Our aim was to assess the hypothesis that a high-dose regimen of ibuprofen is more effective than the standard-dose regimen in closing patent ductus arteriosus (PDA) without increasing adverse effects. Infants of gestational age <29 weeks, with respiratory distress syndrome (RDS) and echocardiographic evidence of significant PDA at 12-24 h of life, were randomized to receive a standard (10-5-5 mg/kg/day) or high-dose (20-10-10 mg/kg/day) course of ibuprofen. We studied 70 infants, 35 of whom received the standard dose of ibuprofen and the other 35 the high dose. Of the infants treated with the standard-dose regimen, 37% had persistent PDA as compared with 14% of those treated with the high-dose regimen (P = 0.03). No differences in the occurrence of adverse effects were observed between the two groups. The high-dose ibuprofen regimen is more effective than the standard-dose regimen in closing PDA in preterm infants <29 weeks of gestation without increasing the adverse effect rate.
In a previous study, it was found that the decrease in the total plasma bilirubin level (Btot) in preterm infants was associated with the decrease in oxidative stress. We hypothesized that this occurs as a result of a pro-oxidant effect of heme oxygenase (HO), which outcompetes with the antioxidant properties of bilirubin. In this study we studied 12 preterm infants in whom the plasma levels of Btot, total hydroperoxide (TH), protein SH groups, HO activity, non-transferrin-bound iron (NTBI), and erythrocyte CuZn superoxide dismutase (CuZn SOD) activity were concurrently measured when the Btot was Ͼ220 M and after a Btot drop of Ͼ34 M. The Btot decrease was concurrent with the TH decrease, protein SH groups increase, and the HO and CuZn SOD activity increase and was not associated with an NTBI increase. We concluded that 1) Btot does not exert a meaningful antioxidant effect in vivo; 2) HO does not exert a pro-oxidant effect involving an NTBI increase and that, on the contrary, it could exert an antioxidant effect; and 3) the concurrent HO and CuZn SOD activity increase could indicate a synergic antioxidant effect of the two enzymes. Many illnesses in preterm infants, including chronic lung disease, necrotizing enterocolitis, retinopathy of prematurity, and intracranial hemorrhage, are thought to be related to the action of reactive oxygen species. This presumably occurs because the antioxidant system of preterm infants is at the same time highly stressed and incompletely developed (1). Moreover, it is well known that during the first days of life, the catabolism of fetal Hb results in a tissue burden of heme that is a potentially pro-oxidant damaging molecule that not only provides a lipophilic form of iron but can itself directly attack the lipid bilayer, the cytoskeleton, and DNA (2,3). Several reports have emphasized the antioxidant role of bilirubin, which in human neonatal plasma seems to have a greater antioxidant potency than urates, ␣-tocopherol, or ascorbates (4). Nevertheless, although the antioxidant effect of bilirubin as a scavenger of reactive oxygen species is well documented in vitro (5-8) as well as in animal studies (9), its role in vivo has not been definitively clarified in preterm infants (10 -13). Even less is known about the role of heme oxygenase (HO) in oxidative stress of the newborn infant. Heme oxygenase is the enzyme responsible for physiologic heme degradation into equimolar amounts of CO and biliverdin and the release of free iron (14). It has been suggested that its inducible form, HO-1, might represent a generalized response to oxidative stress (15)(16)(17) and that HO-1 could confer cellular protection against oxidant stress (14,18 -20). However, recent studies suggest that HO-1 induction might not always be beneficial and that the release of redox-active iron from heme might induce enhance oxidative stress (21,22).In a previous study, we found that in jaundiced preterm infants, a decrease of bilirubin plasma level (Btot) was asso-
Lipoprotein abnormalities are common in patients with chronic renal failure (CRF) on either dialysis or conservative therapy. In order to investigate the changes in lipid and apoli-poprotein pattern from early CRF to dialysis treatment, plasma lipids with apoproteins AI, B, E, CII, CIII, CII/CIII ratio, E/CII ratio, parathyroid hormone (PTH) and insulin levels were examined in 72 patients with different degrees of CRF and 31 patients on hemodialysis (HD), and compared the values of 28 controls. A significant decrease in the Apo CII/CIII ratio was the earliest lipoprotein abnormality to occur in CRF. Hypertriglyceridemia (HTG) with reduced high-density lipoprotein cholesterol levels, increased Apo CIII and decreased Apo E/Apo CIII ratio only occurred in more advanced renal failure (creatinine clearance < 31 ml/min). HD patients showed a general worsening of the lipoprotein profile with elevated Apo E levels and indirect evidence of remnant accumulation. While PTH did not have any significant influence on lipoprotein pattern, increased insulin levels during HD might partly account for the HTG of these patients. Our results point to elevated Apo CIII, reduced Apo CII/Apo CIII and Apo E/ Apo CIII ratios as typical features of uremic hyperlipidemia and show that a defective triglyceride removal is the major pathogenetic mechanism of uremic HTG. HD treatment seems generally to worsen the lipid and apolipoprotein pattern observed in the predialytic stage of CRF.
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