Laboratory method predicting the maximal effective NSAID's in management of rheumatoid arthritis

Macrophages were isolated from 32 patients with acute rheumatoid arthritis [RA]. Macrophages of each patient were separately treated in-vitro with different NSAID's in the presence of immune complex [IC]. Cells inhibition was determined by measuring intracellular enzymes and number of FC receptors before and after treating the cell with NSAID's. Drug that caused maximal inhibition of FC receptors of the macrophages in-vitro was given to the patient for two weeks. Clinical assessment was done for each patient before and after treatment. The same previous procedures were followed for another 15 patients with acute RA as a control group. That group of patients were treated for two weeks by the drug that showed minimal FC receptors inhibition, It was found that the percentage of FC receptors inhibition is proportional to the clinical improvement of the disease parameters. Accordingly, this method can be used to predict the optimal effective NSAIDs for each patient before starting treatment

Anti-Fc-receptors and macrophage function in patients with brucellosis

Chronicity and arthritis are the main complications of brucellosis. To clarify the causes of these complications, 80 patients with brucellosis, acute and chronic with or without arthritis and 20 normal control subjects were studied. The mean value of rheumatoid factor [RF], alpha-1 - antitrypsin [alpha 1-AT], C3, C4 and fibrinogen did not show significant changes between different groups of patients and normal control, while anti-Fc-receptor antibodies showed significant increased levels in all groups of patients. This increase was more significant in patients with chronic brucellosis who had arthritis. The absence of acute reactive phase proteins with the presence of anti-receptor peptide could be attributed to the disease chronicity. Immune complexes [ICs] also showed significant increased levels in the all groups of patients compared with normal control. Evidence of activation of C3 and C4 was observed in patients who had increased IC levels and who had arthritis. Arthritis did not develop in some patients with high IC levels probably due to decreased level of anti-Fc-R antibodies. Also there was no evidence of complement activation in this group of patients