The Effect of Corticosteroid Injections on Postoperative Infections in Trigger Finger Release.

BACKGROUND: Corticosteroid injections have proven benefit in the treatment of symptomatic trigger finger; however, the immune system and tissue repair modulating properties of corticosteroids justify further consideration in surgical candidates. The aim of this study was to assess the relationship between corticosteroid injections and postoperative infection in trigger finger release. METHODS: A single-center retrospective review was conducted of patients seen from 2010 to 2019 to identify those who underwent trigger finger release with subsequent antibiotic prescription for chart-documented wound infection. A demographic matched cohort of 100 patients was identified for comparison. Preoperative corticosteroid injection history including timing, frequency, and dose was collected for all patients. Patient demographics, comorbidities, and presence of postoperative infection were collected from patient medical records. Superficial infection was defined as those requiring antibiotics for resolution without return to the operating room; deep infection was defined as infections that required irrigation and debridement. RESULTS: Of 3234 patients who underwent trigger finger release, 58 (1.8%) were identified with postoperative infections, 6 (0.2%) of which were deep infections. History of corticosteroid injection was significantly more common in patients with postoperative infection. Compared with an age-matched, gender-matched, and body mass index-matched cohort, patients with postoperative infection had significantly increased rate of diabetes mellitus at 34.5% to 19% (P = .04). CONCLUSIONS: While corticosteroid injection in the preoperative period is associated with a higher rate of postoperative infection, the time before surgery and the corticosteroid dose do not appear to have an effect.

BCG-Induced Tumor Immunity Requires Tumor-Intrinsic CIITA Independent of MHC-II.

For decades, BCG immunotherapy has been the standard of care for non-muscle-invasive bladder cancer. Despite this clinical experience, the mechanism by which BCG stimulates tumor-eliminating immunity is unclear, and there is still a need for more accurate prediction of clinical outcomes in advance of treatment initiation. We have shown that BCG stimulates tumor-specific T-cell immunity that requires tumor cell expression of the IFNγ receptor (IFNGR); however, the downstream components of IFNGR signaling responsible for responsiveness to BCG are unknown. Here, we demonstrate that the IFNγ-driven, tumor cell intrinsic expression of the class II transactivator CIITA is required for activation of a tumor-specific CD4 T-cell response and BCG-induced tumor immunity. Despite the established role for CIITA in controlling MHC-II antigen presentation machinery, the requirement for CIITA is independent of MHC-II and associated genes. Rather, we find that CIITA is required for a broader tumor-intrinsic transcriptional program linked to critical pathways of tumor immunity via mechanisms that remain to be determined. Tumor cell intrinsic expression of CIITA is not required for a response to immunotherapy targeting programmed cell death protein 1 (PD-1), suggesting that different modalities of immunotherapy for bladder cancer could be employed based on tumor-intrinsic characteristics.