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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and radiological features in 100 patients with collagen diseases (rheumatoid arthritis, lupus, sclerodermia, dermatomyositis, and panarteritis nodosa) were compared with respiratory performance. 56 patients were drawn from the series of Pende et Al. and 44 from a personal series. The results are set out in tables and graphs. It was found that lung lesions due to collagen disease have no special clinical and radiological features. Respiratory performance is that of a restrictive syndrome that gradually progresses from A.R. to E.S., S. and P.M., accompanied by obstruction of the large airways, as shown by hyperinsufflation in sclerodermia and reduced specific conductance in rheumatoid arthritis.
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PMID:[Clinico-radiological and functional aspects of respiratory syndromes caused by collagen diseases]. 99 94

Skin lesions from six patients with systemic lupus erythematosus, five patients with discoid lupus erythematosus, twelve patients with systemic sclerosis, five patients with localized morphoea and twenty controls were examined by immunohistological techniques using fluorescein-labelled anti-human IgG, anti-human C3 and anti-human renal glomerulus antisera. The major immunohistological changes in systemic sclerosis and in localized morphoea consisted of foci of intercollagenous staining for connective tissue antigens in the reticular layer of the dermis. It is suggested that these findings indicate collagen neogenesis. In lupus erythematosus the major changes occur in the dermo-epidermal junction and consist of deposits of IgG and C3 and thickening and disruption of the membrane as demonstrated by the use of heterologous sera containing antibasement membrane antibodies. Immunohistological techniques are useful in the diagnostic differentiation between scleroderma and lupus erythematosus.
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PMID:Immunohistological studies, with anti-connective tissue and anti-immunoglobulin antisera, of the skin in lupus erythematosus and scleroderma. 108 2

Prevalence of lupus anticoagulant (LA) in patients with systemic lupus erythematosus (SLE) and clinical manifestations vary widely between different clinical series. We investigated the relation between LA, autoimmune hemolytic anemia (AIHA), thrombocytopenia and platelet dysfunction in 80 unselected patients with SLE. AIHA was found in 6 patients (7.5%) and thrombocytopenia in 10 patients (12.5%), which was not related to platelet aggregation abnormalities. Compared to controls, patients with SLE showed significantly prolonged aPTT and kaolin clotting time (KCT), but platelet aggregation induced by both collagen and thrombin was not impaired. LA activity as defined by Rosner et al. (index for LA/ICA) was found in 15 patients (18.9%). Only 7 of these patients showed a positive platelet neutralization test (Triplett) and 9a positive tissue thromboplastin inhibition test (Schleider). In our SLE patients 23.7% have suffered from at least one thrombotic complication. In patients with LA activity thromboembolic complications were increased (p < 0.05). Thrombocytopenia was found in 6% of LA-negative but in 20% of LA-positive patients.
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PMID:[Prevalence of lupus anticoagulant, autoimmune hemolysis, thrombocytopenia and disorders of platelet function in unselected patients with SLE]. 128 63

The effect of circulating lupus anticoagulant on platelet interaction with collagen and other proteins was tested, with the aim of understanding the role of membrane phospholipids in platelet function. Plasma samples from 26 systemic lupus erythematosus (SLE) patients, containing circulating lupus anticoagulant (LAC), were examined for their effect on adhesion and aggregation of normal human platelets. We find that SLE plasma, but not normal plasma, inhibits platelet adhesion to collagen in a concentration-dependent manner. At a plasma concentration of 1% the inhibition was 73 +/- 9% (mean +/- SD). In sharp contrast, there was no effect on platelet adhesion to fibronectin. Purified IgG from the same plasma samples also had an inhibitory effect. At 15 micrograms/ml (comparable in IgG concentration to 0.1% plasma) it inhibited adhesion to collagen by 33 +/- 11%. Inhibition could be abolished by preincubation of the LAC-containing plasma with cardiolipin (CL), phosphatidylinositol (PI), and, to a lesser extent, phosphatidylserine (PS) but not with phosphatidylcholine (PC) or phosphatidylethanolamine (PE). Inhibition could also be abolished by preincubation of the LAC-containing plasma with a 10-fold excess of washed normal platelets. The effect of 1% LAC plasma on platelet aggregation was as striking, showing 79 +/- 26% inhibition of collagen-induced aggregation, and it could also be abolished by preincubation of the LAC plasma with cardiolipin. In contrast, the effect of LAC plasma on thrombin-induced aggregation was rather modest. Our results indicate that antiphospholipid antibodies interfere with platelet adhesion and stimulation by collagen in vitro and point to an important role of external plasma membrane phospholipids, particularly PI, in collagen-induced platelet activation.
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PMID:Lupus anticoagulant antibodies inhibit collagen-induced adhesion and aggregation of human platelets in vitro. 128 33

