DOI: 10.1148/rg.242035092
RadioGraphics 2004;24:435-452
© RSNA, 2004
CT and MR Imaging of the Adrenal Glands in ACTH-independent Cushing Syndrome1
Andrea G. Rockall, FRCR,
Syed A. Babar, FRCR,
S. A. Aslam Sohaib, FRCR2,
Andrea M. Isidori, MD,
Salvador Diaz-Cano, MD, PhD,
John P. Monson, MD,
Ashley B. Grossman, MD and
Rodney H. Reznek, FRCR
1 From the Departments of Academic Radiology (A.G.R., S.A.B., S.A.A.S., R.H.R.), Endocrinology (A.M.I., J.P.M., A.B.G.), and Histopathology (S.D.C.), St Bartholomew's Hospital, Dominion House, St Bartholomew's Close, London EC1A 7ED, England. Presented as an education exhibit at the 2002 RSNA scientific assembly. Received April 2, 2003; revision requested May 7 and received June 12; accepted June 13. All authors have no financial relationships to disclose. Address correspondence to A.G.R. (e-mail: a.g.rockall@qmul.ac.uk).
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Abstract
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Adrenocorticotropic hormone (ACTH)–independent hypercortisolism accounts for 15%–20% of cases of Cushing syndrome and always arises from primary adrenal disease. Computed tomographic (CT) and magnetic resonance (MR) imaging findings in 37 patients with primary adrenal Cushing syndrome were analyzed and correlated with pathologic findings. Hyperfunctioning adenomas (n = 24), together with functioning carcinomas (n = 10), accounted for 92% of cases. Adenomas had a significantly smaller mean size (3.5 vs 14.5 cm) and lower mean unenhanced CT attenuation value (11 vs 28 HU) than did carcinomas. The presence of necrosis, hemorrhage, and calcification favored a diagnosis of carcinoma. Six of 10 carcinoma patients had metastases at presentation. Two adenomas were seen within a myelolipoma, which was recognized at both CT and MR imaging due to its fat content, and two adenomas were of uncertain malignant potential. Bilateral disease—primary pigmented nodular adrenal dysplasia (PPNAD) (n = 2) and ACTH-independent macronodular adrenal hyperplasia (AIMAH) (n = 1)—had characteristic imaging features. In PPNAD, multiple tiny (2–5-mm) nodules were visible bilaterally, with no overall glandular enlargement and normal intervening adrenal tissue. In AIMAH, both glands were grossly enlarged and contained nodules up to 3 cm in diameter. Familiarity with the range of imaging appearances of the adrenal glands in primary adrenal Cushing syndrome may help establish the underlying diagnosis.
© RSNA, 2004
Index Terms: Adrenal gland, CT, 86.1211 • Adrenal gland, diseases, 86.54 • Adrenal gland, MR, 86.12141 • Adrenal gland, neoplasms, 86.31, 86.32 • Cushing syndrome, 86.541
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LEARNING OBJECTIVES FOR TEST 4
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After reading this article and taking the test, the reader will be able to:
- List the primary adrenal diseases that may cause ACTH-independent Cushing syndrome.
- Describe the characteristic imaging features of these diseases.
- Discuss the correlation between the imaging and histologic features of these diseases.
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Introduction
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Cushing syndrome is the clinical manifestation of hypercortisolism and is most frequently iatrogenic. Endogenous Cushing syndrome is a relatively rare disease and may be adrenocorticotropic hormone (ACTH)–dependent (80%–85% of cases) or ACTH-independent (15%–20%) (1). ACTH-dependent Cushing syndrome is due to an ACTH-secreting pituitary adenoma (Cushing disease) in approximately 75%–85% of cases. Rarely, an ectopic source of ACTH may cause ACTH-dependent Cushing syndrome (1,2). The appearance of the adrenal glands in ACTH-dependent Cushing syndrome has been described previously (2).
ACTH-independent Cushing syndrome is always caused by primary adrenal disease (1). The hyperfunctioning primary adrenal disease secretes cortisol and results in Cushing syndrome. ACTH-independent Cushing syndrome is due to an adenoma or carcinoma in the majority of cases but on rare occasions may be caused by other diseases, including primary pigmented nodular adrenal dysplasia (PPNAD) and ACTH-independent macronodular hyperplasia (AIMAH) (3,4). Cross-sectional imaging is used to identify adrenal disease in the investigation of Cushing syndrome. To our knowledge, however, there are no large series describing the imaging features of ACTH-independent Cushing syndrome.
In this article, we describe the range of imaging appearances of primary adrenal diseases that can cause ACTH-independent Cushing syndrome. We discuss and illustrate both unilateral disease (adenoma, adenoma within a myelolipoma, adenoma of uncertain malignant potential, carcinoma) and bilateral disease (PPNAD, AIMAH).
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Patients and Procedures
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Patients
Cases were drawn from those entered in the database of patients with Cushing syndrome in the Department of Endocrinology at our institution. Between January 1964 and October 2001, 413 patients with Cushing syndrome were evaluated in the Department of Endocrinology, and the case notes were entered in the database according to the cause of hypercortisolism. Patients without a definitive diagnosis for the cause of hypercortisolism (ie, Cushing syndrome of "unknown etiology") were not included. Of these 413 patients, 95 (23%) had ACTH-independent Cushing syndrome, and of these 95 patients, 60 (63%) had an adrenal adenoma, 30 (32%) had an adrenal carcinoma, five (5%) had AIMAH, and two (2%) had PPNAD. Results of cross-sectional imaging were available in 37 patients, who formed the study population. Several cases in the database had been referred from outside hospitals, and the scans were not available for review. The gender, mean age, and age range of these 37 patients are summarized in Table 1.
