Accumulation of plasma triiodothyronine sulfate in rats treated with propylthiouracil.

Triiodothyronine sulfate (T3S) is rapidly deiodinated by the propylthiouracil (PTU)-sensitive type I deiodinase. Here we examined the effects of PTU on plasma T3S levels in rats after intravenous administration of radiolabeled T3 or T3S. Sephadex LH-20 chromatography and high-performance liquid chromatography were used to quantify conjugated and nonconjugated iodothyronines, and iodide was measured as the TCA-soluble radioactivity.

Pirprofen-associated hepatic injury.

Four cases of hepatic injury attributed to the use of pirprofen (Rengasil) were reported to the Monitoring Centres for Adverse Reactions of Belgium, The Netherlands and the German Medical Association. One man and three women developed severe hepatic injury between 3 1/2 and 6 1/2 months after starting treatment with 400-1200 mg pirprofen daily. Histology showed acute hepatocellular damage, often with bridging necrosis.

Rapid and bacteria-dependent in vitro hydrolysis of iodothyronine-conjugates by intestinal contents of humans and rats.

Faecal suspensions from healthy humans, conventional (CV), germ-free (GF) and intestine-decontaminated (ID) rats were tested for the in vitro hydrolysis of 125I-labelled iodothyronine sulphates and 3,3',5-triiodothyronine glucuronide (T3G). Whereas 20-fold diluted human and CV rat faecal suspensions hydrolyzed up to 90% of the sulphates, no hydrolysis was observed in 5 times diluted faecal suspensions of GF and ID rats. These results add further weight to the assumption that intestinal iodothyronine sulphatase activity is of bacterial origin.