scholarly journals Background retinopathy

2020 ◽  
Author(s):  
Author(s):  
Hamideh Shajari ◽  
Mohammadamin Ghadyani ◽  
Seyed Hamed Hosseini-Jangjou ◽  
Reza Bahrami ◽  
Seyed Alireza Dastgheib ◽  
...  

Background: Retinopathy of prematurity (ROP) is an important cause of preventable blindness in children. The aim of this study was to examine the association of the polymorphisms at Factor V Leiden (FVL) and methylene tetrahydrofolate reductase (MTHFR) gene with risk of ROP. Methods: A total of 106 neonates with ROP and 110 healthy neonates were enrolled. The FVL G1691A and MTHFR C677T and A1298C polymorphisms were genotyped by PCR-RFLP assay. Results: There was a significant association between FVL G1691A polymorphism and an increased risk of ROP. However, the MTHFR C677T and A1298C polymorphisms were not associated with risk of ROP. Conclusion: FVL G1691A polymorphism may be risk factor for development of ROP in neonates. However, there was no significant association between MTHFR C677T and A1298C polymorphisms and risk of ROP. However, it is critical that larger and well-designed studies in different ethnicities are needed to confirm our conclusions.


2016 ◽  
Vol 45 (6) ◽  
pp. 270
Author(s):  
Rinawati Rohsiswatmo

Background Retinopathy of prematurity (ROP) is one of the ma-jor causes of infant blindness. There are several factors known asrisk factors for ROP. Recent studies show ROP as a disease ofmultifactorial origin.Objective To report the prevalence of ROP in Cipto MangunkusumoHospital, Jakarta and its relation to several risk factors.Methods A cross-sectional descriptive study was conducted fromDecember 2003-May 2005. All infants with birth weight 2500 gramsor less, or gestational age 37 weeks or less, were enrolled con-secutively and underwent the screening of ROP at 4 to 6 weeks ofchronological age or 31 to 33 weeks of postconceptional age.Result Of 73 infant who met the inclusion criteria, 26% (19 out of73 infant) had ROP in various degrees. About 36.8% (7 out of 19infants) were in stage III or more/threshold ROP. No ROP wasnoted in infants born >35 weeks of gestational age, and birth weight>2100 grams. No severe ROP was found in gestational age >34weeks and birth weight >1600 grams. None of full-term, small forgestational age infants experienced ROP. Birth weight, sepsis,apneu, asphyxia, multiple blood transfusions, and oxygen therapyfor more than 7 days were statistically significant with the develop-ment of ROP. However, using multivariate analysis, only asphyxia,multiple blood transfusions, and oxygen therapy for more than 7days were statistically significant with the development of ROP.Conclusion Screening of ROP should be performed in infantsborn 34 weeks of gestational age and/or birth weight <1600 grams.Infants with birth weight from 1600-<2100 grams need to bescreened only if supplemental oxygen is necessary or with clini-cally severe illness


1985 ◽  
Vol 8 (4) ◽  
pp. 249-255 ◽  
Author(s):  
G. Soubrane ◽  
J. Canivet ◽  
G. Coscas

1987 ◽  
Author(s):  
M B Grant ◽  
T Daniels ◽  
D Claire ◽  
R Lottenberg

The increase in von Willebrand factor (vWF) following desmopressin (DDAVP) (1-desamino-8-D-arginine vasopressin) infusion was markedly blunted in severe hemophiliacs who had high vWF levels after treatment with vWF rich plasma concentrates. Diabetics with microangiopathy appear to have disease-induced elevation of vWF. In the current study, the vWF response to DDAVP infusion was measured in 30 diabetics (12 type I, 18 type II) and 16 controls, matched for age, sex and weight. Extent of nephropathy, macroangiopathy, and neuropathy was evaluated. Diabetic retinopathy was assessed by indirect ophthalmoscopy and fluorescein angiography (n=8 proliferative retinopathy, n=6 background retinopathy, n=16 no retinopathy). Plasma samples were collected in the supine, overnight-fasted state. DDAVP (0.3 μg/kg) was infused over 30 min and samples obtained at 0-60 min. vWF antigen was assayed by Laurell rocket electrophoresis. Tissue plasminogen activator (t-PA) activity was measured by a coupled chromogenic substrate assay. Results; Basal vWF levels for type I diabetics (124±16%, MeantSEM) and type II (178±14%) were increased as compared to controls (94±6%), p<.05 and p<.005, respectively. vWF levels for diabetics with proliferative retinopathy (194±29%) were significantly higher than for diabetics with background retinopathy (106±13%) p<.01. Diabetics with elevated basal levels of vWF (>150%) showed less of an increase in vWF following DDAVP infusion than diabetics with normal basal levels (p<.01). The percent increase in vWF following DDAVP administration inversely correlated with basal vWF levels (type I, r=.51; p<.01 and type II, r=.46; p<.01). The basal vWF level was the significant determinant of DDAVP response, not the presence or absence of diabetic complications. Peak t-PA levels showed no difference in controls or diabetics. In contrast to the vWF response, a normal t-PA response to DDAVP infusion was observed in diabetics. Conclusion: Diabetics with microvascular complications and high circulating levels of vWF demonstrate a blunted vWF response to DDAVP. This supports the existence of a negative feedback mechanism as previously reported for the transfused hemophiliacs.


Author(s):  
Mohammadamin Ghadyani ◽  
Mahmood Noorishadkam ◽  
Seyed Hamed Hosseini-Jangjou ◽  
Reza Bahrami ◽  
Elahe Akbarian ◽  
...  

Background: Retinopathy of prematurity (ROP) is a major cause of blindness in newborn infants worldwide. It is well known that neovascularization of the retina is prominent in the proliferative stages of ROP. It is suggested that vascular endothelial growth factor (VEGF) may play a role in the development of ROP. The aim of this study was to evaluate the association of the VEGF -634C/G polymorphism at VEGF with risk of ROP. Methods: In the study 54 neonates diagnosed with ROP and 55 healthy neonates served as controls. The VEGF -634 C/G polymorphism was genotyped by restriction fragment length polymorphism (PCR-RFLP) technique. Results: The CC, CG, and GG genotypes of VEGF -634C/G polymorphism were found in 33.3%, 38.9%, and 27.8% of neonates with ROP, respectively. In controls, CC, CG, and GG genotypes were seen in 43.6%, 45.4%, and 10.9%, respectively. Frequency of mutant allele (C) was 52.8% in neonates with ROP and 66.4% in healthy neonates. There was a significant difference in the distribution of VEGF -634C/G polymorphisms between cases and controls. Moreover, there was a significant association between VEGF -634C/G polymorphisms and ROP risk (OR = 3.141, 95% CI 1.115-8.851, P = 0.030). Conclusion: This study results revealed that VEGF -634C/G polymorphism might serve as a risk factor for development of ROP. Thus, clinicians should be aware of the ROP risk in infant with the VEGF -634C/G polymorphism and ROP risk in infants. However, large sample size and well-designed studies are necessary to validate our findings.


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