and 9 pseudocysts. On the basis of these results, we conclude that a careful hormonal, morpho-functional and instrumental evaluation is indicated in all adrenal cysts, even if the available diagnostic procedures, even when combined, cannot always define their nature. Surgical excision, when possible by laparoscopic approach, is indicated in presence of symptoms, endocrine abnormalities (even when subclinic), complications, suspicion of malignancy and/or large size (>5 cm). Adrenal gland must be excised en bloc, also because of the possible presence of other adrenal lesions.

Abdominal Pain↗
PubMed1998

Cardiomyopathy due to a pheochromocytoma. A reversible entity.

A 45-year-old male presented with acute pulmonary oedema, chest pain and electrocardiographic manifestations of acute myocardial ischaemia in the setting of hypertension crisis from a hyperfunctioning large left-sided pheochromocytoma. Coronary artery disease was excluded on the basis of thallium stress testing and coronary angiography. The latter revealed a picture consistent with dilated cardiomyopathy. After surgical resection of the tumour, both the hypercatecholaminaemia and the arterial hypertension subsided promptly with gradual improvement of the cardiomyopathy and complete resolution of the congestive heart failure symptoms.

Adrenal Gland Neoplasms↗
PubMed1986

Adrenal tissue characterization using MR imaging.

Using a superconducting magnet operating at 0.35 T, the authors investigated the adrenal tissue characterization potential of magnetic resonance (MR) in 28 patients with 33 adrenal masses. There were 13 adrenal adenomas (12 non-hyperfunctioning, one aldosteronoma), nine adrenal metastases, four pheochromocytomas, two neuroblastomas, two adrenal lymphomas, two myelolipomas, and one adrenal cortical carcinoma. Spin-echo pulse sequences were obtained at TR 0.5, 2.0 sec and TE 28, 56 msec. Both qualitative (visual assessment) and quantitative (absolute signal intensity, intensity ratios, T1, T2) data were used for tissue characterization. The results suggest that non-hyperfunctioning adrenal adenomas can be distinguished from non-adenomas using both qualitative and quantitative data: 16/19 non-adenomas were visually hyperintense compared with liver at TR 2.0 sec, TE 56 msec, while none of the non-hyperfunctioning adenomas was relatively hyperintense at any pulse sequence used. Of the quantitative data, the intensity ratios of adrenal lesion/liver at TR 0.5 sec, TE 56 msec were most useful in diagnosis: all adenomas had ratios less than 0.83, while 19/20 non-adenomas had ratios exceeding this value. It is concluded that MR has considerable promise in adrenal tissue characterization.

Adenoma↗
PubMed1977

[Alteration of systemic hemodynamics in dogs with adrenal hypertension].

Arterial hypertension was reproduced in 20 dogs by suturing the adrenal glands with ligature. Arterial pressure showed a significant fall in 2 weeks; cardiac output diminished, and the general peripheral resistance displayed a sharp elevation. The phasic syndrome of hypodynamia, a reduction of the contractility index, of the volumetric rate of cardiac output, of the cardiac index, and of the rate of increase of the intraventricular pressure pointed to reduction of the myocardial contractility. Three months after the suturing there was an even greater elevation of arterial pressure, and hemodynamic shifts were analogous to the two-week hypertension period.

Adrenocortical Hyperfunction↗
PubMed1998

[Imaging of adrenal incidentalomas].

Imaging plays an important role in evaluating fortuitously discovered adrenal masses. These unanticipated masses (incidentalomas) are usually discovered at CT examinations. Although most incidentally discovered adrenal tumors are non-hyperfunctioning adenomas, they must be distinguished from primary or secondary malignant lesions. Recent studies have established that both unenhanced CT scans and chemical shift MR imaging can accurately differentiate benign adenomas from nonadenomatous masses by features that reflect the large amount of lipid found in most adenomas and absent in most nonadenomas. We review here the current imaging issues concerning adrenal incidentalomas including diagnostic approaches and management.

Adenoma↗
PubMed1995

Results of adrenalectomy in 36 dogs with hyperadrenocorticism caused by adreno-cortical tumour.

A total of 38 adrenocortical tumours were removed from 36 dogs with hyperadrenocorticism. The surgical approach was by way of a unilateral flank laparotomy (32 dogs; 14 left and 18 right), a bilateral flank laparotomy (3 dogs) or a midline celiotomy (1 dog). Two dogs were euthanized during surgery because their tumours could not be resected. Eight dogs died from post-operative complications. Pancreatic necrosis with peritonitis was the most common cause of death. Eight of the 26 dogs that survived had signs of recurrence of hyperadrenocorticism. Unsuppressible hyperadrenocorticism was found in four dogs; one dog had probably pre-existent pituitary-dependent hyperadrenocorticism, and adrenocortical function could not be re-examined in the remaining three dogs. Among the 37 tumours examined microscopically expansion of neoplastic tissue into blood vessels was found in 22 of them. Four adrenal glands with adrenocortical tumours also contained phaeochromocytomas. Necropsy was performed in eight dogs. Metastases were found in the lungs of two dogs and in the lungs and liver in one dog. In combination with the data of previous reports, it is suggested that histological findings in surgery specimens are not good predictors for the clinical outcome.

