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CD 34 + cell therapy is safe and effective in slowing the decline of hepatic reserve function in patients with decompensated liver cirrhosis
Author(s) -
Nakamura Toru,
Torimura Takuji,
Iwamoto Hideki,
Kurogi Jyunichi,
Inoue Hiroto,
Hori Yukie,
Sumie Shuji,
Fukushima Nobuyoshi,
Sakata Masahiro,
Koga Hironori,
Abe Mitsuhiko,
Ikezono Yu,
Hashimoto Osamu,
Ueno Takato,
Oho Kazuhiko,
Okamura Takashi,
Okuda Seiya,
Kawamoto Atsuhiko,
Ii Masaaki,
Asahara Takayuki,
Sata Michio
Publication year - 2014
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12622
Subject(s) - medicine , cirrhosis , gastroenterology , hepatic stellate cell , liver function , liver transplantation , leukapheresis , hepatic fibrosis , transplantation , white blood cell , adverse effect , granulocyte colony stimulating factor , liver regeneration , chemotherapy , cd34 , stem cell , regeneration (biology) , biology , genetics , microbiology and biotechnology
Abstract Background and Aim Preclinical studies in rodent models of chronic liver fibrosis have shown that transplantation of peripheral blood ( PB ) C D 34 + cells leads to hepatic regeneration and a reduction of liver fibrosis by suppressing hepatic stellate cell activity and increasing matrix metalloproteinase activity. The aim of this study was to examine the safety and clinical efficacy of intrahepatic transplantation of autologous granulocyte colony‐stimulating factor ( G ‐ CSF )‐mobilized PB ‐ CD 34 + cells in patients with decompensated liver cirrhosis. Methods PB ‐ CD 34 + cells were isolated from G ‐ CSF ‐mobilized apheresis products. Ten patients were treated with G ‐ CSF ‐mobilized PB ‐ CD 34 + cells (treatment group) and seven patients were treated with standard medical therapy. For mobilization, patients in the treatment group received subcutaneous injections of 10 μg G ‐ CSF /kg/day for 5 days. The cells were then injected at three different doses (5 × 10 5 , 1 × 10 6 and 2 × 10 6 cells/kg) through the hepatic artery. Thereafter, all patients were followed up for 24 months. Results G ‐ CSF treatment and leukapheresis were well tolerated, and no serious adverse events were observed. Patients in the treatment group had a significant but transient splenomegaly. After 24 weeks, serum albumin was significantly increased in patients who had received middle or high doses of CD 34 + cells compared with baseline. Doppler ultrasound showed a significant increase in hepatic blood flow velocity and blood flow volume after CD 34 + cell therapy. The hepatic vein pressure gradient decreased in two patients who received high‐dose CD 34 + cells at week 16. Conclusions CD 34 + cell therapy is feasible, safe and effective in slowing the decline of hepatic reserve function.