Diagnosis of ACTH-independent Cushing Syndrome
The diagnosis of Cushing syndrome was based on the clinical features of hypercortisolism, absence of serum cortisol diurnal rhythm, elevated midnight sleeping cortisol levels, and incomplete suppression of cortisol after an oral 2-mg 48-hour low-dose dexamethasone suppression test (standard protocol) to test for suppression of plasma cortisol or urinary steroids (5). A diagnosis of primary adrenal Cushing syndrome was made on the basis of clinical, biochemical, hormonal, and histopathologic criteria. The diagnostic biochemical feature was taken to be the presence of persistently undetectable (<10 pg/mL) levels of ACTH on several samples obtained throughout the day and, when available, after corticotropin-releasing hormone stimulation. Other features that suggested adrenal Cushing syndrome included (a) failure to suppress urinary or plasma cortisol levels during both low- and high-dose dexamethasone suppression tests and (b) failure of serum cortisol to respond to the corticotropin-releasing hormone stimulation test.
Imaging Considerations
The computed tomographic (CT) and magnetic resonance (MR) imaging techniques varied considerably due to the long period over which the data were collected. CT scans and MR images were both available in 15 patients, CT scans alone in 19, and MR images alone in three. CT scans and MR images were reviewed either on hard copy or, if the equipment was available, loaded onto an independent viewing console (GE Medical Systems, Waukesha, Wis) from the digital archives. The images were reviewed by two experienced observers, who arrived at a consensus. Imaging characteristics were recorded, including lesion size and shape; presence or absence of calcification, hemorrhage, and necrosis; enhancement pattern; and signal intensity change at chemical shift imaging.
Histologic Analysis
Results of histopathologic analysis were available in 36 of the 37 patients. Surgery was not considered appropriate in one patient because she presented with a large necrotic adrenal mass with extensive metastases and had clinical findings that were consistent with an adrenal carcinoma. All surgical specimens were fixed in 10% buffered formaldehyde and routinely processed for histologic diagnosis. The lesions were sampled by taking at least one block per centimeter of maximum diameter. All microscopic slides were reviewed to assess the morphologic criteria of malignancy while keeping the presence of metastases as the main criterion for malignancy (6). The morphologic classification of adrenal cortical hyperplasia took into account the nodule size, pattern of distribution, color, and architectural pattern (7).
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Results
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Of the 37 patients, 20 had an adenoma, two had an adenoma within a myelolipoma, two had an adenoma of uncertain malignant potential, 10 had a carcinoma, two had PPNAD, and one had AIMAH. The mean age and age range for patients in each category are shown in Table 1. Mean age did not differ significantly between categories, although the mean age of the two patients with PPNAD was lower than that of patients in the other categories. However, the numbers were too small for formal statistical analysis.
The CT and MR imaging features of the various adrenal lesions are shown in Tables 2–4.
Unilateral Adrenal Disease
The observers were able to identify the nodule or mass in every case of unilateral adrenal disease (Tables 2, 4).
Adenoma.—
An adenoma was confirmed in 20 of 37 cases. The adenomas had a female predilection, and the mean age of affected patients was 45 years (range, 5–66 years). The lesion was usually ovoid, with a mean diameter of 3.5 cm (range, 2–7 cm). The mean CT attenuation value was low (11 HU; range, -16–41 HU); one-half of the nodules were homogeneous, whereas one-half were slightly heterogeneous. A trace of blood was seen in only one case (at MR imaging). Calcification and necrosis were absent in all cases. Following intravenous administration of contrast material, either at CT or MR imaging, there was only mild to moderate and slightly heterogeneous enhancement in all cases (Fig 1). At chemical shift imaging, the mean signal dropout was 43.7% (range, 0%–73%) (Fig 1). In one adenoma, there was no signal dropout, and histologic analysis revealed a markedly pigmented and lipid-poor cortical adenoma (Fig 2). In one case, the patient presented with Conn syndrome and was also found to be hypercortisolemic; a cortical adrenal adenoma that was secreting both cortisol and al-dosterone was identified (9). In this case, there was marked signal dropout at chemical shift imaging, a finding that is typical of a lipid-rich adenoma.
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Figure 1a. Adrenal adenoma in a 68-year-old man. (a) Unenhanced CT scan shows a smooth, ovoid, well-defined low-attenuation mass (arrow). The CT attenuation value was -5 HU, indicating the presence of intracellular lipid. Korobkin et al (8) demonstrated a cut-off point of 18 HU, below which an adrenal lesion may be designated as a benign adenoma with a specificity of 85% and a sensitivity of 100%. (b) Contrast material-enhanced CT scan shows moderate enhancement of the mass (arrow), which gives the lesion a slightly heterogeneous appearance. (c) Axial in-phase (repetition time msec/echo time msec = 150/4.2) (top) and out-of-phase (150/1.8) (bottom) fast multiplanar spoiled gradient-echo (FMPSPGR) T1-weighted MR images (flip angle = 90°) show the mass with classic signal dropout (arrow), a finding that suggests the presence of intracellular lipid, a characteristic feature of benign adenomas. (d) On an axial fast spin-echo T2-weighted MR image (6,000/105), the adenoma (arrow) is isointense relative to the liver. (e) High-power photomicrograph (original magnification, x400; hematoxylin-eosin [H-E] stain) demonstrates a lipid-rich adrenal adenoma with abundant intracellular fat (arrow).
