Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In forty-five patients, who had an arthrodesis because of failed total knee arthroplasty, the cause was infection in forty, instability in two, failure of the prosthesis in two, and loosening in one. The arthrodesis succeeded in twenty-nine (81%) of thirty-six patients who had had a minimally or partially constrained arthroplasty and in five (56%) of nine who had had a hinge-type prosthesis inserted. The reasons for failure were severe bone loss, persistent sepsis, and loss of bone apposition after manipulation. The technique of arthrodesis did not seem to influence the final result. External fixation most commonly had to be used because of the infections and the device was kept in place for an average of ten weeks, after which immobilization in a cast was used until the arthrodesis healed.
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PMID:Arthrodesis of the knee following failed total knee arthroplasty. 42 3

Experience with the GUEPAR prosthesis in 292 cases of which 103 have been followed for more than 2 years, suggests that: implanting a hinge prosthesis is major surgery on elderly patients in whom severe complications have occurred and for this reason, the operations should be reserved for extremely damaged and unstable knees; the most important local complications have been deep sepsis for which we have noted a rate of 6.6 per cent; in the treatment of sepsis, everything must be done to preserve the prosthesis because arthrodesis is difficult to obtain; pain relief has been significant as a result of the operation. The prosthetic design allows flexion of more than 90 degrees in 85 per cent of the cases and 120 degrees in 26 per cent; after two years, the results seem relatively stable. We have not observed aseptic loosening after this period but a longer observation period is necessary to be reassured on this point; patellar pain remains a major concern because this arthroplasty has not solved the problem, and other solutions will have to be found.
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PMID:Guepar hinge prosthesis: complications and results with two years' follow-up. 97 66

The first fifty kinematic rotating-hinge total knee arthroplasties that were done at the Mayo Clinic were reviewed. The indication for use of this prosthesis was either ligamentous instability or loss of bone, or both. At a mean length of follow-up of fifty months (range, twenty-nine to seventy-nine months), the clinical results of thirty-eight knees in thirty-six patients were evaluated. Fifteen of the thirty-eight knees had had a primary arthroplasty and twenty-three had had a revision arthroplasty using the kinematic rotating-hinge prosthesis. Using the knee-rating score of The Hospital for Special Surgery, there were fourteen excellent, twelve good, five fair, and five poor results. For two knees there was inadequate information to calculate a knee-rating score. Lucent lines that were more than one millimeter in width were seen with 25 per cent of the femoral and 50 per cent of the tibial components. Progression of lucent lines was observed in thirteen knees, and five knees showed probable radiographic loosening. The high incidence of complications was distressing, with a 16 per cent rate of sepsis, a 22 per cent rate of patellar instability, and a 6 per cent rate of breakage of the implant. In our opinion, this implant should be used only in knees in which there is functional absence of a collateral ligament that cannot be managed by soft-tissue reconstruction.
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PMID:Kinematic rotating-hinge total knee arthroplasty. 357 6

On hundred and ninety-five hinge prostheses have been inserted between 1970 and 1981, most of them of the G.U.E.P.A.R. type. One hundred and forty-three were followed up. The etiology of five per-operative deaths is discussed. It is concluded that this dramatic event was related to gas embolism. Precautions necessary to avoid such accidents are described particularly at the time of release of the tourniquet. There were 11 cases of sepsis, eight loosenings and four post-operative fractures of the femur or tibia. The functional results were found to be satisfactory but better with the G.U.E.P.A.R. type than with the Shiers prosthesis. Most of the post-operative pain originated from the patella; this aspect of the pain should be able to be avoided by systematic use of patellar resurfacing. The authors conclude that a hinge prosthesis should be used only in cases of severe deformity, of severe instability or in cases of failure of resurfacing procedures.
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PMID:[Hinge prosthesis of the knee. Apropos of 185 cases]. 622 49

Deep sepsis is a serious postoperative complication of total knee hinge arthroplasty. Measures to eradicate the infection are time-consuming, expensive and often a threat to the limb and occasionally the life of the patient. At best, a successful result is a short leg with an arthrodesed knee. More often the patient is left with a painful fibrous ankylosis, or an above-knee amputation. The Hoffman external skeletal fixation device provides rigid fixation and allows early ambulation. Its use in combination with debridement and bone grafting can result in a successful arthrodesis with a minimum amount of shortening.
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PMID:Knee fusion with external skeletal fixation after an infected hinge prosthesis: a case report. 699 34

Fusion proteins of the human 55-kDa TNF receptor extracellular domain with hinge and C2/C3 constant domains of human IgG1 or IgG3 heavy chains were tested in a primate sepsis model. Twenty-four baboons received 4.6, or 0.2 mg/kg of TNFR5-G1,3, or placebo, before the administration of a lethal dose of live Escherichia coli. Treatment with TNFR5-G1,3 decreased 5-day mortality from 88% in the placebo group to 12% in the TNFR5-G1,3-treated animals (p < 0.01 by Fisher's exact test). Treatments with TNR5-G1 and TNFR5-G3 in doses from 0.2 to 4.6 mg/kg were efficacious. Free plasma TNF was neutralized by all treatments, but inactive TNF/TNFR5-G1,3 complexes remained in circulation for prolonged periods. TNFR5-1,3 treatments attenuated the hemodynamic disturbances, reduced fluid requirements, and decreased the systemic IL-1 beta, IL-6, and IL-8 responses. In addition, TNFR5-G1,3 treatment shortened the granulocytopenia and reduced the loss of cellular TNF receptors from granulocytes. The decrease in fibrinogen concentrations and increase in prothrombin and partial thromboplastin times were significantly attenuated by TNFR5-G1,3 treatment. TNFR5-G1,3 treatment markedly attenuated the rise in plasma lactate concentration. Histologic studies of TNFR5-G1,3 revealed dose-dependent protection against tissue injury by Escherichia coli administration.
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PMID:Protection against lethal Escherichia coli bacteremia in baboons (Papio anubis) by pretreatment with a 55-kDa TNF receptor (CD120a)-Ig fusion protein, Ro 45-2081. 869 Sep 12

