Urate oxidase (rasburicase) for treatment of severe acute gout: a case report.

A 73-year-old female patient was referred to our department because of gouty arthritis in the right first toe. The patient suffered from progressive renal failure because of pauci-immune necrotising glomerulonephritis. As severe hyperuricaemia would further worsen progredient renal insufficiency and therapy with allopurinol was contraindicated because of renal insufficiency and previous pancytopenia, the patient was treated twice with intravenous rasburicase. This therapy was well tolerated by the patient and led to the decrease of serum uric acid below the detection limit within 24 hours.

Influence of hypotonic stress on the biliary excretion of doxorubicin in Wistar and TR- rats.

In tumor cells, doxorubicin (DOX) is excreted by P-glycoprotein (P-gp) and the multidrug resistance-associated protein (mrp). Both transporters might also be involved in cellular regulatory volume decrease (RVD). To study the hepatobiliary excretion of DOX during RVD, isolated livers of Wistar and multidrug resistance-associated protein 2 (mrp2)-deficient TR- rats were first perfused with an isotonic and later with a hypotonic medium. In both rat strains, DOX is effectively excreted into the bile. Within 30 minutes, the biliary excretion of DOX-derived fluorescence steadily increased to 1.1+/-0.11 and 0.84+/-0.05 nmoles/min . g liver in Wistar and TR- rats, respectively. Under hypotonic conditions, DOX excretion followed the biphasic-increase in bile flow. Excretion was increased to 136+/-19% and 176+/-9% (first peak) and to 141+/-11% and 157+/-14% (second peak) in Wistar and TR- rats, respectively. Our data show that in the liver of both strains, exposure to a hypotonic medium stimulates DOX excretion, presumably by activation of P-gp and mrp2 during RVD.

Decrease of proteinuria in a patient with adult-onset Still's disease and glomerulonephritis after anti-TNFalpha therapy.

We report the case of a 41-year-old man diagnosed with Still's disease. Multiple disease-modifying anti-rheumatic drug (DMARD) therapies failed to induce disease remission or to prevent progressive joint destruction. The man presented with active arthritis and classical Still's rash accompanied by fever. Anti-tumour necrosis factor-alpha (TNFalpha) therapy was planned but during the medical check-up prior to the biological therapy, renal insufficiency with marked proteinuria (PU) was discovered. With PU of 912 mg/24 h a renal biopsy was performed and a histopathological evaluation revealed the diagnosis of a residual mesangio-proliferative immunocomplex-based glomerulonephritis (GN). After excluding contraindications, infliximab therapy was initiated and a good response of the arthritis was documented after 6 weeks. A significant decrease in PU (279 mg/24 h) was noted after the third infliximab infusion. Because of an allergic reaction during the fifth dose, the infliximab was discontinued. During the time frame without anti-TNFalpha therapy, active joint disease reoccurred and the proteinuria increased significantly. Because of the active disease entanercept therapy was initiated. The arthritis diminished and the PU was reduced markedly within 4 weeks. In the follow-up period of 12 months a good response to therapy was sustained. As described by other investigators, the joint disease showed a rapid and sustained response to anti-TNFalpha therapy. The decrease in proteinuria during biological therapy was notable. It was concluded that the significant decrease in PU in this patient was achieved by eliminating the inflammatory activity of the underlying kidney disease.