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Figure 1b. Adrenal adenoma in a 68-year-old man. (a) Unenhanced CT scan shows a smooth, ovoid, well-defined low-attenuation mass (arrow). The CT attenuation value was -5 HU, indicating the presence of intracellular lipid. Korobkin et al (8) demonstrated a cut-off point of 18 HU, below which an adrenal lesion may be designated as a benign adenoma with a specificity of 85% and a sensitivity of 100%. (b) Contrast material-enhanced CT scan shows moderate enhancement of the mass (arrow), which gives the lesion a slightly heterogeneous appearance. (c) Axial in-phase (repetition time msec/echo time msec = 150/4.2) (top) and out-of-phase (150/1.8) (bottom) fast multiplanar spoiled gradient-echo (FMPSPGR) T1-weighted MR images (flip angle = 90°) show the mass with classic signal dropout (arrow), a finding that suggests the presence of intracellular lipid, a characteristic feature of benign adenomas. (d) On an axial fast spin-echo T2-weighted MR image (6,000/105), the adenoma (arrow) is isointense relative to the liver. (e) High-power photomicrograph (original magnification, x400; hematoxylin-eosin [H-E] stain) demonstrates a lipid-rich adrenal adenoma with abundant intracellular fat (arrow).
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Figure 1c. Adrenal adenoma in a 68-year-old man. (a) Unenhanced CT scan shows a smooth, ovoid, well-defined low-attenuation mass (arrow). The CT attenuation value was -5 HU, indicating the presence of intracellular lipid. Korobkin et al (8) demonstrated a cut-off point of 18 HU, below which an adrenal lesion may be designated as a benign adenoma with a specificity of 85% and a sensitivity of 100%. (b) Contrast material-enhanced CT scan shows moderate enhancement of the mass (arrow), which gives the lesion a slightly heterogeneous appearance. (c) Axial in-phase (repetition time msec/echo time msec = 150/4.2) (top) and out-of-phase (150/1.8) (bottom) fast multiplanar spoiled gradient-echo (FMPSPGR) T1-weighted MR images (flip angle = 90°) show the mass with classic signal dropout (arrow), a finding that suggests the presence of intracellular lipid, a characteristic feature of benign adenomas. (d) On an axial fast spin-echo T2-weighted MR image (6,000/105), the adenoma (arrow) is isointense relative to the liver. (e) High-power photomicrograph (original magnification, x400; hematoxylin-eosin [H-E] stain) demonstrates a lipid-rich adrenal adenoma with abundant intracellular fat (arrow).
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Figure 1d. Adrenal adenoma in a 68-year-old man. (a) Unenhanced CT scan shows a smooth, ovoid, well-defined low-attenuation mass (arrow). The CT attenuation value was -5 HU, indicating the presence of intracellular lipid. Korobkin et al (8) demonstrated a cut-off point of 18 HU, below which an adrenal lesion may be designated as a benign adenoma with a specificity of 85% and a sensitivity of 100%. (b) Contrast material-enhanced CT scan shows moderate enhancement of the mass (arrow), which gives the lesion a slightly heterogeneous appearance. (c) Axial in-phase (repetition time msec/echo time msec = 150/4.2) (top) and out-of-phase (150/1.8) (bottom) fast multiplanar spoiled gradient-echo (FMPSPGR) T1-weighted MR images (flip angle = 90°) show the mass with classic signal dropout (arrow), a finding that suggests the presence of intracellular lipid, a characteristic feature of benign adenomas. (d) On an axial fast spin-echo T2-weighted MR image (6,000/105), the adenoma (arrow) is isointense relative to the liver. (e) High-power photomicrograph (original magnification, x400; hematoxylin-eosin [H-E] stain) demonstrates a lipid-rich adrenal adenoma with abundant intracellular fat (arrow).
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Figure 1e. Adrenal adenoma in a 68-year-old man. (a) Unenhanced CT scan shows a smooth, ovoid, well-defined low-attenuation mass (arrow). The CT attenuation value was -5 HU, indicating the presence of intracellular lipid. Korobkin et al (8) demonstrated a cut-off point of 18 HU, below which an adrenal lesion may be designated as a benign adenoma with a specificity of 85% and a sensitivity of 100%. (b) Contrast material-enhanced CT scan shows moderate enhancement of the mass (arrow), which gives the lesion a slightly heterogeneous appearance. (c) Axial in-phase (repetition time msec/echo time msec = 150/4.2) (top) and out-of-phase (150/1.8) (bottom) fast multiplanar spoiled gradient-echo (FMPSPGR) T1-weighted MR images (flip angle = 90°) show the mass with classic signal dropout (arrow), a finding that suggests the presence of intracellular lipid, a characteristic feature of benign adenomas. (d) On an axial fast spin-echo T2-weighted MR image (6,000/105), the adenoma (arrow) is isointense relative to the liver. (e) High-power photomicrograph (original magnification, x400; hematoxylin-eosin [H-E] stain) demonstrates a lipid-rich adrenal adenoma with abundant intracellular fat (arrow).
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Figure 2a. Small adenoma in a 51-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows an ovoid mass that arises from the medial limb of the left adrenal gland (arrow). A large hemangioma (*) was seen incidentally in the liver (L). (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) shows no signal dropout in the mass (arrow). This finding is uncharacteristic of adenomas, which classically show signal dropout with the out-of-phase sequence. L = liver, * = hemangioma. (c) Photomicrograph (original magnification, x400; H-E stain) shows a lipid-poor adrenal adenoma that contains predominantly eosinophilic compact cells with abundant lipofuscin pigment, which appears brown (arrow). These histologic findings may account for the lack of signal dropout in b.
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Figure 2b. Small adenoma in a 51-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows an ovoid mass that arises from the medial limb of the left adrenal gland (arrow). A large hemangioma (*) was seen incidentally in the liver (L). (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) shows no signal dropout in the mass (arrow). This finding is uncharacteristic of adenomas, which classically show signal dropout with the out-of-phase sequence. L = liver, * = hemangioma. (c) Photomicrograph (original magnification, x400; H-E stain) shows a lipid-poor adrenal adenoma that contains predominantly eosinophilic compact cells with abundant lipofuscin pigment, which appears brown (arrow). These histologic findings may account for the lack of signal dropout in b.
