ASSESSMENT OF ONCOSTATIN M PROTEIN, RESISTIN, AND RESISTIN-LIKE MOLECULE BETA (RELM-Β) LEVELS IN PATIENTS WITH ACUTE PANCREATITIS


Batal S., Başkol G., Başkol M., Yenişekerci E., Taka D., Tanriverdi A. N., ...Daha Fazla

ASES V. INTERNATIONAL KAYSERI SCIENTIFIC RESEARCH CONGRESS JUNE 20-22, 2025, KAYSERI, TURKIYE, Kayseri, Türkiye, 20 - 22 Haziran 2025, ss.499-501, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Kayseri
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.499-501
  • Erciyes Üniversitesi Adresli: Evet

Özet

Acute pancreatitis (AP) is an inflammatory condition that can lead to high mortality in severe

cases, involving a multifaceted cytokine response. However, the underlying pathogenic

mechanisms are still not fully understood. Resistin is a protein expressed in adipocytes,

monocytes, and macrophages; Resistin-Like Molecule beta (RELM-β), another member of the

resistin family, is secreted by intestinal colonic goblet cells. Interleukin-6 (IL-6) functions as a

multifaceted cytokine, while Oncostatin M (OSM) represents an IL-6 family member released

from monocytes and macrophages. This study aimed to evaluate serum levels of OSM, resistin,

RELM-β, and IL-6 in AP patients compared to healthy individuals and to investigate changes

over the disease course.

A total of 34 patients and 31 healthy controls were included. Serum levels of OSM, resistin,

RELM-β, and IL-6 were measured via ELISA on day one, at 48 hours, and prior to discharge

using commercial kits. On day one, levels of all four markers were significantly higher in

patients than in controls (OSM: p<0.003; Resistin: p<0.001; RELM-β: p<0.006; IL-6: p<0.000).

Over time, resistin levels significantly increased by discharge (p<0.006), while IL-6 levels

significantly decreased (p<0.033). No significant changes were observed in OSM or RELM-β

levels (p>0.05; p>0.064).

Patient groups were categorized by Balthazar stages (A-D), with only group D showing

statistically significant elevation in initial day IL-6 levels relative to group A (p<0.047).

Additionally, patients were grouped by Ranson scores (0-2 versus 3-4), where only predischarge

OSM levels proved statistically higher in the elevated score group (p<0.017).

Our findings demonstrate that elevated resistin and RELM-β levels in AP patients suggest these

molecules may participate in the inflammatory response accompanying AP. Data regarding

OSM remains considerably limited. As a pleiotropic cytokine within the IL-6 family, OSM is

recognized for its involvement in inflammation and tissue repair processes. The increased OSM

levels observed in our study can be interpreted as a response to acute inflammation and tissue

stress associated with AP. Notably, the parallel increase in pre-discharge OSM levels withRanson scores suggests OSM may correlate with disease severity. The elevation of OSM levels

alongside increasing Ranson scores indicates this cytokine might serve as a biomarker

contributing not only to inflammatory processes but also to prognostic assessment. This pattern

supports the notion that OSM provides a sensitive response to inflammation intensity and tissue

stress in acute pancreatitis.