[Clinico-immunological aspects of antinuclear antibodies in systemic lupus erythematosus].
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Anti-Sm and anti-ribosomal P protein antibodies show a high degree of specificity for the disease SLE. To determine whether a relationship between these two autoantibodies existed, the frequency of anti-P was determined in sera with and without anti-Sm activity. Of sera from lupus patients with anti-Sm 18/65 (28%), and 6/55 (11%) of sera without anti-Sm had anti-P as determined by an ELISA using a recombinant P2-beta-galactosidase fusion protein as Ag (p less than 0.05). The levels of anti-P were significantly higher in sera containing anti-Sm (0.37 +/- 0.45) than in sera without anti-Sm antibodies (0.18 +/- 0.20) (p less than 0.01). Similarly, a significantly higher proportion of anti-P positivity was found in autoimmune MRL/Mp-lpr/lpr mice positive for anti-Sm (11/53 = 21%) compared to age- and sex-matched mice without anti-Sm (3/53 = 6%) (p less than 0.05). The IgG subclass distributions for anti-Sm and anti-P antibodies were similar in the MRL mice (IgG2a greater than IgG2b greater than IgG3 greater than IgG1). The association did not reflect polyclonal B cell activation in a proportion of MRL mice because no significant differences were observed in anti-DNA, antichromatin or total serum IgG levels in mice with and without anti-Sm or, in mice positive for both anti-P and anti-Sm compared to mice positive for anti-Sm alone. Cross-inhibition experiments excluded the possibility that the Sm and P protein Ag shared a common epitope. Longitudinal measurement of anti-P and anti-Sm antibody levels by ELISA in three mice indicated that both antibodies first appeared at about 3 to 4 mo of age and fluctuated two- to threefold over 3 to 8 mo with independent peaks of activity. Recent observations regarding a relationship between anti-Sm and autoantibodies to other ribosomal proteins suggest that the association may be explained by an immune response to epitopes coassociated on the ribosome.
Lupus nephritis is the archetype of diseases caused by the deposition of immune complexes. The characteristics which render only a portion of circulating immune complexes nephritogenic are not well delineated, but cat-ionic charge of antigen and/or antibody may contribute. Lupus nephritis is characterized by extreme diversity of clinical manifestations and pathologic features. Scrupulous monitoring of urinary sediment and renal function tests is necessary to identify renal involvement in a phase which is amenable to therapeutic intervention. Evaluation of renal biopsies also assists in development of indications for therapy. The pathology of lupus nephritis is classified primarily as mesangial, focal proliferative, diffuse proliferative, and membranous nephropathy. Indexes of activity and of chronicity provide a succinet description of the balance of reversible and irreversible disease. The activity index incorporates glomerular hypercellularity, karyorrhexis/fibrinoid necrosis, leucocyte exudation, hyaline thrombi, cellular crescents, and interstitial inflammation. The chronicity index incorporates glomerular sclerosis, fibrous crescents, tubular atrophy, and interstitial fibrosis. Delineation of the activity and chronicity indexes also facilitates the assessment of prognosis and the ordering of indications for therapy.
Issues concerning contraception, fertility, and pregnancy usually arise during a typical lupus patient's disease course. Pregnancy superimposed on established lupus may alter the course of the disease, and, conversely, lupus may affect the natural history of pregnancy. Two recently described autoantibody markers, anti-SSA (Ro) and anticardiolipin, have provided new insights concerning fetal risks in these patients. Furthermore, they should lead to improved understanding of mechanisms of tissue injury and to new ideas about therapeutic interventions and/or prevention of pregnancy complications.
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A study of the state of the humoral immunity in 36 SLE patients made it possible to detect an increase in the level of autoantibodies to type I collagen in comparison to the level of autoantibodies in healthy donors. It showed correlation with the activity of a process, its course, clinical signs of disease, progression of renal pathology and the levels of antinuclear factor and gamma globulins.
To determine feasibility of using quantitative histochemical assessment of platelet anaerobic metabolism in lupus nephritis (LN) prognostication and elucidation of its activity, the authors examined 23 SLE patients. 20 of them developed renal lesions. Anaerobic metabolism of platelets was measured according to lactate dehydrogenase levels. All the SLE patients had significantly higher levels of the enzyme than healthy controls showed. Maximal LDG activity was registered in rapidly progressive LN with thrombocytopenia. The findings support activation of platelet hemostatic component in SLE patients and valid utilization of a new quantitative histochemical technique for determination of intracellular metabolism enzymes content.