Clinical variables and stone detection in patients with flank pain.

INTRODUCTION: Non-contrast CT (NCT) is commonly used to evaluate flank pain (FP). We sought to evaluate incidence of ureteral calculi on NCT in patients with FP, and to determine if clinical variables are associated with higher detection rates. MATERIALS AND METHODS: Retrospective review identified 613 patients undergoing NCT for FP. Patient clinical data, NCT findings, and intervention were analyzed. Focus was placed on variables commonly associated with urolithiasis (Vstone), comprising hematuria, nausea/vomiting, and prior stone history. Statistical analysis was performed to identify risk of ureteral stones based on number and type of Vstone. RESULTS: No stone disease was identified on NCT in 175 patients (28.5%). NCT demonstrated 214 (35%), 72 (12%), and 152 (25%) patients with stones located in the kidney, ureter, or both, respectively. Only 33 (5%) patients had FP as their sole Vstone, with ureteral calculi identified in 6% of this cohort. The rate of ureteral calculi increased with more Vstone. Patients having all four Vstone were found to have the highest rate of ureteral stones (59%). Statistical analysis demonstrated a statistically significantly increased relative risk of stone formation given three or four Vstone when compared with FP alone. CONCLUSIONS: Whereas isolated FP is associated with a lower rate of ureteral calculus detection, a significant increased relative risk of ureteral calculus is seen in patients with additional clinical variables associated with stone disease. Accordingly, it may be possible to improve detection rates of ureteral stones through the use of additional clinical variables to guide NCT selection.

Cutting edge: central nervous system plasmacytoid dendritic cells regulate the severity of relapsing experimental autoimmune encephalomyelitis.

Plasmacytoid dendritic cells (pDCs) have both stimulatory and regulatory effects on T cells. pDCs are a major CNS-infiltrating dendritic cell population during experimental autoimmune encephalomyelitis but, unlike myeloid dendritic cells, have a minor role in T cell activation and epitope spreading. We show that depletion of pDCs during either the acute or relapse phases of experimental autoimmune encephalomyelitis resulted in exacerbation of disease severity. pDC depletion significantly enhanced CNS but not peripheral CD4(+) T cell activation, as well as IL-17 and IFN-gamma production. Moreover, CNS pDCs suppressed CNS myeloid dendritic cell-driven production of IL-17, IFN-gamma, and IL-10 in an IDO-independent manner. The data demonstrate that pDCs play a critical regulatory role in negatively regulating pathogenic CNS CD4(+) T cell responses, highlighting a new role for pDCs in inflammatory autoimmune disease.