# The Impact of Hemolytic Processes Due to Extracorporeal Support Therapy on the Serum Concentration of the Neuronal Marker Protein NSE

**Authors:** Daniel Ebert, Kurt Henrik Janke, Julia Schumann

PMC · DOI: 10.3390/ijms27041910 · International Journal of Molecular Sciences · 2026-02-17

## TL;DR

This study shows that high NSE levels in ECMO patients may be due to blood cell damage, not brain injury, limiting NSE's usefulness as a brain damage marker during ECMO therapy.

## Contribution

The study demonstrates that ECMO-induced hemolysis, not brain damage, can elevate NSE levels, challenging its use as a reliable neurological marker in ECMO patients.

## Key findings

- Serum NSE levels in ECMO patients showed significant intrapersonal variability.
- No significant difference in NSE levels was found between ECMO patients with and without brain damage.
- A strong positive correlation was observed between serum NSE and LDH levels, indicating hemolysis as a source of elevated NSE.

## Abstract

Neuron-specific enolase (NSE) is a marker used to assess neurological impairment. Notwithstanding, the release of NSE into the circulation can also originate from erythrocytes and thrombocytes, signifying that even mild instances of hemolysis have the potential to induce heightened serum NSE levels. The present study addresses the question of whether the serum NSE level is a reliable parameter for assessing potential brain damage in patients undergoing extracorporeal membrane oxygenation (ECMO). To this end, NSE values of all non-resuscitated ECMO patients treated at our clinic from January 2020 to March 2022 were retrospectively evaluated. Serum NSE levels were found to be median 35.95 µg/L, with significant intrapersonal variability during ECMO therapy. A comparative analysis in ECMO patients with and without diagnosed brain damage revealed no statistically significant differences. In contrast, the concurrent measurement of serum LDH and NSE levels exhibited a significant positive correlation (Spearman Rho 0.69), indicating that the elevated serum NSE levels exhibited by patients devoid of cerebral impairment were attributable to the occurrence of ECMO-induced hemolysis. Consequently, the prognostic value of serum NSE levels in patients undergoing ECMO is restricted. The data also demonstrate that individual measurements of serum NSE levels in ECMO patients should be regarded as snapshots with only limited significance.

## Linked entities

- **Proteins:** ENO2 (enolase 2)

## Full-text entities

- **Genes:** HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, ENO2 (enolase 2) [NCBI Gene 2026] {aka HEL-S-279, NSE}
- **Diseases:** neurological impairment (MESH:D009422), hypoxemia (MESH:D000860), hemolysis (MESH:D006461), ARDS (MESH:D012128), hepatic coma (MESH:D006501), stroke (MESH:D020521), neuronal damage (MESH:D009410), respiratory failure (MESH:D012131), anoxic brain damage (MESH:D002534), cardiac arrest (MESH:D006323), ICD (OMIM:252500), neurological complications (MESH:D002493), cardiogenic shock (MESH:D012770), ischemic stroke (MESH:D002544), malignancies (MESH:D009369), International Classification (MESH:D008310), brain injury (MESH:D001930), neurological damage (MESH:D020196), clouding of consciousness (MESH:D003244), compression of the brain (MESH:D009408), Brain damage (MESH:D001925), intracerebral hemorrhage (MESH:D002543), hepatic dysfunction (MESH:D008107), Diseases (MESH:D004194), injury to (MESH:D014947), critically ill (MESH:D016638), cerebral impairment (MESH:D002547)
- **Chemicals:** glucose (MESH:D005947), bilirubin (MESH:D001663), Impella (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC12940368/full.md

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Source: https://tomesphere.com/paper/PMC12940368