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Figure 2c. Small adenoma in a 51-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows an ovoid mass that arises from the medial limb of the left adrenal gland (arrow). A large hemangioma (*) was seen incidentally in the liver (L). (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) shows no signal dropout in the mass (arrow). This finding is uncharacteristic of adenomas, which classically show signal dropout with the out-of-phase sequence. L = liver, * = hemangioma. (c) Photomicrograph (original magnification, x400; H-E stain) shows a lipid-poor adrenal adenoma that contains predominantly eosinophilic compact cells with abundant lipofuscin pigment, which appears brown (arrow). These histologic findings may account for the lack of signal dropout in b.
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Adenoma within a Myelolipoma.—
In two of 37 cases, imaging demonstrated an adrenal myelolipoma. In both cases, an adrenal cortical adenoma was found within the myelolipoma at histologic analysis. The diagnosis of myelolipoma was made at imaging based on the presence of clearly visible fat in the lesion (Fig 3). However, in both cases, there had been concern at the time of diagnosis over the relatively large amount of soft tissue within these lesions and the size of the lesions (7.2 and 7.6 cm, respectively), findings that raise the possibility of malignant potential (Fig 4). At histologic analysis, the nonfatty soft-tissue component was seen to represent a cortical adenoma in both cases, although in one case, histopathologic findings suggested that the lesion was of uncertain malignant potential due to its size.
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Figure 3a. Adenoma within a myelolipoma in a 44-year-old woman with Cushing syndrome. (a) Longitudinal ultrasonographic image shows a hyperechoic suprarenal mass (arrow) with an appearance consistent with that of a predominantly fat-containing lesion. (b) Unenhanced CT scan helps confirm the fatty nature of the mass (arrow). However, a relatively large soft-tissue component (*) can also be seen within the lesion. (c) Coronal spin-echo T1-weighted MR images (740/25) show a predominantly fat-containing high-signal-intensity mass (short arrows) with areas of intermediate signal intensity (long arrow). (d) Axial short inversion time inversion-recovery MR image (1,800/25, inversion time msec = 100) shows a large mass with marked signal dropout (arrow), a finding that confirms the predominantly fatty nature of the lesion. At histologic analysis, the lesion proved to be a myelolipoma containing an adenoma.
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Figure 3b. Adenoma within a myelolipoma in a 44-year-old woman with Cushing syndrome. (a) Longitudinal ultrasonographic image shows a hyperechoic suprarenal mass (arrow) with an appearance consistent with that of a predominantly fat-containing lesion. (b) Unenhanced CT scan helps confirm the fatty nature of the mass (arrow). However, a relatively large soft-tissue component (*) can also be seen within the lesion. (c) Coronal spin-echo T1-weighted MR images (740/25) show a predominantly fat-containing high-signal-intensity mass (short arrows) with areas of intermediate signal intensity (long arrow). (d) Axial short inversion time inversion-recovery MR image (1,800/25, inversion time msec = 100) shows a large mass with marked signal dropout (arrow), a finding that confirms the predominantly fatty nature of the lesion. At histologic analysis, the lesion proved to be a myelolipoma containing an adenoma.
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Figure 3c. Adenoma within a myelolipoma in a 44-year-old woman with Cushing syndrome. (a) Longitudinal ultrasonographic image shows a hyperechoic suprarenal mass (arrow) with an appearance consistent with that of a predominantly fat-containing lesion. (b) Unenhanced CT scan helps confirm the fatty nature of the mass (arrow). However, a relatively large soft-tissue component (*) can also be seen within the lesion. (c) Coronal spin-echo T1-weighted MR images (740/25) show a predominantly fat-containing high-signal-intensity mass (short arrows) with areas of intermediate signal intensity (long arrow). (d) Axial short inversion time inversion-recovery MR image (1,800/25, inversion time msec = 100) shows a large mass with marked signal dropout (arrow), a finding that confirms the predominantly fatty nature of the lesion. At histologic analysis, the lesion proved to be a myelolipoma containing an adenoma.
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Figure 3d. Adenoma within a myelolipoma in a 44-year-old woman with Cushing syndrome. (a) Longitudinal ultrasonographic image shows a hyperechoic suprarenal mass (arrow) with an appearance consistent with that of a predominantly fat-containing lesion. (b) Unenhanced CT scan helps confirm the fatty nature of the mass (arrow). However, a relatively large soft-tissue component (*) can also be seen within the lesion. (c) Coronal spin-echo T1-weighted MR images (740/25) show a predominantly fat-containing high-signal-intensity mass (short arrows) with areas of intermediate signal intensity (long arrow). (d) Axial short inversion time inversion-recovery MR image (1,800/25, inversion time msec = 100) shows a large mass with marked signal dropout (arrow), a finding that confirms the predominantly fatty nature of the lesion. At histologic analysis, the lesion proved to be a myelolipoma containing an adenoma.
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Figure 4a. Adenoma associated with a myelolipoma in a 64-year-old woman with Cushing syndrome. (a) Axial unenhanced CT scan shows a large left adrenal mass with multiple low-attenuation areas centrally (horizontal arrow) that represent pockets of fat. A speck of calcification (vertical arrow) is also noted adjacent to the fatty component. (b) Contrast-enhanced arterial-phase CT scan shows mild enhancement of the mass. (c) Axial spin-echo T1-weighted MR image (500/16) shows the mass with small central foci of high signal intensity (arrow) that correspond to the foci of fat seen at CT. (d) Axial fast spin-echo T2-weighted MR image (6,000/102) shows the mass with mixed signal intensity. Multiple high-signal-intensity foci of varying size are seen within the mass and correspond to the hematopoietic component of a myelolipoma, which in this case forms a large part of the mass (cf e). (e) Photomicrograph (original magnification, x100; H-E stain) (left) shows a myelolipoma with a capsule (C) superior to adrenocortical tissue (A), the hyperfunctioning part of the lesion. More inferiorly, there is a mixture of vacuolated fat cells (F) and hematopoietic (bone marrow) cells (H), which make up a large part of the myelolipoma. A higher-power photomicrograph of the same lesion (original magnification, x200; H-E stain) (right) demonstrates a vacuolated fat cell (F) surrounded by markedly hyperchromatic hematopoietic cells.
