Raised serum ferritin predicts non-response to interferon and ribavirin treatment in patients with chronic hepatitis C infection

被引:65
作者
Distante, S [1 ]
Bjoro, K
Hellum, KB
Myrvang, B
Berg, JP
Skaug, K
Raknerud, N
Bell, H
机构
[1] Aker Univ Hosp, Dept Med, Hepatol Unit, N-0514 Oslo, Norway
[2] Natl Hosp, Dept Med, Oslo, Norway
[3] Cent Hosp, Dept Med, Akershus, Norway
[4] Ullevaal Univ Hosp, Dept Infect Dis, Oslo, Norway
[5] Aker Univ Hosp, Hormone Lab, Oslo, Norway
[6] Natl Inst Publ Hlth, Dept Virol, Oslo, Norway
[7] Aker Univ Hosp, Dept Pathol, Oslo, Norway
来源
LIVER | 2002年 / 22卷 / 03期
关键词
ferritin; hepatitis C virus; interferon treatment; ribavirin treatment; hemochromatosis; HFE-C282Y gene mutation;
D O I
10.1046/j.0106-9543.2002.01672.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/Aim: Previous studies have indicated that response to interferon therapy is inversely proportional to the amount of body iron stores. We have studied the relationship between serum ferritin, transferrin saturation, liver iron, presence of HFE-C282Y gene mutation and response to treatment in patients with chronic hepatitis C infection. Methods: Two hundred and fifty-six naive, HCV-RNA positive patients (60% males, median age 38 years, range 21-70) were treated with interferon and ribavirin for 6 months. Iron indices and the presence of the C282Y mutation were measured. In 242 (94%) patients iron deposition were determined by Perls staining method. Patients with negative HCV-RNA at 6 months after the end of treatment were defined as sustained viral responders. Results: Non-responders (n = 127) had significantly higher median s-ferritin values compared with sustained viral responders (130 mug/L vs. 75 mug/L P < 0.001). There was no difference in transferrin saturation among the two response groups. Only 23% (4/7) of patients with Perls grade 1 in liver biopsies responded to treatment vs. 54% (122/225) patients without iron deposition (P = 0.02), however, 10/13-non-responders had HCV genotype one. Two patients (0.8%) were homozygous for the C282Y mutation, 36 patients were heterozygous (14%). Among mutation carriers 26/38 achieved sustained response compared with 102/216 non-carriers (68% vs. 48%, P = 0.02). In a multivariate analysis s-ferritin (P = 0.030) and C282Y carrier status (P = 0.012) remained independent predict of sustained response. Conclusions: Raised s-ferritin values predicate non-response to interferon-ribavirin therapy in hepatitis C patients. Response rate in C282Y mutation carriers seems greater than in non-carriers.
引用
收藏
页码:269 / 275
页数:7
相关论文
共 35 条
[21]  
Lechmann M, 1999, EUR J CLIN INVEST, V29, P337
[22]  
LEGGETT BA, 1990, CLIN CHEM, V36, P1350
[23]   Are haemochromatosis mutations related to the severity of liver disease in hepatitis C virus infection? [J].
Martinelli, ALC ;
Franco, RF ;
Villanova, MG ;
Figueiredo, JFC ;
Secaf, M ;
Tavella, MH ;
Ramalho, LNZ ;
Zucoloto, S ;
Zago, MA .
ACTA HAEMATOLOGICA, 1999, 102 (03) :152-156
[24]  
Ohnishi K, 1996, AM J GASTROENTEROL, V91, P1374
[25]   HEPATIC IRON CONCENTRATION AS A PREDICTOR OF RESPONSE TO INTERFERON-ALFA THERAPY IN CHRONIC HEPATITIS-C [J].
OLYNYK, JK ;
REDDY, KR ;
DIBISCEGLIE, AM ;
JEFFERS, LJ ;
PARKER, TI ;
RADICK, JL ;
SCHIFF, ER ;
BACON, BR .
GASTROENTEROLOGY, 1995, 108 (04) :1104-1109
[26]  
PEREZ R, 1993, GUT, V34, P139
[27]   LIVER-DAMAGE IN ITALIAN PATIENTS WITH HEREDITARY HEMOCHROMATOSIS IS HIGHLY INFLUENCED BY HEPATITIS-B AND HEPATITIS-C VIRUS-INFECTION [J].
PIPERNO, A ;
FARGION, S ;
DALBA, R ;
ROFFI, L ;
FRACANZANI, AL ;
VECCHI, L ;
FAILLA, M ;
FIORELLI, G .
JOURNAL OF HEPATOLOGY, 1992, 16 (03) :364-368
[28]  
Piperno A, 1995, EUR J GASTROEN HEPAT, V7, P1203
[29]  
Riggio O, 1997, AM J GASTROENTEROL, V92, P1298
[30]   Heterozygosity for hereditary hemochromatosis is associated with more fibrosis in chronic hepatitis C [J].
Smith, BC ;
Grove, J ;
Guzail, MA ;
Day, CP ;
Daly, AK ;
Burt, AD ;
Bassendine, MF .
HEPATOLOGY, 1998, 27 (06) :1695-1699