Increased epidermal growth factor expression in amyotrophic lateral sclerosis patients: A potential protective mechanism against pressure ulcers

Abstract

Objectives: This study aimed to investigate epidermal growth factor (EGF) and keratinocyte growth factor (KGF) expression in proximal (gluteal) and distal (ankle) skin biopsies of individuals diagnosed with amyotrophic lateral sclerosis (ALS) compared to controls and to explore whether these factors may contribute to the relative sparing of pressure ulcers in ALS.

Patients and methods: In this prospective cohort study, 10 patients with limb-onset ALS and 16 age- and sex-matched controls with other neurological diseases underwent skin biopsies between April 2015 and December 2016. Immunohistochemical staining for EGF, KGF, and PGP9.5 was performed. Growth-factor expression was semiquantitatively scored; intraepidermal nerve fiber density quantification followed established protocol.

Results: The ALS group (7 male, 3 female; mean age: 52.9 ± 13.5 years; range, 31 to 72 years) and the control group (10 male, 6 female; mean age: 51.8 ± 12.8 years; range, 29 to 73 years) had similar demographic characteristics (p > 0.05). Proximal EGF expression was significantly higher in patients with ALS (p < 0.05). Distal EGF expression did not differ between groups. Across all participants, proximal EGF levels were higher compared to distal levels (p < 0.05). Expression of KGF showed no intergroup difference at either anatomical biopsy site. Patients with ALS demonstrated reduced intraepidermal nerve fiber density both in proximal and distal samples compared to established normative values consistent with small-fiber involvement. No associations were found between EGF and KGF levels and age, sex, or disease duration.

Conclusion: Increased EGF expression in pressure-prone gluteal skin of patients with ALS suggests that EGF-mediated wound-healing pathways may contribute to the unexpectedly low incidence of pressure ulcers in ALS. Larger prospective studies incorporating biochemical, histological, and functional assays are required to establish the mechanistic basis of this growth factor dysregulation in ALS.

*These authors contributed equally to this work.

Cite this article as: Arslan D, Kurt E, Ergül-Ülger Z, Erdem-Özdamar S, Tan E, Bekircan-Kurt CE. Increased epidermal growth factor expression in amyotrophic lateral sclerosis patients: A potential protective mechanism against pressure ulcers. Turk J Neurol 2026;32(3):230-236. https://doi.org/10.55697/tnd.2026.731.

The data that support the findings of this study are available from the corresponding author upon reasonable request.

E.K., S.E.Ö., C.E.B.K., E.T.: Idea/concept; S.E.Ö., C.E.B.K., E.T.: Design, references and fundings; D.A., S.E.Ö., C.E.B.K., E.T.: Control/supervision; D.A., E.K., Z.E.Ü., C.E.B.K.: Data collection and/or processing; D.A., E.K., C.E.B.K.: Analysis and/or interpretation; D.A., E.K.: Literature review; D.A., C.E.B.K.: Writing the article; D.A., E.K., Z.E.Ü., S.E.Ö., C.E.B.K., E.T.: Critical review; Z.E.Ü., S.E.Ö., C.E.B.K., E.T.: Materials.

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

The authors received no financial support for the research and/or authorship of this article.

The authors declare that artificial intelligence (AI) tools were not used, or were used solely for language editing, and had no role in data analysis, interpretation, or the formulation of conclusions. All scientific content, data interpretation, and conclusions are the sole responsibility of the authors. The authors further confirm that AI tools were not used to generate, fabricate, or ‘hallucinate’ references, and that all references have been carefully verified for accuracy.