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Anti‐thymocyte globulin treatment of marrow aplasia associated with paroxysmal nocturnal haemoglobinuria (PNH) resulted in haematological improvement due to an expansion of the PNH clone
Author(s) -
Cheung W. C.,
Lam C. C. K.,
Kwong Y. L.
Publication year - 2003
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2003.04046.x
Subject(s) - clone (java method) , aplastic anemia , bone marrow failure , pancytopenia , immunology , anti thymocyte globulin , bone marrow aplasia , haematopoiesis , medicine , paroxysmal nocturnal hemoglobinuria , globulin , biology , bone marrow , stem cell , gene , genetics
Summary. A patient with aplastic anaemia developed paroxysmal nocturnal haemoglobinuria (PNH) 4 years after diagnosis, with an ensuing haematopoietic improvement. The PNH clone subsequently declined, leading to pancytopenia again. Anti‐thymocyte globulin had to be administered 14 years later, which resulted in haematopoietic improvement once more. Flow cytometric analysis showed that this was attributable to expansion of the PNH clone, owing probably to alleviation of its suppression by immune‐mediated mechanisms. PIG‐A gene analysis showed that the same PNH clone had waned and waxed in the clinical course. Our results suggest that the PNH clone might rarely be an immune target as well.

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