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

Sera from patients with systemic lupus erythematosus (SLE) and clinically related diseases were examined for cold-reactive lymphocytotoxic antibodies (LCA). The incidence of LCA was significantly increased in SLE (93%), discoid lupus (50%), and "lupus-like" syndromes associated with congenital complement deficiencies (63%) as compared to normal controls (3%) and patients with drug-induced lupus (11%), mixed connective tissue disease (MCTD) (17%), and necrotizing vasculitis (19%). The diagnostic and pathogenetic implications of these differences are discussed.
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PMID:Lymphocytotoxic antibodies in systemic lupus erythematosus and clinically related diseases. 3 65

Cold-reactive antibodies cytotoxic for peripheral monocytes from more than half of normal donors were found in the sera of 2 of 25 patients with systemic lupus erythematosus (SLE) and 1 of 26 with rheumatoid arthritis (RA), and they were absent in 25 normal sera. In contrast, lymphocytotoxic activity for T or B lymphocytes was found in over half of the lupus sera. The antibodies to monocytes were primarily IgM and exhibited varying specificities. Some of the antibodies were directed against antigenic determinants common to monocytes, T and B cells, or against determinants shared between monocytes and one lymphocyte type. One serum possessed a high titer of antibodies that were specific for monocytes. The clinical significance of antimonocyte antibodies remains to be established.
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PMID:Monocyte-reactive antibodies in patients with systemic lupus erythematosus. 6 77

Sera from 11 (65%) of 17 patients with newly diagnosed procainamide-induced lupus contained cold-reactive lymphocytotoxic antibodies to normal human lymphocytes in titres of 1/2 to 1/128. In contrast, only 3 of 15 patients on long-term procainamide therapy without lupus and 3 of 65 normal men had serum lymphocytotoxic antibodies, none at a titre higher than 1/2. Antibody levels in the lupus patients declined quickly after procainamide was stopped, in parallel with their clinical improvement. Procainamide (3.75 x 10(-3) mol/l) suppressed by more than 80% in-vitro phytohaemagglutinin-induced 3H-thymidine incorporation by normal human blood lymphocytes. At 3.75 x 10(-4) mol/l, procainamide enhanced the mitogenic response to 160 +/- 20% of normal. Thus procainamide may interact with the lymphocyte membrane, possibly producing a lupus syndrome directly, by altering lymphocyte function, or indirectly, by generating autoantibodies reactive with normal membrane structures.
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PMID:Lymphocyte alteration by procainamide: relation to drug-induced lupus erythematosus syndrome. 9 Sep 17

In a retrospective multicenter study 106 patients with systemic lupus erythematosis were analyzed who had had the disease for an average of 8.6 years, and from whom an average of 8 sera were tested within 3 years for current immunologic parameters. Cumulative clinical data showed arthropathies in 86% of the patients, exanthema (67%), cytopenia (58%), and involvement of the kidney (45%), lung (43%) and heart (24%). In at least 1 serum per patient the following immune abnormalities were found: antinuclear antibodies (98%), anti-native DNA (92%), low C3 (71%), low C4 (82%), circulated immunocomplexes (70%) and cold lymphocytotoxins (46%). A clinical score and an immunological score was introduced and the two items were compared: the immune data from a single serum do not provide long-range prognostic information. The present disease state is best reflected by the total immune score, C3 and C4 with, however, many exceptions. Within the disease course of some SLE patients, periods were observed during which no pathological immune serologic data are measureable. This phenomenon may pose diagnostic problems.
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PMID:[Systemic lupus erythematosus--clinical aspects and laboratory findings]. 38 95

A prospective clinical study of cold-reactive lymphocytotoxic antibodies in systemic lupus erythematosus has been completed. A highly significant association between serum lymphocytotoxicity and the development of cerebral manifestations was observed. While lymphocytotoxic antibodies from patients with cerebral lupus were absorbed by homogenates of human brain, those from patients who at no time had evidence of cerebral disease failed to cross-react with brain. It is suggested that subpopulations of lymphocytotoxic antibodies differ in their brain reactivity, and that one population may be causally related to the development of some of the features of cerebral lupus.
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PMID:Brain reactivity of lymphocytotoxic antibodies in systemic lupus erythematosus with and without cerebral involvement. 60 49

