Subject(s)
Cyclophosphamide/adverse effects , Cyclosporine/therapeutic use , Granulomatosis with Polyangiitis/complications , Granulomatosis with Polyangiitis/drug therapy , Immunosuppressive Agents/therapeutic use , Adult , Cyclophosphamide/therapeutic use , Cystitis/chemically induced , Disease Progression , Female , Humans , Neural Tube Defects/chemically induced , Recurrence , Treatment Refusal , Urinary Bladder Neoplasms/chemically inducedABSTRACT
Rheumatoid arthritis (RA) is a chronic polyarticular joint disease associated with massive synovial proliferation, inflammation, and angiogenesis. PPAR-gamma ligands, both 15-deoxy-Delta(12,14)-prostaglandin J2 (15d- PGJ2) and troglitazone (TRO), can inhibit the growth of RA synoviocytes in vitro, and suppress the chronic inflammation of adjuvant-induced arthritis in rats, but the potency of 15d-PGJ2 is higher than TRO. Prostaglandin (PG) E2 plays important roles in joint erosion and synovial inflammation. In the present study, 15d-PGJ2, but not TRO and other prostanoids, suppressed interleukin (IL)-1beta-induced PGE2 synthesis in rheumatoid synovial fibroblasts (RSFs) through the inhibition of cyclooxygenase (COX-2) and cytosolic phospholipase A2 (cPLA2) expression. Furthermore, the inhibition was not affected by pretreatment with anti-PPAR-gamma antibody. It means that this anti-inflammatory effect of 15d-PGJ2 for PG synthesis may be independent of PPAR-gamma and 15d-PGJ2 is a key regulator of negative feedback of the arachidonate cascade on the COX pathway. These findings provide new insight into the feedback mechanism of the arachidonate cascade.
Subject(s)
Arachidonic Acid/metabolism , Arthritis, Rheumatoid/metabolism , Feedback , Prostaglandin D2/metabolism , Synovial Membrane/metabolism , Thiazolidinediones , Arthritis, Rheumatoid/pathology , Chromans/pharmacology , Cyclooxygenase 2 , Cysteine/antagonists & inhibitors , Cysteine/biosynthesis , Dinoprostone/antagonists & inhibitors , Dinoprostone/biosynthesis , Humans , Isoenzymes/immunology , Isoenzymes/metabolism , Leukotriene Antagonists , Leukotriene B4/antagonists & inhibitors , Leukotriene B4/biosynthesis , Leukotrienes/biosynthesis , Membrane Proteins , Prostaglandin D2/analogs & derivatives , Prostaglandin-Endoperoxide Synthases/immunology , Prostaglandin-Endoperoxide Synthases/metabolism , Receptors, Cytoplasmic and Nuclear/immunology , Thiazoles/pharmacology , Transcription Factors/immunology , TroglitazoneABSTRACT
A tumor-like lesion in the anterior mediastinum was recognized in a 21-year-old female patient with Graves' disease. A CT examination and MRI suggested a thymoma. A subtotal thyroidectomy and a total thymectomy were therefore performed simultaneously. A pathological study of the thymic mass showed thymic hyperplasia. These findings suggest that an enlarged anterior mediastinal mass in a Graves' disease could thus sometimes turn out to be thymic hyperplasia and not a thymoma.
