Goodpasture’s Syndrome: A Case Presentation

Dr. Murat Morgül, Yedikule Chest Diseases Hospital and Chest Surgery Center, TR-34760 Zeytinburnu-Istanbul (Turkey) Dear Sir, Goodpasture’s syndrome is a disease which is characterized by an increase in anti-GBM (glomerular basement membrane) antibodies, pulmonary hemorrhage, and glomerulonephritis [1]. We have reached the conclusion that our patient is suffering from this particular disease because he had a high concentration of anti-GBM antibodies in his serum, presence of hemoptysis and a pathology with crescentic glomerulonephritis features. We have used corticosteroids, immunosup-pressives, plasmapheresis, anticoagulants, and hemodialysis, as derived from a recent study on this rare disease. The 24-year-old male patient, who had no complaints at all up until 2 months before admission when he developed hemoptysis together with a color change of his urine, getting reddish. He was hospitalized immediately. Physical examination revealed blood pressure 120/80 mm Hg and pulse 80/min. During the clinical observation the blood pressure had been found to be 210/120 mm Hg, so nifedipine was administered orally. During the systematic examination of the patient no particular features had been found except for the following: facial edema, pretibial edema and painful hepatomegaly (4 cm). His complaints on hemoptysis had continued after he was hospitalized. Anti-GBM antibodies (1,280 U) normalized to 0-10 U after treatment. There were no special features on chest roentgenography. Crescentic glomerulonephritis and sclerosis ( > 80% of the glomeruli) was found on kidney biopsy and light microscopy. The above-mentioned clinical and laboratory findings were indicative of Goodpasture’s syndrome, and he was treated with corticosteroids, immunosuppressives, plasmapheresis, anticoagulants and hemodialysis. Goodpasture’s syndrome had been defined as a disease with presence of anti-GBM antibodies or an accumulation of im-munoglobin deposits in the glomeruli and/or alveoli [2]. Radioimmunoassay is the most sensitive and specific method in the exploration of anti-GBM antibodies in the serum [1]. Immunofluorescent microscopy may be used for detecting antiGBM antibodies in the tissue and for the diagnosis of the disease it is important to prove the presence of linear im-munoglobulins [3]. Since the 70 s considerable extension of the survival rate had been achieved with high doses of corticosteroids, pulse treatment with cyclophosphamide, and plasmapheresis [4-6]. Renal transplantation may be possible if the