Faculty Bibliography

RATIONALE AND OBJECTIVES: To assess the American College of Radiology Incidental Findings Committee's (ACR-IFC) recommendations for defining and following up abnormal incidental abdominopelvic lymph nodes. MATERIALS AND METHODS: A total of 59 lymph nodes satisfying ACR-IFC criteria as incidental (no malignancy or lymphoproliferative disorder) and with sufficient follow-up to classify as benign (biopsy, decreased size, >/=12-month stability) or malignant (biopsy, detection of primary malignancy combined with either fluorodeoxyglucose hyperactivity or increase in size of the node) were included. Two radiologists independently assessed nodes for suspicious features by ACR-IFC criteria (round with indistinct hilum, hypervascularity, necrosis, cluster >/=3 nodes, cluster >/=2 nodes in >/=2 stations, size >/=1 cm in retroperitoneum). Outcomes were assessed with attention to ACR-IFC's recommendation for initial 3-month follow-up. RESULTS: A total of 8.5% of nodes were malignant; 91.5% were benign. Two of six malignant nodes were stable at 3 to <6-month follow-up before diagnosis; diagnosis of four of five malignant nodes was facilitated by later development of non-nodal sites of tumor. A total of 13, 5, 8, and 9 nodes were deemed benign given a decrease at <3 months, 3-5 months, 6-11 months, or >/=12 months of follow-up. No ACR-IFC feature differentiated benign and malignant nodes (P = 0.164-1.0). A cluster >/=3 nodes was present in 88.1%-93.2% of nodes. A total of 96.6%-98.3% had >/=1 suspicious feature for both readers. Necrosis and hypervascularity were not identified in any node. CONCLUSIONS: ACR-IFC imaging features overwhelmingly classified incidental nodes as abnormal, although did not differentiate benign and malignant nodes. Nodes stable at the ACR-IFC's advised initial 3-month follow-up were occasionally proven malignant or decreased on further imaging. Refinement of imaging criteria to define nodes of particularly high risk, integrated with other clinical criteria, may help optimize the follow-up of incidental abdominopelvic lymph nodes.

OBJECTIVE: The purpose of this study is to evaluate the roles of self-directed learning and continual feedback in the learning curve for tumor detection by novice readers of prostate MRI. MATERIALS AND METHODS: A total of 124 prostate MRI examinations classified as positive (n = 52; single Prostate Imaging Reporting and Data System [PI-RADS] category 3 or higher lesion showing Gleason score >/= 7 tumor at MRI-targeted biopsy) or negative (n = 72; PI-RADS category 2 or lower and negative biopsy) for detectable tumor were included. These were divided into four equal-sized batches, each with matching numbers of positive and negative examinations. Six second-year radiology residents reviewed examinations to localize tumors. Three of the six readers received feedback after each examination showing the preceding case's solution. The learning curve, plotting accuracy over time, was assessed by the Akaike information criterion (AIC). Logistic regression and mixed-model ANOVA were performed. RESULTS: For readers with and without feedback, the learning curve exhibited an initial rapid improvement that slowed after 40 examinations (change in AIC > 0.2%). Accuracy improved from 58.1% (batch 1) to 71.0-75.3% (batches 2-4) without feedback and from 58.1% to 72.0-77.4% with feedback (p = 0.027-0.046), without a difference in the extent of improvement (p = 0.800). Specificity improved from 53.7% to 68.5-81.5% without feedback and from 55.6% to 74.1-81.5% with feedback (p = 0.006-0.010), without a difference in the extent of improvement (p = 0.891). Sensitivity improved from 59.0-61.5% (batches 1-2) to 71.8-76.9% (batches 3-4) with feedback (p = 0.052), though did not improve without feedback (p = 0.602). Sensitivity for transition zone tumors exhibited larger changes (p = 0.024) with feedback than without feedback. Sensitivity for peripheral zone tumors did not improve in either group (p > 0.3). Reader confidence increased only with feedback (p < 0.001). CONCLUSION: The learning curve in prostate tumor detection largely reflected self-directed learning. Continual feedback had a lesser effect. Clinical prostate MRI interpretation by novice radiologists warrants caution.

BACKGROUND: Common variable immunodeficiency (CVID) is a heterogeneous disorder commonly presenting with recurrent sinopulmonary infections. In all, 6%-10% of CVID patients develop an inflammatory bowel disease (IBD)-like disorder, making these patients a unique population to investigate immune-mediated gastrointestinal disease. This study examined whether defects in peripheral and/or intestinal lymphocytes are involved in disruption of the intestinal mucosa in CVID patients with inflammatory intestinal diseases. METHODS: Peripheral blood (PB) T cells from healthy controls; CD or UC; CVID; and CVID with IBD were stimulated for 48 hours with anti-CD3+CD28 or phytohemagglutinin (PHA) + phorbol 12-myristate 13-acetate (PMA); cytokine production was measured by enzyme-linked immunosorbent assay (ELISA). Cytokine expression from unstimulated lamina propria lymphocytes (LPLs) was compared by real-time polymerase chain reaction (PCR). Immunohistochemistry of mucosal biopsies was performed. Cell populations were quantified by morphometry. RESULTS: CVID/IBD PB T cells stimulated by anti-CD3+CD28 had trends for reduced IL-2, IL-10, IFN-gamma, and TNF-alpha compared to controls. These differences were not apparent following stimulation by PHA/PMA. Constitutive production of inflammatory cytokines by LPLs was not detected. Histologically, CVID patients had reduced/absent plasma cells with reductions in intestinal IgM and IgA. CVID patients with and without gastrointestinal (GI) disease exhibited increased CD3+ T cells, specifically CD8+, in the colon compared to normal and IBD controls, suggesting immune dysregulation. CONCLUSIONS: Intestinal inflammation in CVID patients with IBD-like disease may be mediated by abnormal cytokine production through a T-cell receptor-mediated pathway. However, the variability observed suggests multiple, rather than singular, mechanisms are involved. Histologic features such as reduced intestinal plasma cells and lack of intestinal immunoglobulins may be useful markers in diagnosing CVID in a patient with GI disease refractory to conventional therapies.