The significance of cold lymphocytotoxins, observed at 15 degreesC, is not clearly understood at the present time. The frequency of their appearance has been studied in normal subjects (blood donors, aged people, vaccinated subjects, post-traumatic splenectomy) and in patients with a neurologic disease (multiple sclerosis), a neoplasic disease (breast cancer)and hematologic diseases (thrombocytopenia, acute leukemia, chronic lymphatic leukemia, Hodgkin disease and systemic lupus erythematosus). There are no antibodies found in the geriatric group; they are found only in 3,9 % of blood donors and in 18 % of the subjects after vaccinations. A range of 17 to 30 % is found in subjects with breast cancer or multiple sclerosis. More than 50 % of the individuals with Hodgkin disease or lupus erythematosus produce these antibodies (52 % and 73 % respectively). In acute leukemias and chronic lymphatic leukemias, lymphocytotoxic antibodies sometimes appear at 37 degrees, reacting with autologous cells and having no HL-A specificity.
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PMID:[Cold lymphocytotoxins: their relationship with various physiological and pathological conditions]. 108 28

Autoimmunity to a 28-29-kDa cell-surface DNA-binding molecule has previously been described in patients with systemic lupus erythematosus and related autoimmune diseases. This report describes experiments that implicate a similar antigen-antibody system in the evolution of autoimmunity in lupus-prone mice. DNA binding to murine spleen cells was found to be a saturable phenomenon that was inhibited by excess cold DNA and trypsinization. The role of autoimmunity to murine cell-surface DNA-binding molecules in lupus-prone mice (MRL lpr/lpr, MRL +/+, BXSB) was compared to normal mice (BALB/c, C3H.SW) by means of an assay that measured the inhibition of cell-surface DNA binding. Only sera from lupus strains had inhibitory activity and this component was shown to be an IgM autoantibody. Furthermore, we isolated a spontaneously occurring IgM monoclonal antibody from the spleen of an MRL/lpr mouse, which inhibited DNA binding to mouse cells. Time-course studies indicated that young female MRL/lpr mice lacked detectable activity against cell-surface DNA-binding molecules; however, by 8-10 weeks maximal inhibitory activity was observed. This response occurred prior to the development of significant antinuclear antibody activity. With the appearance of overt disease and anti-DNA antibodies, inhibition of DNA-binding activity became undetectable. These findings mirror previous studies on autoimmunity to a cell-surface DNA-binding molecule on human leucocytes, but have the added advantage of permitting the study of the temporal evolution of this inhibitory activity in relation to disease expression.
Lupus 1992 May
PMID:DNA binding to mouse cells is mediated by cell-surface molecules: the role of these DNA-binding molecules as target antigens in murine lupus. 130 77

Chilblains represents an idiopathic vascular cutaneous benign acral syndrome. Epidemiology and basic mechanisms remain hypothetic and the treatment is controversial. The patients exhibit pruritic, redness painful, burning acral patches or plaques on the toes and/or fingers. The disease is bilateral, youthful and influenced by exposure to cold. Spontaneous healing is common when spring arrives and relapse is frequent on the following winters. There is no systemic symptom and laboratory studies are normal. The physical examination is sufficient for diagnosis. Histologic examination shows vascular and perivascular capillary and venular lymphocyte infiltrates without necrosis nor leukocytoclasia. The differential diagnosis includes: lupus, cold urticaria, acrocyanosis, erythermalgia, vasculitis and the Blue Toe Syndrome. Treatment includes prophylactic measures against cold and calcium channel inhibiting drug. In more severe cases thyrocalcitonin and hemodilution might be helpful.
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PMID:[Chilblains]. 143 11

Over 12 months of general internal medicine practice in a small community, three premenopausal women, and a man presented with peripheral circulatory complaints. All were found to have cryofibrinogen, a cold-precipitable abnormal fibrinogen complex, in their blood. None had cryofibrinogen levels above 100mg per 100ml. The plasma of 195 other patients were screened. Cryofibrinogen was found in only one of these samples, that of a 23 year old women with active lupus erythematosis. These case reports suggest a relationship between low levels of cryofibrinogenaemia and mild circulatory disorders.
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PMID:Low levels of cryofibrinogenaemia and peripheral circulatory dysfunction. 189 2

A case of lupus cystitis in a 23-year-old male is reported. The patient began to complain of diarrhea and vomiting in October, 1985. When the diagnosis of systemic lupus erythematosus (SLE) was established at the Department of Internal Medicine in our hospital, he was referred to our clinic for examination of pollakisuria on November 22. DIP revealed a loss of bladder distensibility, and bilateral hydronephrosis and hydroureter. Transurethral cold cup biopsies revealed subcutaneous edema. A diagnosis of lupus cystitis was made and he was treated with steroids, which resulted in symptomatic and radiographic improvement.
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PMID:[A case of lupus cystitis]. 273 71


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