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At least 1,243 records · Page 69Linked to original sources
PubMed1997

Some studies of the complement system during total hip replacement using bone cement under general anaesthesia.

Fourteen patients who underwent Charnley or Howse total hip replacement using CMW bone cement were studied. Mean values of C4 and C3 determined before the induction of anaesthesia and insertion of bone cement and also after this procedure showed no significant difference and were within the normal range. Furthermore, no evidence of C3 breakdown products was found. It was therefore concluded that neither the general anaesthetic technique nor the insertion of bone cement activated the classical or alternative complement pathways and such a mechanism was not responsible for the hypotension which occurred shortly after the insertion of bone cement in 10 cases studied.

Aged↗
PubMed2001

Complement activation by apoptotic endothelial cells following hypoxia/reoxygenation.

Reperfusion of ischaemic tissue initiates an inflammatory reaction that increases tissue injury. Complement activation at the endothelium contributes to this inflammation. This study investigated the mechanism of complement activation following reoxygenation of hypoxic human umbilical vein endothelial cells (HUVEC) as a model for complement activation observed on endothelium in reperfused ischaemic tissue. HUVEC cultured in 1% oxygen followed by reoxygenation activated the classical complement pathway resulting in C3 deposition. There was an increase in apoptotic cells in these cultures that was demonstrated by binding of fluorescein isothiocyanate-Annexin V and staining for hypodiploid nuclei. To determine if apoptotic HUVEC activate complement, uniformly apoptotic cells were produced by serum and growth factor deprivation. These cells, but not the control HUVEC, activated the classical complement pathway in the absence of antibody or other serum factors. To determine if apoptotic cells in the reoxygenated cultures were activating complement, fluorescent analysis was done. Annexin V binding and C3d deposition on cells from reoxygenated cultures showed complete concordance on the subpopulation of apoptotic cells. In addition, complement activation following reoxygenation of HUVEC was eliminated by treatment of the cultures with a caspase inhibitor during reoxygenation. These results suggest that oxidative damage to endothelial cells during reoxygenation initiates apoptosis with exposure of phosphatidylserine. Apoptotic cells directly activate the classical pathway of complement by binding C1. Activation of complement at the endothelium may contribute to the inflammatory response as well as clearance and repair.

Amino Acid Chloromethyl Ketones↗
PubMed1999

Plasmapheresis with a substitution solution of human serum protein (5%) versus plasmapheresis with a substitution solution of human albumin (5%) in patients suffering from autoimmune diseases.

Therapeutic plasma exchange (TPE) has been used extensively for over 2 decades to treat a variety of autoimmune and congenital diseases and is now widely accepted. The primary objective of this study was to compare the clinical efficacy of two plasma exchange preparations, human serum protein (HSP) and human albumin (HA). Twenty-four patients in the following disease categories underwent TPE using either HSP (Biseko, 5%) or HA (5%): systemic lupus erythematosus, 8; glomerulonephritis, 8; myasthenia gravis, 2; Guillain-Barré-syndrome, 2; recurrent iritis, 1; pemphigoid, 1; uveitis, 1; and vascular retinitis, 1. There was no statistically significant difference in the average number of TPEs needed in the HSP group (13.5) and HA (13.8) measured over the first 6 weeks of treatment. The secondary parameters, in particular the immunological parameters IgG and IgA, provided evidence that plasma exchange with HSP may have some advantages over HA, and confirmatory studies in a larger group of patients are indicated. Adverse events during TPE occurred in both the HAS group (4 patients) and the HA group (4 patients). However, patients in the HSP group were older (12.3 years), were suffering from more complicated autoimmune diseases, and the number of occasions (days) on which these were reported (6 days) was less than in the HA group (11 days). One patient in the HA group died from septic-toxic circulatory collapse on Day 49 due to an infection with resistant strains of Staphylococcus aureus. Infections in other patients did not occur; all showed considerable improvement in their symptoms and completed the study in good general condition.

Adult↗
PubMed1997

Complement activation during storage of whole blood, red cells, plasma, and buffy coat.

