title: Mannose-binding lectin and the prognosis of fulminant hepatic failure caused by HBV infection.
abstract: OBJECTIVE
  The mannose-binding lectin (MBL) gene was reported to play an important role in determining the clinical outcome of persistent hepatitis B virus (HBV) infection. We investigated serum MBL concentrations and MBL gene mutations to determine whether they were related to the prognosis of patients with fulminant hepatic failure (FHF) caused by HBV infection.
  
  
  METHODS
  We investigated serum MBL concentrations and MBL gene mutations in 43 HBV-infected Japanese patients with FHF and 260 HBsAg-negative healthy controls. Serum MBL concentrations were measured by an enzyme-linked immunosorbent assay, and mutations in the MBL gene were analysed by nested PCR and direct DNA sequencing.
  
  
  RESULTS
  Only a mutation in codon 54 of the MBL gene was found. The frequency of this mutation in nonsurvivors (40%, 8/20) was higher than in survivors (13%, 3/23), and the difference was slightly significant (p = 0.043). The H allele frequency in survivors (70.5%, 31/44) was higher than in nonsurvivors (39.5%, 15/38) (p = 0.0048). Because of these factors the mean serum MBL concentration in survivors, 1.61 ,micro/ml (range 0.3-3.86), was significantly higher than in nonsurvivors, 0.79 microg/ml (range 0.04-1.51) (p < 0.0001). The likelihood ratio for nonsurvival was 0 for over 2.0 microg/ml, 0.67 for 1.0-2.0 microg/ml, and 2.24 for 0-1.0 microg/ml.
  
  
  CONCLUSIONS
  The mutation in codon 54 of the MBL gene tended to be higher in nonsurvivors than in survivors. The H allele frequency (high producing allele in H/Y) in survivors was higher than that in nonsurvivors. High levels of serum MBL correlated with the survival of patients with FHF due to HBV infection. Serum MBL may be useful as a predictive factor for the survival of patients with FHF caused by HBV.
authors.affiliation: Department of Internal Medicine, Japan Defense Forces Central Hospital, Tokyo, Japan. HZF02141@nifty.ne.jp
authors.forename: Yukiya
authors.initials: Y
authors.lastname: Hakozaki
authors.forename: Makoto
authors.initials: M
authors.lastname: Yoshiba
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Sekiyama
authors.forename: Eiji
authors.initials: E
authors.lastname: Seike
authors.forename: Junichi
authors.initials: J
authors.lastname: Iwamoto
authors.forename: Keiji
authors.initials: K
authors.lastname: Mitani
authors.forename: Masafumi
authors.initials: M
authors.lastname: Mine
authors.forename: Toshio
authors.initials: T
authors.lastname: Morizane
authors.forename: Katsuki
authors.initials: K
authors.lastname: Ohtani
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Wakamiya
mesh_terms: D000328:Adult; D002352:Carrier Proteins / Q000097:blood / Q000235:genetics*; D016022:Case-Control Studies; D037222:Collectins; D004247:DNA / Q000032:analysis; D004252:DNA Mutational Analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D019694:Hepatitis B, Chronic / Q000150:complications*; D006801:Humans; D017093:Liver Failure / Q000097:blood / Q000209:etiology* / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D016133:Polymerase Chain Reaction; D011379:Prognosis
chemical_list: D002352:Carrier Proteins; D037222:Collectins; D004247:DNA