[Effect of propyphenazone on drug biotransformation in the liver. A comparison with phenylbutazone using the aminopyrine breath test]. / Zum Einfluss von Propyphenazon auf die Arzneimittelbiotransformation in der Leber. Eine Vergleichsstudie mit Phenylbutazon unter Verwendung des Aminopyrin-Atemtestes.

By means of the aminopyrine breath analysis the influence of phenylbutazone, propyphenazone and of the combination preparation Wofapyrin "new" on the aminopyrine-N-demethylation, a hepatic microsomal performance of biotransformation in patients with diseases of the rheumatic circle of forms was examined. The enzyme-inducing effect of phenylbutazone known from literature could be confirmed. On the other hand despite a relatively highly dosed one-week treatment propyphenazone did not lead to changes of the demethylation capacity of the liver in the majority of the patients. In individual cases increases of the capacity are possible. In general, however, the doses of propyphenazone usual in the practice for the treatment of acute feverish infections no disturbing effects of induction or inhibition on the metabolic liver functions represented by the amino-N-demethylation are to be expected. The enzyme-inducing effect of Wofapyrin "new" is to be ascribed to the phenyl-butazone component.

Synovial protease/inhibitor ratios in erosive and nonerosive arthropathies.

Although rheumatoid joint fluids contain numerous polymorphs capable of secreting neutral proteases known to be able to digest cartilage, the high level of inhibitors (mainly alpha 1-antitrypsin and alpha 2-macroglobulin) has always been considered to be more than sufficient to inhibit their activity completely. Consequently little interest has been paid to the potential role of these enzymes in cartilage damage. Four arthropathies of different erosive potential are here compared: spondyloarthropathies, rheumatoid arthritis with and without gold or D-penicillamine therapy, and septic arthritis. The synovial concentration of the inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin has been compared with the polymorph enzyme output, as measured by beta-glucuronidase. Total haemolytic complement, white cell count, and C-reactive protein have also been measured in the joint fluid. The range of white cell count and inhibitors was the same in all 4 groups, while the enzyme output varied substantially from low levels in the spondyloarthropathies to very high levels in the septic joints. The higher the erosive potential of the disease, therefore, the more disadvantageous is the inhibitor/enzyme ratio. It is also pointed out that cartilage has physiochemical properties which facilitate and enhance polymorph enzyme output while severely curtailing the activity of the inhibitors. The observation that synovial fluid is inhibitory in vitro may therefore bear little relationship to the situation at the cartilage surface in vivo.