BACKGROUND: The process of separating whole blood into components and the storage of blood components may cause the release of toxic metabolites from the complement cascade. The aim of this study was to determine whether the storage of blood components leads to the activation of the complement cascade and the release of anaphylatoxins. STUDY DESIGN AND METHODS: Blood from 12 healthy volunteers was collected and stored either as whole blood or as components: red cells in saline-adenine-glucose-mannitol solution, plasma, and buffy coat. The concentrations of anaphylatoxins and other complement proteins in the various blood components were intermittently analyzed during a 5-week storage period. RESULTS: Increasing levels of anaphylatoxins were demonstrated during the storage of whole blood and plasma. Elevated concentrations of the anaphylatoxins C3a and C5a were observed during the storage of whole blood. Increased C5a levels were observed after 7 days of storage. High concentrations of C3a were found in plasma after 14 days of storage. Low or non-detectable levels of C3a; C5a, and other complement components were found in red cells stores in saline-adenine-glucose-mannitol solution. CONCLUSION: The study demonstrated activation of complement during the storage of whole blood and plasma but not in red cells in storage solution. The transfusion of larger volumes of stored whole blood or plasma may contribute to the risk of development of organ dysfunction. Therefore, it is advisable to use red cells in storage solution.

Anaphylatoxins↗
PubMed2002

C1r-C1s-C1inhibitor (C1rs-C1inh) complex measurements in tears of patients before and after penetrating keratoplasty.

PURPOSE: The aim of this pilot study was to determine the presence of complement activation products in tears from pre- and postkeratoplasty eyes and the fellow eyes in order to investigate the activation of the classical and alternative pathways of the complement system in the early postkeratoplasty period. METHODS: Tear samples from both eyes of 19 prekeratoplasty patients were tested. From 10 patients, samples were taken before operation, one week and 3 weeks after penetrating keratoplasty. Only baseline and 1 weak samples, and baseline and 3 week samples were available from 5 and 2 patients, respectively, while only baseline tear samples were collected from 2 patients. Tear concentration of two complement activation products, C1rs-C1inh and C3bBbP were determined by enzyme-linked immunosorbent assay. RESULTS: There was no difference (p = 0.339) between baseline samples of the eyes waiting for operation (0.93 +/- 0.51 AU/ml, mean +/- SEM) and the fellow eyes (0.33 +/- 0.33 AU/ml) in respect of mean C1rs-C1inh complex concentration. The one-week samples of the operated eyes revealed significantly (p = 0.006) elevated levels of C1rs-C1inh complexes (18.8. +/- 6.37 AU/ml), compared to their baseline samples (1.18 +/- 0.64 AU/ml), whereas the one-week values of the fellow eyes did not differ from the baseline values. Compared to the increased one-week values, the three-week values decreased to the baseline values in the operated eyes. C3bBbP could be detected in 3/68 tear samples. CONCLUSIONS: In our study we demonstrated the increased concentration of C1rs-C1inh complex in several tear samples taken early after human penetrating keratoplasty. These findings provide direct evidence that the classical pathway of complement may be activated in the early postoperative period after penetrating keratoplasty.

Adult↗
PubMed1999

Complement activation in patients with systemic lupus erythematosus without nephritis.

OBJECTIVE: To study the association between disease activity and complement activation prospectively in patients with systemic lupus erythematosus (SLE). PATIENTS AND METHODS: Twenty-one SLE patients were examined monthly for 1 yr. Disease activity, autoantibodies, conventional complement tests and the following complement activation products were investigated: C1rs-C1inh complexes, C4bc, Bb, C3a, C3bc, C5a and the terminal SC5b-9 complement complex (TCC). RESULTS: Modest variation in disease activity was noted. None of the patients had nephritis. Flare was observed at 27 visits. Four patients had anti-C1q antibodies in conjunction with modestly low C1q concentrations. The complement parameters were rather constant during the observation period. Slightly to moderately decreased C4 (0.05-0.10 g/l) was found in 10 patients and severely decreased C4 (<0.05 g/l) in seven patients. Decreased C4 was not associated with increased complement activation. Complement activation products were either normal or slightly elevated. TCC was the only activation product correlating significantly with score for disease activity at flare. None of the variables tested predicted flares. CONCLUSION: Complement tests are of limited importance in routine examination of SLE without nephritis, although TCC is suggested to be one of the most sensitive markers for disease activity.

Adult↗
PubMed1982

Effect of nonviable tissue and abscesses on complement depletion and the development of bacteremia.

Complement concentrations and blood cultures were compared in 58 patients within 24 hours of injury and weekly thereafter. Extensive amounts of nonviable tissue (n = 40) were associated with a mean depletion of C4, C3, and C5 by 56%, and minor injuries (n = 18) by 22% of normal concentration within 14 hours after injury. The C4, C3, and C5 concentrations returned to normal or above within a week after minor injuries, but not following major injuries. However, C4, c3, and C5 levels remained depressed after major injuries unless necrotic tissue was removed or abscesses were drained. If complement concentration was below 50% of normal for more than a week all patients developed bacteremia. Following debridement or drainage complement returned to normal in 11 patients and blood cultures became negative in seven. Possible consequences by activation and altered availability of complement for chemotaxis, opsonization, and lysis of bacteria have been analyzed and related to the development of bacteremia.

