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• W2083223442 abstract "Recently there has been a spate of reports of autoimmune haemolytic anaemia (AIHA) following treatment of chronic lymphocytic leukaemia (CLL) with fludarabine. We reported 12 cases among 52 patients treated by our group up to June 1995 (Myint et al, 1995) and a further series of 24 cases has been assembledd by culling the Spontaneous Reporting System of the Food and Drug Administration in America (Weiss et al, 1998). As more reports accumulate, the picture is becoming clearer. AIHA is unlikely to occur in patients with de novo CLL treated for the first time with fludarabine (Leporrier et al. 1997). However, in patients who have been treated with multiple courses of alkylating agents, exposure to fludarabine triggers AIHA in about 20% of cases. The haemolysis is usually severe, difficult to treat, and may prove fatal. Autoimmune thrombocytopenia (AITP) may also be triggered by fludarabine in a similar group of patients (Montillo et al, 1994). patients with AIHA following fludarabine are liable to relapse if they are re-exposed to fludarabine (Myint et al, 1995). or to the other purine analogues, cladribine (Hamblin et al, 1998) or pentostatin (Bryd et al. 1995). We report here two patients with lymphoid tumours whose fludarabine-triggered autoimmune disease relapsed after further exposure to conventional chemotherapy. Patient A presented in December 1989 at the age of 58 with stage C CLL and responded rapidly to treatment with intermittent chlorambucil and prednisolone. Over the next 8 years he remained well, but required up to six courses of intermittent chlorambucil each year to control his progressive disease. By the beginning of 1997 his disease was relapsing rapidly after completing courses of chlorambucil, and therefore between January and March we treated him with three 5 d courses of fludarabine 25 mg/m2. Direct antiglobulin test was negative at this time. His response to fludarabine was minor. After three courses his spleen had shrunk from 10 to 8 cm below the costal margin, his platelet count had risen from 48 to 110 times 109/l, his lymphocyte count had reduced from 43 times 109/l to 7times 109/l, but his Hb had declined from 12·7 g/dl to 7·7 g/dl. His direct antiglobulin test remained negative. 6 weeks after completing the third course he developed Pneumocystis carinii pneumonia which responded to treatment with high-dose co-trimoxazole. During this illness his direct antiglobulin test first became positive, although without overt haemolysis. He made a good recovery from the infection, but 19 weeks after the last course of fludarabine, while no longer receiving co-trimaxazole, he developed severe AIHA, and his Hb fell to 5·8 g/dl. he did not respond to treatment with steroids and splenectomy was undertakin, following which his Hb returned to normal. Three months after the splenectomy, when the WBC had risen to 200 times 109/l and with the patient otherwise well with a normal Hb and platelet count, he was treated with chlorambucil, 10 mg/d. After 9d treatment he was seen by his GP with a normal Hb. but the next day he was admitted in a moribund state with an Hb of 5· g/dl and evidence of severe haemolysis. Despite treatment with steroids his Hb fell further and he died. Patient B presented in November 1992 at the age of 68 with stage III follicle centre cell lymphoma. She responded well to treatment with six courses of mitozantrone, chlorambucil and prednisolone but relapsed with enlarged para-aortic glands in May 1994. She then received eight courses of mitozantrone, chlorambucil, vinblastine and prednisolone and achieved a complete remission. The disease relapsed in June 1997 with enlarged para-aortic glands and evidence of hydronephrosis. She was treated with 5 d courses of fludarabine. 25 mg/m2. Ten days after completing the second course of fludarabine she developed bruising and palatal petechiae and her platelet count had fallen to 8 times 109/l. The bone marrow showed increased numbers of megakaryocytes, and direct and indirect tests for platelet antibodies were positive. As there was no response to treatment with high-dose methyl prednisolone or intravenous immunoglobulin, she underwent an emergency splenectomy under platelet transfusion cover. Her platelet count rose to 303 times 109/l. In view of her persistent ureteric compression by paraaortic glands, she was retreated with mitozantrone, chlorambucil, prednisolone and vinblastine 9 weeks after her last course of lludarabine. 4 weeks after completing her second course she was readmitted with severe oral petechiae and widespread bruising. Her platelet count was 10 times 109/l. After a stormy course she eventually responded to vincristine 1 mg i.v., and her platelet count rose to 395 times 109/l. Although the way that purine analogues trigger autoimmune disease is unknown, we have suggested that the profound immune suppression induced by these drugs in CLL disturbs the normal T-cell control of autoreactive lymphocytes. Thus fludarabine exerts its greatest effect in patients with long-standing disease who have received much treatment. Lewis et al (1966) recognized more than 30 years ago that treatment with radiotherapy or alkylating agents could trigger active haemolysis in CLL, but this phenomenon is very rare and has seldom re-appeared in the literature. We have previously recognized the hazard of reintroducing purine analogues after an autoimmune episode (Myint et al, 1995) but had assumed that other forms of treatment would be safe. These cases demonstrate that other forms of chemotherapy may be equally dangerous. Patient B would appear to be the first patient with follicular lymphoma as opposed to CLL in whom an autoimmune complication has been triggered by fludarabine." @default.
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• W2083223442 title "IN PATIENTS WITH LYMPHOID TUMOURS RECOVERING FROM THE AUTOIMMUNE COMPLICATIONS OF FLUDARABINE, RELAPSE MAY BE TRIGGERED BY CONVENTIONAL CHEMOTHERAPY" @default.
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• W2083223442 doi "https://doi.org/10.1046/j.1365-2141.1998.0952e.x" @default.
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