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MR imaging of the adrenals: correlation with computed tomography.

The purpose of this study was to evaluate the role of magnetic resonance (MR) imaging in adrenal disease based on correlative imaging with CT. Fifty lesions in 36 patients with a variety of adrenal diseases were evaluated, at 0.5 T using spin echo (SE) multislice short repetition time (TR) and SE multislice multiecho long TR sequences. It is concluded that MR is capable of identifying most adrenal abnormalities previously detected by CT. The results suggest that MR has a greater specificity for mass lesions and might be useful to differentiate nonfunctioning adenomas from functioning adenomas, metastasis, pheochromocytomas, cysts, and intraadrenal hemorrhage. Magnetic resonance imaging also has the potential to detect aldosteronomas by increased signal intensity in addition to contour distortion using long TR/echo time sequences. The ability to perform multiplanar imaging and the presence of superior contrast as compared with CT are useful for the assessment of origin and extension of large lesions and the detection of pheochromocytomas in complex cases. Considering MR's limitations, we believe that at present its major role in evaluation of adrenal disease should be complementary to CT.

Adenoma↗

CT and MR imaging of massive macronodular adrenocortical disease: a rare cause of autonomous primary adrenal hypercortisolism.

We studied four patients with adrenocorticotropic hormone (ACTH)-independent hypercortisolism due to bilateral massive enlargement of the adrenal glands. The combined weight of the adrenal glands ranged from 69 to 149 g and the adrenal cortex was replaced in three of four patients by multiple nodules ranging from microscopic to 4 cm in diameter. One patient had massive diffuse enlargement. All patients had low or undetectable levels of serum ACTH, absence of petrosal sinus to peripheral gradients of ACTH in bilateral samples from the inferior petrosal sinuses before and after stimulation by corticotropin releasing hormone, and absence of an adenoma on MR imaging of the pituitary gland. The marked degree of adrenocortical enlargement and absence of ACTH dependency separates this massive macronodular disease from the more common ACTH-dependent macronodular hyperplasia encountered in older patients with pituitary-dependent Cushing disease. All patients required bilateral adrenalectomy to control hypercortisolism. We present the spectrum of nodular adrenal disease associated with hypercortisolism and a differential diagnosis based on morphologic criteria.

Adrenal Cortex Diseases↗

Cushing's syndrome: problems in diagnosis.

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.

ACTH Syndrome, Ectopic↗

Psychosocial factors, sex differences, and atherosclerosis: lessons from animal models.

OBJECTIVE: Premenopausal women, compared with men, are relatively spared from coronary heart disease and the underlying atherosclerosis. Our purpose has been to elucidate the reason for this difference and to explore the role of behavioral factors in this phenomenon. METHODS: Studies employed socially housed cynomolgus macaques (Macaca fascicularis) fed an atherogenic diet and subjected to behavioral observations. Ovariectomy, with or without hormone replacement, was used to test specific hypotheses about estrogen's role in the protection of females from atherosclerosis and coronary heart disease. RESULTS: Female macaques, like women, are resistant to atherosclerosis. However, this resistance is modified by social status-dominant monkeys develop little atherosclerosis, whereas subordinates resemble males in the amount of lesion that occurs. Subordinate females also are characterized by hypercortisolemia, behavioral dysfunction, and impaired ovarian function; the resulting low concentrations of circulating estrogen perhaps explain their accelerated atherosclerosis. Notably, atherosclerosis is exacerbated in ovariectomized monkeys but is suppressed in association with pregnancy, a hyperestrogenic state. Moreover, exogenous estrogen (an oral contraceptive) inhibits atherosclerosis in premenopausal social subordinates. CONCLUSIONS: To the extent that our results apply to women, they highlight the potential importance of behavioral stressors and their effects on estrogen activity in the premenopausal development of atherosclerosis. The triad of hypercortisolism, ovarian impairment, and psychiatric morbidity found in monkeys also occurs in women and may represent a high-risk state for disorders of the cardiovascular system and perhaps, other estrogen-sensitive tissues.

Adrenocortical Hyperfunction↗

Hypercortisolemic depression is associated with increased intra-abdominal fat.

