Imaging of Fibrous Dysplasia Protuberans, an Extremely Rare Exophytic Variant of Fibrous Dysplasia.

This paper details the case report of a 26-year-old man who presented with a growing right-sided skull mass evaluated with ultrasound, non-contrast CT, contrast-enhanced MRI and 99mTc-MDP whole body bone scan with SPECT/CT. These studies suggested a broad differential diagnosis favoring benign osseous lesions. Given a more recent increase in the rate of growth, headache and large size, the lesion was excised via craniotomy followed by cranioplasty. Pathology confirmed fibrous dysplasia (FD) as the diagnosis. Interestingly, this report is the imaging evaluation of the exophytic subtype of FD, the so-called FD protuberance, an extremely rare variant of FD, of which only two case reports are found in the literature.

A Unique Case of Increased 18F-FDG Metabolic Activity in the Soft Tissues of the Bilateral Upper Thighs Due to Immunizations in a Pediatric Patient.

A case of a 7-month-old white female who was referred for 18F-fluorodeoxyglucose (FDG) Positron emission tomography/computed tomography (PET/CT) initial evaluation of a lytic skull lesion with presumed diagnosis of Langerhans cell histiocytosis is described. Incidentally, she was found to have hypermetabolic nodules in the soft tissues of her anterior thighs.

Renal cell carcinoma presenting with paraneoplastic hypercalcemic coma: a case report and review of the literature.

We report a case of a 62-year-old woman with renal cell carcinoma (RCC) presenting with a hypercalcemia-induced coma. A laboratory evaluation indicated nonparathyroid-mediated hypercalcemia with an initial serum calcium level of 18.6 mg/dL. Our patient's parathyroid hormone (PTH)-related peptide level was undetectable. Initial imaging was negative, but PET scan identified a mass in the upper pole of the left kidney. Our patient underwent partial nephrectomy, and the mass was identified as RCC on final pathology. After surgery, her hypercalcemia resolved and PTH returned to normal limits. This case report describes a patient with RCC with the unusual presentation of hypercalcemic coma. We review the differential diagnosis of malignant hypercalcemia and the evaluation of hypercalcemia occurring with RCC. This case illustrates the need to carefully review and interpret all available data, especially when conventional testing in the work-up of hypercalcemia is unrevealing.

Apical hypertrophy caused by glycogen storage disease creating artifacts in myocardial perfusion imaging.

A 46-year-old man with atrial fibrillation and coronary artery disease was referred for myocardial perfusion imaging for the evaluation of chest pain. The patient underwent adenosine stress and rest dual-isotope myocardial perfusion imaging. There was no adenosine-induced chest pain or EKG changes specific for ischemia. Myocardial perfusion images demonstrated an apical "hot spot" and decreased tracer activity in the base of the heart. The polar plots showed a bright center with a rim of significant (>2.5 SD) defect around the base of the myocardium. Ischemia in the base of the heart, with the apex of the heart seemingly normal, was rather puzzling and correlation with magnetic resonance images (MRI) showed apical hypertrophy. Examination of the history revealed that the patient was diagnosed with restrictive cardiomyopathy 2 years ago and endocardial biopsy showed intramyocardial glycogen on electron microscopy, suggesting glycogen storage disease. The case illustrates a "hot spot" resulting from apical hypertrophy creating artifactual fixed defects in myocardial perfusion images and in polar maps.