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infection with varicella-zoster virus in a patient with acquired hemophilia. A 16-year-old male presented with a severe
hemorrhagic varicella that resulted in an acquired hemophilia. Within 24 hours of onset of the disease a severe hemophilicthrombocytopenia developed which was rapidly complicated by multiple cerebral infarctions. Following a cytoreductive
treatment with cytostatic steroids, the course of the disease was followed by serial measurements of von Willebrand factor
activity, FVIII antigen, and FVIII ristocetin cofactor assay. A severe pathological decrease in FVIII antigen was documented
repeatedly, concomitantly with the absence of FVIII activity. This patient is presented to emphasize the different clinicalcourses during the course of the varicella infection: severe thrombocytopenia rapidly progressing to intravascular coagulopathyand cerebral infarction vs a mild course with no thrombocytopenia, a transient increase in FVIII antigen, but a rapid decrease in
FVIII activity and bleeding without thrombocytopenia. We suggest, that acquired hemophilia in childhood patients is not a rarephenomenon. The prognosis of varicella-induced acquired hemophilia is determined by the intensity of the clinical course of thevarice

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