Propofol Induced Subacute Cutaneous Lupus Erythematosus: A Case Report.

We report a case of a woman who experienced unexplained recurrent rashes of varying severity after multiple exposures to anesthesia, and then 2 successful surgeries under general anesthesia with no resultant rashes after removing propofol from her anesthetic plans. We infer her previous postanesthetic rashes were likely associated with drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) triggered by propofol.

Pushing the DIEP Envelope with ERAS: 24 Hour Discharge is Safe in Appropriately Selected Patients.

Enhanced recovery after surgery protocols have become increasingly adopted for autologous breast reconstruction, demonstrating improved quality of care and reduced hospital stays. Despite this, average length of stay remains over 3 days. We have found, in appropriately selected patients, hospital length of stay can be safely reduced to less than 48 hours. Methods: Retrospective review was performed of patients who underwent microsurgical breast reconstruction by the senior author (M.H.) from April 2019 to December 2021. Demographics, operative details, length of stay, and postoperative complications are reported to assess for safety of discharge within 48 hours, with the primary outcome measure being flap loss. Results: In total, 188 flaps were performed on 107 patients. Average age was 51.4 years (SD 10.1 years) with average BMI 26.6 kg/m2 (SD 4.8 kg/m2). Average length of stay was 1.97 days (SD 0.61 days), and 96 patients (89.7%) were discharged within 48 hours. Six flaps (3.2%) required operative takebacks. Five of the six (83.3%) takebacks occurred on postoperative days zero or one, and all five of these flaps were salvaged. There were four breast hematomas (2.1%), four breast seromas (2.1%), eight breast infections (4.3%), 13 breasts (6.9%) with wound dehiscence, four flaps (2.1%) with partial flap loss, and 24 breasts (12.8%) with mastectomy flap necrosis. One hundred fifty flaps (79.8%) had no complications. Overall success rate of flap reconstruction was 99.5%. Conclusion: Hospital discharge in 24-48 hours is safe in appropriately selected patients undergoing autologous tissue breast reconstruction.

Requirement of myeloid cell-specific Fas expression for prevention of systemic autoimmunity in mice.

OBJECTIVE: The death receptor Fas is a critical mediator of the extrinsic apoptotic pathway, and its role in mediating lymphoproliferation has been extensively examined. The present study was undertaken to investigate the impact of myeloid cell-specific loss of Fas. METHODS: Mice with Fas flanked by loxP sites (Fas(flox/flox) ) were crossed with mice expressing Cre under control of the murine lysozyme M gene promoter (Cre(LysM) ), which functions in mature lysozyme-expressing cells of the myelomonocytic lineage. The genotype for Cre(LysM) Fas(flox/flox) mice was verified by polymerase chain reaction and flow cytometric analysis. Flow cytometric analysis was also used to characterize myeloid, dendritic, and lymphoid cell distribution and activation in bone marrow, blood, and spleen. Luminex-based assays and enzyme-linked immunosorbent assays were used to measure serum cytokine/chemokine and immunoglobulin levels. Renal damage or dysfunction was examined by immunohistochemical and immunofluorescence analysis. RESULTS: Cre(LysM) Fas(flox/flox) mice exhibited a systemic lupus erythematosus (SLE)-like disease that included leukocytosis, splenomegaly, hypergammaglobulinemia, antinuclear autoantibody and proinflammatory cytokine production, and glomerulonephritis. Loss of Fas in myeloid cells increased levels of both Gr-1(low) and Gr-1(intermediate) blood monocytes and splenic macrophages and, in a paracrine manner, incited activation of conventional dendritic cells and lymphocytes in Cre(LysM) Fas(flox/flox) mice. CONCLUSION: Taken together, these results suggest that loss of Fas in myeloid cells is sufficient to induce inflammatory phenotypes in mice, reminiscent of an SLE-like disease. Thus, Fas in myeloid cells may be considered a suppressor of systemic autoimmunity.