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Inicio Annals of Hepatology O-21 SOLUBLE CD163 PERFORMANCE AS A NON-INVASIVE BIOMARKER OF DIFFERENT LIVER CO...
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Vol. 24. Issue S1.
Abstracts of the 2021 Annual meeting of the ALEH (Asociación Latinoamericana para el Estudio del Hígado)
(September 2021)
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Vol. 24. Issue S1.
Abstracts of the 2021 Annual meeting of the ALEH (Asociación Latinoamericana para el Estudio del Hígado)
(September 2021)
Open Access
O-21 SOLUBLE CD163 PERFORMANCE AS A NON-INVASIVE BIOMARKER OF DIFFERENT LIVER CONDITIONS
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Cairoli Victoria1, Casciato Paola Cecilia2, Giadans Cecilia Graciela1, Ameigeiras Beatriz3, De Matteo Elena1, Preciado Maria Victoria1,#, Valva Pamela1,#
1 Multidisciplinary Institute for Investigation in Pediatric Pathologies (IMIPP), CONICET-GCBA, Laboratory of Molecular Biology, Pathology Division, Ricardo Gutiérrez Children's Hospital, Gallo 1330, CABA, C1425, Argentina
2 Liver Unit, Italian's Hospital of Buenos Aires, Pres. Tte. Gral. Juan Domingo Perón 4190, CABA, C1199 ABH, Argentina
3 Liver Unit, Ramos Mejía Hospital, Gral. Urquiza 609, CABA, CP1221, Argentina
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Vol. 24. Issue S1

Abstracts of the 2021 Annual meeting of the ALEH (Asociación Latinoamericana para el Estudio del Hígado)

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Introduction

Development of noninvasive tests to predict liver injury represents a current goal. Soluble CD163 (sCD163) is a specific plasma biomarker of macrophage activation with promising clinical relevance in estimating damage severity and predicting the outcome in different liver conditions.

Aim

To evaluate sCD163 performance as a non-invasive marker of liver damage.

Materials and Methods

sCD163 was quantified by enzyme-linked-immunosorbent assay in plasma from 123 patients (57 HCV, 20 HCV/HIV, 10 HBV, 36 MAFLD) obtained at time of liver biopsy. 20 healthy donors were included as controls. sCD163 values were compared among disease conditions and related to histological parameters of liver damage. Diagnostic performance was assessed by the area under the receiver operating characteristic curves (AUROC).

Results

Patients´ sCD163 levels [0.579g/L (0.034 -3.596)] were higher than controls´ [0.221g/L (0.116-0.549)] (p<0.0001, Mann-Whitney). However, in a detailed analysis according to disease etiology, only viral conditions showed significantly higher sCD163 levels [HCV+ 0.7520g/L (0.168-3.468), p<0.0001; HCV+/HIV+ 0.964g/L (0.345-3.596), p<0.0001; HBV+ 0.526g/L (0.199-0.802), p=0.0375, Dunn's-multiple-comparisons]. MAFLD patients displayed similar sCD163 levels to the control group [0.345g/L (0.0338-1.804)]. HCV mono- and HIV-coinfected patients shared the highest sCD163 levels. In relation to liver injury, HCV+ and HCV+/HIV+ patients specifically displayed a profile with higher sCD163 levels associated with more severe hepatitis. Remarkably, just in HCV+/HIV+ cases these differences were significant (p=0.0097 Mann-Whitney) and the AUROC analysis demonstrated a good performance in predicting hepatitis severity [AUROC=0.875; cutoff: 0.672g/L (91.67% sensitivity, 83.33% specificity)]. Concerning fibrosis, only HCV+ and HCV+/HIV+ patients with significant fibrosis displayed a profile with high sCD163 level; however, the AUROC analysis showed good performance just for HCV+/HIV+ patients [AUROC=0.825); cutoff: 0.9640g/L (100% sensitivity, 60% specificity)].

Conclusion

Plasmatic sCD163 is elevated in patients with several liver conditions but it can be particularly used as a marker of liver inflammation and fibrosis in HCV/HIV co-infected patients.

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‘These two authors equally contributed to this work’

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