ABSTRACT
Although therapeutic heat and cold measures are widely used in rheumatic diseases, their application in joint inflammations is still broadly empirical. Animal experiments concerning the effects of systemic hyperthermia and of local heat and cold applications upon experimentally induced inflammations (dextran edema, formol edema, kaolin edema, carrageenan edema, adjuvant arthritis) show that some inflammations are significantly depressed, i.e. they are effected by a useful therapeutic influence, but that cold and heat can also act as enhancing inflammatory stimulus. Under certain conditions, whole-body hyperthermia has immuno-suppressive effects. Although the exact points of intervention of heat and cold investigations, acute exsudative inflammations seem to be better influenced by cold; on the contrary, chronic torpid and proliferous inflammations are better influenced by heat. Prostaglandin mediated inflammations can be aggravated by cold, because it stimulates the prostaglandin synthesis; acute exsudative inflammatory processes are most often aggravated by heat. These results show that both therapeutic agents should be applied within a well-defined range and with care.
Subject(s)
Cryotherapy , Hot Temperature/therapeutic use , Rheumatic Diseases/therapy , Animals , Body Temperature , Humans , Hyperthermia, Induced/adverse effects , Inflammation/therapy , Joints/physiology , Rheumatic Diseases/immunology , Time FactorsABSTRACT
In a controlled therapeutic trial 17 patients with active rheumatoid arthritis (stage II and III) were divided in two randomized groups. One group of 9 patients was treated with 900 mg of D(-)penicillamine (Trolovol) plus 1500 mg of salicylate per day, the other group of 8 patients with 10 mg of prednisolone plus 1500 mg of salicylate daily. Before and after 1, 2, 3, 4 and 6 months of treatment IgA, IgG, IgM and caeruloplasmin were estimated with immunodiffusion technique. In both groups the IgA and IgG levels remained unchanged; unter D-penicillamine, on the contrary, a statistically significant and continuous fall of IgM and caeruloplasmin was observed; prednisolone treatment induced only a temporary fall of caeruloplasmin. In the DPA treated patients, a significant correlation of IgM with caeruloplasmin and of caeruloplasmin with ESR was found. In both groups there was no correlation between joint count and caeruloplasmin, joint count and IgM, caeruloplasmin and copper, copper and ESR; in the prednisolone group no correlation between caeruloplasmin, ESR and IgM was observed. The correlations suggest that the remarkable fall of IgM and caeruloplasmin under D(-)penicillamine treatment is caused at least partially by direct interference of DPA with these plasma proteins.
