Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

Weber syndrome, tuberous sclerosis, and multiple endocrine neoplasia (MEN) syndrome. Anatomically, some pheochromocytomacontaining glands are normal in size. Bilateral tumors are more prevalent in both MEN II patients and those with von Hippel-Lindau disease; some of these patients also develop extraadrenal pheochromocytomas. Thus detection of bilateral or familial pheochromocytomas warrants a search for other unsuspected tumors. Of note is that a large minority of these patients with a pheochromocytoma are asymptomatic and have normal blood pressure and normal catecholamine testing. Nevertheless, in patients with von Hippel-Lindau disease and MEN II syndrome, the measurement of plasma normetanephrine and metanephrine achieves a sensitivity and specificity of over 95% in detecting pheochromocytomas (33).

Intravenous ionic contrast may precipitate a hypertensive crisis in a patient with a pheochromocytoma. Premedication with an a-adrener- gic blocking agent appears prudent prior to intravenous (IV) contrast agent administration to prevent an adrenergic crisis, although the need for such blockage is not well established for nonionic contrast agents.

Imaging

A review of 282 patients who underwent pheochromocytoma resection in France between 1980 and 1991, found unilateral tumors

in 67%, bilateral ones in 19%, and extraadrenal in 14% (34); the sensitivities of imaging in detecting these tumors were 89% for CT,98% for MRI, and 81% for I-131-MIBG scintigraphy.

If imaging reveals no adrenal tumor in a patient suspected of a pheochromocytoma, imaging of other extraadrenal sites, including bladder, is necessary. Scintigraphy with I-131- MIBG is useful to detect extraadrenal and bilateral tumors.

Most pheochromocytomas are readily imaged by CT, US, and MRI (Fig. 16.4), yet the clinical and imaging findings are not always straightforward, even in a setting of elevated catecholamines. Intrinsically solid tumors, necrosis, and hemorrhage result in a cystic appearance and, as a result, they have a variable imaging appearances. It is with cystic tumors that the differential diagnosis between cystic pheochromocytomas, necrotic carcinomas, and metastases becomes problematic. An aid to diagnosis is that aside from necrotic regions, these are very hypervascular tumors and postcontrast CT shows marked contrast enhancement.

Another source for confusion is that a minority of adrenal pheochromocytomas contain sufficient microscopic fat to result in a CT attenuation of <10HU and thus mimic an adenoma (35); after contrast enhancement some of these hypodense tumors also reveal >60% contrast washout on 10-min images, similar to adenomas.

Some contain linear or laminated calcifications (Fig. 16.5). Aside from several anecdotal reports, pheochromocytomas do not contain sufficient lipid to influence their imaging appearance.

Nonnecrotic pheochromocytomas tend to be hypointense-to-isointense to liver on T1and hyperintense on T2-weighted images. Their lack of fat reflects their hyperintense T2weighted fat-suppressed appearance. They tend to exhibit progressive enhancement postcontrast MR. Nevertheless, a sufficient number of pheochromocytomas have an atypical low signal intensity on T2-weighted images and not all hyperintense adrenal tumors represent pheochromocytomas, so that reliance on a hyperintense T2-weighted appearance results in a low sensitivity in diagnosing a pheochromocytoma (Fig. 16.6).

Scintigraphy with I-123-MIBG achieves an 80% to 90% detection rate for these tumors; MIBG SPECT sensitivity approaches 100%. This tracer accumulates in adrenergic tissue throughout the body, including metastases. Optimal scan timing is variable, with scans often obtained 24 to 48 hours postinjection. An occasional metastasis is detected only on earlier scans. Indium-111 pentetreotide scintigraphy appears to have similar detection ability as I-123-MIBG, but it has not been studied as extensively.

2-[18F]-fluoro-deoxy-D-glucose PET detected tumors in 76% of patients with pheochromocytomas, with most benign, malignant, and metastatic foci avidly concentrating FDG (36); in fact, several pheochromocytomas not accumulating MIBG showed intense FDG uptake, although MIBG images tended to be as good or better for tumors concentrating both agents. A majority of pheochromocytomas also reveal uptake during (11C)-hydroxyephedrine- PET scanning (37).

