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Biomedical subjects

G K Endresen

Publications and source records attributed to G K Endresen.

At least 19 recordsLinked to original sources
PubMed1991

[Determination of antinuclear antibodies in rheumatic diseases].

The presence of circulating serum antinuclear antibodies (ANA) directed against various nuclear structures is a hallmark of systemic rheumatic diseases. These diseases are characterized by overlapping clinical features and the diagnosis is not always clear-cut. Each disease has a profile of ANA specificities which is more or less specific to that disease. Therefore serological tests that define the precise specificities of ANA are of great importance for establishing the diagnosis.

Antibodies, Antinuclear↗
PubMed1991

Calprotectin (the L1 protein) during surgery in patients with rheumatoid arthritis.

Calprotectin (L1) is a major leukocyte protein which is released during activation or death of neutrophil granulocytes and monocytes. Previous studies have shown that L1 may be a useful marker of disease activity in patients with adult or juvenile rheumatoid arthritis (RA). In the present study, the plasma concentrations of L1 were analysed during shoulder-joint surgery in 16 patients with adult or juvenile RA. Decreased L1 concentrations were found 48 h postoperatively. Thereafter, the L1 concentrations were increased at 72 h, with a following decrease until day 14 postoperatively. In contrast, increased serum concentrations of both C-reactive protein (CRP) and orosomucoid (i.e. alpha 1-acid glycoprotein) were found at 48 h after surgery. Plasma samples obtained before and after surgery were analysed by gel filtration. Approximately 3/4 of the plasma L1 was found in fractions corresponding to the native molecule, while the rest was detected in higher molecular mass fractions. The distribution of L1 antigen in low and high molecular mass regions did not differ between the pre- and postoperative plasma samples. The L1 protein consists of light and heavy chains. Increased serum levels of the cystic fibrosis antigen, which is identical to L1 light chain, have been described in patients with cystic fibrosis. The existence of circulating free L1 chains was presently investigated in plasma obtained before and after surgery. After gel filtration of plasma samples, no free L1 chains were detected by use of enzyme immunoassay and dot blot.

Acute-Phase Reaction↗
PubMed1991

Intraoperative autotransfusion in reconstructive hip joint surgery of patients with rheumatoid arthritis and ankylosing spondylitis.

The efficacy of a simple, low-cost device designed for intraoperative blood salvage and reinfusion, known as the Sorensen system, was studied during 24 hip joint operations in adult patients suffering from rheumatoid arthritis or ankylosing spondylitis. The total need for homologous blood was reduced to 28%, compared with a matched control group of patients who had previously undergone hip surgery by homologous blood replacement. In primary hip-replacement operations, the need for blood was met either completely by autotransfused blood or by the addition of 1 or 2 units of homologous blood. In revision arthroplasties, the maximal need for homologous blood was 6 units owing to a greater blood loss during operation. Postoperative changes in several hematologic variables measured were all very small. The autotransfusion system proved easy and safe to operate. No patients manifested complications. In our experience, the system may be considered an underutilized resource in rheumatological surgery.

Adolescent↗
PubMed1989

Evidence for activation of platelets in the synovial fluid from patients with rheumatoid arthritis.

Platelets were isolated by gel filtration from paired samples of peripheral blood and synovial fluid (SF) aspirated from inflamed knee joints from 20 adult patients with rheumatoid arthritis (RA) as well as from peripheral blood obtained from 20 healthy subjects. The platelets from the three different sources were investigated for quantitative differences in the number of two distinct types of intracellular storage organelles using immunofluorescence staining for platelet factor 4 (PF4) and labelling with the fluorescent substance mepacrine (MC). The number of PF4-stained organelles per cell was the same in the peripheral normal and RA platelets. This number was distinctly lower in the SF platelets. The peripheral and SF platelets from the RA patients had the same number of MC-labelled organelles. This number was distinctly lower than in the normal cells. The results suggest that the peripheral RA platelets had been activated to liberate serotonin and other substances from one type of organelles, and that the SF platelets had been activated to an additional liberation of PF4 from another such type. Liberated PF4, serotonin, and other substances from SF platelets may, in several ways, contribute to the inflammatory responses of RA.

Adult↗
PubMed1987

Studies on the steric relationship between HLA antigens, beta 2-microglobulin and the Fc receptor on human platelets.

