Search PubMed⌕ Search

Biomedical subjects

A Cruchaud

Publications and source records attributed to A Cruchaud.

At least 55 records · Page 3Linked to original sources
PubMed1976

Nonmalignant monoclonal immunoglobulinemia, pernicious anemia and gastric carcinoma. A model of immunologic dysfunction. Report of two cases and review of the literature.

The association of an autoimmune disease with a monoclonal immunoglobulin is not exceptional and most probably results from a dysfunction of the immunologic apparatus. This study describes two patients with monoclonal immunoglobulin A (IgA) and M (IgM) gammopathy, respectively, in whom pernicious anemia and finally gastric carcinoma developed. One patient had autoantibodies to gastric parietal cell and to thyroid microsomal antigen which could not be identified with the M-component. This observation, together with the fact that pernicious anemia occurred in one case before and in the other case after the discovery of M-component, suggests that different clones of cells were responsible for both disorders. Sixteen cases in which the patients had the same association have been collected from the literature and the data are compared with ours.

Aged↗
PubMed1976

Cephalothin-induced immune hemolytic anemia.

A patient with renal disease developed Coombs-positive hemolytic anemia while receiving cephalothin therapy. An anti-cephalothin IgG antibody was detected in the patient's serum and in the eluates from her erythrocytes. In addition, nonimmunologic binding of normal and patient's serum proteins to her own and cephalothin-coated normal red cells was demonstrated. Skin tests and in vitro lymphocyte stimulation revealed that the patient was sensitized to cephalothin and also to ampicillin. Careful investigation of drug-induced hemolytic anemias reveals the complexity of the immune mechanisms involved.

Anemia, Hemolytic↗
PubMed1975

[Antibodies against various nuclear antigens (especially DNA and RNA proteins) in disseminated lupus erythematosus with and without kidney involvement and in other collagen diseases. Preliminary report].

The incidence of autoantibodies to various nuclear antigens was studied in 64 patients with SLE, 137 patients with various connective tissue diseases, 63 other patients and 90 controls. A positive correlation was found between SLE, nephritis, and the presence of antibody against native DNA. Antibody to denatured DNA showed no specificity for SLE and was correlated with the absence of nephritis. Antibody to RNA-protein occurred mainly in SLE, regardless of the presence or absence of nephritis.

Antibodies, Antinuclear↗
PubMed1975

Immune complex deposits in systemic lupus erythematosus kidney without histological or functional alterations.

This study demonstrates that in systemic lupus erythematosus (SLE), the presence of immune complexes on the glomerular basement membrane (GEM) does not invariabley result in histological and/or functional lesions of the kidney. Among a group of 29 lupus patients, six subjects were selected for thorough investigation, because their renal function was normal or only slightly altered though they had suffered from SLE for 20 months to 18 years. All patients had antinuclear factor, anti-native-DNA antibody and a low level of complement; 3 had anti-denatured-DNA antibody, 2 had denatured DNA-anti-denatured-DNA circulating complexes and 3 had anti-RNA-protein antibody. Kidney biopsies disclosed either no histological lesion or minimal changes in five of them and diffuse proliferative glomerulonephritis in one. By contrast, using the immunofluorescent technique, granular deposits containing the third component of complement (C3) were found on the GBM of all patients; IgG was present in 5 cases, IgM in 3, fibrinogen in two cases and around the tubules of one. Electron microscopy confirmed the presence of subendothelial and mesangial deposits. Our results also showed a good correlation between the importance of deposits and the presence of denatured DNA-anti-denatured-DNA circulating complexes. From the data obtained in these 6 cases as well as in the 23 other patients of the group, 3 categories of lupus patients could be distinguished with regard to kidney involvement: 1) patients with insignificant histological lesions, no immune deposits and essentially normal function; 2) patients with definite histological lesions, immune deposits and renal insufficiency and 3) patients with few if any histological lesions and little functional impairment contrasting with important immune deposits. The resistance of some patients to the mephrotoxic effects of immune deposits shows that lupus nephritis depends on intricate pathogenic mechanisms and suggests that these are possible antagonized by "protective" factors.

Adolescent↗
PubMed1975

Catabolism physical, and immunologic properties of endocytosed isologous and heterologous iota-globulins by mouse macrophages.

The catabolism of completely endocytosed isologous and heterologous gamma-globulins by mouse macrophages was studied in vitro. Mouse, human, and rabbit 125-I-IgG were coupled to mouse, human, or sheep erythrocytes either as antibodies or by covalent binding. They were exposed to macrophages for 1 hr and the non-endocytosed erythrocytes were then removed with a Ficoll gradient centrifugation. Catabolism was evaluated after 2, 5, and 18 hr in culture by measuring the radioactivity released into the culture medium as well as the radioactivity that remained associated with cells. It was found that all iota-globulins were catabolized in a similar fashion, and that the type of carrier erythrocytes (isologous or heterologous) had no influence on catabolism. Some of the material that remained associated with macrophages was on the cell membrane and could be removed by trypsin. Some of the material that was released by macrophages was completely degraded but some was either not degraded or only partially degraded. Sucrose density gradient analysis and SDS-polyacrylamide gel electrophoresis showed that this material had kept some physical properties of native iota-globulins. It was also found with the antigen-binding inhibition test and incubation with erythrocytes that the released material contained molecules carrying Fab determinants and was able to bind specifically to erythrocytic antigens. Taken together, these observations show that iota-globulins phagocytosed in the form of antigen-antibody complexes are only incompletely degraded and that the material associated with plasma membrane of macrophages or found in the culture medium is a product of cell catabolism.

Animals↗
PubMed1973

Human smooth muscle autoantibody. Its identification as antiactin antibody and a study of its binding to "nonmuscular" cells.

When human serum containing smooth muscle autoantibodies (SMA) is incubated with extracts containing thrombosthenin (the contractile material of platelets) or thrombosthenin-A (the actin-like moiety of thrombosthenin), it loses its ability to bind to smooth muscle. Such binding is also diminished when SMA serum is incubated with lysed platelets; this effect is not seen if the SMA serum is incubated with intact platelets. The incubation of other autoantibodies (such as antimitochondrial or antinuclear antibodies) with thrombosthenin does not affect their binding to the specific antigens. It appears that SMA is directed against the actin fraction of thrombosthenin-ie, SMA is an antiactin antibody. Hence the name of antiactin autoantibody (AAA) seems more appropriate than smooth muscle autoantibody (SMA). A study of the distribution of antiactin autoantibody binding in rat, rabbit and man shows that several "nonmuscular" structures contain actin under normal conditions; these include megakaryocytes and platelets, normal rat hepatocytes, the brush borders of renal tubules, the periphery of epithelial cells of the intestine, polymorphs and lymphocytes in lymph nodes (but not thymic cortical lymphocytes). In addition, certain cell types (such as granulation tissue fibroblasts, cultivated fibroblasts, hepatocytes or regenerating liver and epidermal cells growing over a skin wound) can reversibly acquire a massive network of actin-containing microfilaments resembling those in smooth muscle.

Absorption↗