BMC Ophthalmol. 2026 Jan 27. doi: 10.1186/s12886-026-04640-z. Online ahead of print.
ABSTRACT
OBJECTIVE: This study aimed to investigate the relationship between systemic fibrosis markers, including the Aspartate Aminotransferase-to-Platelet Ratio Index (APRI) and the Fibrosis-4 Index (FIB-4), and the development of proliferative vitreoretinopathy (PVR).
METHODS: The medical records of patients who underwent surgery for rhegmatogenous retinal detachment between January 2019 and October 2025 were retrospectively reviewed. A total of 394 participants were included and divided into three groups: PVR-positive retinal detachment group (PVR (+) RD; n = 150), PVR-negative retinal detachment group (PVR (-) RD; n = 175), and a healthy control group (n = 69). APRI and FIB-4 scores were calculated using preoperative complete blood count and liver function test parameters. Demographic data and clinical characteristics of the patients were recorded.
RESULTS: The mean age of the 394 participants included in the study was 59.9 ± 13.2 years (range: 22-89 years). Of the patients, 184 (46.7%) were female, and 210 (53.3%) were male. Although the mean FIB-4 and APRI values tended to be higher in the PVR (+) group compared with the PVR (-) and control groups, no statistically significant differences were observed (p = 0.062 and p = 0.835, respectively). In multivariate logistic regression analysis, longer symptom duration was independently associated with an increased risk of proliferative vitreoretinopathy (OR = 1.04, 95% CI: 1.02-1.06; p = 0.001). Diabetes mellitus was also identified as an independent risk factor for PVR development (OR = 2.51, 95% CI: 1.22-5.17; p = 0.013), and inferior rhegmatogenous retinal detachment was significantly associated with PVR (OR = 0.48, 95% CI: 0.25-0.93; p = 0.029).
CONCLUSION: The APRI and FIB-4 indices did not reveal a statistically significant difference in distinguishing the development of proliferative vitreoretinopathy. These findings support that the pathogenesis of PVR is primarily driven by inflammatory and fibroproliferative processes occurring within the local vitreoretinal microenvironment rather than by systemic fibrosis.
PMID:41593573 | DOI:10.1186/s12886-026-04640-z