Therapy

The treatment of choice for most pheochromocytomas is surgical resection, although an occasional one is treated by catecholamine pharmacotherapy. Resection consists of either adrenalectomy or adrenal-sparing surgery, with a laparoscopic approach commonly employed. A pheochromocytoma has been treated with percutaneous radiofrequency ablation (23).

Neuroblastoma/Ganglioneuroma

Clinical

The most common abdominal neoplasm of early childhood, a neuroblastoma originates from neuroblasts in sympathetic ganglia. The adrenal glands are the most common site, with

B

C

those with aneuploid tumors have a much better survival.

Percutaneous biopsy using 15or 16-gauge core biopsy needles provides an alternate approach to open biopsy in children with advanced neuroblastoma. Percutaneous biopsy provides both a histologic diagnosis and enough sample for prognosis.

Imaging

Depending on the site of origin, imaging reveals a suprarenal or paraspinal tumor. Neuroblastomas are poorly encapsulated and compress or invade adjacent structures; aortic or inferior vena caval encasement is often found with larger tumors. In adults, ganglioneuromas tend to surround major blood vessels but do not narrow the lumen. Tumor hemorrhage and necrosis result in a heterogeneous imaging appearance. An occasional neuroblastoma contains a cystic component. Coarse, mottled calcifications are common. They have less CT contrast enhancement than muscle and, similar to neuroblastomas, a heterogeneous, predominantly hyperintense signal is evident on T2weighted MR images. Computed tomography and MRI are preferred over US because of their ability to better image metastases. Bone scans and chest radiographs are obtained preoperatively to detect metastases and establish a baseline.

Gray-scale 2D and 3D US using tissue harmonic imaging identified an adrenal ganglioneuroblastoma in a pregnant woman as an inhomogeneous,encapsulated,solid tumor (38); color and power Doppler showed extensive neovascularity.

Iodine-123-MIBG scintigraphy detects most neuroblastomas but some bone metastases show little or no MIBG uptake (39). SPECT imaging detects more tumors and better defines their location. Both 24-hour and delayed 48hour scanning appear useful; washout can result in some lesions being missed on delayed scans. Occasionally technetium-99m (Tc-99m)– hydroxymethylene diphosphonate (HMDP) bone scintigraphy is positive in an adrenal neuroblastoma.

Although MIBG scintigraphy appears superior to FDG-PET, the latter does detect most

ADVANCED IMAGING OF THE ABDOMEN

primary neuroblastoma foci and metastases. Also, occasionally FDG-PET is positive when a neuroblastoma fails to accumulate MIBG. PET scanning using carbon-11-hydroxyephedrine (HED) will also locate neuroblastomas.

Combined MIBG scintigraphy and MR imaging achieves a better diagnosis of neuroblastoma foci in children than either study individually. A retrospective study found MIBG scintigraphy, MRI and combined MIBG-MRI sensitivities of 69%, 86% and 99% and specificities of 85%, 77% and 95%, respectively (39).

In a newly discovered tumor the differential often includes a Wilms’ tumor. Imaging shows most neuroblastomas to be more inhomogeneous than a Wilms’ tumor. the latter is intrarenal in location, while an adrenal neuroblastoma displaces the kidney inferolaterally. Some paraspinal neuroblastomas extend into the spinal canal, a finding not seen with Wilms’ tumors. At times an adrenal hemorrhage (hematoma) mimics a neuroblastoma. After the initial presentation, US should distinguish an anechoic and avascular hemorrhage from the hyperechoic and vascular neuroblastoma.

Lymphoma

Primary adrenal lymphoma is rare (40). More common is lymphomatous adrenal involvement from adjacent extraperitoneal lymph nodes, either unilateral or bilateral. Clinically silent adrenal involvement is relatively common with the latter, but adrenocortical insufficiency is a late finding with bilateral adrenal involvement.