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Figure 4b. Adenoma associated with a myelolipoma in a 64-year-old woman with Cushing syndrome. (a) Axial unenhanced CT scan shows a large left adrenal mass with multiple low-attenuation areas centrally (horizontal arrow) that represent pockets of fat. A speck of calcification (vertical arrow) is also noted adjacent to the fatty component. (b) Contrast-enhanced arterial-phase CT scan shows mild enhancement of the mass. (c) Axial spin-echo T1-weighted MR image (500/16) shows the mass with small central foci of high signal intensity (arrow) that correspond to the foci of fat seen at CT. (d) Axial fast spin-echo T2-weighted MR image (6,000/102) shows the mass with mixed signal intensity. Multiple high-signal-intensity foci of varying size are seen within the mass and correspond to the hematopoietic component of a myelolipoma, which in this case forms a large part of the mass (cf e). (e) Photomicrograph (original magnification, x100; H-E stain) (left) shows a myelolipoma with a capsule (C) superior to adrenocortical tissue (A), the hyperfunctioning part of the lesion. More inferiorly, there is a mixture of vacuolated fat cells (F) and hematopoietic (bone marrow) cells (H), which make up a large part of the myelolipoma. A higher-power photomicrograph of the same lesion (original magnification, x200; H-E stain) (right) demonstrates a vacuolated fat cell (F) surrounded by markedly hyperchromatic hematopoietic cells.
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Figure 4c. Adenoma associated with a myelolipoma in a 64-year-old woman with Cushing syndrome. (a) Axial unenhanced CT scan shows a large left adrenal mass with multiple low-attenuation areas centrally (horizontal arrow) that represent pockets of fat. A speck of calcification (vertical arrow) is also noted adjacent to the fatty component. (b) Contrast-enhanced arterial-phase CT scan shows mild enhancement of the mass. (c) Axial spin-echo T1-weighted MR image (500/16) shows the mass with small central foci of high signal intensity (arrow) that correspond to the foci of fat seen at CT. (d) Axial fast spin-echo T2-weighted MR image (6,000/102) shows the mass with mixed signal intensity. Multiple high-signal-intensity foci of varying size are seen within the mass and correspond to the hematopoietic component of a myelolipoma, which in this case forms a large part of the mass (cf e). (e) Photomicrograph (original magnification, x100; H-E stain) (left) shows a myelolipoma with a capsule (C) superior to adrenocortical tissue (A), the hyperfunctioning part of the lesion. More inferiorly, there is a mixture of vacuolated fat cells (F) and hematopoietic (bone marrow) cells (H), which make up a large part of the myelolipoma. A higher-power photomicrograph of the same lesion (original magnification, x200; H-E stain) (right) demonstrates a vacuolated fat cell (F) surrounded by markedly hyperchromatic hematopoietic cells.
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Figure 4d. Adenoma associated with a myelolipoma in a 64-year-old woman with Cushing syndrome. (a) Axial unenhanced CT scan shows a large left adrenal mass with multiple low-attenuation areas centrally (horizontal arrow) that represent pockets of fat. A speck of calcification (vertical arrow) is also noted adjacent to the fatty component. (b) Contrast-enhanced arterial-phase CT scan shows mild enhancement of the mass. (c) Axial spin-echo T1-weighted MR image (500/16) shows the mass with small central foci of high signal intensity (arrow) that correspond to the foci of fat seen at CT. (d) Axial fast spin-echo T2-weighted MR image (6,000/102) shows the mass with mixed signal intensity. Multiple high-signal-intensity foci of varying size are seen within the mass and correspond to the hematopoietic component of a myelolipoma, which in this case forms a large part of the mass (cf e). (e) Photomicrograph (original magnification, x100; H-E stain) (left) shows a myelolipoma with a capsule (C) superior to adrenocortical tissue (A), the hyperfunctioning part of the lesion. More inferiorly, there is a mixture of vacuolated fat cells (F) and hematopoietic (bone marrow) cells (H), which make up a large part of the myelolipoma. A higher-power photomicrograph of the same lesion (original magnification, x200; H-E stain) (right) demonstrates a vacuolated fat cell (F) surrounded by markedly hyperchromatic hematopoietic cells.
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Figure 4e. Adenoma associated with a myelolipoma in a 64-year-old woman with Cushing syndrome. (a) Axial unenhanced CT scan shows a large left adrenal mass with multiple low-attenuation areas centrally (horizontal arrow) that represent pockets of fat. A speck of calcification (vertical arrow) is also noted adjacent to the fatty component. (b) Contrast-enhanced arterial-phase CT scan shows mild enhancement of the mass. (c) Axial spin-echo T1-weighted MR image (500/16) shows the mass with small central foci of high signal intensity (arrow) that correspond to the foci of fat seen at CT. (d) Axial fast spin-echo T2-weighted MR image (6,000/102) shows the mass with mixed signal intensity. Multiple high-signal-intensity foci of varying size are seen within the mass and correspond to the hematopoietic component of a myelolipoma, which in this case forms a large part of the mass (cf e). (e) Photomicrograph (original magnification, x100; H-E stain) (left) shows a myelolipoma with a capsule (C) superior to adrenocortical tissue (A), the hyperfunctioning part of the lesion. More inferiorly, there is a mixture of vacuolated fat cells (F) and hematopoietic (bone marrow) cells (H), which make up a large part of the myelolipoma. A higher-power photomicrograph of the same lesion (original magnification, x200; H-E stain) (right) demonstrates a vacuolated fat cell (F) surrounded by markedly hyperchromatic hematopoietic cells.
