ABSTRACT
A 30-year-old woman with primary antiphospholipid syndrome (PAPS) presented with cerebral ischemia, thrombocytopenia, anemia and proteinuria. Administration of warfarin potassium, without concomitant corticosteroid administration, significantly improved all of these symptoms along with a decrease in the titers of antiCL-beta2-GP-I antibodies and a shortening of prolonged APTT. Therefore, the antiphospholipid antibodies in this patient could have been evoked by vitamin-K-dependent coagulation factors or plasma proteins which are assumed to undergo conformational changes exposing cryptic epitopes. This case report provides clues to the mechanisms underlying the production of antiphospholipid antibodies in patients with PAPS.
Subject(s)
Anemia/drug therapy , Anticoagulants/therapeutic use , Antiphospholipid Syndrome/drug therapy , Brain Ischemia/drug therapy , Proteinuria/drug therapy , Thrombocytopenia/drug therapy , Warfarin/therapeutic use , Adult , Anemia/diagnosis , Antiphospholipid Syndrome/diagnosis , Brain Ischemia/diagnosis , Cardiolipins/blood , Female , Glycoproteins/immunology , Humans , Partial Thromboplastin Time , Proteinuria/diagnosis , Thrombocytopenia/diagnosis , beta 2-Glycoprotein IABSTRACT
A 63-year-old man with rheumatoid arthritis presented with rhabdomyolysis and intractable arthritis of acute onset. He was diagnosed to have sepsis due to Staphylococcus aureus infection through of an ulcerated rheumatoid nodule. Staphylococcus aureus isolated from pus in the ulcerated rheumatoid nodule and a blood sample obtained from the heart post-mortem produced the toxic shock syndrome toxin-1 (TSST-1). The TSST-1 and/or unmethylated CpG motifs in the oligonucleotides present in a bacterium, Staphylococcus aureus in this case, might be implicated in the induction of rhabdomyolysis and intractable arthritis.
Subject(s)
Arthritis, Rheumatoid/complications , Rhabdomyolysis/etiology , Staphylococcal Infections/complications , Fatal Outcome , Humans , Male , Middle Aged , Rheumatoid Nodule/complications , Sepsis/complications , Shock, Septic/etiology , Ulcer/complicationsABSTRACT
The properties of a ferric ion-reducing system which catalyzes the reduction of ferric ion with elemental sulfur was investigated with a pure strain of Thiobacillus ferrooxidans. In anaerobic conditions, washed intact cells of the strain reduced 6 mol of Fe with 1 mol of elemental sulfur to give 6 mol of Fe, 1 mol of sulfate, and a small amount of sulfite. In aerobic conditions, the 6 mol of Fe produced was immediately reoxidized by the iron oxidase of the cell, with a consumption of 1.5 mol of oxygen. As a result, Fe production was never observed under aerobic conditions. However, in the presence of 5 mM cyanide, which completely inhibits the iron oxidase of the cell, an amount of Fe production comparable to that formed under anaerobic conditions was observed under aerobic conditions. The ferric ion-reducing system had a pH optimum between 2.0 and 3.8, and the activity was completely destroyed by 10 min of incubation at 60 degrees C. A short treatment of the strain with 0.5% phenol completely destroyed the ferric ion-reducing system of the cell. However, this treatment did not affect the iron oxidase of the cell. Since a concomitant complete loss of the activity of sulfur oxidation by molecular oxygen was observed in 0.5% phenol-treated cells, it was concluded that the ferric ion-reducing system plays an important role in the sulfur oxidation activity of this strain, and a new sulfur-oxidizing route is proposed for T. ferrooxidans.