Imaging findings range from solid nodules to diffuse homogeneous tumors. Adjacent lymphadenopathy is common. Often the adrenal glands are simply replaced by lymphomatous tissue and appear enlarged while maintaining their usual shape. With growth, lymphomas tend to become heterogeneous in appearance. They are hypoechoic with US. Magnetic resonance imaging reveals a signal intensity similar to that of metastases. Increasing enhancement on delayed postcontrast images is typical.

Necrosis and calcifications develop after therapy.

ADRENALS

Less Common Tumors

Rarer adrenal tumors include a bronchogenic cyst, pure lipoma, teratoma, vascular leiomyomas, schwannoma, and even a sarcoma. Occasionally a patient with von Recklinghausen’s disease develops bilateral adrenal neurofibromas, although in this disease adrenal pheochromocytomas are more common. Ectopic tissue is occasionally detected in the adrenal glands (i.e., a choristoma), the most common one being ectopic thyroid tissue (41). Except for the latter, no imaging findings suggest a specific diagnosis.

Hemangioma

Adrenal hemangiomas are rare. Some contain calcifications and often are large. The more typical ones have imaging characteristics similar to those of liver hemangiomas. An occasional adrenal hemangioma contains a central stellate hypointense region on MRI. Hemorrhage and necrosis are relatively common, and these influence their imaging appearance. The gradual tumor enhancement from the periphery inward is not seen as often as with liver hemangiomas. An occasional one presents with extraperitoneal hemorrhage.

An adrenal hemangioma-like appearance in an infant should suggest a hemangioendothelioma. Their imaging appearance is similar to those in the liver.

sisted either of an isolated adrenal myelolipoma (identified by fat evident at CT) or myelolipomatous tissue within other adrenal tumors (consisting of smaller foci containing less fat but more calcifications) (43); larger myelolipomas contained hemorrhage and necrosis. About 20% of these tumors contain small foci of calcifications.

Unenhanced CT should detect most of these tumors. The amount of fat present varies considerably, but a myelolipoma should not contain only fat; a mixture of fat and nonfatty tissue often results in a heterogeneous appearance (Fig. 16.7). Bleeding can obliterate surrounding fat planes (Fig. 16.8). Contrast-enhanced CT can obscure the fat component and miss a tumor.

Ultrasonography shows a highly echogenic tumor.

Magnetic resonance imaging reveals a variable signal with both T1and T2-weighted sequences (Fig. 16.9). The signal decreases with fat suppression. These tumors enhance postcontrast. Their MR characteristics are modified by any hemorrhage and necrosis.

As already mentioned, other adrenal tumors, including a rare adenocarcinoma, contain fat. Differential diagnosis for a fat-containing adrenal lesion also includes a teratoma and liposarcoma. Some cysts contain a fatty component.

A biopsy should be diagnostic. Unless symptoms ensue, most of these tumors can be followed conservatively. With time, they can increase, decrease, or remain unchanged.

Myelolipoma

Adrenal cortical myelolipomas are rare, benign, nonfunctioning tumors composed of fat and bone marrow tissue. They occur bilaterally. Most myelolipomas are small and are discovered incidentally in asymptomatic patients. Anecdotal reports describe extraadrenal perirenal myelolipomas (42). An occasional patient presents with acute pain secondary to intratumoral or extraperitoneal bleeding.

In a minority of patients a myelolipoma is associated with some type of endocrine

Adrenal myelolipomatous tissue reported from the Armed Forces Institute of Pathology con-

Hemorrhage/Hematoma

Some of the more common conditions associated with adrenal hemorrhage are listed in Table 16.2. Usually a hematoma is limited to the adrenal glands, without involving adjacent extraperitoneal tissues.

Adrenal hematomas have an imaging appearance similar to that of hematomas at other locations; their appearance changes and evolves with time.

Neonates

Most adrenal hemorrhage in neonates is idiopathic, although birth stress and related factors

are implicated. Jaundice may be present. Hemorrhage is more common on the right side, except if associated with renal vein thrombosis when it occurs much more often on the left. With an inferior vena cava thrombus hemorrhage tends to be bilateral.

