Was prolonged to 49 (PT-INR 1.

55). In addition to increased T-Bil level of

Was prolonged to 49 (PT-INR 1.55). In addition to increased T-Bil level of 6.9 mg/dL, serum ALT level increased to 131 IU/L. Serum HGF and AFP levels were 1.94 and 22.9 ng/ mL, respectively, and liver volume was 595 mL. Following observation of general condition for 24 hours, treatment with rh-HGF was initiated, and the protocol therapy was continued for 14 days without any severe adverse events. Hepatic encephalopathy disappeared after plasma exchange (PE) on day 2; consciousness level was not impaired throughout the study period. Intravenous rh-HGF reduced systolic BP. The patients with lucidity, however, did not complain any symptom. Although prednisolone (PSL) was administered to reduce ALT, blood biochemical findings and patient condition were stable throughout the 2-Bromo-1,3-difluoro-4-nitrobenzene study period. After the completion of the study, 4-((2-Hydroxyethyl)(methyl)amino)benzaldehyde biochemical findings were gradually improved, and, finally, the patient survived. Additional file 3: Clinical course of patient 3, with LOHF, who died within the observation period. Sixty four-year-old Japanese woman with LOHF of undetermined etiology suffered from advanced hepatic encephalopathy (HE). She presented with platelet count of 9.2 ?104/L, PT of 37 (PT-INR 1.78), T-Bil level of 11.7 mg/dL, ALT level of 260 IU/L, and serum albumin level of 2.9 g/dL. Serum HGF and AFP levels PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8086425 were 1.07 and 3.9 ng/mL, respectively, and liver volume was 640 mL. Because of oliguria (392 mL/day), protocol therapy was discontinued on day 13, resulting in 12-day rh-HGF dosing. Additionally, PSL was administered to reduce serum ALT, and plasma exchange (PE) and/or continuous hemodiafiltration (CHDF) was performed throughout the study period. Serum ALT levels reduced immediately, and hepatic encephalopathy was transiently improved during rh-HGF dosing period. However, hepatic encephalopathy, prolonged PT, and an increase in T-Bil progressed during the observation period, and the patient died during the observation period (28 days after the onset of hepatic encephalopathy). Additional file 4: Clinical course of patient 4, with FHSA caused by a drug, who survived. Forty-year-old Japanese man with FHSA, which was caused by a supplement containing coenzyme Q-10, showed platelet count of 7.0 ?104/L, PT of 43 (PT-INR 1.62), T-Bil level of 27.6 mf/dL, ALT level of 253 IU/L, and serum albumin level of 2.9 g/dL, but not hepatic encephalopathy (HE), which was temporarily observed before enrollment. Serum HGF and AFP levels were 1.88 and 39.7 ng/mL, respectively, and liver volume was PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 1110 mL. Administration of rh-HGF was continued for 14 days, and PSL was administered to reduce ALT throughout the study period. An increase in T-Bil and prolonged PT was modestly improved during rh-HGF dosing, followed by further improvement after the observation period. Ultimately, the patient survived. PE; plasma exchange. Additional file 5: Serum levels of TGF-b were not affected by rhHGF dosing. Serum TGF-b concentrations before and after the rh-HGF dosing period were determined by ELISA. Although patient 2 exhibited an increase in serum TGF-b after 14-day rh-HGF administration, there was no significant difference in serum levels of TGF-b (mean ?SE: 230.4 ?21.0 vs 266.4 ?68.1 pg/ml, p = 0.52).for the data from a nationwide survey of FH and LOHF. This study was supported by funds from the Ministry of Education, Culture, Sports, Science and Technology of Japan. Author details HGF Hepatic Regeneration Therapy Project, 3-b]pyrazine Department of Experimental Therapeutics, Transl.