We performed a retrospective analysis of twenty-five consecutive massive articulating endoprostheses that were inserted at our unit during the management of patients with Giant Cell Tumours of their distal femur. Fifteen of these implants were fixed hinge devices and ten were rotating hinge devices with HA collars (since 1993). None of these cases were revised for sepsis. There had been no cases of recurrent disease or amputation. The mean follow-up was 12 years (range = 5-18 years). The average age at time of insertion was 37 years. Young patients with fixed hinged devices developed a high incidence (33%) of aseptic loosening. They also had a significant rate of re-bushing. Results of the rotating hinge prosthesis with HA collar were much more promising. Functional scores were good after a period of 12 years despite the young age group.
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PMID:Massive endoprostheses for giant cell tumours of the distal femur: A 12-year follow-up. 1684 97

Recently, we provided evidence that PKCalpha depletion in monocytes/macrophages contributes to cellular desensitization during sepsis. We demonstrate that peroxisome proliferator-activated receptor gamma (PPARgamma) agonists dose dependently block PKCalpha depletion in response to the diacylglycerol homologue PMA in RAW 264.7 and human monocyte-derived macrophages. In these cells, we observed PPARgamma-dependent inhibition of nuclear factor-kappaB (NF-kappaB) activation and TNF-alpha expression in response to PMA. Elucidating the underlying mechanism, we found PPARgamma1 expression not only in the nucleus but also in the cytoplasm. Activation of PPARgamma1 wild type, but not an agonist-binding mutant of PPARgamma1, attenuated PMA-mediated PKCalpha cytosol to membrane translocation. Coimmunoprecipitation assays pointed to a protein-protein interaction of PKCalpha and PPARgamma1, which was further substantiated using a mammalian two-hybrid system. Applying PPARgamma1 mutation and deletion constructs, we identified the hinge helix 1 domain of PPARgamma1 that is responsible for PKCalpha binding. Therefore, we conclude that PPARgamma1-dependent inhibition of PKCalpha translocation implies a new model of macrophage desensitization.
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PMID:PPARgamma1 attenuates cytosol to membrane translocation of PKCalpha to desensitize monocytes/macrophages. 1732 8

Revision total knee arthroplasty using a second generation modular rotating hinge design was done on thirty two knees in 30 patients over an 8-year period. Twenty-nine knees in 29 patients were followed up for 4.5-11 years (mean, 58 months). Four prostheses failed and two patients had died and one patient was lost to followup. Indications for revision were recurrent sepsis (five knees), component failure (four knees), ligamentous instability (two knees), aseptic loosening (10 knees), fracture (six knees), and gross bone loss (five knees). Early results have demonstrated improvement in both the Knee Society knee and function Scores and range of movement. The Knee Society knee score improved from 26 preoperatively to 68 postoperatively. The function score improved from 27 preoperatively to 75 postoperatively. One patient had evidence of aseptic loosening on radiographs, and the patellofemoral complication rate was low at 6%. This short-term clinical and radiographic review has demonstrated encouraging results in the use of a custom-made second generation rotating hinge component when used in revision knee surgery.
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PMID:The SMILES prosthesis in salvage revision knee surgery. 1794

The intestinal epithelium is repetitively deformed by shear, peristalsis, and villous motility. Such repetitive deformation stimulates the proliferation of intestinal epithelial cells on collagen or laminin substrates via ERK, but the upstream mediators of this effect are poorly understood. We hypothesized that the phosphatidylinositol 3-kinase (PI3K)/AKT cascade mediates this mitogenic effect. PI3K, AKT, and glycogen synthase kinase-3beta (GSK-3beta) were phosphorylated by 10 cycles/min strain at an average 10% deformation, and pharmacologic blockade of these molecules or reduction by small interfering RNA (siRNA) prevented the mitogenic effect of strain in Caco-2 or IEC-6 intestinal epithelial cells. Strain MAPK activation required PI3K but not AKT. AKT isoform-specific siRNA transfection demonstrated that AKT2 but not AKT1 is required for GSK-3beta phosphorylation and the strain mitogenic effect. Furthermore, overexpression of AKT1 or an AKT chimera including the PH domain and hinge region of AKT2 and the catalytic domain and C-tail of AKT1 prevented strain activation of GSK-3beta, but overexpression of AKT2 or a chimera including the PH domain and hinge region of AKT1 and the catalytic domain and C-tail of AKT2 did not. These data delineate a role for PI3K, AKT2, and GSK-3beta in the mitogenic effect of strain. PI3K is required for both ERK and AKT2 activation, whereas AKT2 is sequentially required for GSK-3beta. Furthermore, AKT2 specificity requires its catalytic domain and tail region. Manipulating this pathway may prevent mucosal atrophy and maintain the mucosal barrier in conditions such as ileus, sepsis, and prolonged fasting when peristalsis and villous motility are decreased and the mucosal barrier fails.
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PMID:Strain-induced proliferation requires the phosphatidylinositol 3-kinase/AKT/glycogen synthase kinase pathway. 1904 55


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