Normal human platelets were investigated by immunofluorescent staining methods for the steric relationship between HLA class I antigens, beta 2-microglobulin and the Fc receptor. IgG antibody to human class I antigens or beta 2-microglobulin, but not their F(ab')2 fragments, blocked the binding of human IgG-Fc fragments to the platelet Fc-receptor. The receptor binding of human IgG-Fc fragments did not prevent the binding of any of the antibodies. This was observed in incubation studies performed both at 4 degrees C, 20 degrees C and 37 degrees C. The results provide evidence that HLA class I antigens and their associated beta 2-microglobulin are in close proximity to the Fc-receptor on human platelets. It is suggested that inhibition of the platelet Fc-receptor was due to binding between the Fc part of surface-bound antibody molecules and the Fc-receptors.

Blood Platelets↗
PubMed1985

Studies on the binding of proteins to the human platelet surface: relation to platelet activation.

Several antibody fractions and sera from patients with rheumatoid arthritis, systemic lupus erythematosus and chronic idiopathic thrombocytopenic purpura were examined for their ability to bind to normal platelets using immunofluorescent staining techniques. Platelet aggregometry was used to study the activating capacity of the samples. Both C1q, C1s, C1 inactivator, fibrinogen, factor VIII-related antigen, alpha 1-acid glycoprotein, alpha 1-antitrypsin, beta 2-microglobulin and isoantigens A and B, as well as fibronectin and plasminogen were found on the platelet surface. Only antibodies to C1q, C1s and beta 2-microglobulin were able to induce platelet aggregation. Sera containing immune complexes or platelet autoantibodies revealed positive surface staining for IgG, or for IgG and IgM. There sera also induced aggregation of platelets. Sera not containing immune complexes or autoantibodies gave negative staining and aggregation results. Thus, only some of the ligand receptor interactions were able to induce platelet aggregation.

Antibodies↗
PubMed1984

Studies on the binding of complement factor C3 to the surface of human blood platelets.

Employing immunofluorescent staining methods, platelets from several adult patients with chronic idiopathic thrombocytopenic purpura, with systemic lupus erythematosus, and with classical rheumatoid arthritis stained positively with antisera to C3(beta 1C) and C3dg(alpha 2D). In some cases, platelet-bound C3dg antigens, but no evidence of other C3 antigens were observed. Platelets that were positive for C3 and/or C3dg were always positive for IgG or for both IgG and IgM. Platelets from normal subjects stained negatively for C3, C3dg, IgG, and IgM. Furthermore, various incubation experiments were performed to investigate the uptake of C3 and its subfragments on normal platelets. Positive platelet staining for C3 was obtained after incubation with normal and C3b-containing sera, but not after incubation with native C3. Platelets incubated with C3c(beta 1A)/C3dg-containing serum gave a positive staining for C3dg, but not for C3c. None of the sera stained positively for IgG or IgM. Thus, in contrast to platelets from several of the patients, no in vivo binding of C3 antigens on normal platelets could be established. However, in vitro they could take up both C3b and C3dg, apparently by specific binding to platelet surface structures.

Arthritis, Rheumatoid↗
PubMed1984

Studies on the binding of complement factor C4 in human platelets. Complement activation by means of cold agglutinins.

Normal human platelets were investigated by immunofluorescence techniques for the natural occurrence of and uptake capacity for complement factor C4. Fractions of human platelets were found to carry none or very little C4. Activated C4 was readily taken up by the majority of platelets in vitro. Complement could be activated with pathological cold agglutinins (CA) of mono- or polyclonal types, all with specificity for the I antigen. Complement activation seen in normal human sera was probably due to naturally occurring CA with anti-I specificity. Thrombin potentiated the complement-activating capacity of CA, and complement factor C1 enhanced and stabilized the binding of CA to platelets.

Agglutinins↗
PubMed1984

Demonstration of fibronectin associated with platelets in synovial fluid from patients with rheumatoid arthritis.

