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PubMed1990

Sub-clinical Cushing's syndrome in patients with adrenal gland incidentalomas. Pitfalls in diagnosis and management.

Widespread use of contemporary imaging techniques (ultrasound, computerized axial tomography, and magnetic resonance imaging scans) have led to the incidental discovery of asymptomatic adrenal neoplasms with increasing frequency. Patients with such adrenal "incidentalomas" typically have no clinical manifestations of adrenal cortical hyperfunction at the time of discovery. We have studied 122 patients with asymptomatic adrenal masses ranging in size from 2 to 7 cm in diameter from 1978 to 1988. Selected patients, after adrenal metastases, pheochromocytoma, myelolipomas, and cysts were ruled out, were further evaluated for adrenal cortical hyperfunction by measuring urinary 17-hydroxysteroids, 17-ketosteroids, and free cortisol, serum A.M., P.M. cortisol, and plasma ACTH levels. These values were also measured before and after dexamethasone suppression. NP-59 adrenal scintiscans were performed on all patients. Six patients were identified with sub-clinical Cushing's syndrome. Baseline cortisol levels were normal in each of these patients. Loss of diurnal rhythm appeared to be the most sensitive indicator of abnormal adrenal cortical function. When adrenalectomy is performed in such patients, especially when contralateral adrenal gland suppression is evidenced by NP-59 scanning or other biochemical assessment, perioperative steroids should be administered in a manner similar to that used for patients with symptomatic Cushing's syndrome. Unilateral adrenalectomy in a patient with an asymptomatic adrenal adenoma, insufficiently studied, may result in Addisonian crisis.

Adenoma↗
PubMed1988

Early diagnosis of and surgical strategy for adrenal medullary disease in MEN II gene carriers.

Sixteen multiple endocrine neoplasia type II (MEN II) gene carriers--12 who had undergone thyroidectomy because of medullary carcinoma of the thyroid and 4 whose thyroid glands had been removed because of C cell hyperplasia--were examined for the presence of pheochromocytomas. No patient had sought medical advice for pheochromocytoma symptoms. Fourteen patients had MEN IIa syndromes, one patient had a MEN IIb and another patient had a mixed syndrome of von Recklinghausen's neurofibromatosis and MEN II. Eight patients had undergone unilateral adrenalectomy for pheochromocytoma 11 +/- 4 years before. The patients underwent clinical examination, determination of the urinary excretion of catecholamines and metabolites, and 131I-metaiodobenzylguanidine (131I-MIBG) and CAT scans. 131I-MIBG scanning was performed with images 1, 4, and 7 days after the radionuclide injection. In seven of eight patients who had undergone unilateral adrenalectomies, the 131I-MIBG scans showed accumulation of the radionuclide in the remaining adrenal gland. Bilateral adrenal accumulation of the radionuclide was demonstrated in seven of eight MEN IIa gene carriers who had not undergone adrenalectomy. Five patients, two of whom had undergone adrenalectomy, were found to have unilateral pheochromocytomas less than 2 cm in diameter. Only one of these five patients had an elevated excretion of urinary catecholamines. Between day 4 and day 7 after 131I-MIBG injection, adrenal glands with pheochromocytomas increased their relative accumulation of the radionuclide significantly more (p less than 0.02) than did adrenal glands without any demonstrable pheochromocytomas. All the pheochromocytomas were viewed by means of CAT scans. Only one MEN IIa patient had bilateral pheochromocytomas, but our findings indicate that there is a tendency to bilateral adrenal medullary hyperfunction in most MEN II gene carriers. As 131I-MIBG and CAT scans can facilitate the early diagnosis of pheochromocytomas, unilateral adrenalectomy can safely be performed in most MEN IIa patients. Bilateral pheochromocytomas develop in a majority of patients with MEN IIb syndromes. Bilateral adrenalectomy should therefore be performed in these patients.

3-Iodobenzylguanidine↗
PubMed1995

Transperitoneal laparoscopic versus open adrenalectomy for benign hyperfunctioning adrenal tumors: a comparative study.