Adrenal Cortex Neoplasms↗
PubMed2002

Development of overt Cushing's syndrome in patients with adrenal incidentaloma.

OBJECTIVE: The natural course of adrenal incidentalomas, especially those with subclinical autonomous glucocorticoid production, i.e. subclinical Cushing's syndrome, and the risk that such conditions will evolve towards overt Cushing's syndrome are unknown. DESIGN: Longitudinal follow-up evaluation of a series of 284 consecutive patients with adrenal incidentaloma. METHODS AND RESULTS: Out of 284 consecutive patients with adrenal incidentaloma studied at our Institution in the last 15 years, 98 patients (23 with subclinical hypercortisolism) underwent surgery. Of 130 non-operated patients with a follow-up of at least 1 year, eight had subclinical hypercortisolism at diagnosis. We describe in detail four patients who developed overt Cushing's syndrome after 1-3 years of follow-up. Only one of these patients had subclinical hypercortisolism at first diagnosis. Estimated cumulative risk for a non-secreting adrenal incidentaloma to develop subclinical hyperfunction was 3.8% after 1 year and 6.6% after 5 years. For patients with masses with subclinical autonomous glucocorticoid overproduction, estimated cumulative risk to develop overt Cushing's syndrome was 12.5% after 1 year. CONCLUSIONS: In patients with adrenal incidentalomas the risk of progression towards overt Cushing's syndrome is not low, at variance with previous reports. A careful biochemical and hormonal follow-up is advisable in all patients who do not need surgery at first presentation.

Adolescent↗
PubMed2003

[Primary hyperaldosteronism].

Primary hyperaldosteronism (PHA), autonomic secretion of aldosterone by the adrenal gland, is rare. PHA usually results in therapy-resistant hypertension and is often but not always accompanied by hypokalaemia. Common causes of PHA are an aldosterone-producing adenoma, idiopathic aldosterone hypersecretion, unilateral hyperplasia or a genetic variant: glucocorticoid-remediable aldosteronism (GRA). The diagnosis should be phased and first of all requires a biochemical confirmation of the presence of PHA. In PHA patients, plasma renin is invariably suppressed. Blood should be collected under standardised conditions while the patient is not using beta-blockers or centrally-acting antihypertensive medication. Patients with a suppressed plasma renin and an elevated plasma aldosterone concentration have PHA. In patients with a suppressed plasma renin and a high-normal plasma aldosterone concentration a confirming test should be performed in which PHA is diagnosed if aldosterone is not suppressed following volume expansion with sodium chloride. The cause of PHA is determined by means of a CT scan or MRI of the adrenal glands to find a unilateral adenoma. If the CT scan or MRI is normal, adrenal vein aldosterone sampling may be considered as a next step in order to demonstrate lateralisation of aldosterone production. The hypertension and hypokalaemia of all forms of PHA respond well to spironolactone therapy. In the case of a unilateral adenoma or unilateral hyperplasia, adrenalectomy is the treatment of choice. For GRA, dexamethasone in doses that reduce the corticotropin (ACTH) level is indicated.

Adenoma↗
PubMed1992

[Arterial hypertension secondary to Conn's disease: an infrequent pathology in nephrology. Report of a clinical case].

In this work we describe a case of Conn's syndrome caused by a suprarenal adenoma in a sixty-one year female. The patient had come to our observation because of severe hypertension and hypokalemia. Primary aldosteronism resulting from the secretion of excessive amounts of aldosterone caused by autonomous hyperfunction of the adrenal cortex usually by a solitary adenoma. In most series of unselected patients, it is found in fewer than 0.5% of hypertensives. In our study we demonstrated the circadian changes of arterial blood pressure but we failed to demonstrate the presence of hypertrophic cardiomyopathy as recently emphasized in the literature. Regardless of its rarity, primary aldosteronism is a fascinating disease, protean in its manifestations, logical in its pathophysiology.

Adenoma↗
PubMed1999

Progesterone secreting adrenal mass in a cat with clinical signs of hyperadrenocorticism.

