# Evaluation of soluble suppression of tumorigenicity 2 (sST2) as serum marker for liver fibrosis

**Authors:** Florian F. Hildenbrand, Barbara Illi, Stefanie von Felten, Jacqueline Bachofner, Joanna Gawinecka, Arnold von Eckardstein, Beat Müllhaupt, Joachim C. Mertens, Sena Blümel

PMC · DOI: 10.1186/s12876-023-03116-4 · BMC Gastroenterology · 2024-01-30

## TL;DR

This study evaluates sST2 as a blood marker for liver fibrosis in patients treated for hepatitis C, finding it useful alone and in combination with other tests.

## Contribution

The study demonstrates that sST2 is a stable serum marker for liver fibrosis, unaffected by inflammation and useful in combination with existing tests.

## Key findings

- Median sST2 values increased with fibrosis stages and remained stable after treatment, indicating stability.
- sST2 showed fair correlation with VCTE and improved diagnostic performance when combined with APRI or FIB-4.
- sST2 had an AUROC of 0.74 for detecting advanced fibrosis before treatment.

## Abstract

With the increase in patients at risk of advanced liver disease due to the obesity epidemic, there will be a need for simple screening tools for advanced liver fibrosis. Soluble suppression of tumorigenicity 2 (sST2) is a serum biomarker for fibrotic processes. The aim of this study was to evaluate sST2 as marker for liver fibrosis in patients successfully treated for chronic hepatitis C.

424 patients from the Swiss Hepatitis C Cohort Study were screened for inclusion in this post-hoc cohort study. Inclusion criteria were sustained virological response (SVR), available elastography (VCTE) and serum samples for biomarker analysis before and after treatment. For the validation of sST2, values were compared to VCTE, FIB-4 and APRI using Spearman’s correlation and AUROC analyses.

Data of 164 subjects were finally analyzed. Median sST2 values slightly increased with VCTE-derived fibrosis stages and remained stable after reaching SVR within the respective fibrosis stage, suggesting that sST2 is not influenced by liver inflammation. However, correlation of sST2 pre- and post-treatment with VCTE was fair (Spearman’s rho = 0.39 and rho = 0.36). The area under the curve (AUROC) for sST2 in detecting VCTE-defined F4 fibrosis (vs. F0-F3) before therapy was 0.74 (95%CI 0.65–0.83), and 0.67(95%CI 0.56–0.78) for the discrimination of F3/F4 fibrosis vs. F0-F2. Adding sST2 to either APRI or FIB-4, respectively, increased diagnostic performance of both tests.

sST2 can potentially identify patients with advanced fibrosis as a single serum marker and in combination with APRI and FIB-4.

## Linked entities

- **Proteins:** CORT (cortistatin)

## Full-text entities

- **Genes:** GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}, ST2 (suppression of tumorigenicity 2) [NCBI Gene 6761], GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, RHO (rhodopsin) [NCBI Gene 6010] {aka CSNBAD1, OPN2, RP4}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** HCV (MESH:D006526), obese (MESH:D009765), non-alcoholic steatohepatitis (MESH:D005235), inflammation (MESH:D007249), VCTE (MESH:D053421), lung disease (MESH:D008171), End-Stage Liver Disease (MESH:D058625), ALD (MESH:D000326), HA (MESH:D011015), autoimmune diseases (MESH:D001327), metabolic dysfunction associated steatohepatitis (MESH:D005234), heart failure (MESH:D006333), Liver stiffness (MESH:D017093), bleeding (MESH:D006470), CHC (MESH:D019698), autoimmune and metabolic liver diseases (MESH:D008107), Metabolic dysfunction (MESH:D008659), kidney disease (MESH:D007674), Fibrosis (MESH:D005355), Chronic Hepatits C infection (MESH:D000088562), necrosis (MESH:D009336), non-alcoholic fatty liver disease (MESH:D065626), pulmonary fibrosis (MESH:D011658), HIV (MESH:D015658), hepatocyte injury (MESH:D014947), hepatitis B (MESH:D006509), HCC (MESH:D006528), liver cirrhosis (MESH:D008103), Alcoholic liver disease (MESH:D008108)
- **Chemicals:** HA (MESH:D006820), LED (-), Sofosbuvir/Ledipasvir (MESH:C000595958), ribavirin (MESH:D012254), glycosaminoglycan (MESH:D006025), SOF (MESH:D000069474)
- **Species:** Homo sapiens (human, species) [taxon 9606], Hepatitis C Virus [taxon 11103]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10825988/full.md

## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC10825988/full.md

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Source: https://tomesphere.com/paper/PMC10825988