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Tom Pettersson, Fourth Department of Medicine, Helsinki University Central Hospital, U. Unioninkatu 38, SF-00170 Helsinki (Finland) Auto-immune haemolytic anaemia and auto-immune thrombocytopenia are well-known manifestations of systemic lupus erythematosus (SLE), but occur much less often in the other connective tissue diseases. We report the case of a patient with scleroderma, who developed severe auto-immune thrombocytopenia, leucopenia and, later, fulminant auto-immune haemolytic anaemia. In 1972, a 16-year-old man presented with polyar-thralgia and Raynaud’s phenomenon. Over the time he developed thinned lips and a narrowed mouth, ul-cerations of the fingertips and atrophy of the soft tissue of his fingers, which became fixed in a claw-like position. These findings together with difficulties in swallowing, and facial teleangiectasia led to the diagnosis of scleroderma. Laboratory investigations revealed rheumatoid factor, anti-nuclear antibodies up to 1/10,000 with speckled pattern and anti-RNP antibodies, but no anti-Scl-70 antibodies, no antiSm antibodies and no increased levels of anti-dsDNA antibodies. The patient was treated with prednisone in small doses. In 1981, the patient was admitted because of spontaneous bleeding and petechiae. He had a very low platelet count (2 × 109/1), no anaemia, but a moderate leucopenia, with a normal differential count. A bone marrow aspirate contained an increased amount of megakaryocytes. Platelet antibodies were detectable in the patient’s serum with an indirect Coombs’ test. Treatment with 40 mg of prednisone daily resulted in normalization of the platelet count within a month. Two years later, the patient presented with fever, jaundice, fatigue and dark urine. Laboratory examination showed a haemoglobin value of 73 g/l, reticu-locytosis, neutrophilic leucocytosis and thrombocyto-sis. A direct Coombs’ test was positive with IgG, IgA, IgM, C3 and C4 on the surface of the erythrocytes. The plasma haemoglobin concentration increased to 2,033 mg/l (reference range < 50 mg/l). A test for cold agglutinins was negative. A bone marrow aspirate showed erythroid hyperplasia. Prednisone treatment (80 mg/day) and methylprednisolone pulse therapy (1 g intravenously for 3 subsequent days) had no effect on the haemolysis. On days 7–11 of hospitalization, intravenous immunoglobulin infusions (San-doglobulin® 0.4 g/kg body weight/day) were given. The patient’s need for erythrocyte transfusions, however, continued, his condition deteriorated and he became oliguric. In this situation, plasmapheresis treatment (performed with a membrane filtration technique) was started on day 9 of hospitalization. After the first plasmapheresis, the haemoglobin value stabilized, and began to rise 2 weeks later, after five plas-maphereses and an