A 7-year-old 7-kg (16-lb) neutered male Himalayan cat had nonpruritic progressive alopecia of 9 months' duration. The cat had hyperglycemia and glucosuria. Physical examination revealed complete alopecia along the abdomen, inguinal area, medial and caudal areas of the thighs, ventral area of the thorax, and axilla. Clinical signs were consistent with endocrine-induced alopecia and hyperadrenocorticism, however, results of diagnostic tests (ACTH stimulation and low-dose dexamethasone suppression) were not supportive of hyperadrenocorticism. Abdominal ultrasonography revealed a mass cranial to the left kidney. Blood samples were obtained before and after ACTH stimulation to measure sex hormone concentrations. Analysis revealed markedly high blood progesterone concentrations before and after ACTH stimulation. An adrenalectomy was performed and histologic examination of the mass revealed a well-differentiated adrenocortical carcinoma. The right adrenal gland could not be viewed during surgery and was assumed to be atrophic. Following surgery, the hyperglycemia and glucosuria resolved. Within 4 months of surgery, the hyperprogesteronemia had resolved, and at 12 months the cat's coat quality appeared normal. Findings suggest that cats with signs of hyperadrenocorticism should be evaluated not only for abnormal cortisol concentrations, but also for sex hormone abnormalities.

Adrenal Cortex Function Tests↗
PubMed1994

[Distinction between adrenal adenomas and metastases using 0.5 Telsa MR imaging: diagnosis with out-of-phase T2*-weighted gradient-field-echo image].

The purpose of this study was to investigate the ability of MR imaging with a 0.5-T apparatus to distinguish adrenal adenomas from adrenal metastases. The series included 23 adrenal adenomas (18 non-hyperfunctioning adenomas, 5 hyperfunctioning) and 23 adrenal metastases (14 from lung, 5 liver, 3 colon, and 1 stomach cancer). The signal intensity (SI) ratio (adrenal tumor/liver) on T1-, T2-, and T2*-weighted MR images was calculated for adrenal tissue characterization. Adrenal adenomas were more precisely distinguished from adrenal metastases on T2*-weighted images (21/23, 91%) than on T2-weighted images (15/23, 65%). In conclusion, T2*-weighted images were better than routine T2-weighted images in distinguishing adrenal adenomas from adrenal metastases. The reason could be that the total signal intensity of adrenal adenomas which contained some fat components decreased on T2*-weighted images due to an out-of-phase effect.

Adenoma↗
PubMed1993

[Adrenal incidentaloma].

Recent increased use of ultrasonography and computed tomography (CT) has detected a substantial number of incidentally discovered adrenal tumor (incidentaloma). In our institute the discovery rate of adrenal incidentaloma per number of abdominal CT examinations was 0.43%. Those incidentalomas were incidentally found during examination for abdominal discomfort and lumbar pains or evaluation of the cause of hypertension. In the group study by the research committee on "Disorders of Adrenal Steroid Hormones" under the sponsorship of the Ministry of Health and Welfare of Japan, in 53 of 149 patients with incidentaloma, surgical resection was done during 5 years between 1983 and 1989. The pathological examination of those tumors revealed 67.9% of non-hyperfunctioning adrenocortical adenoma, 9.4% of adrenal cancer, 9.4% of ganglioneuroma, 5.7% of pheochromocytoma, 5.7% of adrenal cyst and 1.9% of myelolipoma. The criteria for resection of adrenal incidentaloma have not been established. However, tumors having a diameter of over 5 cm are generally excised in most institutes. Tumors having a diameter of between 3 cm and 5 cm are usually resected if the shape of the tumor is ambiguous and the margin of the tumor is irregular. Tumors having a diameter of less than 3 cm should be carefully followed up by abdominal CT examination every 6 months.

Adrenal Gland Neoplasms↗
PubMed2003

Prevalence and natural history of adrenal incidentalomas.

Clinically silent adrenal masses discovered by imaging studies performed for unrelated reasons, i.e. adrenal incidentalomas, have become a rather common finding in clinical practice. However, only limited studies of incidence, prevalence, and natural history of adrenal incidentalomas are available. A comprehensive review of the literature shows the prevalence of adrenal incidentalomas to be 2.3% at autopsy and 0.5-2% at abdominal computed tomography scan. Most lesions are adrenocortical adenomas at histology, whereas the prevalence of adrenocortical carcinomas is relatively low. The risk of malignancy over time for masses defined as benign at diagnosis is estimated at about 1/1000, even though 5-25% of masses increase in size during follow-up. Hyperfunction develops in about 1.7% of cases and the risk is higher in patients with lesions larger than 3 cm. Cortisol hypersecretion is the most likely disorder that may ensue, and it remains subclinical in about two-thirds of cases. The lack of controlled studies precludes making specific management recommendations. Large perspective controlled studies to define the epidemiology, natural history, and possible associated morbidity of adrenal incidentalomas and their impact on the quality of life of patients are needed.

Adenoma↗