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3Department of Pathology, Brooke Army Medical Center, Fort Sam Houston, TX 78234. 41-year-old woman undergoing clinical and imaging evaluation for adrenocorticotropic hormone (ACTH)-independent Cushing’s syndrome was found to have a lipid-poor left adrenal adenoma on abdominal CT. Further evaluation with PET/CT supported a diagnosis of lipid-poor adrenal adenoma but also revealed a spiculated 3-cm soft-tissue mass in the right inguinal region that exhibited intense (standardized uptake value, 4.0) 18F-FDG activity (Fig. 1A). MRI showed the lesion to have intermediate T1 (Fig. 1B) and markedly low T2 (Fig. 1C) signal characteristics, extending through the right inguinal canal into the right lateral mons pubis (Fig. 1C). Sonography-guided core biopsy was performed, and histologic findings were consistent with endometriosis (Fig. 1D). Low T2 signal intensity characteristic of a soft-tissue lesion is of considerable aid in narrowing the radiologist’s differential diagnosis. The mnemonic CHAFT (calcification, hemosiderin, amyloid/air, fibrous lesions, and tophaceous gout) can be used to easily formulate a differential diagnosis in such lesions. Correlation with conventional radiographs and CT plays an important role in distinguishing among these entities through more precise identification of calcifications, air, and tophi. In addition, clinical presentation and anatomic location can effectively exclude tophaceous gout from differential consideration. Inguinal hernia, fibrous neoplasm, and extrapelvic endometriosis remain in the differential diagnosis. Although PET/CT is a valuable technique in evaluating for neoplasms, this case illustrates the importance of correlating increased 18F-FDG activity with cross-sectional imaging examinations. Infection, inflammation, physiologic muscular activity, brown fat, and metabolically active lesions (i.e., endometriosis) all can show markedly increased 18F-FDG uptake. Endometriosis is a common gynecologic disease affecting 1–2% of all women. Classically, it is characterized by implantation of endometrial tissue outside the uterine cavity, resulting in bleeding, cyclical pain, and scarring. Typically, endometriosis occurs within the ovaries and peritoneum [1]. However, rarer cases have been reported in the vagina, rectum, lung (potentially leading to catamenial pneumothorax), subcutaneous tissues, and inguinal canal [2, 3]. The prevailing theory to explain the mechanism of endometriosis is retrograde menstruation (implantation theory), which proposes that viable endometrial tissue is refluxed through the fallopian tube during menstruation and deposited on the peritoneal surface or pelvic organs [1]. The gubernaculum testis, which is embryologically a cord of fibrous and muscular tissue, A

Campbell SE, Reed CM, Bui-Mansfield LT, Fillman E 64-year-old woman with a history of sarcoidosis presented with back and abdominal pain and was unresponsive to nonsteroidal antiinflammatory medications. In addition, the patient complained of weakness in her right arm. Physical examination of the abdomen was unremarkable, and examination of the spine revealed normal flexion and extension and no focal tenderness. Neurologic examination revealed slightly decreased strength in the right arm and hand. A posteroanterior chest radiograph showed a bilateral diffuse reticulonodular pulmonary parenchymal pattern, right paratracheal stripe thickening, and bilateral hilar lymphadenopathy (Fig. 1A). CT of the chest confirmed bilateral hilar, right paratracheal, and subcarinal lymphadenopathy and interstitial pulmonary disease. CT also revealed widespread retroperitoneal lymphadenopathy and multiple lytic lesions within the vertebral bodies and posterior elements of the thoracolumbar spine. Subsequent MRI of the spine revealed decreased T1 signal intensity and increased T2 signal intensity scattered throughout the spine (Fig. 1B). After IV sodium gadopentate was administered to the patient, multiple brightly enhancing lesions within the vertebral bodies, pedicles, laminae, and spinous processes were identified. Diffuse leptomeningeal and nerve root enhancement and an enhancing parenchymal spinal cord mass were also present (Fig. 1C). Biopsy of a vertebral lesion revealed noncaseating granuloma consistent with sarcoidosis without evidence of malignancy (Fig. 1D). Gram stains and cultures for fungi, aerobic and anaerobic organisms, and acid-fast bacilli were all negative. The differential diagnosis for diffuse marrow infiltration, enhancing intraaxial spinal cord mass, diffuse meningeal and nerve root enhancement, and mediastinal and retroperitoneal lymphadenopathy includes metastatic disease, lymphoma, leukemia, hematogenous osteomyelitis (tuberculous, fungal), and sarcoidosis [1]. Sarcoidosis is a systemic granulomatous disease of unknown etiology that has been shown to affect nearly every organ system. Osseous involvement occurs in 1–13% of cases, typically in the small tubular bones of the hands and feet [2, 3]. Sarcoidosis may affect either the vertebral column or the spinal cord. Typical vertebral column manifestations are lytic lesions with sclerotic borders that enhance on MRI and enhancement of the intervertebral disk [1, 3–5]. Typical spinal cord manifestations are leptomeningeal enhancement, enhancing spinal cord mass, nerve root “clumping,” and enhancing nerve root [4]. The most common spinal cord manifestation is leptomeningeal disease [4]. Given the variable manifestations of sarcoidosis within the spine, this disease should be considered in the differential diagnosis along with multiple sclerosis [4]; tuberculous meningitis [4]; and widespread vertebral involvement of metastatic disease, infection, or lymphoma [1]. Sarcoidosis is typically treated with corticosteroid therapy, after which clinical symptoms and even MRI findings may completely or partially resolve in 29% of the patients [6]. Prednisone