Serum Prolidase and Ischemia-Modified Albumin Levels in Neural Tube Defects: A Comparative Study of Myelomeningocele, Meningocele, and Myeloschisis

BACKGROUND Neural tube defects (NTDs) are congenital malformations resulting from incomplete neural tube closure, leading to severe neurological impairments. Despite advances in prenatal screening and surgical interventions, the biochemical mechanisms underlying NTDs remain unclear. Prolidase, an enzyme involved in collagen metabolism, and ischemia-modified albumin (IMA), a marker of oxidative stress, may play roles in NTD pathogenesis. This study aimed to compare serum prolidase and IMA levels in infants with NTDs and healthy controls to assess their potential contribution to NTD development. MATERIAL AND METHODS A case-control study was conducted, including 45 infants diagnosed with NTDs (myelomeningocele, meningocele, and myeloschisis) and 45 age- and sex-matched healthy controls. Serum prolidase and IMA levels were measured using validated spectrophotometric methods. Statistical analyses were performed to compare biomarker levels between groups and among NTD subtypes. RESULTS Serum prolidase levels were significantly elevated in NTD patients (2.21±0.06 IU/L) compared to controls (1.07±0.04 IU/L, p<0.001). Similarly, serum IMA levels were higher in NTD patients (0.40±0.01 ABSU) than in controls (0.22±0.01 ABSU, p<0.001). No significant differences were observed in biomarker levels among the different NTD subtypes (p>0.05). CONCLUSIONS Elevated prolidase and IMA levels in NTD patients suggest a potential role in NTD pathogenesis, possibly through impaired collagen metabolism and oxidative stress. Further research is needed to explore their diagnostic and therapeutic implications in neural tube defect management.