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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the proliferative lesion of rheumatoid arthritis becomes polarized and invasion of articular cartilage and subchondral bone begins, it is likely that many mesenchymal cells, including periosteal and perichondral cells, and perhaps even the chondrocytes and osteoblasts themselves can be activated to produce destructive enzymes. Early in the course of RA cartilage proteoglycans are depleted, leaving the remaining collagen more susceptible to mechanical breakdown as well as to enzymatic breakdown. Specific collagenases are released by synovial cells and, in addition, by polymorphonuclear leukocytes. The latter enzyme may account for free collagenase found in synovial fluid, a finding possibly related to saturation of inhibitory proteins by proteases with greater affinity for them, leaving collagenase active. At this time in the course of rheumatoid arthritis, a joint would be under double jeopardy from enzymes released by the invading pannus as well as by collagenase free and active in the synovial fluid. Rapid destruction could occur. Although cartilage collagen has an intrinsic resistance to collagenase conferred by its primary structure and by higher order structure (e.g. intermolecular cross-links), it seems wise to cool down hot joints because increased temperature may increase the rate of collagen degradation and, therefore, cartilage destruction. In addition, superimposed sepsis or acute flares of rheumatoid disease result in enough influx of polymorphonuclear leukocytes into the joints to result in free collagenolytic activity being present. This provides a rationale for frequent aspiration of any joint fluid, septic or otherwise, containing high polymorphonuclear leukocyte counts.
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PMID:Collagenolytic systems in rheumatoid arthritis. 16 97

The results obtained with early surgical treatment of burns have been re-examined from various aspects. Early escharectomy, which tranforms the necrobiotic tissue into a surgical lesion, reduces the chemical factors of inflammation, lowers the lactic acid level and depresses the activity and disordered proliferation of the fibroblasts and the consequent laying down of immature collagen which is responsible for the pathological evolution of the burn scar. The removal of toxic material with proteasic activity, the reduction in the risk of sepsis, the saving of work for the immunopoietic mechanism, a reduction in the weight loss through improved nitrogen balance and an increase in the anabolic phase of muscular metabolism by early movement as well as a shortening of the period of hospitalization--all are factors in favour of the early surgical technique. Better healing is obtained by the elimination of the necrotic tissue, a reduction in the haematologic tissue inflammation mediators, an increase in the antibacterial defence following the reconstruction of the skin surface with covering materials and the rapid articular reduction; not to mention the inhibition of the formation of granulation tissue.
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PMID:Considerations on early surgery in the treatment of extensive burns. 22 68

Mounting evidence supports efforts to preserve splenic function. This evidence indicates (1) that the problem of postsplenectomy sepsis warrants splenic preservation whenever possible, and (2) that the spleen, as a whole or in part, and its function, can be preserved in cirmustances which formerly seemed to necessitate removal of the entire spleen. Nine patients with splenic injuries in whom splenic function was preserved successfully are presented. Approaches to management of the splenic injuries included (1) nonoperative management, (2) hemostasis by application of microfibrillar collagen (Avitene), (3) partial splenic resection, and (4) preservation of accessory spleen. Since reliable prevention and treatment of postsplenectomy sepsis do not seem attainable in the near future, continuing efforts to preserve function of the spleen whenever possible, in patients with injured spleens, seem justified and desirable.
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PMID:Preservation of splenic function in adults and children with injured spleens. 42 96

Serial measurements of coagulation activity, platelet counts, and platelet aggregation were done in patients with full-thickness burns involving 25% or more of body surface area to detect specific changes that might correlate with the onset of septicemia. Mean and maximal values for prothrombin time, partial thromboplastin time, thrombin time, activities of factor V and factor VIII, and concentrations of fibrinogen and fibrinogen-related antigens observed in the presence of bacterial septicemia did not differ significantly from those observed in the absence of septicemia. Mean platelet counts were significantly less with sepsis, but values in individual subjects were not indicative of the presence of septicemia. By contrast, platelet aggregation in response to adenosine diphosphate, epinephrine, and collagen always became severely abnormal with the onset of septicemia but not in the absence of sepsis.
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PMID:Platelet aggregation as a sign of septicemia in thermal injury. A prospective study. 94 30