The aims of this study were to investigate whether anticardiolipin antibodies (aCL) bind to intact (resting or activated) platelets in vitro. Suspensions of resting, activated (with a mixture of thrombin and collagen) and freeze-thawed platelets from healthy subjects were incubated with either affinity-purified aCL or pooled normal human immunoglobulin G (IgG). Platelet-bound IgG was measured by flow cytometric analysis of platelets incubated with a fluorescein-conjugated polyclonal goat anti-human IgG. There was no significant binding of IgG aCL to intact resting or activated platelets, while significant specific binding to freeze-thawed platelets was demonstrated. These results question the theory that aCL bind/activate intact platelets in vivo.
Lupus 1992 Dec
PMID:Lack of specific binding of anticardiolipin antibodies to intact platelets. 130 7

Collagen failure has been shown to result in synovitis, joint adhesions, and internal joint derangement. This case report illustrates the similarities between patients with systemic lupus erythematosus and an internally deranged temporomandibular joint and patients with internal derangement with no lupus erythematosus. If abnormalities in intra-articular collagen tissue lead to adhesion formation and restrict normal mobility during translatory movements, joint mechanics would be compromised. Arthritic changes, vasculitis, and synovitis of systemic lupus erythematosus appear to be contributory factors in this pathophysiologic process. Diagnostic and therapeutic arthroscopic surgery was performed. Acute and chronic signs of synovitis were observed during surgery, and tissue samples were obtained for histologic interpretation.
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PMID:Acute closed lock in a patient with lupus erythematosus: case review. 140 Nov 39

Platelet adhesion to collagen under flow conditions was studied in 18 patients with lupus anticoagulant, seven of which showed a prolonged bleeding time in the presence of a normal platelet count. The effect of patient plasma, IgG and purified anticardiolipin antibodies on platelet adhesion was also examined. We found a significant reduction of platelet adhesion in patients with lupus anticoagulant, which was more evident in patients with prolonged bleeding time. This platelet adhesion defect could be attributed to a plasma factor. In fact, patients' platelets regained normal adhesion when mixed with normal plasma, whereas controls' platelets showed abnormal adhesion in the presence of patient plasma. A causative role of antiphospholipid antibodies was demonstrated in experiments using purified immunoglobulins and anticardiolipin antibodies.
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PMID:Prolonged bleeding time in patients with lupus anticoagulant. 145 93

Secondary mucinosis is a common finding in connective tissue diseases, especially in lupus erythematosus and dermatomyositis, but is seen only rarely in morphea. We report the case of a 9-year-old boy who presented with linearly arranged, flesh-colored to erythematous, indurated, very tender plaques on his right arm. He had similar lesions on his midchest and upper back. Histopathology revealed the characteristic findings of morphea and mucin deposition between thickened collagen bundles. This is an unusual case of linear morphea with hyaluronic acid deposition.
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PMID:Linear morphea with secondary cutaneous mucinosis. 147 50

The authors report the case of a 37-year-old man with bilateral posterior tibial artery aneurysms and concomitant collagen vascular disease. The patient initially presented with pain and swelling of the calves. The diagnosis was made by duplex scan and confirmed with arteriography. Diagnostic studies later verified the presence of a lupus-like syndrome. To date, 10 patients with aneurysms of the infrapopliteal arteries have been reported in the literature; four of these have had associated systemic diseases. These reports are reviewed; their clinical manifestations are discussed, and a treatment plan for these uncommon lesions is presented.
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PMID:Bilateral infrapopliteal artery aneurysms. 159 36

The production of relatively high quantities of autoantibodies (autoAb) that react with DNA and other intranuclear antigens is characteristic of individuals with systemic lupus erythematosus and other autoimmune diseases. However, the capacity of these Ab to penetrate cells and induce functional perturbations in vivo is not well appreciated. To address this issue, monoclonal (m) anti-DNA Ab (mAb), derived from MRL-lpr/lpr and (NZB x SWR)F1 mice, were administered to normal mice, and the animals were examined for morphologic and functional abnormalities. A subset of five mAb produced intranuclear immunoglobulin deposits in multiple organs. Intranuclear immunoglobulin deposits were also observed after cross-linking the tissue before direct immunofluorescence and after i.v. injection of F(ab')2 fragments of one anti-DNA Ab. This phenomenon was reproducible and was only associated with this subset of autoAb. Furthermore, intranuclear deposits of anti-DNA Ab within glomeruli were associated with morphologic and functional abnormalities including: hypercellularity, epithelial foot process fusion, new fiber bundle formation within the mesangium suggestive of new collagen synthesis, and proteinuria. These results indicate that a subset of autoAb may penetrate cells in vivo to influence normal cellular and nuclear function and to contribute to functional and pathologic abnormalities in individuals with systemic lupus.
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PMID:Murine monoclonal anti-DNA antibodies penetrate cells, bind to nuclei, and induce glomerular proliferation and proteinuria in vivo. 162 59


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