Sulfapyridine and sulfones decrease glycosaminoglycans viscosity in dermatitis herpetiformis, ulcerative colitis, and pyoderma gangrenosum.

Shortly after the introduction of sulfa drugs, sulfapyridine was found to have unique therapeutic properties, unrelated to antibacterial activity. Later, sulfones were found to share the same properties. The disorders initially improved were dermatitis herpetiformis, pyoderma gangrenosum, subcorneal pustular dermatosis, acrodermatitis continua, impetigo herpetiformis and ulcerative colitis. They were also sometimes helpful in many other disorders. They are effective in select disorders characterized by edema followed by granulocytic inflammation or edema followed by vesicle or bullae formation. The sulfones work in low doses in leprosy and their mode of action is not fully understood. Several pieces of experimental information are available. It is proposed that these drugs are entering or influencing the protein moiety of glycosaminoglycans and decreasing tissue viscosity. This decreased tissue viscosity prevents edema and dilution of tissue fluid and decreases acute inflammation and vesicle and bullae formation.

Autoantibodies--a mechanism of microdebridement.

Antibodies to foreign debris are generally beneficial because they speed inflammation and debridement of tissue. Intracellular components are debris if they reach extracellular space. If not rapidly debrided from extracellular space, intracellular components stimulate autoantibody production. If not debrided, cellular constituents like other foreign material can initiate a chronic tissue response. Antibodies will speed removal of debris if an effective microdebridement mechanism is present. This is their general biologic significance. If the patient has a defective microdebridement system as in lupus erythematosus or rheumatoid arthritis, the autoantibodies occur to large numbers of intracellular substances and accumulate and contribute to tissue damage. Tissue damage occurs and autoantibodies accumulate in lupus erythematosus and rheumatoid arthritis because of inadequate microdebridement. This should not detract from the fact that autoantibodies are a common secondary phenomenon which plays an important part in maintaining tissue microdebridement.