Sulfasalazine: II. Some notes on the discovery and development of salazopyrin.

In summing up: salazopyrin is an effective drug, particularly in ulcerative colitis. Serious adverse effects are remarkably rare. Salazopyrin provoked an improvement in 75-80% of cases of UC. It is excellently adapted for long-term treatment and, in this respect, is clearly superior to corticosteroids. It prevents relapses, particularly if the dosage is increased. The main indication for corticosteroids in UC is for acute attacks early in the course of the disease and to influence allergic symptoms during the disease. For acute swelling of the rectum, local treatment with corticosteroids or salazopyrin is often effective. Adverse effects occur in about 15% of cases treated with salazopyrin. They are due primarily to hypersensitivity to the drug. With very few exceptions, they disappear spontaneously or are controlled by corticosteroids or by some other treatment. The allergic pulmonary changes may give rise to a modest dyspnea, which is not fatal. The cyanotic and the yellow-coloring of the skin are harmless side effects. As to sulfa crystals in the kidneys and the urine, for the most part, they can be avoided by simple treatment. Agranulocytosis is a rare complication in the course of treatment with salazopyrin. During the 35 yr that the drug has been used, only 14 cases have been published in the literature. Of this number, three have died, but the treatment of the agranulocytosis is known in only one of them. Nonpublished cases probably exist, but this number does not seem to be great in my experience. In comparison with many other drugs (certain chemotherapeutics and antibiotics), the frequency of serious side effects caused by salazopyrin is remarkably low.

The origin of rheumatoid arthritis.

The origin of rheumatoid arthritis (RA) is in our opinion a bacterial infection. The infection gives rise to changes in the macrophages, with release of enzymes, etc., and secondarily abnormal immune processes occur. In favor of this opinion is, among other things, the similarity with rheumatic fever, which is caused by streptococci group A, as well as experience gained in connection with experimentally provoked arthritis. In experimental arthritis, produced by streptococci group B (Svartz), there appears in rats the same type of joint disease as in human RA and, besides, a rheumatoid factor (RF)-like macroglobulin, which cannot be distinguished by available methods from human RF macroglobulin. A 7 S hemagglutinating RF (RF II) was also produced in animals, as well as some other immunoglobulins. The RF II has a much weaker hemagglutinating capacity than the usual RF macroglobulin which for comparison could be termed RF I. The streptococci B used in our investigations were mostly isolated from the nasopharynx of RA patients.