OBJECTIVE: Similar to patients with a metabolic syndrome, patients with major depression are at increased risk of developing cardiovascular disorders. Interestingly, both disorders share a specific endocrine syndrome that promotes the accumulation of visceral fat, which again is considered a marker of increased cardiovascular morbidity and mortality. METHODS: Intra-abdominal fat was measured in 22 postmenopausal depressed women and 23 age-matched healthy women by computer tomography at the level of lumbar vertebrae 1 (L1) and 4 (L4). Saliva was taken in patients and control subjects at 08:00 hours over a period of 7 drug-free days for the measurement of free cortisol. In patients only we performed an oral glucose tolerance test. RESULTS: Compared with control subjects, depressed patients with elevated free cortisol concentrations showed similar visceral fat depots at L1 (113.0 +/- 41.6 vs. 94.3 +/- 53.2 cm(2)). Hypercortisolemic depressed patients also showed greater fat depots in this area (74.5 +/- 55.5 cm(2), p =.04) than the normocortisolemic patients. However, a comparison of all patients with control subjects revealed no difference in fat accumulation at either L1 or L4. Finally, glucose concentrations during the glucose tolerance test were higher in hypercortisolemic than in normocortisolemic patients, whereas their insulin levels showed only a tendency toward being increased. CONCLUSIONS: Hypercortisolemic depressed patients suffer from resistance to insulin and increased visceral fat. The fact that hypercortisolemia reverses depression-related fat loss, particularly in the visceral area, might partially explain why major depression can be considered a risk factor for cardiovascular disorders.

Abdomen↗

Clinically significant hypercorticism secondary to local steroid therapy.

Multiple gastric ulcers developed secondary to systemic absorption of the topical synthetic steroid in this case. Rapid healing occurred as well as the resolution of the moon facies and hypertension on cessation of topical steroid administration and routine treatment for ulcers.

Administration, Topical↗

Hypercortisolism, diarrhea with steatorrhea, and massive proteinuria due to pheochromocytoma.

Amelioration or cure of hypertension, hypercortisolism, diarrhea with steatorrhea, and massive proteinuria resulted from excision of a pheochromocytoma that contained immunoreactive ACTH, VIP, and somatostatin. Ectopic ACTH production by the tumor was clearly the cause of the hypercortisolism, and the possible involvement of VIP and somatostatin in the diarrhea and steatorrhea was considered. The response to tumor removal suggested that the mesangioproliferative glomerulonephritis shown on renal biopsy was also a paraneoplastic phenomenon.

Adrenal Gland Neoplasms↗

Long-term medical treatment of ectopic ACTH syndrome.

BACKGROUND: The morbidity of hypercortisolemia due to ectopic production of ACTH by various tumors may be greater than the morbidity of the tumor itself. METHODS: We report three cases of long-term treatment of ectopic ACTH syndrome due to metastatic bronchial carcinoid, islet cell carcinoma, and malignant thymoma tumors. Clinical and biochemical eucortisolemia was achieved in each case and was sustained from 24 to 55 months. We review the therapeutic options and their reported efficacy. RESULTS: Cessation of therapy resulted in recurrence of hypercortisolemia in each case, showing the effectiveness of therapy. CONCLUSION: Long-term treatment of ectopic ACTH-induced hypercortisolemia by blocking adrenal steroidogenesis is clinically effective and well tolerated.

ACTH Syndrome, Ectopic↗

Endocrine disorders and orthopedic problems in children.

Endocrine excesses or deficiencies frequently result in alterations of height as compared with age-matched children. Less clinically obvious are significant alterations in bone metabolism leading to osteoporosis, which can affect the child and may affect the patient as an adult. Slipped capital femoral epiphysis appears to be associated with a variety of endocrine disorders, particularly hypothyroidism. The hormonal treatment of various endocrine and nonendocrine disorders has been associated with alterations of bone metabolism, or of bone maturation, as well as with producing or aggravating orthopedic disorders.

Adrenocortical Hyperfunction↗

Effects of inactivity and hormonal mediators on skeletal muscle during recovery from trauma.

Severe injury profoundly alters two important hormonal mediators of skeletal muscle. Cortisol production, and the subsequent effect on muscle catabolism, is immediately and persistently elevated. To the contrary, testosterone, a primary anabolic stimulus of skeletal muscle, is considerably suppressed with trauma. The result is a dramatically increased catabolic/anabolic hormonal profile that is further exacerbated by the prolonged inactivity that occurs with severe injury. These factors combine to produce a conspicuous loss of lean body mass throughout hospitalization. Emerging evidence suggests that one approach to ameliorating the loss of skeletal muscle nitrogen is restoration of the anabolic influence. The safe and effective normalization of testosterone concentrations after severe injury attenuates the loss of muscle protein. The retention of lean body mass will positively affect clinical and rehabilitative outcomes.

Adrenocortical Hyperfunction↗