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diffuse leukoaraiosis. Initial hematological and biochemical values were normal, including coagulation tests. Fluid intake was reduced and intravenous antihypertensive medication was introduced (nicardipine) in association with omeprazole, polyvitamin and aminopenicillin for a pulmonary infection due to swallowing dysfunction. This ICH was considered as related to the untreated severe hypertension. Two weeks later, after an initial partial clinical recovery, marked neurological deterioration occurred, leading to coma associated with a right hemiparesis associated with the preexisting left hemiplegia. At the same time, gastrointestinal bleeding appeared. Blood pressure ranged between 150/70 and 170/90 mm Hg. Laboratory findings showed prolonged prothrombin time (PT ! 10%) and activated partial thromboplastin time (aPTT 1 120 s; control 35 s), both normal on admission 14 days before. PT and aPTT were prolonged on a 1: 1 mixture of patient and normal plasma, suggesting the presence of an acquired coagulation inhibitor. The factor V activity level was undetectable ( ! 3%), while the activity levels of the other clotting factors were within the normal range, as well as the fibrinogen level, thrombin time and platelet count. Fibrin degradation products were undetectable. These abnormalities were related to a specific factor V inhibitor titrating 13 Bethesda Dear Sir, Spontaneous intracerebral hemorrhages (ICH) are frequent and associated with high morbidity and mortality [1, 2] . Classical risk factors for ICH are hypertension, age, male sex and high alcohol intake [1] . Secondary ICH worsening occurs in up to 20–40% of patients [2–5] . Progression of mass effect is mainly described at 2 time points: within the 2 first days associated with extension of the hematoma, and during the second and third weeks associated with progression of the edema [2–5] . We report herein a late clinical deterioration following ICH, due to the development of a severe acquired coagulation abnormal ity.

Late and Fatal Deterioration of an Intracerebral Hemorrhage Attributable to the Onset of a High Titer of Acquired Factor V Inhibitor