Metallosis and metal-induced synovitis are well-recognized complications of metal-backed polyethylene joint prostheses and have been frequently described in the orthopedic surgery literature; however, relatively fewer articles discussing the radiologic aspects of this complication have been published. To illustrate the importance of radiologic findings in the diagnosis and management of these patients, we present a case of metallosis and metal-induced synovitis complicating two revisions of a total knee arthroplasty, caused by polyethylene liner wear and dissociation of the polyethylene liner from the metal-backed patellar prosthesis. Specific attention is given to reviewing signs that aid in diagnosis, such as the "bubble sign," "cloud sign," and "metal-line signs."
To investigate the role of interferon regulatory factor-1 (IRF-1) in the development of lupus nephritis, IRF-1 -/-genotype mice were bred onto the MRL/lpJfas lpr (MRL/lpr) background. We examined kidney mesangial cell function and disease progression. Endpoints evaluated included inflammatory mediators, autoantibody production, immune complex deposition, renal pathology, T cell subset analysis, and duration of survival. Mesangial cells cultured from IRF-1 -/-mice produced significantly lower levels of nitric oxide and IL-12 but not TNF-a when stimulated with LPS + IFN-c. IRF-1 -/-mice showed less aggravated dermatitis compared to the wild-type mice. Anti-doublestranded DNA production and proteinuria were significantly decreased in IRF-1 -/-mice compared to IRF-1 +/+ mice. IgG and C3 deposition as well as glomerulonephritis were decreased in IRF-1 -/-mice at 26 wk of age compared to the IRF-1 +/+ mice. Splenic CD4 -CD8 -CD44 + T cells were decreased while CD4 + CD25 + T cells were increased in the IRF-1 -/-mice when compared to IRF-1 +/+ mice. Survival rates (ED 50 ) were 22 wk for IRF-1 +/+ mice and 45 wk for IRF-1 -/-mice. These findings suggest an important role of IRF-1 in mediating renal disease in MRL/lpr mice. IntroductionThe etiology of systemic lupus erythematosus remains an enigma although genetic factors influenced by environmental agents appear to trigger the disease. Clearly, B cells, T cells, and macrophages play important roles in the development of lupus pathology [1][2][3].Chronic expression of Th1 cytokines secreted by Th cells is particularly harmful due to their influence on the initiation and promotion of tissue destruction [4,5]. Cytokines, including IFN-c, promote inflammation and provide a positive amplification loop responsible for escalating autoimmune kidney damage [6].MRL/lpr mice develop glomerulonephritis and vasculitis at an early age (4-5 months) [7]. Renal disease is characterized by the early influx of activated T cells and macrophages into the kidney. Activated T cells secrete IFN-c, which induces macrophages to express CSF-1, IL-1b, and TNF-a. Macrophages accumulate in the kidney during inflammation and generate IFN-a, TNF-a, and reactive oxygen species. Locally produced chemokines, particularly monocyte chemoattractant protein (MCP)-1, are also instrumental in attracting and maintaining cellular influx [8] -12 [20]. In the IRF-1 -/-NOD mouse, insulitis and diabetes were decreased accompanied by an increased survival [21]. Additional studies have suggested a role of IRF-1 and IFN-regulated genes in mediating human lupus [22][23][24]. Based on the knowledge that IRF-1 modulates inflammatory mediator production, we sought to determine whether IRF-1 gene deletion alters the severity of lupus nephritis in MRL/lpr mice. Results IRF-1 MRL/lpr mouse phenotypeTo determine the role of IRF-1 in autoimmune disease, IRF-1-knockout mice were backcrossed for eight generations to the MRL/lpr mice. After eight backcrosses, the littermates were intercrossed to yield cohorts for these studies....
SUMMARY:We describe the case of a patient with aseptic meningoencephalitis after intrathecal iohexol injection for myelography and review the previous literature on similar cases of contrastinduced neurotoxicity.A septic meningoencephalitis is a rare complication of myelography with nonionic, iodinated, water-soluble contrast agents. We describe a case of a 69-year-old woman in whom aseptic meningoencephalitis developed after she underwent iohexol myelography. Case ReportA 69-year-old white woman underwent a technically successful outpatient CT myelogram with 10 mL of iohexol (Omnipaque 300; GE Healthcare, Cork, Ireland). The CSF was clear and colorless, and myelogram revealed degenerative osteoarthritis and severe central canal stenosis at L3-L4 secondary to short pedicles, facet and ligamentum flavum hypertrophy, and diffuse disk bulging. Approximately 12 hours after the injection, she experienced fever, headache, confusion, agitation, and aphasia. She was brought to the emergency department 20 hours after the myelogram.In the emergency department, her initial temperature was 102.5°F, and she was agitated and unable to speak, though she could shake and nod her head for "yes" or "no" responses. She complained of a severe headache and low back pain but denied incontinence or lower extremity numbness. On physical examination, she had mild symmetric lower extremity weakness that measured 4 of 5 bilaterally. Her serum white blood cell count (WBC) was 24,300 cells/L (90% neutrophils). Head CT revealed moderate to severe, chronic, smallvessel ischemic disease. Lumbar puncture and CSF analysis approximately 30 hours after the iohexol injection revealed turbid-appearing fluid with 300 white cells/L (61% polymorphonuclear cells and 1% monocytes), 5200 red cells/L, glucose level of 63 mg/dL, and elevated total protein level of 624 mg/dL. A second tube of CSF from the same lumbar puncture revealed 220 white cells/L (94% polymorphonuclear cells and 2% lymphocytes) and 1545 red cells/L. Results of CSF bacterial and cryptococcal antigens were negative. CSF culture revealed no growth at 5 days.She was initially started on intravenous ceftriaxone (2000 mg) and vancomycin (1000 mg) every 12 hours. The following day, approximately 48 hours after the myelogram, she was afebrile, and her mental status and neurologic examination had returned to near baseline with fluent speech. She was alert and oriented, with no recollection of the previous day, and complained only of a bandlike headache. An infectious disease consultation was obtained, and the patient was diagnosed with an allergic reaction to the iohexol. Diagnosis was based on the negative Gram stain result, negative culture result, and rapid resolution. Antibiotics were discontinued after results of CSF tests, blood tests, and urine cultures remained negative.
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