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Massive ascites of donor T-cell origin in a patient with acute GVHD after a reduced-intensity allograft for CLL

Bone Marrow Transplantation volume 32, pages 961–963 (2003)Cite this article

It is not known if the features of GVHD following reduced-intensity conditioning (RIC) allograft differ from those following a conventional allograft. Ascites, pleural and pericardial effusions have been previously reported following myeloablative allografts. VOD, infections, cardiac insufficiency,1 postconditioning and G-CSF toxicity,2 and disease relapse3 can cause effusions after BMT. Extensive chronic GVHD (cGVHD) with laboratory features of autoimmunity has been found to be a cause of sterile effusions.4,5,6,7 In a review of 1905 patients, Seber et al8 evaluated seven cases presenting with large recurrent sterile pleural and/or pericardial effusions following myeloablative alloBMT and felt that these were possibly associated with acute/chronic GVHD and CMV infection. Silberstein et al9 recently described a patient with Hodgkin's disease who developed extensive cGVHD following an RIC allograft and DLI, and presented with polymyositis, polyserositis with large pericardial effusion and constrictive pericarditis.

We performed an RIC PBSCT from an HLA-identical brother in a 52-year-old woman with CLL Rai IV. Conditioning consisted of fludarabine, busulphan and ATG. Cyclosporin A (CsA) as GVHD prophylaxis was started on D−2. Engraftment was fast but lymphocytosis increased rapidly with 40 000 lymphocytes/mm3 in blood and 52% in the marrow on D+30. At that time, the patient had 45% donor CD3+ cells in the blood. The post-transplant period was uneventful except for skin acute GVHD (aGVHD) grade 2 from D+15 that was effectively treated with a short-course prednisolone. The patient was discharged from the hospital 1 month after transplantation without aGVHD and Karnovsky index of 100%. Owing to persistent CLL, CsA was withdrawn on D+63. On D+70, the patient developed grade 4 skin and grade 3 gut aGVHD. Combined immunosupression with CSA, steroids and an anti-IL2-receptor antibody was started with skin GVHD amelioration, but intestinal symptoms did not improve. On D+80, patient started complaining of abdominal distension. Ultrasound on D+84 confirmed the presence of ascites (approximately 2 l) with normal flow in the portal vein without hepatosplenomegaly. Bilirubin and transaminases were normal. Usual causes of ascites (VOD, cardiac, bacterial, tuberculosis, viral, fungal causes and significant hypoalbuminemia with concomitant fluid retention) were excluded by appropriate tests. Autoantibodies that are commonly present in cGVHD (antinuclear (ANA), antismooth muscle, antimitochondrial, anti-RO/SSA, anti-La/SSB, anti-SM, anti-Scl70, antithyroid, anti-LKM, Farr test) were all negative. During the next 5 months, the patient was drained of 1–4 l of ascitic fluid on five occasions (Table 1). The first paracentesis at +3 months demonstrated clear ascitic fluid with a protein level of 25 g/l and 96% of lymphocytes. The cellular composition of the ascitic fluid was similar in all aspirates: cytological and phenotypic analysis revealed high prevalence of T cells (86%) and no CLL. Donor origin of the ascitic T cells was confirmed by FISH (98% 46XY). Interestingly, at that time, blood and marrow showed heavy infiltration with monoclonal CLL B cells. In spite of significant residual disease, the amount of donor chimaerism was on the rise in the blood (48% of all cells and 94% of CD3+ cells).

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  1. Institut Paoli-Calmettes, Marseille, France

    V Ivanov, C Faucher, K Bilger, N Vey, D Sainty, B Calmels, C Chabannon, M Lafage-Pochitaloff, M J Mozziconacci, M Mohty, M A Chrestian & D Blaise

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  1. V Ivanov
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Ivanov, V., Faucher, C., Bilger, K. et al. Massive ascites of donor T-cell origin in a patient with acute GVHD after a reduced-intensity allograft for CLL. Bone Marrow Transplant 32, 961–963 (2003). https://doi.org/10.1038/sj.bmt.1704242

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