Primary retroperitoneal masses include a diverse, and often rare, group of neoplastic and non-neoplastic entities that arise within the retroperitoneum but do not originate from any retroperitoneal organ. Their overlapping appearances on cross-sectional imaging may pose a diagnostic challenge to the radiologist; familiarity with characteristic imaging features, together with relevant clinical information, helps to narrow the differential diagnosis. In this article, a systematic approach to identifying and classifying primary retroperitoneal masses is described. The normal anatomy of the retroperitoneum is reviewed with an emphasis on fascial planes, retroperitoneal compartments, and their contents using cross-sectional imaging. Specific radiologic signs to accurately identify an intra-abdominal mass as primary retroperitoneal are presented, first by confirming the location as retroperitoneal and secondly by excluding an organ of origin. A differential diagnosis based on a predominantly solid or cystic appearance, including neoplastic and non-neoplastic entities, is elaborated. Finally, key diagnostic clues based on characteristic imaging findings are described, which help to narrow the differential diagnosis. This article provides a comprehensive overview of the cross-sectional imaging features of primary retroperitoneal masses, including normal retroperitoneal anatomy, radiologic signs of retroperitoneal masses and the differential diagnosis of solid and cystic, neoplastic and non-neoplastic retroperitoneal masses, with a view to assist the radiologist in narrowing the differential diagnosis.

Among patients with PsA, MetS and IR are highly prevalent, and are independently associated with the severity of underlying PsA.

No abstract

Different HLA susceptibility genes were associated with particular features that defined the PsA phenotype of a given patient. Additive interactions between different susceptibility HLA alleles defined the propensity for a more severe or milder musculoskeletal phenotype.

Objective. To examine the effect of tumor necrosis factor (TNF) blocking therapy on hypoxia in vivo, macroscopic and microscopic inflammation, and magnetic resonance imaging (MRI) results in patients with inflammatory arthritis.Methods. Patients with inflammatory arthritis (n ‫؍‬ 20) underwent full clinical assessment, arthroscopy, synovial biopsy, and MRI before and after initiation of biologic therapy. Macroscopic synovitis/vascularity was assessed with a visual analog scale, and tissue PO 2 (tPO 2 ) was measured at arthroscopy using a Licox probe. Cell-specific markers (CD4, CD8, CD68, CD20, and CD19) and blood vessel maturity were quantified by immunohistologic analysis and dual-immunofluorescence factor VIII/␣-smooth muscle actin staining, respectively. Contiguous gadoteric acid-enhanced MRI of the target knee was used to assess synovial enhancement.Results. Biologic therapy responders showed a significant increase of tPO 2 in vivo (P < 0.05). This response was associated with significant reductions in 28-joint Disease Activity Score using the C-reactive protein level (DAS28-CRP) (P ‫؍‬ 0.012), macroscopic synovitis (P ‫؍‬ 0.017), macroscopic vascularity (P ‫؍‬ 0.05), CD4؉ T cells (P < 0.041), and CD68؉ macrophages (P < 0.011). Blood vessel numbers were also reduced in responders; however, this did not reach statistical significance. Strong inverse correlations were demonstrated between changes in tPo 2 levels and changes in DAS28-CRP (r ‫؍‬ ؊0.53, P < 0.001), CD4 (r ‫؍‬ ؊0.44, P < 0.026), CD68 (r ‫؍‬ ؊0.46, P < 0.003), and macroscopic vascularity (r ‫؍‬ ؊0.314, P ‫؍‬ 0.049) after therapy. Furthermore, changes in inflammation as measured by MRI showed a strong inverse correlation with tPO 2 levels (r ‫؍‬ ؊0.688, P < 0.002) and positive correlations with CRP levels (r ‫؍‬ 0.707, P ‫؍‬ 0.001), macroscopic synovitis (r ‫؍‬ 0.457, P ‫؍‬ 0.056), macroscopic vascularity (r ‫؍‬ 0.528, P‫؍‬ 0.017), CD4 (r ‫؍‬ 0.553, P < 0.032), and CD68 (r ‫؍‬ 0.670, P < 0.002) after therapy.Conclusion. This is the first study to show that successful biologic therapy significantly improves in vivo synovial hypoxia. Changes are strongly associated with changes in macroscopic and microscopic measures of joint inflammation and MRI improvement. These data further strengthen the concept that hypoxia is an important event driving synovial inflammation.