Paired samples of peripheral blood and synovial fluid (SF) aspirated from inflamed knee joints from 15 adult patients with classical rheumatoid arthritis, as well as peripheral blood obtained from 15 healthy subjects, were anticoagulated with ACD. Peripheral blood platelets were separated from other plasma constituents by gel filtration of platelet-rich plasma on Sepharose 2B. When using this technique on SF, it was found that platelets could be isolated from other SF constituents, and that each of the SF's gave a high yield of eluted platelets. Direct immunofluorescent staining for human fibronectin was performed with isolated and suspended platelets obtained from the three different sources. Aliquots of both intact and permeabilized platelets were stained. Intact peripheral platelets from all patients and normal subjects revealed a weakly positive staining, whereas the staining of intact SF platelets from all patients was clear and bright. The fluorescence of intact cells was surface-located and speckled. For permeabilized platelets, the staining had a punctate intracellular pattern, with a varying number of discrete and bright fluorescent foci per cell. Counting of the foci in each platelet specimen revealed that this number, which was also found in peripheral platelets from all patients and normal subjects, was distinctly greater than the number of foci in all the SF platelet specimens. No relationship was found between the various staining results and medical treatment or Waaler-Rose serology of the patients. The findings indicate that the SF platelets had large amounts of surface-bound and small amounts of intracellular fibronectin, whereas the converse was found in the case of peripheral platelets from the patients and normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Studies on the binding of immunoglobulins and immune complexes to the surface of human platelets: IgG molecules react with platelet Fc receptors with the CH3 domain.

Suspensions of human platelets were incubated with various immunoglobulin preparations and subsequently stained with FITC-conjugated antisera. Incubation with monomeric, IgG, but not with monomeric IgM, IgA, IgD nor with IgE, gave a positive staining of the platelets. Incubation of platelets with monomeric IgG1 and IgG3 as well as with Fc and pFc'-fragments from IgG3 also gave a positive staining while incubation with monomeric IgG2 and IgG4 did not. Thus, IgG binds to Fc receptors on the surface of human platelets with the CH3 domain of the Fc region. Heat aggregation also caused binding of IgG2 but not with IgG4 proteins to human platelet Fc receptors. The majority of platelet preparations both from ITP and SLE patients gave a positive staining using direct immunofluorescence technique. Incubation of normal human platelets with sera from ITP and SLE patients gave a strong surface staining of normal platelets. Strong staining was also obtained with pepsin-digested sera from most patients with ITP while pepsin-digested sera from patients with SLE did not give a positive staining. It is therefore concluded that the majority of sera from patients with ITP contain antibodies with specificities for platelet surface antigens while sera from patients with SLE contain immune complexes that react with platelet Fc receptors through the Fc parts of the IgG antibodies.

Animals↗
PubMed1981

Investigation of blood platelets in synovial fluid from patients with rheumatoid arthritis.

Synovial fluid (SF) aspirated from inflamed knee joints from each of 13 patients with adult rheumatoid arthritis (RA) was mixed with ACD in the ratio SF/ACD=9:1 with subsequent addition of an equivalent amount of an edta-tris buffer. The mixture was centrifuged to obtain a platelet-rich supernatant. The platelets were washed three times and counted. The same procedure was performed with SF from non-inflamed knee-joints from 3 patients with osteoarthrosis (OA). Direct immunofluorescence (IF) studies were performed with aliquots of platelet suspensions from each SF. In most RA specimens observed under the microscope before separation of platelets, a few small platelet aggregates were observed and platelets were seen in contact with lymphocytes. In all instances, the platelet count appeared to be positively correlated to the total number of white blood cells. In the OA specimens, relatively few platelets were detected, a few lymphocytes were seen in contact with platelets, but no platelet aggregates or correlation between platelets and white blood cell counts were found. Results of the IF studies of RA specimens provide evidence that IgG, IgM and C3 are located on the platelet surface. On the surface of OA platelets, however, only IgG and C3 were detected. Identical staining results were found with washed peripheral platelets from 3 of the RA and 1 of the OA patients. Neither medical treatment nor Waaler serology influenced the staining results. In inflamed SF from RA patients, both IgG aggregates, immune complexes, collagen, and prostaglandins can induce a platelet release reaction with liberation of vasoactive compounds, chemotactic substances and enzymes which can destroy connective tissue, cartilage and bone structures. Interpretations and the significance of the different results are discussed.

Adult↗
PubMed1977

Platelet count and disease activity in juvenile rheumatoid arthritis.

Blood samples from 41 children with juvenile rheumatoid arthritis (JRA) were studied. The platelet count was tested for possible relationship and correlation with a number of clinical and laboratory parameters. High platelet count was associated with active disease, presence of secondary amyloidosis, and poor functional capacity. The platelet count was positively correlated with the erythrocyte sedimentation rate, anemia, and granulocytosis. The platelet count thus seems to provide an additional parameter of disease activity in patients with JRA.

Adolescent↗