We report the case of a 59-years-old woman who presented a metastatic breast cancer relapse and a known congenital hypofibrinogenemia . On admission the patient presented with subcutaneous hematomas and the biologic work-up put into evidence an undetectable level of fibrinogen, a slightly reduced level of FV, Alpha-2-antiplasmin, Plasminogen Activator Inhibitor (PAI1) and a strongly prolonged Reptilase time. A grade III thrombocytopenia was also present. This constellation of biologic findings suggested the presence of a hyperfibrinolytic environment. The patient was therefore started on tranexamic acid on continuous infusion. Because of the spurious laboratory frame, could have been also consistent with a Disseminated Intravascular Coagulation with hyperfibrinolytic phenotype, an Unfractioned Heparin Infusion was introduced at the second day of treatment. Over the following weeks an improvement of the lab tests occurred and no bleeding appeared. Despite the introduction of a chemotherapeutic regimen for the underlying disease, the platelets count increased and the patient could be discharged on oral tranexamic acid.
With this brief case report we want to highlight the importance to recognize a hyperfibrinolytic phenotype in order to choose the adequate treatment and to minimize the bleeding as well the thrombotic risks. Indeed, although hyperfibrinolysis remains a quite rare manifestation apart from coagulation impairment of traumatic origin, it can be triggered by some conditions such as M3 Acute Myeloid Leukemia or some Adenocarcinomas. It´s intriguing to think that in our case the presence of a congenital hypofibrinogenemia could have played a role in the setting of the hyperfibrinolysis.
