Mannose binding lectin levels are not related to radiographic damage in ankylosing spondylitis

Sibel Zehra Aydin1, Pamir Atagunduz, Burak Erer

  • 1Marmara University Faculty of Medicine, Istanbul, Turkey. drsibelaydin@gmail.com

Insights

This study found no link between mannose-binding lectin (MBL) deficiency and spinal radiographic damage in ankylosing spondylitis (AS) patients. MBL deficiency prevalence and severity scores were similar in AS patients and healthy controls.

Area of Science:

  • Immunology
  • Rheumatology
  • Radiology

Background:

  • Mannose-binding lectin (MBL) plays a role in innate immunity.
  • MBL deficiency has been investigated in various autoimmune diseases.
  • Its role in the pathogenesis and radiographic progression of ankylosing spondylitis (AS) remains unclear.

Purpose of the Study:

  • To investigate the association between MBL deficiency and radiographic spinal damage in a large cohort of AS patients.
  • To compare MBL levels and deficiency prevalence between AS patients and healthy controls.
  • To determine if MBL levels correlate with disease activity or radiographic scores in AS.

Main Methods:

  • A cohort of 191 AS patients and 85 healthy controls were studied.
  • MBL levels were quantified using standard ELISA kits.
  • Radiographic spinal damage was assessed using BASRI (Bath Ankylosing Spondylitis Radiology Index) and mSASSS (modified Stoke Ankylosing Spondylitis Spinal Score) scores.

Main Results:

  • Median MBL levels were comparable between AS patients and healthy controls (2,530 vs. 3,415 ng/ml, p=0.1).
  • The prevalence of MBL deficiency (<500 ng/ml) was similar in both groups (21.5% in AS vs. 17.6%, p=0.5).
  • No significant association was found between MBL levels and disease activity, clinical features, therapies, or radiographic scores (BASRI and mSASSS) in AS patients.

Conclusions:

  • MBL deficiency is not more prevalent in AS patients compared to healthy individuals.
  • MBL deficiency does not appear to be a contributing factor to severe radiographic spinal damage in AS.
  • Further research may explore other immune pathways in AS pathogenesis.

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