The "switch-off" mechanism of spontaneous resolution of acute gout attack.

Urate crystal size change and the modification of coated proteins by oxygen radicals released by stimulated polymorphonuclear cells (PMN) could represent a likely "switch-off" mechanism of the spontaneous resolution of acute gout attack. The absorption spectra and the uric acid, allantoin and urea concentrations were determined before and after in vitro exposition of monosodium urate (MSU) crystals to superoxide anion (O2) photochemically generated. The results showed a complete dissolution of MSU crystals after incubation under O2-, with decrease of uric acid and increase of allantoin and urea concentrations. Our results were confirmed by polarizing, electron microscopy and calorimetric techniques. The results obtained seem to confirm that the spontaneous resolution of acute gout attack could be attributed to the dissolving effect on urate crystals and the modification of coated proteins by O2- released by phagocytizing PMN.

[Possible mechanism of action of drugs in the basic therapy of rheumatoid arthritis: effect on platelet aggregation]. / Possible meccanismo d'azione dei farmaci della terapia di fondo dell'artri te reumatoide: effetto sulla aggregazione piastrinica.

As it is known that platelets play an important role in arising and maintaining the inflammation, the authors have studied "in vitro", the effect on platelet aggregation of three drugs (Sodium Aurothiomalate, Auranofin and Penicillamine) used in basic therapy of Rheumatoid Arthritis (RA). The drugs are used in different concentrations and at different times of preincubation. The study was based on the principle of Born and using the Coagg-Salus aggregometer. The platelet aggregation was induced by ADP 2.5 microM. The authors have demonstrated that the above-named drugs inhibit the platelet aggregation induced by ADP in different percentile, according to the concentrations adopted and the time of preincubation with platelets rich plasma. This study seems particularly interesting because it can offer a possible interpretation on the mechanism of action of basic therapy in RA.

[Drug-induced changes in chemotaxis under normal conditions and in rheumatoid arthritis]. / Modificazioni farmacologicamente indotte della chemiotassi in condizioni normali e nell'artrite reumatoide.

The effects of agents used in RA treatment, various drugs, RF, rheumatoid nodule and synovial fluid was studied on chemotaxis of PMNs. NSAIDS, corticosteroids, theophylline, colchicine, SOD, RF, rheumatoid nodule and synovial fluid were found to inhibit the chemotactic responsiveness while AMPc, GMPc, PGEI and immunodulator drugs enhanced chemotaxis. The results support the hypothesis that drugs tested may modulate chemotactic function by affecting cellular microtubules assembly and/or GMPc accumulation.

[The production of superoxide anion (O2-) by polymorphonuclear cells in patients with rheumatoid arthritis]. / La produzione di superossido anione (O2-) da parte dei polimorfonucleati di pazienti con artrite reumatoide.

Superoxide anion production has been determined in controls and RA patients PMNs stimulated with zymosan, rheumatoid synovial membrane, nodule and synovial fluid, rheumatoid factor, aggregated gamma-globulins, Mycoplasma and Epstein-Barr virus. Patients with RA showed an increased production of O2- after incubation with zymosan and rheumatoid tissue extracts or synovial fluid in comparison to normal controls. The findings indicate that rheumatoid PMNs become activated by different stimuli to produce an excess of O2- which can contribute to chronic inflammatory process.

[Inhibition of fructose-induced hyperuricacidemia by pretreatment with phosphates]. / Inibizione dell'iperuricemia da fruttoso mediante pretrattamento con fosfati.

To test the hypothesis that intravenous injections of fructose rapidly decreases liver ATP and Pi and results in the rapid degradation of adenine nucleotides and hyperuricemia, fructose was administered intravenously to a group of normal and gouty subjects; 4 gouty patients were treated with a phosphate solution prior fructose loading. The results obtained show that fructose administration plus phosphate solution prevents Pi depletion and inhibits fructose-induced hyperuricemia.