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Adenoma of Uncertain Malignant Potential.—
In two of 37 cases, the adrenal lesion was classified histologically as an adenoma of uncertain malignant potential because some dysplastic features were identified (Fig 5). Both patients were over 70 years old, which is older than the mean age for patients with simple benign adenomas (45 years). The imaging features in these two cases were intermediate between benign and malignant features. The maximum diameters of the lesions (3.5 and 6.5 cm, respectively) were less than that of the smallest carcinoma. However, the unenhanced CT attenuation value was relatively high (38 HU) in the case in which CT findings were available, and there was minimal signal dropout at chemical shift imaging (4% and 9%, respectively). One patient subsequently developed metastases and died of the disease, indicating that the lesion was indeed malignant.
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Figure 5a. Adenoma of uncertain malignant potential in a 73-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows a large (6.5-cm) mass in the left adrenal gland (arrow). There was neither hemorrhage nor necrosis within the mass, nor metastases at presentation. (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) demonstrates no significant signal dropout (arrow). (c) On an axial fast spin-echo T2-weighted MR image (7,500/105), the mass (arrow) is isointense relative to the spleen.
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Figure 5b. Adenoma of uncertain malignant potential in a 73-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows a large (6.5-cm) mass in the left adrenal gland (arrow). There was neither hemorrhage nor necrosis within the mass, nor metastases at presentation. (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) demonstrates no significant signal dropout (arrow). (c) On an axial fast spin-echo T2-weighted MR image (7,500/105), the mass (arrow) is isointense relative to the spleen.
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Figure 5c. Adenoma of uncertain malignant potential in a 73-year-old woman. (a) Axial in-phase FMPSPGR T1-weighted MR image (150/4.2, flip angle = 90°) shows a large (6.5-cm) mass in the left adrenal gland (arrow). There was neither hemorrhage nor necrosis within the mass, nor metastases at presentation. (b) Axial out-of-phase FMPSPGR T1-weighted MR image (150/1.8, flip angle = 90°) demonstrates no significant signal dropout (arrow). (c) On an axial fast spin-echo T2-weighted MR image (7,500/105), the mass (arrow) is isointense relative to the spleen.
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Carcinoma.—
In 10 of 37 cases (27%), the adrenal lesion was a carcinoma. These carcinomas had a female predilection, and the mean patient age was similar to that of patients with adrenal adenomas (Tables 1, 2). All lesions had a maximum transverse diameter over 7.5 cm (mean, 14.5 cm; range, 7.5–21 cm), making them significantly larger than the adenomas (P < .0001) and adenomas of uncertain malignant potential (P = .03). The unenhanced CT attenuation values of the solid (nonnecrotic) parts of the tumor (mean, 28.1 HU; range, 20–31 HU) were significantly higher than those of the adenomas (P = .048). The tumors usually had a markedly heterogeneous texture at both CT and MR imaging (Figs 6–8). Necrosis was seen in nine of 10 cases (Fig 6), and hemorrhage (n = 4) (Fig 6) or calcification (n = 3) was frequently identified. Contrast enhancement was mild and markedly heterogeneous (Figs 6, 8). At the time of presentation, six patients had lung or liver metastases (Fig 7) and four patients had tumor thrombus extending into the IVC and, in one case, invading the IVC wall (Fig 8).
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Figure 6a. Adrenal carcinoma in a 32-year-old woman with Cushing syndrome. (a) Unenhanced CT scan demonstrates a large, low-attenuation suprarenal mass (short arrows) containing areas of high attenuation (long arrows) that are consistent with hemorrhage. (b) Contrast-enhanced CT scan demonstrates the mass with heterogeneous enhancement. Large areas of necrosis are also seen (*). Note the anterior displacement and compression of the inferior vena cava (IVC) (arrow). (c) Axial T1-weighted MR image (500/14) demonstrates high-signal-intensity areas within the mass (arrow), a finding that is consistent with hemorrhage. (d) Axial fast spin-echo T2-weighted MR image (7,500/100) also demonstrates extensive high-signal-intensity areas within the mass (arrow), a finding that is consistent with necrosis. (e) Photomicrograph (original magnification, x100; H-E stain) demonstrates amorphous necrosis (arrows), a finding that is seen in the majority of adrenal carcinomas.
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Figure 6b. Adrenal carcinoma in a 32-year-old woman with Cushing syndrome. (a) Unenhanced CT scan demonstrates a large, low-attenuation suprarenal mass (short arrows) containing areas of high attenuation (long arrows) that are consistent with hemorrhage. (b) Contrast-enhanced CT scan demonstrates the mass with heterogeneous enhancement. Large areas of necrosis are also seen (*). Note the anterior displacement and compression of the inferior vena cava (IVC) (arrow). (c) Axial T1-weighted MR image (500/14) demonstrates high-signal-intensity areas within the mass (arrow), a finding that is consistent with hemorrhage. (d) Axial fast spin-echo T2-weighted MR image (7,500/100) also demonstrates extensive high-signal-intensity areas within the mass (arrow), a finding that is consistent with necrosis. (e) Photomicrograph (original magnification, x100; H-E stain) demonstrates amorphous necrosis (arrows), a finding that is seen in the majority of adrenal carcinomas.