A retrospective study of 116 children with Hodgkin's disease diagnosed in the period 1935-1970 was undertaken to assess the prognostic role of histopathologic classiciation and clinical extent of the disease. The ages of the 80 boys and 36 girls ranged from 2.5 years to 15.0 years (mean, 10.0 years). The histopathologic diagnosis by lymph node biopsy revealed lymphocyte predominance in 22, nodular sclerosis in 67, mixed cellularity in 24, and lymphocyte depletion in 3. Within the subgroup of nodular sclerosis, 47 biopsies had classic well-developed collagenous bands, whereas 20 were in the cellular phase (10 without collagenous bands and 10 with minimal collagen). The clinical extent of disease was determined. There were 33 patients with Stage I disease, 38 with Stage IIA, 12 with Stage IIB, 24 with Stage III, and 9 with Stage IV. Survival correlated with histopathologic type and clinical stage, but not with age or sex. Survival was not dependent on the degree of collagenization in nodular sclerosis. There were 28 patients who survived for more than 10 years. Four of these 29 subsequently died owing to acute myelomonocytic leukemia, carcinoma of the breast, sepsis, and progression of Hodgkin's disease, respectively. Neoplasms developed in two other long-term survivors (thyroid carcinoma in one, and multiple basal cell carcinomas in the other).
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PMID:Hodgkin's disease in childhood. 120 66

Eighteen immuno-compromised children (malignancies, hematological diseases, collagen diseases) with neutropenia and infections were treated with imipenem/cilastatin sodium (IPM/CS), and the efficacy and the safety of the drug were evaluated. 1. Responses to IPM/CS were excellent in 13 patients, good in 1, and fair in 4. None of the patients displayed a poor response to the treatment thus the efficacy rate was 77.8%. 2. Of 5 patients with sepsis, 4 had excellent or good responses. IPM/CS was effective against sepsis caused by Enterococcus faecalis and Pseudomonas aeruginosa. 3. In patients with severe neutropenia (WBC less than 100/mm3), the efficacy rate was 70%. 4. As for side effects, elevations of GOT and GPT were observed in 1 patient with liver cirrhosis. These results indicate that IPM/CS is safe and effective in immuno-compromised children with neutropenia and infections.
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PMID:[Clinical evaluation of imipenem/cilastatin sodium against infections in compromised children (malignancy, hematological disease, collagen disease)]. 143 90

Dermatosparaxis is a recessively inherited connective-tissue disorder that results from lack of the activity of type I procollagen N-proteinase, the enzyme that removes the amino-terminal propeptides from type I procollagen. Initially identified in cattle more than 20 years ago, the disorder was subsequently characterized in sheep, cats, and dogs. Affected animals have fragile skin, lax joints, and often die prematurely because of sepsis following avulsion of portions of skin. We recently identified two children with soft, lax, and fragile skin, which, when examined by transmission electron microscopy, contained the twisted, ribbon-like collagen fibrils characteristic of dermatosparaxis. Skin extracts from one child contained collagen precursors with amino-terminal extensions. Cultured fibroblasts from both children failed to cleave the amino-terminal propeptides from the pro alpha 1(I) and pro alpha 2(I) chains in type I procollagen molecules. Extracts of normal cells cleaved to collagen, the type I procollagen synthesized by cells from both children, demonstrating that the enzyme, not the substrate, was defective. These findings distinguish dermatosparaxis from Ehlers-Danlos syndrome type VII, which results from substrate mutations that prevent proteolytic processing of type I procollagen molecules.
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PMID:Human dermatosparaxis: a form of Ehlers-Danlos syndrome that results from failure to remove the amino-terminal propeptide of type I procollagen. 164 26

