@article {Dornbcr0420091816, author = {Isabel Dorn and Ulrich Budde and Michael C Fr{\"u}hwald and Monika P{\"o}ppelmann and Ulrike Nowak-G{\"o}ttl}, title = {Acquired von Willebrand syndrome in a 10-year-old girl with acute lymphoblastic leukaemia}, volume = {2009}, elocation-id = {bcr0420091816}, year = {2009}, doi = {10.1136/bcr.04.2009.1816}, publisher = {BMJ Publishing Group}, abstract = {Following diagnosis of acute lymphoblastic leukaemia (ALL) in a 10-year-old girl, routine coagulation screening including von Willebrand factor antigen (VWF:Ag), ristocetin cofactor activity (VWF:RCo) and factor VIIIC (FVIII:C) detected no pathological findings. After the first HR2' element of the high-risk group of the ALL-BFM 2000 protocol, the patient demonstrated extensive bleeding symptoms and acquired von Willebrand syndrome was diagnosed. VWF:Ag (13\%), VWF:RCo (13\%) and FVIII:C (27\%) were decreased. Multimer analysis showed a loss of large multimers and a loss in triplet structures. The observed pattern was thought to be typical for monoclonal IgG gammopathy; however, in this case, unexpectedly, biclonal IgM gammopathy (κ and λ) was detected. After treatment with intravenous immunoglobulin over 5 days, coagulation factors increased to normal levels. Although this effect was assumed to be at best only temporary, especially in a case of IgM gammopathy, no further bleeding symptoms have been observed. Trial registration number: M208}, URL = {https://casereports.bmj.com/content/2009/bcr.04.2009.1816}, eprint = {https://casereports.bmj.com/content}, journal = {Case Reports} }