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Figure 6c. Adrenal carcinoma in a 32-year-old woman with Cushing syndrome. (a) Unenhanced CT scan demonstrates a large, low-attenuation suprarenal mass (short arrows) containing areas of high attenuation (long arrows) that are consistent with hemorrhage. (b) Contrast-enhanced CT scan demonstrates the mass with heterogeneous enhancement. Large areas of necrosis are also seen (*). Note the anterior displacement and compression of the inferior vena cava (IVC) (arrow). (c) Axial T1-weighted MR image (500/14) demonstrates high-signal-intensity areas within the mass (arrow), a finding that is consistent with hemorrhage. (d) Axial fast spin-echo T2-weighted MR image (7,500/100) also demonstrates extensive high-signal-intensity areas within the mass (arrow), a finding that is consistent with necrosis. (e) Photomicrograph (original magnification, x100; H-E stain) demonstrates amorphous necrosis (arrows), a finding that is seen in the majority of adrenal carcinomas.
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Figure 6d. Adrenal carcinoma in a 32-year-old woman with Cushing syndrome. (a) Unenhanced CT scan demonstrates a large, low-attenuation suprarenal mass (short arrows) containing areas of high attenuation (long arrows) that are consistent with hemorrhage. (b) Contrast-enhanced CT scan demonstrates the mass with heterogeneous enhancement. Large areas of necrosis are also seen (*). Note the anterior displacement and compression of the inferior vena cava (IVC) (arrow). (c) Axial T1-weighted MR image (500/14) demonstrates high-signal-intensity areas within the mass (arrow), a finding that is consistent with hemorrhage. (d) Axial fast spin-echo T2-weighted MR image (7,500/100) also demonstrates extensive high-signal-intensity areas within the mass (arrow), a finding that is consistent with necrosis. (e) Photomicrograph (original magnification, x100; H-E stain) demonstrates amorphous necrosis (arrows), a finding that is seen in the majority of adrenal carcinomas.
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Figure 6e. Adrenal carcinoma in a 32-year-old woman with Cushing syndrome. (a) Unenhanced CT scan demonstrates a large, low-attenuation suprarenal mass (short arrows) containing areas of high attenuation (long arrows) that are consistent with hemorrhage. (b) Contrast-enhanced CT scan demonstrates the mass with heterogeneous enhancement. Large areas of necrosis are also seen (*). Note the anterior displacement and compression of the inferior vena cava (IVC) (arrow). (c) Axial T1-weighted MR image (500/14) demonstrates high-signal-intensity areas within the mass (arrow), a finding that is consistent with hemorrhage. (d) Axial fast spin-echo T2-weighted MR image (7,500/100) also demonstrates extensive high-signal-intensity areas within the mass (arrow), a finding that is consistent with necrosis. (e) Photomicrograph (original magnification, x100; H-E stain) demonstrates amorphous necrosis (arrows), a finding that is seen in the majority of adrenal carcinomas.
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Figure 7a. Adrenal carcinoma in an 11-year-old girl with Cushing syndrome and virilization. (a) Axial fast spin-echo T2-weighted MR image (5,000/105) shows a large, left-sided adrenocortical carcinoma (black arrow) and a liver metastasis (white arrow). (b) Chest CT scan shows extensive lung metastases.
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Figure 7b. Adrenal carcinoma in an 11-year-old girl with Cushing syndrome and virilization. (a) Axial fast spin-echo T2-weighted MR image (5,000/105) shows a large, left-sided adrenocortical carcinoma (black arrow) and a liver metastasis (white arrow). (b) Chest CT scan shows extensive lung metastases.
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Figure 8a. Adrenocortical carcinoma in a 45-year-old woman with a history of hypertension. (a) Contrast-enhanced CT scan demonstrates a large, heterogeneously enhancing mass in the right suprarenal region (arrow) with extension into the IVC (*). (b) Sagittal thin-section reformatted image elegantly demonstrates tumor extension into the IVC and right atrium (arrow).
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Figure 8b. Adrenocortical carcinoma in a 45-year-old woman with a history of hypertension. (a) Contrast-enhanced CT scan demonstrates a large, heterogeneously enhancing mass in the right suprarenal region (arrow) with extension into the IVC (*). (b) Sagittal thin-section reformatted image elegantly demonstrates tumor extension into the IVC and right atrium (arrow).
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Bilateral Adrenal Disease
The imaging features of these bilateral diseases are summarized in Tables 3 and 4.
PPNAD.—
PPNAD was seen in two of 37 cases, both involving relatively young patients (10 and 28 years, respectively) (Fig 9). The adrenal glands manifested with bilateral small discrete nodules between 2 and 5 mm in size. The glands were not enlarged overall. In both cases, the diagnosis was confirmed histologically. In one case, the appearance was classical, with 2–5-mm pigmented nodules with atrophic intervening adrenal tissue (Fig 9). In the second case, the nodules were not pigmented but the features were otherwise characteristic. In this latter case, chemical shift imaging was available, and signal dropout was clearly visible.
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Figure 9a. PPNAD in a 28-year-old man. (a, b) Delayed contrast-enhanced CT scans show small nodules in the left (a) and right (b) adrenal glands (arrows). The remaining portions of the glands do not appear hyperplastic. (c) Photomicrograph (original magnification, x200; H-E stain) (left) shows nodules of enlarged and hyperchromatic cells (hyperplastic adrenocortical cells) (arrowhead) alternating with normal adrenocortical parenchyma (A). Photomicrograph (original magnification, x200; H-E stain) (right) reveals deeply eosinophilic cells with an abundance of lipofuscin pigment (arrows) and a focal cluster of hyperchromatic cells with dark blue staining (H). The latter are hematopoietic cells and are commonly seen incidentally in normal adrenal tissue. These findings indicate the presence of PPNAD, also known as micronodular hyperplasia.
