ABSTRACT
In early June 2004, a 50-year-old female was admitted to the hospital for slight fever, general fatigue, hemoptysis, dyspnea, and renal dysfunction (serum creatinine[Cr] : 6.05 mg/dL). She had been treated with prednisolone (PSL : 10-20 mg/day) for RA. She was diagnosed with Goodpasture syndrome based on a high titer of anti-glomerular basement membrane antibody (87 EU), and pulmonary hemorrhage. The renal and pulmonary impairments were markedly improved by the pulse therapy, plasma exchange and temporary hemodialysis. However, the Cr level remained at 2.0 mg/dL, indicating nephrotic syndrome. Light microscopy with Periodic acid-Shiff(PAS) staining demonstrated global sclerosis in three of ten glomeruli. Five glomeruli showed the formation of cellular, and fibrocellular crescents, and the formation of fibrous crescents. Tubular damage and interstitial fibrosis were severe. Immunofluorescence microscopy disclosed major depositions of IgG in a linear pattern along the glomerular basement membrane(GBM). Electron microscopy revealed foot process effacement (>50%)and no electron-dense deposits. Therefore, we diagnosed Goodpasture syndrome associated with minimal change nephrotic syndrome (MCNS). Some reports have dealt with the association of RA and Goodpasture syndrome with D-penicillamine, and of RA and antineutrophil cytoplasmic antibodies (ANCA)-related vasculitis with pulmonary hemorrhage, but none has dealt with cases complicated with RA and Goodpasture syndrome associated with MCNS. Accordingly, whether or not there is a causal relationship between RA and Goodpasture syndrome remains obscure, but since the number of reported cases is small, experience with more cases is necessary to clarify this matter.
Subject(s)
Anti-Glomerular Basement Membrane Disease/etiology , Arthritis, Rheumatoid/complications , Nephrosis, Lipoid/etiology , Anti-Glomerular Basement Membrane Disease/diagnosis , Anti-Glomerular Basement Membrane Disease/therapy , Arthritis, Rheumatoid/drug therapy , Female , Humans , Kidney/pathology , Methylprednisolone/administration & dosage , Middle Aged , Nephrosis, Lipoid/diagnosis , Nephrosis, Lipoid/pathology , Plasma Exchange , Prednisolone/administration & dosage , Pulse Therapy, Drug , Renal Dialysis , Treatment OutcomeABSTRACT
A 61-year-old man with incomplete Behçet's disease was admitted to our hospital because of weakness and muscle pain in August 2001. The patient was diagnosed as having incomplete Behçet's disease because of oral aphtha, genital ulcer and uveitis. He had been administered with colchicine since December 1999. Cyclosporin was added in June 2000, because of repeated ocular attacks. In May 2001, he noticed weakness of proximal limb muscles. In three months, severe generalized muscle pain and numbness in his hands progressed. Laboratory findings showed elevation of muscular enzyme, serum creatinine, and hepatic transaminases. Electromyography and nerve conduction studies indicated myopathy and mild polyneuropathy, respectively. On diagnosis as drug induced neuromyopathy, colchicine administration was stopped. But, severe muscle pain continued. Thus, the cyclosporin dose was also reduced. Seven days later, weakness and muscle pain disappeared and laboratory findings markedly improved. These data indicate that the pathogenesis of neuromyopathy in this case was closely related to colchicine and cyclosporin. Caution will be needed in using these drugs for patients with Behçet's disease.
Subject(s)
Behcet Syndrome/drug therapy , Colchicine/administration & dosage , Colchicine/adverse effects , Cyclosporine/administration & dosage , Cyclosporine/adverse effects , Neuromuscular Diseases/chemically induced , Behcet Syndrome/complications , Drug Therapy, Combination , Humans , Male , Middle AgedABSTRACT
Calcium level is maintained by parathyroid hormone, 1alpha, 25 (OH)(2)D(3) and calcitonin in cooperation with bone, kidney and intestine. In the kidney activation of vitamin D and transcellular calcium transport in distal tubule regulate calcium concentlation. In the parathyroid glands calcium-sensing receptor sense extracellular calcium and secretes parathyroid hormone. It is received negative feedback from 1alpha, 25 (OH)(2)D(3) and phosphate.