Figure 16.8. Bleeding adrenal myelolipoma. Contrastenhanced CT reveals a fat-containing tumor superior to the right kidney (arrows). Angiography performed shortly after this study identified a hypovascular tumor. (Courtesy of Patrick Fultz, M.D., University of Rochester.)

Typically, these neonates do not develop adrenal insufficiency. A scrotal hematoma is occasionally the initial presentation of adrenal hemorrhage in neonates.

The primary differential diagnosis in a neonate is a neuroblastoma, although MRI will differentiate these, with the exception of a hemorrhagic, cystic-appearing neuroblastoma (see also the description in Neuroblastoma/ Ganglioneuroma, above). Also, hemorrhage should change its appearance over time, become anechoic, and decrease in size. Neonatal adrenal hemorrhage should also be differentiated from adrenal congestion, which develops in perinatal asphyxia and other perinatal stress conditions. Ultrasonography in the latter identifies diffuse adrenal enlargement, a smooth surface, and loss of the central hyperechoic stripe (44); histology in five neonates who died revealed diffuse sinusoidal congestion.

Adults

In adults, spontaneous adrenal hemorrhage ranges from unilateral to bilateral. Aside from trauma, most are associated with stress or a severe illness and are more often unilateral. In a setting of anticoagulant therapy a hematoma usually develops early in the course. If associated with a neoplasm, imaging

should detect tumor enhancement. Adrenal hemorrhage is relatively common in patients with meningococcal sepsis (WaterhouseFriderichsen syndrome); some hemorrhages

Table 16.2. Conditions associated with adrenal hemorrhage

Neonates

Idiopathic

Stress

Renal vein thrombosis

Inferior vena cava thrombosis

Adults Idiopathic Stress

Surgery Hypotension Sepsis

Trauma

Anticoagulant therapy Underlying neoplasm Postpartum period

Meningococcal sepsis (Waterhouse-Friderichsen syndrome)

Primary antiphospholipid syndrome Adrenal vein thrombosis

Inferior vena cava thrombosis

Vasculitis leading to hypercoagulable state and venous thrombosis

Associated with liver transplantation Adrenomyeloneuropathy

extend into adjacent extraperitoneal tissues. In some patients with primary antiphospholipid syndrome hemorrhage is probably due to adrenal vein thrombosis. A right adrenal hemorrhage is a complication of liver transplantation, a not surprising finding because these patients undergo inferior vena caval division and ligation of right adrenal veins.

Imaging findings of adrenal hemorrhage are varied and consist of either unilateral or bilateral gland enlargement, at times asymmetrical, or a focal tumor. A typical CT appearance is a heterogeneous tumor having a density of 50 to 90HU. Some hemorrhages are associated with periadrenal fat infiltration or even involve adjacent diaphragmatic crus. They are hyperintense on both T1and T2-weighted MR images. A hematoma shows no contrast enhancement with either CT or MRI. Angiography, although rarely performed, identifies a hypovascular tumor. With time, the involved gland shrinks and the hematoma decreases in density.

While unilateral hemorrhage generally has few sequelae, bilateral involvement can result in adrenal insufficiency. In either case, an adrenal hemorrhage should be followed until resolution to exclude an underlying neoplasm. With time, some involved glands atrophy and calcify. Presumably in some adults adrenal calcifications represent sequelae of neonatal hemorrhage. The

hallmark of a remote hemorrhage is an extensively calcified gland with no significant soft tissue component. Prior granulomatous disease usually results in more patchy calcifications.

ADVANCED IMAGING OF THE ABDOMEN

Adrenal vein thrombosis can develop in a setting of heparin-induced thrombocytopenia (45).

Insufficiency

Most of the adrenal cortex must be destroyed before adrenal insufficiency (Addison’s disease) manifests clinically. Most often insufficiency is idiopathic, although an autoimmune disorder is often suspected. Other less common etiologies include adrenal hemorrhage, tuberculosis, histoplasmosis, rare adrenal involvement by North American blastomycosis, and sarcoidosis. Infiltration by lymphoma or metastatic carcinoma, when extensive, can also lead to adrenal insufficiency.