Prior studies of vascular rejection in transplanted human hearts have stressed the importance of accelerated coronary arteriosclerosis (chronic vascular rejection). We, however, have had four patients with sudden onset of acute heart failure within 90 days of transplantation who have died without significant myocardial interstitial rejection or the concentric intimal thickening with dense collagen that is typical of chronic vascular rejection. In contrast, the coronary arteries in our patients had a prominent lymphocytic infiltrate, a loosely organized intimal thickening composed of smooth muscle cells, and extensive endothelial injury. We believe that these changes define acute vascular rejection of the coronary artery. In 14 transplanted hearts obtained consecutively, at autopsy or at a second transplant procedure, graft failure was caused by acute coronary vascular rejection in six cases and by chronic coronary vascular rejection in one case. The remaining seven patients showed no evidence of vascular rejection and died primarily of sepsis. Cytomegalovirus (CMV) disease was present in 6 of 7 patients with vascular rejection, of which 43% were CMV-negative recipients of hearts from CMV-positive donors. The adoption of a triple-drug protocol, in which azathioprine was added to cyclosporine and prednisone, reduced the incidence of acute vascular rejection from 27% to 8%. We conclude that acute coronary vascular rejection may be initially seen as global cardiac ischemia in the absence of significant interstitial myocardial rejection. Further, acute vascular rejection should be pathologically distinguished from chronic vascular rejection, although both are probably stages in the natural history of immune-mediated vascular injury.
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PMID:Acute vascular rejection of the coronary arteries in human heart transplantation: pathology and correlations with immunosuppression and cytomegalovirus infection. 165 3

The objective of this study was to test the efficacy of bonding rifampin to double-velour Dacron grafts with collagen to prevent graft sepsis. Fifty 6.0 mm Dacron grafts (length 5.0 cm) impregnated with either collagen (control) or collagen plus rifampin (experimental) were implanted in dogs end-to-end into the infrarenal aorta. The dogs were divided into four groups (each with an experimental and control subdivision) as a function of time between grafting and bacterial challenge. At 2, 7, 10, or 12 days after graft implantation, sequential groups were challenged with 1.2 x 10(8) colony forming units of Staphylococcus aureus (clinical isolate) intravenously suspended in 250 ml normal saline. Three weeks after hematogenous seeding, the grafts were sterilely harvested. One-tailed Fisher's exact test was used to compare the patency and culture-proven infection of control and antibiotic coated grafts as a function of implantation time before bacteremic challenge. In the 2-day group, four of six control grafts were infected compared with zero of six experimental grafts (p less than 0.030). In the 7-day group, five of six control grafts were infected with S. aureus versus zero of six in the experimental group (p less than 0.008). In the 10-day group, one of six experimental grafts was infected, but the control group had only two of six graft infections. In the 12-day group two of six experimental grafts and one of five control grafts were infected. These results indicate that rifampin bonded with collagen to knitted Dacron grafts will protect the graft from bacteremic infection for 7 days after implantation in a highly challenging model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of graft infection by use of prostheses bonded with a rifampin/collagen release system. 183 64

Hemorrhage in patients with Lassa fever is associated with the presence of a circulating plasma inhibitor of platelet aggregation. This study was to determine whether patients with Argentine hemorrhagic fever (AHF) develop a similar inhibitor. Normal platelets showed significantly weaker aggregation responses to a sub-maximal dose of adenosine diphosphate (ADP) when mixed with plasma from 10 patients with AHF (mean percent of control +/- 1 SE = 57.2 +/- 6.7%) compared to those mixed with plasma from 9 viral control patients (79.5 +/- 4.1%; P less than 0.05) and 9 febrile patients with septicemia (103.8 +/- 3%; P less than 0.001). Plasma from 3 patients with severe AHF inhibited in a dose-dependent fashion the aggregation responses of normal platelets to collagen, sodium arachidonate, a calcium ionophore (A23187), and ristocetin; none of 4 samples from convalescent AHF patients showed this inhibitory activity. The platelet inhibition was sudden in onset and unaffected by a 30 min pre-incubation, not neutralized by convalescent plasma with high titer antibody to Junin virus, and abolished after heating plasma from an AHF patient at 56 degrees C for 30 min. Hemorrhage in AHF is associated with the presence of a circulating inhibitor of platelet aggregation, and disturbed hemostasis in arenavirus-induced hemorrhagic fevers may have a common basis.
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PMID:A plasma inhibitor of platelet aggregation in patients with Argentine hemorrhagic fever. 216 Jan 97


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