In our retrospective study we compare the effectiveness and safety of transperitoneal laparoscopic versus open adrenalectomy in 40 patients with benign hyperfunctioning unilateral adrenal tumors. Patients 1 to 20 underwent open adrenalectomy between July 1988 and July 1992, and patients 21 to 40 underwent the laparoscopic procedure between September 1992 and January 1994. Student's t test for unpaired data was used to compare intraoperative and postoperative results, and morbidity observed in the 2 groups. The affected adrenal gland was successfully removed in all cases. Mean operative time was significantly longer for laparoscopy, although it shortened progressively due to the learning curve effect. Blood loss was significantly less with laparoscopy, while only 3 patients undergoing open surgery required blood transfusions. Overall invasiveness and analgesic requirement were significantly lower with laparoscopy. The intervals to oral intake and ambulation, hospital stay and return to preoperative normal activity were shorter with laparoscopy. Major complications were noted only in open surgery patients. At 3 months all patients in both groups were cured of the underlying adrenal disease. We conclude that transperitoneal laparoscopic adrenalectomy is equally effective and less invasive than open surgery, and that it should be considered the first choice therapy for benign hyperfunctioning adrenal tumors.

Adrenal Gland Neoplasms↗
PubMed1952

Operations on the adrenal glands.

Various conditions of the adrenal gland are amenable to surgical treatment. Removal of a pheochromocytoma is almost always indicated when the tumor is diagnosed. The results of extirpation have been excellent in cases in which patients were operated upon before the onset of chronic hypertension. Removal of the "nerve cell" tumors of the adrenal is indicated if metastasis cannot be demonstrated. Hypofunction of the adrenal cortex may be partially alleviated by the repeated implantation of pellets of desoxycorticosterone acetate. Hyperfunction of the adrenal cortex causes a variety of clinical manifestations depending upon which of the numerous hormones are affected. Removal of a cortical tumor alleviates these symptoms. These tumors are malignant in more than 50 per cent of cases, and recurrence is frequent. Bilateral hyperplasia of the glands rather than a tumor may be present. In such circumstances, resection of 95 per cent of the adrenal tissue is effective in controlling the symptoms of the disease. Total bilateral excision of the adrenals is, at present, under investigation as a means of treatment for a variety of conditions.

Adrenal Cortex Neoplasms↗
PubMed1998

[Polyglandular autoimmune syndrome in 14-year-old boy].

A case of polyglandular autoimmune syndrome (PGA) in a 14-year-old boy presented is. The case syndromes included hyperthyreosis with a high titre of antithyreoglobulin and antimicrosomal antibodies and hypofunction of adrenal glands confirmed by the test with ACTH. The boy was admitted to the clinic in an average general condition. Marked insufficiency of the body mass in comparison to the height, many pigmented moles on the skin and features of thyroid hyperfunction confirmed by laboratory examinations were observed. Thyreostatic and b-blocker were applied for treatment. The boy was discharged in the condition of clinical and biochemical euthyreosis. After two months of follow-up in the Endocrinologic Outpatient Department there was no weight gain, no appetite and general weakness. The anamnesis showed multiple faintings. The boy was hospitalized again. Suspecting adrenal hypofunction, a test with ACTH was carried out but it did not give any result. Substitutive treatment was applied resulting in a gradual improvement of the general condition and disappearance of complaints. The case is presented due to the rare incidence of the syndrome and due to the diagnostic difficulties.

English Abstract↗
PubMed1987

[Diagnosis of adrenal medullary diseases in patients with sporadic or hereditary medullary thyroid carcinoma. A report of 37 cases with 8-year follow-up study].