In an acute setting of shock, adrenal insufficiency should be considered if CT reveals bilateral, enlarged, hematoma-density adrenal glands. In a setting of septicemia, however, shock may be induced by septicemia rather than adrenal insufficiency. Also, at times adrenal gland enlargement in the face of adrenal insufficiency is due to tumors such as lymphoma or metastases.

Imaging in patients with more chronic adrenal insufficiency shows that about half have bilateral adrenal enlargement, at times containing regions of necrosis and calcification. Enlarged glands tend to decrease in size after appropriate therapy. Some patients have calcified, atrophic glands. Noncalcified atrophic glands are difficult to visualize with imaging.

Iron deposition in the adrenal glands in patients with hemochromatosis eventually results in mild adrenal insufficiency. Computed tomography reveals small glands having increased attenuation.

Vascular Lesions

An aneurysm of an adrenal artery is rare; rupture leads to a periadrenal hematoma. Imaging reveals a cystic tumor, hematoma, and possible thrombus in the artery. These aneurysms can be diagnosed by angiography and are amenable to embolization.

Immunosuppression

Both fungal and viral adrenal infections are more common in AIDS patients than in the general population. Sufficient gland destruction results in adrenal insufficiency.

Lymphoma predominates among adrenal tumors in AIDS patients. Kaposi’s sarcoma is less common. Several adrenal adenocarcinomas have been reported, although the association may be fortuitous.

Postoperative Changes

An adrenalectomy is performed using either an open or laparoscopic approach and either an anterior, posterior, or a thoracoabdominal incision. A transthoracic approach is preferred by some. Using anterior transabdominal approach the left adrenal gland is reached by either mobilizing the spleen and pancreatic tail, or using the lesser sac as a pathway and displacing the pancreas away from the adrenal gland. An open adrenalectomy is generally performed in patients with a suspected malignancy and for tumors larger than about 6cm. A laparoscopic adrenalectomy is considered for others; it requires minimal access, is least painful to the patient, and results in a shorter hospitalization than an anterior approach.

References

1.Karampekios S, Hatjidakis AA, Drositis J, Gourtsoyiannis N. Artificial paravertebral widening for percutaneous CT-guided adrenal biopsy. [Review] J Comput Assist Tomogr 1998;22:308–310.

2.Konig CW, Pereira PL, Trubenbach J, et al. MR imagingguided adrenal biopsy using an open low-field-strength scanner and MR fluoroscopy. AJR 2003;180:1567–1570.

3.Shafaie FF, Katz ME, Hannaway CD.A horseshoe adrenal gland in an infant with asplenia. Pediatr Radiol 1997;27:591–593.

4.Akata D, Haliloglu M, Ozmen MN, Akhan O. Bilateral cystic adrenal masses in the neonate associated with the incomplete form of Beckwith-Wiedemann syndrome. Pediatr Radiol 1997;27:184–185.

5.Moore EE, Malangoni MA, Cogbill TH, et al. Organ injury scaling VII: cervical vascular, peripheral vascular,

ADRENALS

adrenal, penis, testis, and scrotum. J Trauma 1996;41: 523–524.

6.Ferrozzi F, Cademartiri F, Tognini G. [Adrenal hydatidosis. The computed tomographic picture in a case.] [Review] [Italian] Radiol Med 1999;98:430–431.

7.Hahn ST, Park SH, Kim CY, Shinn KS. Adrenal paragonimiasis simulating adrenal tumor—a case report. J Korean Med Sci 1996;11:275–277.

8.Wang LJ, Wong YC, Chen CJ, Chu SH. Imaging spectrum of adrenal pseudocysts on CT. Eur Radiol 2003;13:531–535.

9.Barzon L, Scaroni C, Sonino N, et al. Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates. J Clin Endocrinol Metab 1998;83:55–62.

