Concentration and microheterogeneity of acute-phase glycoproteins in patients with systemic lupus erythematosus.

PURPOSE: To determinate glycosylation of selected acute-phase glycoproteins (AGP, ACT, CP) and serum concentration of this proteins in Systemic Lupus Erythematosus (SLE) patients. PATIENTS AND METHODS: The study was carried out on 35 patients with active SLE and 15 healthy volunteers. The immunological measurements were performed at first day of hospitalisation, before receiving treatment. The concentration of CRP, AGP, ACT and CP were evaluated by electroimmunoassay using anti-AGP, anti-ACT, anti-CP antibodies. CRP levels were determined by radial immunodiffusion with anti-CRP antibodies. The microheterogeneity of the acute phase proteins was assessed by agarose affinity electrophoresis using Con A as a ligand, as was described by Bøg-Hansen. RESULTS: Between SLE patients and control group statistically significant differences (p < 0.01) were observed in serum concentration of all investigated parameters. There were no significant differences in serum acute-phase proteins levels with regards to patient's age, sex and disease activity. The reactivity coefficients: AGP-RC, ACT-RC, CP-RC in SLE patients were similar to the healthy group. The precipitate curves were similar in both groups. The main difference was in the area of the precipitant, which was bigger in the SLE patients. CONCLUSIONS: Configuration of analysis serum concentration and heterogeneity of acute-phase proteins is one of important diagnostic tests in SLE.

The human C3b receptor: function and role in human diseases.

The human C3b receptor (CR1) is a polymorphic glycoprotein which functions regulating the complement system by inhibiting the activation of C3 and C5, through its effect on their convertases, and serving as cofactor for factor I in mediating the degradation of C3b to its inactive fragment C3bi and further to C3d-g. The latter are then ligands for their respective receptors on leukocytes, CR3 and CR2. Additionally, CR1 on erythrocytes endows these cells with the capacity to deliver immune complexes (IC) to the reticuloendothelial system, resulting in their clearance from the circulation. On phagocytes, this receptor participates in the process of endocytosis of foreign particles. There is a wide inherited variation of CR1 expression on erythrocytes (CR1/E) of different individuals. Patients with diseases which feature elevated levels of IC, such as systemic lupus erythematosus, leprosy, and AIDS, have a marked decrease of CR1/E, which may result in an altered clearance. This reduction appears to be related to disease activity, and the most probable site for CR1/E loss is during the transfer of IC to macrophages. Healthy neutrophils increase tenfold their expression of CR1 in response to the effect of chemoattractant peptides. Neutrophils from patients with AIDS display an altered response to stimulation. This defect may be of relevance in the process of endocytosis.

Survey of the human acetylator polymorphism in spontaneous disorders.

There is ample evidence that the human acetylator phenotypes are associated with drug induced phenomena. It is principally the slow acetylators who exhibit toxic adverse effects because of their relative inability to detoxify the original drug compounds. In rare instances, however, it is the rapid acetylators who are at a disadvantage. In the matter of association of spontaneous disease with either acetylator phenotype, there are two groups of disorders to consider. First, disorders in which carcinogenic amines are known to be an aetiological factor. This is because these amines are substrates for the polymorphic N-acetyltransferase activity and hence there is a possible rational basis for searching for an association. Secondly, other disorders where searches for associations are based more on hunches. In the first group there is a definite statistical association between cancer of the bladder and the slow acetylator phenotype. In prevalence studies the slow phenotype is 39% more associated with bladder cancer than is the rapid phenotype. On the basis of the evidence now available it is not possible to say whether this association is because slow acetylators develop the disease more frequently or whether they survive longer. In the second group the relevant studies show (1) a greatly increased prevalence of slow acetylators in Gilbert's disease; (2) a confirmed association between the rapid acetylator phenotype and diabetes; (3) a possible association between the rapid acetylator phenotype and breast cancer; (4) a possible association between the slow acetylator phenotype and leprosy in Chinese patients; (5) an earlier age of onset of thyrotoxicosis (Graves' disease) in slow acetylators than in rapid acetylators; (6) no evidence of an association between either phenotype and spontaneous systemic lupus erythematosus.