Thirty-seven patients with medullary thyroid carcinoma were investigated to determine the status of adrenal medulla by computed tomography and 131I-metaiodobenzylguanidine (131I-MIBG) scintigraphy as well as measurements of urinary catecholamine excretion. Patients were followed up for 8 years in maximum. Fifteen patients belonged to multiple endocrine neoplasia type 2 including patients with incomplete phenotype. Computed tomography demonstrated adrenal tumors or enlargement in all 6 patients with urinary epinephrine (E) more than 30 micrograms/day, 4 of them were confirmed to have pheochromocytoma or adrenal medullary hyperplasia by surgery. In 2 patients with E less than 30 micrograms/day and epinephrine to norepinephrine (E/N) ratio more than 0.3 suggesting adrenal medullary hyperfunction, computed tomography revealed small adrenal tumors. Three of the remaining 7 patients with E less than 30 micrograms/day and E/N ratio less than 0.3 had equivocal enlargement of unilateral gland on computed tomography. 131I-MIBG scintigraphy demonstrated tracer uptake in adrenal glands with tumor more than 1cm in diameter. One of 2 adrenal glands with medullary hyperplasia showed a faint adrenal image on the scintiscan, but the other showed no tracer uptake. Pheochromocytoma became manifest in 4 patients during the follow-up period, 4, 13, 14 and 34 years after thyroid surgery. None of 22 patients with sporadic medullary thyroid carcinoma showed adrenal abnormalities on the examinations mentioned above.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

[Functional morphology of the hypothalamo-hypophyseal-adrenal system in acute coronary failure]].

Histological and morphometric studies of large-cell and small-cell hypothalamic nuclei, adenohypophysis, and adrenal cortex of patients who died from acute coronary failure revealed signs of persistent hyperfunction of small-cell nuclei of the hypothalamus, bundle and retinal adrenocortical zones, and signs of short-term hyperfunction of pituitary adenocytes. These changes indicate disorders in the hypothalamic regulation of adrenal activity.

Adrenal Glands↗
PubMed1985

Effect of o,p'DDD therapy on endogenous ACTH concentrations in dogs with hypophysis-dependent hyperadrenocorticism.

The effect of o,p'DDD therapy on the endogenous plasma ACTH concentration was evaluated in 15 dogs with hypophysis-dependent hyperadrenocorticism. Adequate control of hyperadrenocorticism with o,p'DDD was based on the reduction of water consumption to within the normal range, disappearance of clinical signs of lethargy, weakness, alopecia, thin skin, or pendulous abdomen, and an increase in blood cortisol below the normal range after exogenous ACTH administration. Endogenous ACTH concentrations were determined for each dog after the disease was controlled and while they were given o,p'DDD on a maintenance schedule. Endogenous ACTH concentrations increased in 14 of 15 dogs after o,p'DDD therapy, indicating a lack of suppressive effects of o,p'DDD on hypophysis ACTH secreting cells.

Adrenal Cortex Function Tests↗
PubMed1993

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

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 (< 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.

Adenoma↗
PubMed2000

Dietary protein restriction stress in the domestic chicken (Gallus gallus domesticus) induces remodeling of adrenal steroidogenic tissue that supports hyperfunction.

The stress of dietary protein restriction in the immature domestic turkey (Meleagris gallopavo) induces adrenal steroidogenic hypofunction that is associated with an alteration in the proportion of density-dependent subpopulations of steroidogenic cells within the adrenal gland. In contrast, when imposed on immature chickens, this nutritional stressor induces long-term enhancement of adrenal steroidogenic function. However, whether this alteration in function is accompanied by a remodeling of chicken adrenal steroidogenic tissue as in the turkey is not known. To address this question, immature cockerels (2 weeks old) were fed established isocaloric synthetic diets containing either 20% (control) or 8% (restriction) soy protein for 4 weeks. Adrenal glands were processed for the isolation of defined, density-separable, adrenal steroidogenic cell subpopulations: three low-density adrenal steroidogenic cell subpopulations [LDAC-1 (rho = 1.0285-1.0430 g/ml), LDAC-2 (rho = 1. 0430-1.0485 g/ml), and LDAC-3 (rho = 1.0485-1.0500 g/ml)] and one high-density subpopulation [HDAC (rho = 1.0510-1.0840 g/ml)]. The steroidogenic function of these cell subpopulations was assessed. Protein restriction consistently, but differentially, enhanced maximal ACTH-induced corticosterone production by the subpopulations: values of LDAC-1, -2, and -3 and HDAC from protein restricted birds were, respectively, 116, 43, 33, and 20% greater than those of corresponding cell subpopulations from control birds. However, it had contrasting influences on maximal ACTH-induced aldosterone production by the cell subpopulations. Whereas the value of LDAC-1 from protein-restricted birds was 70% greater than that from control birds, the values for LDAC-2 and -3 were not different from those of the control, and the value for HDAC was 22% less than that of the control. Protein restriction also altered the cell subpopulation composition of the adrenal gland: compared to control, it increased the proportion of LDAC-1 by 46% and decreased the proportion of LDAC-3 and HDAC by 34 and 20%, respectively. Thus, dietary protein restriction increased the proportion of cells (i.e., LDAC-1) having the greatest enhancement in corticosteroid production. This pattern of remodeling of chicken adrenal steroidogenic tissue in response to dietary protein restriction contrasts sharply with the pattern that occurs in another galliform species, the domestic turkey.

