Phenotypic alterations of regulatory T cells in autoimmune hepatitis: Causal or associated with treatment and remission?
Phenotypic alterations of regulatory T cells in autoimmune hepatitis: Causal or associated with treatment and remission?
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DOI:
10.1002/hep.27301
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发表时间:
2015-02
期刊:
影响因子:
13.5
通讯作者:
M. Sebode;M. Peiseler;C. Weiler-Normann;C. Schramm;A. Lohse;J. Herkel
中科院分区:
文献类型:
--
作者:
M. Sebode;M. Peiseler;C. Weiler-Normann;C. Schramm;A. Lohse;J. Herkel
for disease progression in chronic viral hepatitis. However, this is in contrast with the findings of Kuniholm et al. In a recent study from our group, HCV patients with cirrhosis, as assessed by transient elastography, had higher levels of sCD163 and sCD206 (the shed mannose receptor), compared to those with no/mild fibrosis. However, sCD206 was inferior to sCD163 in cirrhosis prediction, supporting the notion that sCD163 may be the best macrophagespecific biomarker in chronic viral hepatitis. In our published report, liver biopsy data were available for all patients and we focused on the relationship between sCD163 and the histological scores for inflammation and fibrosis. For this reason, the associations between sCD163 and APRI/FIB-4 were omitted, but we are pleased to present them here. Consistent with the data by Kuniholm et al., sCD163 (logarithmically transformed) was strongly associated with APRI (r 5 0.64; P< 0.001) and FIB-4 (r 5 0.59; P< 0.001) in our 551 HCV patients. In the 203 HBV patients, sCD163 was associated with APRI (r 5 0.51; P< 0.001) and showed a trend toward association with FIB-4 (r 5 0.14; P 5 0.09). To investigate the adjusted relationship between sCD163 and fibrosis, we performed multiple ordered logistic regression analysis with the fibrosis score as the dependent variable and sCD163, APRI, and FIB-4 (all logarithmically transformed) as the explanatory. In this model, we observed a clear significant association between sCD163 and the fibrosis score after adjustment for APRI and FIB-4, both in patients with HCV and HBV infection (Table 1). Taken together, the data indicate that sCD163 correlates with APRI and FIB-4, but possesses the capability for fibrosis prediction beyond both models, and this is further illustrated by the very good performance of sCD163-based fibrosis scores, particularly in HCV patients. Finally, we entirely agree with Kuniholm et al. that longitudinal studies of sCD163 and other macrophage markers, preferably under antiviral treatment with repeated liver biopsies, are needed to further elucidate the role of macrophages and the prognostic value of macrophage markers in chronic viral hepatitis. KONSTANTIN KAZANKOV, M.D. HOLGER JON MØLLER, M.D., PH.D., D.Sc. BO MARTIN BIBBY, M.Sc., PH.D. HENDRIK VILSTRUP, M.D., D.Sc., FRCP, FEBGH JACOB GEORGE, MBBS, Ph.D., FRACP HENNING GRØNBÆK, M.D., PH.D. Department of Hepatology and Gastroenterology Aarhus University Hospital Aarhus, Denmark Department of Clinical Biochemistry Aarhus University Hospital Aarhus, Denmark Department of Biostatistics Aarhus University Aarhus, Denmark The Storr Liver Unit University of Sydney and Westmead Hospital Westmead, Australia