Re. Re. Dabigatran overdose: a case report of acute hepatitis. Extracorporeal treatment and review of the literature

Excerpt

In 2017, we published a case of dabigatran overdose in a patient affected by heart and renal failure who developed acute hepatitis and coma [1]. Recently, we have read with interest the comments of Caruso et al. [2], who raised some concerns on the potential dabigatran toxicity in our patient. In particular, the authors asked for information on several points: the first of these was, “Were the serum direct thrombin inhibitor levels available prior to starting CVVHD?” As described in the manuscript, 24 h after admission but before CVVHDF treatment, the dabigatran concentration was measured at trough, and showed a very high plasmatic concentration (989 ng/ml). A critical dabigatran overdose was confirmed. The second question regarded whether the ammonia level was documented. The serum ammonia level was carried out at hospital admission and was within the normal range [46 μg/dl (n.r. 31–123)]. The patient had no history of hepatic disease and its laboratory tests, a few months prior to admission at our Internal Medicine ward, were normal. Lastly, Caryuso inquired whether we considered sepsis as a cause of hemodynamic instability, renal dysfunction and hepatic injury. We considered sepsis as a possible diagnosis, but we did not find clinical or laboratory evidence of infection. In particular, the procalcitonin [0.1 ng/ml (n.r. < 0.5)], fibrinogen [216 mg/dl (150–450)] and WBC levels [11.1 × 10³/mm³ (4–11.2)] were all normal. Serological investigations for HBV, HCV, HSV, VZV, EBV and CMV were negative. Moreover, during the patient’s admission in the Intensive Care Unit, urine and bronchial secretions cultures were performed, but these too were negative. Thus, we were confident in ruling out sepsis as a cause of organ dysfunction, following Singer et al. [3]. …