Related Experiment Video
Updated: May 31, 2026

Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
Serum fructosamine and retinopathy of prematurity
Senol Bozdag1, Serife Suna Oguz, Tulin Gokmen
1Department of Neonatology, Zekai Tahir Burak Maternity and Teaching Hospital, Ankara, Turkey. senolbozdag@hotmail.com
Insights
Serum fructosamine does not predict retinopathy of prematurity in very low birth weight infants. However, the duration of hyperglycemia is linked to the development of this condition in premature infants.
Area of Science:
- Neonatal Medicine
- Ophthalmology
- Endocrinology
Background:
- Retinopathy of prematurity (ROP) is a significant cause of visual impairment in premature infants.
- Hyperglycemia is a common complication in very low birth weight (VLBW) infants and has been implicated in ROP development.
- Serum fructosamine is a marker of glycemic control over the preceding 2-3 weeks.
Purpose of the Study:
- To evaluate the predictive value of serum fructosamine for ROP development in VLBW infants.
- To investigate the association between hyperglycemia duration and ROP in this population.
Main Methods:
- A cohort of 167 premature infants (birth weight < 1500g, gestational age < 32 weeks) was studied.
- Serum fructosamine levels were measured at birth and one month postnatally.
- Hyperglycemia was defined as mean blood glucose > 150 mg/dL, and ROP was assessed by ophthalmologists.
Main Results:
- Serum fructosamine levels did not differ significantly between infants who developed ROP and those who did not.
- The duration of hyperglycemia was significantly longer in infants who developed ROP (3.05 days vs 1.69 days).
- Multivariate analysis showed a significant correlation between hyperglycemia duration and ROP development (OR 3.26, p=0.035).
Conclusions:
- Serum corrected fructosamine is not a reliable predictor of ROP in VLBW infants.
- The duration of hyperglycemia, rather than fructosamine levels, appears to be a contributing factor to ROP development in this vulnerable group.
Objective:
To determine whether serum fructosamine which is a good marker for detecting hyperglycemia during the previous 2 to 3 wk in infants could predict the development of retinopathy of prematurity in very low birth weight infants.
Methods:
One hundred sixty seven premature infants who had a birth weight of < 1500 g and a gestational age of less than 32 wk were investigated in the present study. Blood glucose was measured at the bedside and infants were recorded as hyperglycemic if their mean blood glucose levels were higher than 150 mg/dL. Serum corrected fructosamine level was obtained from the cord blood at birth and after the first month of life. The infants' eyes were examined by ophthalmologists to detect retinopathy of prematurity at the gestational age of 32 wk or at four wk after birth, whichever came first.
Results:
Corrected fructosamine was 319.6 ± 59.6 and 272.8 ± 50.6 mmol/l for group 1 on 1(st) and 30(th) day respectively; 320 ± 61.7 and 268.2 ± 47.3 mmol/l for groups 2 + 3 on 1(st) and 30(th) day respectively which did not differ between groups (p = 0.766 and p = 0.665), whereas duration of hyperglycemia was 1.69 ± 1.1 day in group 1 compared with 3.05 ± 2.4 day in groups 2 + 3 which was significantly different (p = 0.019). The multivariate regression analysis indicated that the duration of hyperglycemia in days was significantly correlated with the development of retinopathy of prematurity (OR 3.26; 95% CI 1.09-9.80; p = 0.035).
Conclusions:
Although the duration of hyperglycemia may contribute to the development of retinopathy of prematurity, serum corrected fructosamine does not have a good predictive value in developing retinopathy of prematurity in very-low-birth-weight (VLBW) infants.
Related Concept Videos
Diabetic Retinopathy
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis
Serum Studies: Renal Function Tests
Glucose Transporters
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Diabetes Mellitus: Type 2 and Gestational
Diabetic Nephropathy

