Therapeutic effect of Agaricus brasiliensis on phenylhydrazine-induced neonatal jaundice in rats.

The present study was designed to investigate the effect of Agaricus brasiliensis extract (ABE) on phenylhydrazine-induced neonatal jaundice in rats. Administration of ABE dose-dependently reduced the elevated bilirubin level induced by phenylhydrazine. It can be somewhat supported from the results of in vitro bilirubin degradation experiment. ABE treatment also reduced the total antioxidant status (TAOS), cascade O2(-)/SOD, level of NF-κB protein, and adrenomedullin (AM). Overall, the results of this study demonstrated that Agaricus brasiliensis extract may be beneficial to reducing bilirubin level without causing hepatotoxicity in neonatal jaundice.

Abordagem clinica, laboratorial e terapeutica do recém-nascido icterico / Clinical, laboratorial and therapeutic management of the neonatal jaundice

O objetivo desta revisäo/atualizaçäo a respeito da abordagem clinica, laboratorial e terapeutica do recém-nascido icterico foi apresentar um roteiro didático, com a finalidade de se tentar esclarecer algumas dúvidas sobre a conduta na hiperbilirrubinemia neonatal, dando enfase aos pontos polêmicos da terapeutica

Patologías del recién nacido en relación con la edad materna / The pathology of the born according to the mother ly age

Las patologías de recién nacido según la edad materna es una problemática vigente en nuestros hospitales. Se realizó un estudio prospectivo con una muestra de 500 recién nacidos, seleccionados al azar, atendidos en el Hospital General del Oeste "Dr. José Gregorio Hernández", quienes posteriormente fueron trasladados a retén de niño sano o patológico, dependiendo de las condiciones del mismo posterior al nacimiento, y los datos maternos fueron recopilados de las historias obstétricas. El mayor porcentaje de nacimientos se registró en madres con edades conprendidas entre 16-20 años, representando 36,6 por ciento coincidiendo a su vez con el mayor número de patologías más frecuentes: ictericia del recién nacido (23,4 por ciento) y síndrome de dificultad respiratoria (22,8 por ciento). Con este estudio se trata de resaltar la importancia que tiene el llevar a cabo un buen control prenatal y adecuada educación sexual, logrando disminuir la incidencia de embarazos en gestantes jóvenez y las complicaciones neonatales que ello acarrea

Oxidation of parenteral lipid emulsion by ambient and phototherapy lights: potential toxicity of routine parenteral feeding.

Vitamin E can be a prooxidant in isolated lipoprotein suspensions. Because lipid emulsions used in parenteral nutrition are lipoprotein-like suspensions rich in polyunsaturated fatty acids and vitamin E, we hypothesized that vitamin E may act as a prooxidant in lipid emulsions, as it is in lipoprotein suspensions. We therefore exposed an intravenously administered lipid emulsion (Intralipid) to a single spotlight commonly used in the treatment of neonatal jaundice, and measured the formation of triglyceride hydroperoxides by using high-performance liquid chromatography with postcolumn chemiluminescence detection. Concentrations of these hydroperoxides in different batches of fresh intralipid were usually approximately 10 mumol/L but increased up to 60 times after exposure to phototherapy light for a period of 24 hours, even though significant amounts of vitamin E were present at the end of the exposure. Triglyceride hydroperoxides were formed during phototherapy light exposure whether the intralipid was in plastic tubing used routinely for infusion or in glass containers. Ambient light also caused significant peroxidation of the formula lipids, although to a much lesser extent than observed with phototherapy light. For infants in the neonatal intensive care unit who were receiving intralipid but not phototherapy, solutions being infused at the end of 24 hours contained a mean of 40 mumol/L hydroperoxides. For infants receiving phototherapy, the mean was 97 mumol/L. Phototherapy light-induced formation of triglyceride hydroperoxides was prevented by covering the intralipid with aluminum foil or supplementation with sodium ascorbate before light exposure. We conclude that intralipid is highly susceptible to oxidation and that elevated levels of oxidized lipids can be formed during its clinical use, especially when intralipid infusion is combined with phototherapy. Because lipid hydroperoxides are cytotoxic and can cause adverse effects, inadvertent infusion of rancid intralipid may add to the numerous problems encountered by premature neonates.