10.Honigschnabl S, Gallo S, Niederle B, et al. How accurate is MR imaging in characterisation of adrenal masses: update of a long-term study. Eur J Radiol 2002; 41:113–122.

11.Cataldi A, Cortese G, Corradino R, Porpiglia F, Ali A, Fava C. [Characterization of non-secreting adrenal nodules (incidentalomas): role of multiphasic spiral computerized tomography.] [Italian] Radiol Med 2000;100:257–261.

12.Namimoto T, Yamashita Y, Mitsuzaki K, et al. Adrenal masses: quantification of fat content with double-echo chemical shift in-phase and opposed-phase FLASH MR images for differentiation of adrenal adenomas. Radiology 2001;218:642–646.

13.Fujiyoshi F, Nakajo M, Fukukura Y, Tsuchimochi S. Char-

acterization of adrenal tumors by chemical shift fast low-angle shot MR imaging: comparison of four methods of quantitative evaluation. AJR 2003;180: 1649–1657.

14.Israel GM, Korobkin M, Wang C, Hecht EN, Krinsky GA. Comparison of unenhanced CT and chemical shift MRI in evaluating lipid-rich adrenal adenomas. AJR 2004;183:215–219.

15.Szolar DH, Kammerhuber FH. Adrenal adenomas and nonadenomas: assessment of washout at delayed contrast-enhanced CT. Radiology 1998;207:369–375.

16.Peña CS, Boland GW, Hahn PF, Lee MJ, Mueller PR. Characterization of indeterminate (lipid-poor) adrenal masses: use of washout characteristics at contrastenhanced CT. Radiology 2000;217:798–802.

17.Caoili EM, Korobkin M, Francis IR, Cohan RH, Dunnick NR. Delayed enhanced CT of lipid-poor adrenal adenomas. AJR 2000;175:1411–1415.

18.Chung JJ, Semelka RC, Martin DR. Adrenal adenomas: characteristic postgadolinium capillary blush on dynamic MR imaging. J Magn Reson Imaging 2001;13: 242–248.

19.Hofle G, Gasser RW, Lhotta K, Janetschek G, Kreczy A, Finkenstedt G. Adrenocortical carcinoma evolving after diagnosis of preclinical Cushing’s syndrome in an adrenal incidentaloma. A case report. Horm Res 1998;50:237–242.

20.Joual A, Patard JJ, Chopin D, Abbou CC. [Contralateral aneurysm-like adrenal gland metastasis of a renal adenocarcinoma.] [French] Prog Urol 1998;8:89–91.

21.Tsukamoto E, Itoh K, Kanegae K, Kobayashi S, Koyanagi T, Tamaki N. Accumulation of iodine- 131–iodocholesterol in renal cell carcinoma adrenal metastases. J Nucl Med 1998;39:656–658.

22.Shibata T, Maetani Y, Ametani F, Itoh K, Konishi J. Percutaneous ethanol injection for treatment of adrenal

metastasis from hepatocellular carcinoma. AJR 2000; 174:333–335.

23.Mayo-Smith WW, Dupuy DE. Adrenal neoplasms: CTguided radiofrequency ablation–preliminary results. Radiology 2004;231:225–230.

24Sohaib SA, Hanson JA, Newell-Price JD, et al. CT appearance of the adrenal glands in adrenocorticotrophic hormone-dependent Cushing’s syndrome. AJR 1999; 172:997–1002.

25.Midorikawa S, Hashimoto S, Kuriki M, et al. A patient with preclinical Cushing’s syndrome and excessive DHEA-S secretion having unilateral adrenal carcinoma and contralateral adenoma. Endocr J 1999;46: 59–66.

26.Otsuka F, Ogura T, Nakao K, et al. Cushing’s syndrome due to unilateral adrenocortical hyperplasia. Intern Med 1998;37:385–390.

27.Doppman JL, Chrousos GP, Papanicolaou DA, Stratakis CA, Alexander HR, Nieman LK. Adrenocorticotropinindependent macronodular adrenal hyperplasia: an uncommon cause of primary adrenal hypercortisolism. Radiology 2000;216:797–802.

