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To the Editor—A 47-year-old man was admitted to our institution with severe acute hepatitis B (SAHB). The patient had suffered deep venous thrombosis of both lower extremities 2 years previously, and 2 mutations (C677T and A1298C) in the gene for methylenetetrahydrofolate reductase (MTHFR) were detected. Moreover, the family history was positive for thrombophilic states—his mother had thrombosis of the central retinal vein. The clinical course demonstrated a gradual worsening, with encephalopathy and progression to fulminant hepatic failure occurring during the first week after admission. The bilirubin level rose to 314 mmol/ L (reference range, 0–20 mmol/L), and the alanine aminotransferase level rose to 87.5 mkat/L (reference range, 0–0.8 mkat/L). Moreover, a significant deterioration in coagulation parameters was apparent: the prothrombin time was 21.3 s (reference range, 10.9–15.3 s), the international normalized ratio was 1.85 (reference range, 0.80–1.20), the D-dimer level was 1380.0 ng/mL (reference range, 0–250 ng/mL), and the antithrombin III (AT III) level was 31% (reference range, 81%–130%). The initial therapy was aimed at combining antiviral treatment with improvement of the coagulation disorder. The patient received low-molecular-weight heparin, intravenous vitamin K, and 4 transfusion units (1000 mL) of fresh frozen plasma followed by 2000 IU of AT III concentrate and 100 mg of lamivudine (Zeffix) daily for viral suppression. This therapeutic approach led to a prompt correction of coagulopathy and to favorable clinical, biochemical, and virological responses over the next several days. Seroconversion to antibody against hepatitis B e antigen was recorded on the 11th day of lamivudine therapy; 5 weeks later, the biochemical and coagulation test results were normal, and hepatitis B surface antigen was undetectable. Lamivudine therapy was stopped after the second negative hepatitis B surface antigen test result, which was obtained 1 month later. SAHB is an intermediate state between acute hepatitis B with a moderate course and progression to fulminant hepatic failure. The following criteria for the diagnosis of SAHB have been proposed by Schmilovitz-Weiss et al [1]: (1) the presence of hepatic encephalopathy, (2) a serum bilirubin level 10.0 mg/dL ( 170 mmol/L), and (3) an international normalized ratio 1.6. The combination of 2 or more of these criteria is considered to be diagnostic. According to Tillmann et al [2], only 1 criterion is required for the diagnosis of SAHB: a prothrombin time 36% of normal (or either an international normalized ratio 12.0 or an absolute prothrombin time 23 s). The disturbances in blood coagulation are sequelae of the involvement of the coagulation and fibrinolysis pathways. Hemorrhage complicating the course of SAHB is due to reduced synthesis of clotting factors and inhibitors of coagulation and fibrinolysis. Less is known about AT III levels during the course of SAHB; AT III supplementation is therefore debatable. However, we chose more aggressive anticoagulation therapy for our patient with extremely low AT III levels and a potential thrombophilic state (ie, MTHFR deficiency and a history of deep venous thrombosis), and this therapy led to a rapid improvement in clinical status and laboratory parameters. It is worth noting that the fulminant course of SAHB is associated with an exaggerated immune response, which might be modulated by the strong anti-inflammatory effects of AT III [3]. Thus, the close monitoring of AT III levels and the combination of antiviral agents and AT III concentrate in the treatment of SAHB could be beneficial.

Favorable Outcome of Severe Acute Hepatitis B in a Patient Treated with Antithrombin III and Antiviral Therapy