ABSTRACT
Eight patients with systemic sclerosis previously exposed to organic chemical agents were investigated. Laboratory and clinical data of these patients were evaluated. The interval between the beginning of exposition and symptoms was 6.1 +/- 4.9 years. Considering the laboratory findings, a slight decrease in OKT4 positive T cell number was found. The antinucleolar and fine speckled antinuclear antibody pattern was found simultaneously in five cases. The possible role of chemical agents in the development of sclerodermic changes is discussed.
Subject(s)
Dermatitis, Occupational/chemically induced , Scleroderma, Systemic/chemically induced , Adult , Antibodies, Antinuclear , Dermatitis, Occupational/drug therapy , Female , Humans , Middle Aged , Nifedipine/therapeutic use , Penicillamine/therapeutic use , Prednisone/therapeutic use , Scleroderma, Systemic/drug therapyABSTRACT
The binding of 125I-labelled anti-bovine serum albumin (BSA)-BSA immune complexes (IC), giving a final molar antibody to antigen ratio of 1:1, to monocytes isolated from 18 patients with systemic lupus erythematosus (SLE) and from 10 normal healthy donors was quantitatively investigated. The degradation of the bound IC by the same monocytes was kinetically determined at the same time. The assays were performed on monocyte monolayers. Scatchard plots at 4 degrees C demonstrated that monocytes from patients with active SLE expressed a mean Fc gamma receptor (FcR) number that was 22% higher than that of the controls, although this did not reach statistical significance. The FcR number of normal monocytes and the degradation rate of anti-BSA-BSA complexes by the same cells showed a positive correlation. At the same time, the digestion of anti-BSA-BSA complexes by monocytes of SLE patients with active disease was prolonged, despite their enhanced FcR-ligand binding. The dissociation of FcR-ligand binding and FcR-mediated degradation suggests that the IC degradation is controlled by altered biochemical mechanisms in the monocytes of SLE patients.
Subject(s)
Antigen-Antibody Complex/metabolism , Lupus Erythematosus, Systemic/immunology , Monocytes/metabolism , Female , Humans , Male , Receptors, Fc/analysis , Receptors, Fc/metabolism , Serum Albumin, Bovine/immunologyABSTRACT
The authors review the theoretical basis of human antilymphocyte globulin (ALG) and human antihymocyte globulin (ATG) treatment in myasthenia gravis. Ten selected seriously ill myasthenic patients were treated with ALG and/or ATG. Three of the patients improved significantly and a further four moderately, whereas the condition of three patients did not change. ALG therapy is effective in the suppression of cellular immune mechanism, therefore it can be assumed that it exerts its effect in myasthenia gravis by inhibiting thymus hormone stimulation.
