Idiopathic pulmonary haemosiderosis treated by plasmapheresis.

A 52-year-old woman was admitted to our hospital with severe haemoptysis and dyspnoea. She had had repeated haemoptysis starting 18 months before admission and for the last eight months this had cccurred almost daily. Fibreoptic bronchoscopy and a bronchogram had been normal. Several sputa samples were negative for acid-fast bacilli. On admission physical examination showed tachycardia, tachypncea, and normal arterial and central venous pressure. Bilateral diffuse crackles were present. The heart sounds were normal. Chest radiographs showed a moderate alveolar infiltrate at both lung bases. The white cell count was 14000, haemoglobin 8-8 g, haematocrit 34%, MCH 22 pg, MCV 81 ,um3, MCHC 26-20%, serum iron 82 gg, reticulocytes 75000, ESR 65 mm in one hour, total bilirubin 1-2 mg, LDH 581 ,, total protein and electrophoresis, urea and creatinine were normal. ANA, LE cells, rheumatoid factor, Coombs' test and HBsA antigen were negative. There was no proteinuria and the urine sediment was normal. Arterial Pao9 was 55 mmHg on breathing 35% oxygen. Forty-eight hours after admission the patient's condition worsened, dyspnoea and haemoptysis increased, hypoxia was severe and alveolar infiltration becarre widespread. Treatment with antituberculous drugs, methylprednisone 1 g, and azathioprine ICO mg, daily was started. On the sixth hospital day a transbronchial lung biopsy was performed. This showed pulmonary haemorrhage but no infection, vasculitis, necrosis, granulomata, or deposit of immunoglobulins as observed by immunofluorescence. The next day methylprednisolone was reduced to 100