28.Stewart PM. Mineralocorticoid hypertension. [Review] Lancet 1999;353:1341–1347.

29.Lingam RK, Sohaib SA, Vlahos I, et al. CT of primary

hyperaldosteronism (Conn’s syndrome): the value of measuring the adrenal gland. AJR 2003;181:843– 849.

30.Lorenzo Romero JG, Salinas Sanchez AS, Segura Martin M, et al. [The Conn syndrome. The clinical and surgical aspects of 18 cases of adrenal adenoma.] [Spanish] Actas Urol Esp 1999;23:14–21.

31.Sohaib SA, Peppercorn PD,Allan C, et al. Primary hyperaldosteronism (Conn syndrome): MR imaging findings. Radiology 2000;214:527–531.

32.Liang HL, Pan HB, Lee YH, et al. Small functional adrenal cortical adenoma: treatment with CT-guided percutaneous acetic acid injection–report of three cases. Radiology 1999;213:612–615.

33.Eisenhofer G, Lenders JW, Linehan WM, Walther MM, Goldstein DS, Keiser HR. Plasma normetanephrine and metanephrine for detecting pheochromocytoma in von Hippel-Lindau disease and multiple endocrine neoplasia type 2. N Engl J Med 1999;340:1872–1879.

34.Jalil ND, Pattou FN, Combemale F, et al. Effectiveness and limits of preoperative imaging studies for the localisation of pheochromocytomas and paragangliomas: a review of 282 cases. French Association of Surgery (AFC), and The French Association of Endocrine Surgeons (AFCE). Eur J Surg 1998;164:23– 28.

35.Blake MA, Krishnamoorthy SK, Boland GW, et al. Lowdensity pheochromocytoma on CT: a mimicker of adrenal adenoma. AJR 2003;181:1663–1668.

36.Shulkin BL, Thompson NW, Shapiro B, Francis IR, Sisson JC. Pheochromocytomas: imaging with 2– [fluorine-18]fluoro-2-deoxy-D-glucose PET Radiology 1999;212:35–41.

37.Trampal C, Engler H, Juhlin C, Bergstrom M, Langstrom B. Pheochromocytomas: detection with 11C hydroxyephedrine PET. Radiology 2004;230:423–428.

38.Slapa RZ, Jakubowski W, Kasperlik-Zaluska AA, et al. Adrenal ganglioneuroblastoma in pregnant woman: diagnosis with three-dimensional ultrasound. Eur Radiol 2002;12 Suppl 3:S121–126.

39.Pfluger T, Schmied C, Porn U, et al. Integrated imaging using MRI and 123I metaiodobenzylguanidine scintigraphy to improve sensitivity and specificity in the diagnosis of pediatric neuroblastoma. AJR 2003;181:1115–1124.

40.Tazi K, Achour A, Koutani A, Ibn Attya A, Hachimi M, Lakrissa A. [Primary non-Hodgkin’s malignant lymphoma of the adrenal gland. Case report and review of the literature.] [Review] [French] Prog Urol 1999;9: 1102–1105.

41.Shiraishi T, Imai H, Fukutome K, Watanabe M, Yatani R. Ectopic thyroid in the adrenal gland. Hum Pathol 1999;30:105–108.

42.Kumar M, Duerinckx AJ. Bilateral extraadrenal perirenal myelolipomas: an imaging challenge. AJR 2004;183:833–836.

43.Kenney PJ, Wagner BJ, Rao P, Heffess CS. Myelolipoma: CT and pathologic features. Radiology 1998;208:87–95.

44.Koplewitz BZ, Daneman A, Cutz E, Hellmann J. Neonatal adrenal congestion: a sonographic-pathologic correlation. Pediatr Radiol 1998;28:958–962.

45.Bolter S, Meier M, Roeren T. [Adrenal vein thrombosis in heparin-induced thrombocytopenia.] [German] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2000;172:100–101.