Myocrisin-mediated oxidative stress.

This study reports on the ability of myocrisin to mediate in the production and detoxification of oxidants (principally hydrogen peroxide) in the monocyte in-vivo and in-vitro. The hydrogen peroxide produced by the monocyte derived from rheumatoid arthritis patients being treated with myocrisin was found to be 14.9 +/- 1.6 nmoles/10(6) cells and is elevated above levels found in monocytes obtained from patients either being treated with non-steroidal anti-inflammatory drugs (NSAIDs) (11.3 +/- 0.4 nmoles/10(6) cells; P < 0.01) or normal healthy volunteers (11.2 +/- 1.2 nmoles/10(6) cells; P < 0.01). A comparative study on glutathione (GSH) oxidation indicated that levels of monocyte GSH were elevated in myocrisin-treated patients (2.4 +/- 0.49 mmol/l) over normal healthy volunteers (0.83 +/- 0.18 mM; P < 0.01) and that levels of monocyte diglutathione (GSSG) were depressed (myocrisin, 0.97 +/- 0.41 micromol/l; normal, 5.71 +/- 0.73 micromol/l; P < 0.01). The non-inhibition of glutathione reductase and the inhibition of glutathione peroxidase by gold provides the link between these two observations. Thus, gold therapy would seem to elevate monocyte hydrogen peroxide, increase monocyte reduced glutathione and decrease plasma glutathione peroxidase activity. Subsequently, the data from this small group of patients (n = 10) provides an indication that, in-vivo, myocrisin contributes to an increase in oxidative stress.

Maroteaux-Lamy syndrome, mild form--MPS vi b.

Mucopolysaccharidosis VI (Maroteaux-Lamy Syndrome) form B is a rare disease occurring in siblings. It may present with radiological features like Perthes' disease or hypothyroidism. We report two such cases, and discuss the differential diagnosis of the spondylo-epiphyseal dysplasias. We stress the importance of final diagnosis by identifying a particular glycosaminoglycan excess in the urine and an enzyme deficiency in the fibroblasts aryl sulphatase B and N-acetylgalactosamine-4-sulphatase.

Calf haematoma following anticoagulants in synovial rupture.

Four cases of calf haematoma are described in which an incorrect diagnosis of deep vein thrombosis (DVT) was made of rupture of the knee synovium, and led to inappropriate anticoagulant therapy. Awareness of how closely synovial rupture of the knee can simulate DVT should prevent such mistakes. Where there is doubt venography and/or arthrography are advocated before prescribing anticoagulants which can be dangerous as there may already be bleeding from the rupture site.