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Chatarina Lofqvist, Ingrid Hansen Pupp, Jing Chen, Colman J. Hatton, Aimee Juan, David Ley, Gunnel Hellgren, Lois E. Smith, Ann Hellstrom; Proliferative Retinopathy of Prematurity is Associated with Low Serum Levels of Adiponectin. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4687.
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Adiponectin (APN) is almost exclusively produced by adipose tissue. Adiponectin production is downregulated by weight gain, angiotensin II, oxidative stress, and testosterone as well as proinflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (IL)-6. In the oxygen-induced mouse model of ROP APN suppresses TNF-α-induced inflammatory changes and blocks retinal neovascularization. Furthermore, an association between APN serum levels and postnatal growth of preterm infants has been reported. Since we have found previously a link between poor postnatal growth and later development of proliferative ROP, these results suggest a potential link between APN and development of ROP. The aim of this study was to investigate if there is a link between postnatal longitudinal development of serum adiponectin levels after birth and ROP.
A prospective cohort study was performed in twenty-four extremely preterm infants (median (range) gestational age (GA) 25.2 (23.0-27.00) weeks with weekly blood sampling of adiponectin from birth to PMA 36 weeks. ROP was determined according to the International ROP classification.
Sixteen children had no signs of any ROP and eight infants had proliferative ROP. Adiponectin levels at birth were low in both groups and showed a similar continuous increase occurring up to postmenstrual age (PMA) 30 weeks irrespective of GA at birth (Fig). For both groups between PMA 24 to 31 weeks adiponectin levels increased 10-fold, then rapidly decreased. There was a significant correlation between mean adiponectin levels at PMA 33-36 weeks and mean weight SDS at PMA 33-36 weeks (r2=0.40 p=0.001). Furthermore infants who developed proliferative ROP, had significantly lower levels of adiponectin between PMA 33-36 weeks (corresponding to the time for the induction of proliferative ROP) compared to the group with no ROP, p=0.019.
Our results show that the serum level of adiponectin is lower during the proliferative phase, in infants who develop severe ROP. Further studies of the mechanism of action and expression are necessary to determine if the correlation between circulating levels of adiponectin and retinal neovascularization is causal or merely secondary to postnatal weight gain.
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