Localized amyloidosis is a rare condition, especially that involving the ureter. Because of its rarity and the difficulty in differentiating this condition from urothelial carcinoma by intravenous urography and computed tomography, nephroureterectomy has often been performed unnecessarily for this disease. The authors encountered two cases of this disease, both of which showed a negative urine cytology, no obvious mass effect, and a hypointensity on T2-weighted imaging. Because these findings are very rare in urothelial carcinoma, ureteroscopy-guided biopsy was performed, which yielded the diagnosis of amyloidosis. The patients were then treated and followed up at our institute. Primary localized amyloidosis of the ureter should be considered when evaluating ureteric lesions visualized as hypointensities on T2-weighted images that do not show an obvious mass effect, which could help in the avoidance of unnecessary surgery.
Juvenile idiopathic arthritis (JIA) is a collective term for pediatric inflammatory arthritis of unknown etiology, which presents diverse clinical and imaging findings. The pathogenesis is complex; however, most cases stem from an autoimmune mechanism. Herein we provide a short review of imaging findings of JIA. Imaging assessment begins with plain radiography demonstrating joint swelling, periarticular osteopenia, and juxtaarticular bone erosion. Bone erosion occurs later in JIA. Instead, aberrant epimetaphyseal growth often gives the first clue to the diagnosis. US and MRI can demonstrate the details of the synovium, cartilage, and subchondral bone. JIA is subdivided into oligoarthritis, polyarthritis (rheumatoid factor-negative and positive), psoriatic arthritis, enthesitis-related arthritis, and systemic JIA. Awareness of the different clinical characteristics, pathogenic background, and prognosis of each subtype facilitates a more advanced, imaging-based diagnosis. Unlike the other types, systemic JIA is an autoinflammatory disease accompanied by inflammatory cytokinemia and systemic symptoms stemming from aberrant activation of the innate immunity. Other autoinflammatory diseases, both monogenic (e.g., NOMID/CINCA) and multifactorial (e.g., CRMO), are also discussed.
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