Adrenal Cortex Hormones↗
PubMed2004

Case of combined adrenal cortical adenoma and myelolipoma.

We report a case of myelolipoma 10 mm in size within a functional cortical adenoma that was 33 x 22 x 17 mm in size. A 29-year-old woman was referred to hospital for transient hypertension. A right adrenal tumor was detected by computed tomography (CT) scan and magnetic resonance imaging (MRI). Her cortisol levels indicated a loss of the normal diurnal pattern, and urinary 17-hydroxycorticosteroids was elevated. She underwent a right adrenalectomy under the diagnosis of adrenal adenoma with Cushing's syndrome. The tumor was fairly well encapsulated by a thin layer of connective tissue. The major tumor portion was composed of two distinct cell types, clear cells and eosinophilic cells, arranged in an alveolar structure. These findings were representative of cortical adenoma. The adrenal cortical adenoma centrally included well-demarcated adipose tissue admixed with scattered islands of myelopoietic elements: erythroblasts, myeloid cell series and lymphocytic cells, which was eventually recognized as myelolipoma. Recently, adrenal myelolipoma has commonly been found because of the ease of detecting it as an incidentaloma by CT scan or MRI. However, the present adrenal myelolipoma case is uncommon because it is combined with a functioning cortical adenoma. Only six similar cases have previously been reported in English and Japanese publications. Furthermore, in the present case, the myelolipoma formed a tumor nodule, and to our knowledge, this is the first reported case of a radiographically recognizable tumor nodule. We discuss the etiology of myelolipoma and suggest that myelolipoma can develop in the course of endocrine hyperfunction.

Adenoma↗
PubMed1992

Corticotropin-releasing hormone and adrenocorticotropic hormone concentrations in cerebrospinal fluid of dogs with pituitary-dependent hyperadrenocorticism.

There is still some controversy concerning the question of whether Cushing's disease in man is caused by a primary dysfunction of the pituitary or a hypothalamic disorder. In the latter option, excessive hypothalamic stimulation of pituitary corticotropes would cause or contribute to the genesis of POMC-secreting adenomas. In the present study cerebrospinal fluid (CSF) CRH levels and levels of ACTH and cortisol in CSF and plasma were measured in clinically healthy dogs, in dogs with pituitary-dependent hyperadrenocorticism (PDH), and in dogs with hyperadrenocorticism due to an adrenocortical tumor (ATH). In CSF from dogs with PDH, CRH concentrations (226.6 +/- 14.4 ng/liter) were significantly (P < 0.05) lower than those in control dogs (309.5 +/- 20.3 ng/liter). In the dogs with ATH, CSF CRH concentrations (211.0 +/- 40.3 ng/liter) were in the range of those in PDH dogs. In dogs with ATH, CSF ACTH levels (13.0 +/- 3.0 ng/liter) were significantly (P < 0.05) lower than those in control dogs (63.4 +/- 3.5 ng/liter), whereas in dogs with PDH, the levels (116.8 +/- 47.5 ng/liter) were not different from those in the control group. In control dogs, the concentrations of CSF CRH and plasma ACTH were significantly correlated (r = 0.635; P < 0.01). This functional dependency appeared to be disturbed in dogs with PDH, as in these dogs CSF CRH concentrations did not correlate with plasma ACTH concentrations. It is concluded that continuous hyperstimulation of pituitary corticotropes with hypothalamic CRH is probably not the cause of excessive ACTH secretion in dogs with pituitary-dependent hyperadrenocorticism.

Adrenal Cortex Neoplasms↗