Abscess↗
PubMed1984

Inherited complement deficiencies.

Isolated genetic deficiencies of individual components of the complementary system have been described in man for all the components of the classical pathway and the membrane attack complex as well as for Factor I, Factor H and properdin. It is only for Factor B and Factor D of the alternative pathway that homozygous deficiency states are not so far known. Complement deficiency states provide the most direct way of looking at the role of the complement system in vivo and emphasize the importance of complement in resistance to bacterial infection and in particular to infection with Neisseria. This association is not unexpected since in vitro studies have shown complement to be an efficient enhancer of phagocytosis and inflammation. The particularly frequent occurrence of neisserial infection may be ascribed to the ability of these organisms to survive in phagocytic cells so that the plasma cytolytic activity provided by complement is needed to kill them. On the other hand the strong association between complement deficiencies and immune-complex diseases--especially systemic lupus erythematosus--was unexpected and seems paradoxical in view of the large part played by complement in the pathogenesis of immune complex mediated tissue damage. The paradox can be explained in part by the necessity for an intact complement system in the solubilization and the proper handling of immune complexes. It is also likely that complement deficiency can allow the persistence of low virulence organisms that produce disease solely by an immune complex mechanism. Recently described deficiencies of complement receptors and their effects in vivo are described.

Blood Donors↗
PubMed1977

Haemostatic and complement changes in a family with 'allergic' disorders.

A family with allergic manifestations, haemostatic disturbances, total absence of haemolytic activity of the complement system and low IgG levels is described. It is suggested that this functional abnormality of the complement system and the decreased level of immunoglobulin G may be due to immune complex reactions.

Adolescent↗
PubMed1992

An association between homozygous C3 deficiency and low levels of anti-pneumococcal capsular polysaccharide antibodies.

Inherited deficiencies of complement components are associated with an increased risk of infection by encapsulated, high grade bacterial pathogens such as Streptococcus pneumoniae, Haemophilus influenzae type b and Neisseria meningitidis. Hence, the levels of antibodies to bacterial capsular polysaccharide antigens were measured using ELISA in 65 patients with inherited deficiencies covering the classical, alternative and terminal components of the complement cascade. Three of the four C3-deficient individuals studied were found to be almost totally deficient in specific anti-pneumococcal capsular polysaccharide (PCP) antibodies. These individuals had a history of recurrent pneumococcal sepsis. While single individuals with C1r, C2 and C1Inh deficiency were found to have low anti-PCP antibody levels, no other group of complement deficiency had significantly reduced anti-PCP antibody levels compared with 100 controls. Antibody levels to the other two polysaccharides were not significantly lower in the patient groups. These findings suggest that C3 may be able to provide a stimulatory signal to promote the production of anti-PCP antibodies.

Adolescent↗
PubMed1992

Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils.

Neutrophils activated by soluble particulate stimuli generate superoxide anion and subsequently form hydrogen peroxide and other oxygen radicals. The effect of hydrogen peroxide on the complement system in normal serum was investigated. Treatment of normal serum with hydrogen peroxide resulted in a diminution of the haemolytic activity of the total and alternative complement pathways and the haemolytic titres of C3 and C5 but not of C2, in normal serum. These decreases in complement activity depended on the concentration of hydrogen peroxide added to the serum. Immunoelectrophoretic analysis of hydrogen peroxide-treated serum showed that C3 and C5 proteins were activated. Complement degradation products C3a and C5a were produced in normal serum treated with hydrogen peroxide, and 20 mM EDTA abolished C3a and C5a production in hydrogen peroxide-treated serum but 20 mM Mg-EGTA did not. Catalase completely abolished and dimethylsulphoxide and D-mannitol, hydroxyl radical scavengers, partially inhibited the hydrogen peroxide-mediated complement activation. Hypochlorite, incubated with normal serum, significantly inhibited serum haemolytic activity, and sodium thiosulphate, a reducing agent, abolished the effect of hypochlorite. Normal serum incubated with activated neutrophils showed neutrophil chemotactic activity and decreased serum haemolytic activity, and the addition of catalase or methionine (5 mM) completely abolished the effects of activated neutrophils. These results suggest that hydrogen peroxide activates complement via an alternative pathway of complement activation and that hydroxyl radicals and other hydrogen peroxide-related species such as hypochlorite are most likely involved in hydrogen peroxide-mediated complement activation. Complement activation by oxygen radicals produced by activated neutrophils may be one of the mechanisms by which complement is activated in human immune complex diseases.

Complement Activation↗