Effect of heparin dose and infusion rate on lipid clearance and bilirubin binding in premature infants receiving intravenous fat emulsions.

The effect of heparin dose and infusion rate on plasma lipids, lipases, and unbound bilirubin was investigated in 22 premature infants with physiologic jaundice. Infants were randomly assigned to receive low or high intravenous doses (24 vs 137.3 U/day) of heparin. Each patient then received 2 g/kg/day of 10% Intralipid on 2 successive days: one day during a 15-hour period and the other day over 24 hours, with the order assigned randomly. The results demonstrate a significantly greater change in serum-free fatty acids in infants receiving the high heparin dose during the 15-hour lipid infusion period. Lipoprotein lipase activity rose more with the high heparin dose and equally at either infusion rate. We conclude that lipid infusions of 2 g/kg/day with low heparin dosage infused over 24 hours resulted in less elevation in serum-free fatty acids. There were no adverse effects on unbound bilirubin at either infusion rate or heparin dosage.

Fecal bilirubin excretion and serum bilirubin concentrations in breast-fed and bottle-fed infants.

To assess the rate of excretion of bilirubin in the stools and its effects on serum bilirubin concentrations, we studied 24 breast-fed and 13 bottle-fed infants during the first 3 days after birth. Bottle-fed infants passed significantly more stool (3-day totals, 82 vs 58 gm, P less than 0.001), excreted more bilirubin (3-day totals, 23.8 vs 15.7 mg, P less than 0.05), and had lower serum bilirubin values (day 3, 6.8 vs 9.5 mg/dl, P less than 0.02). Among the breast-fed infants, greater stool output was associated with greater fecal bilirubin excretion (r = 0.56, P less than 0.05) and lower serum bilirubin concentrations (r = 0.66, P less than 0.001). Our data suggest that hyperbilirubinemia in breast-fed infants may be related to a delay in bilirubin clearance resulting from low stool output.

Development of bilirubin transport and metabolism in the newborn rhesus monkey.

Hepatic transport and metabolism of bilirubin have been examined in term, premature, and postmature newborn Macaca mulatta (rhesus) monkeys with and without prior phenobarbital treatment of pregnant mother and neonate. In untreated neonates a biphasic pattern of physiologic unconjugated hyperbilirubinemia has been observed. Phase I was characterized by a rapid increase in serum bilirubin concentration to 4.5 mg/dl by 19 hours and an equally rapid decline to 1.0 mg/dl by 48 hours of age. Phase II was characterized by a stable elevation at 1.0 mg/dl (four times greater than in the adult) from 48 to 96 hourse of age, followed by a decline to normal adult concentrations thereafter. An identical pattern was observed in 29 normal, term human neonates, but the duration of each phase was approximately three times as long as that in the monkey. Phase I hyperbilirubinemia appears to result from a sixfold increase in bilirubin load presented to the liver in the neonatal period, combined with marked deficieny in hepatic bilirubin conjugation, the rate-limiting step during Phase I. Hepatic uptake of bilirubin is not rate limiting during Phase I but may contribute to Phase II hyperbilirubinemia. An increased bilirubin load persists throughout the first 19 days of life in the monkey. Phase I physiologic jaundice in the monkey neonate was completely eliminated by prenatal maternal and neonatal administration of phenobarbital. A threefold enhancement of hepatic conjugation of bilirubin (glucuronyl transferase activity) during Phase I entirely accounted for the prevention of hyperbilirubinemia. The bilirubin load was unaffected by administration of phenobarbital. Whereas in control neonates the bilirubin load slightly exceeded hepatic bilirubin conjugating capacity and resulted in retention of bilirubin, in phenobarbital-treated neonates, hepatic conjugating capacity slightly exceeded that required for the bilirubin load. Administration of phenobarbital failed to alter Phase II hyperbilirubinemia and did not enhance either maximal hepatic uptake or excretion of bilirubin. Hepatic glucuronly transferase activity was increased threefold during Phase II and during the remainder of the neonatal period. Premature birth retarded maturation of hepatic glucuronyl transferase activity. In one phenobarbital-treated premature monkey neonate, there was no apparent response to treatment. Accelerated maturation of bilirubin uptake, conjugation, and excretion of bilirubin was observed in one postmature monkey neonate.