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F AMILIAL amyloidotic polyneuropathy (FAP) ATTRMet 30 is the result of an inherited disorder of transthyretin metabolism. Both amyloid transthyretin and normal transthyretin are produced in the liver and the transplantation is a successful therapy for this disease and is performed in spite of the completely normal liver function of these patients.1 A high incidence of hyperfibrinolysis was reported during liver transplantation but these studies were performed in patients with previous liver insufficiency and the relative role of preoperative factors (liver disease, coagulation disorders, increased fibrinolytic activity) and intraoperative factors (surgical trauma, hypotension, and graft reperfusion) is not clearly established.2,3 As far as we know, the incidence and the severity of hyperfibrinolysis during liver transplantation in patients without preoperative liver insufficiency has not yet been studied. The aim of this study was to evaluate the incidence of hyperfibrinolysis during liver transplantation in FAP and to correlate these findings with several perioperative factors. PATIENTSGroup I included 75 FAP ATTR Met 30 recipients of first liver transplants during a 6-year period, 41 male and 34 female, with age of 35.1 Ϯ 7.2 years, body mass index (BMI) of 20.7 Ϯ 4.1 kg/m 2 , disease duration (since the first symptom) of 4.4 Ϯ 2.4 years and neurologic score of 32.7 Ϯ 11.3 in the scale of Macedo et al. 4 Every patient in this group received prophylactic antifibrinolytic therapy. For a control, 102 patients with liver diseases transplanted during the same period were used as follows: 21 patients that did not receive prophylactic antifibrinolytic therapy were considered as group IIA; 81 patients that received high-dose aprotinin during all the surgical procedure were considered as group IIB. Not different concerning sex, both group IIA (43.2 Ϯ 13.8 years, P Ͻ .01) and group IIB (43.2 Ϯ 12.5 years, P Ͻ .001) were older than group I. Group I patients had normal liver tests: AST, 26.0 Ϯ 12.2 U/L; ALT, 25.3 Ϯ 15.7 U/L; total bilirubin 0.8 Ϯ 0.4 mg/dL; direct bilirubin 0.1 Ϯ 0.1 mg/dL. The same was not observed in the other groups: AST was 124 Ϯ 228 U/L in group IIA (P ϭ ns) and 191 Ϯ 467 U/L in group IIB (P Ͻ .01); ALT, 100 Ϯ 156 U/L in group IIA (P ϭ ns) and 169 Ϯ 419 U/L in group IIB (P Ͻ .01); total bilirubin 5.3 Ϯ 9.9 mg/dL in group IIA (P ϭ ns) and 10.1 Ϯ 12.5 mg/dL in group IIB (P Ͻ .001); direct bilirubin 3.0 Ϯ 6.5 mg/dL in group IIA (P ϭ ns) and 5.1 Ϯ 7.7 mg/dL in group IIB (P Ͻ .001). The values of P account comparisons with group I. METHODAnesthesia, monitoring, circulatory, and coagulation goals and treatments were the same in the three groups. Thrombelastograms (TEG) were retrospectively evaluated in a blind fashion by two independent observers. As standardized, one intraoperative value of a60/ma (whole blood clot lysis index) less than 0.8 was considered a signal of hyperfibrinolysis. Before the evaluation of any TEG of this study, we decided to consider one intraoperative value of F (whole blood clot l...

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