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Figure 9b. PPNAD in a 28-year-old man. (a, b) Delayed contrast-enhanced CT scans show small nodules in the left (a) and right (b) adrenal glands (arrows). The remaining portions of the glands do not appear hyperplastic. (c) Photomicrograph (original magnification, x200; H-E stain) (left) shows nodules of enlarged and hyperchromatic cells (hyperplastic adrenocortical cells) (arrowhead) alternating with normal adrenocortical parenchyma (A). Photomicrograph (original magnification, x200; H-E stain) (right) reveals deeply eosinophilic cells with an abundance of lipofuscin pigment (arrows) and a focal cluster of hyperchromatic cells with dark blue staining (H). The latter are hematopoietic cells and are commonly seen incidentally in normal adrenal tissue. These findings indicate the presence of PPNAD, also known as micronodular hyperplasia.
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Figure 9c. PPNAD in a 28-year-old man. (a, b) Delayed contrast-enhanced CT scans show small nodules in the left (a) and right (b) adrenal glands (arrows). The remaining portions of the glands do not appear hyperplastic. (c) Photomicrograph (original magnification, x200; H-E stain) (left) shows nodules of enlarged and hyperchromatic cells (hyperplastic adrenocortical cells) (arrowhead) alternating with normal adrenocortical parenchyma (A). Photomicrograph (original magnification, x200; H-E stain) (right) reveals deeply eosinophilic cells with an abundance of lipofuscin pigment (arrows) and a focal cluster of hyperchromatic cells with dark blue staining (H). The latter are hematopoietic cells and are commonly seen incidentally in normal adrenal tissue. These findings indicate the presence of PPNAD, also known as micronodular hyperplasia.
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AIMAH.—
Imaging findings were available in only one case of AIMAH and were characteristic, with massively enlarged adrenal glands bilaterally, in this case retaining the normal adreniform shape. The adrenal limb width and maximum nodule size were 30 mm. Unlike with the adrenal adenomas and carcinomas, there was marked enhancement, predominantly of the periphery of the glands, at contrast-enhanced imaging (Fig 10a–10c). At MR imaging, the glands were isointense relative to the spleen and hypointense relative to the liver on T1-weighted images and hyperintense relative to both the spleen and the liver on T2-weighted images. The glands demonstrated 42% signal dropout at chemical shift imaging, suggesting the presence of intracellular lipid (Fig 10d, 10e). At histologic analysis, there were multiple large nodules interspersed with markedly hyperplastic adrenal tissue between the nodules. There was no pigmentation.
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Figure 10a. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) (e) FMPSPGR T1-weighted MR images (flip angle = 90°) demonstrate 42% signal dropout within the glands with the out-of-phase sequence, a finding that indicates the presence of intracellular lipid. (f) Sectioned gross resected specimen of the left adrenal gland shows marked cortical expansion with multiple nodules (arrows). (g) Photomicrograph (original magnification, x200; H-E stain) reveals sheets of largely fascicular zone cells and areas of glomerular zone cells, which have a more compact trabecular pattern. No malignant or pigmented cells are seen.
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Figure 10b. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) (e) FMPSPGR T1-weighted MR images (flip angle = 90°) demonstrate 42% signal dropout within the glands with the out-of-phase sequence, a finding that indicates the presence of intracellular lipid. (f) Sectioned gross resected specimen of the left adrenal gland shows marked cortical expansion with multiple nodules (arrows). (g) Photomicrograph (original magnification, x200; H-E stain) reveals sheets of largely fascicular zone cells and areas of glomerular zone cells, which have a more compact trabecular pattern. No malignant or pigmented cells are seen.
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Figure 10c. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) (e) FMPSPGR T1-weighted MR images (flip angle = 90°) demonstrate 42% signal dropout within the glands with the out-of-phase sequence, a finding that indicates the presence of intracellular lipid. (f) Sectioned gross resected specimen of the left adrenal gland shows marked cortical expansion with multiple nodules (arrows). (g) Photomicrograph (original magnification, x200; H-E stain) reveals sheets of largely fascicular zone cells and areas of glomerular zone cells, which have a more compact trabecular pattern. No malignant or pigmented cells are seen.
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Figure 10d. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) (e) FMPSPGR T1-weighted MR images (flip angle = 90°) demonstrate 42% signal dropout within the glands with the out-of-phase sequence, a finding that indicates the presence of intracellular lipid. (f) Sectioned gross resected specimen of the left adrenal gland shows marked cortical expansion with multiple nodules (arrows). (g) Photomicrograph (original magnification, x200; H-E stain) reveals sheets of largely fascicular zone cells and areas of glomerular zone cells, which have a more compact trabecular pattern. No malignant or pigmented cells are seen.
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Figure 10e. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) (e) FMPSPGR T1-weighted MR images (flip angle = 90°) demonstrate 42% signal dropout within the glands with the out-of-phase sequence, a finding that indicates the presence of intracellular lipid. (f) Sectioned gross resected specimen of the left adrenal gland shows marked cortical expansion with multiple nodules (arrows). (g) Photomicrograph (original magnification, x200; H-E stain) reveals sheets of largely fascicular zone cells and areas of glomerular zone cells, which have a more compact trabecular pattern. No malignant or pigmented cells are seen.
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Figure 10f. AIMAH in a 50-year-old man with Cushing syndrome. (a) Contrast-enhanced CT scan shows massive hyperplasia of both adrenal glands (arrows), which still retain their adreniform contour. (b, c) Axial unenhanced (b) and contrast-enhanced (c) fat-saturated spin-echo T1-weighted MR images (500/16) show intense homogeneous enhancement of the hyperplastic nodular glands. (d, e) Axial in-phase (150/4.2) (d) and out-of-phase (150/2.3) < | |
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Abstract
LEARNING OBJECTIVES FOR TEST...
