Biomedical subjects

Talkad S Raghuveer

Publications and source records attributed to Talkad S Raghuveer.

5 recordsLinked to original sources

PubMed2006

Inborn errors of metabolism in infancy and early childhood: an update.

Recent innovations in medical technology have changed newborn screening programs in the United States. The widespread use of tandem mass spectrometry is helping to identify more inborn errors of metabolism. Primary care physicians often are the first to be contacted by state and reference laboratories when neonatal screening detects the possibility of an inborn error of metabolism. Physicians must take immediate steps to evaluate the infant and should be able to access a regional metabolic disorder subspecialty center. Detailed knowledge of biochemical pathways is not necessary to treat patients during the initial evaluation. Nonspecific metabolic abnormalities (e.g., hypoglycemia, metabolic acidosis, hyperammonemia) must be treated urgently even if the specific underlying metabolic disorder is not yet known. Similarly, physicians still must recognize inborn errors of metabolism that are not detected reliably by tandem mass spectrometry and know when to pursue additional diagnostic testing. The early and specific diagnosis of inborn errors of metabolism and prompt initiation of appropriate therapy are still the best determinants of outcome for these patients.

Child, Preschool↗

PubMed2005

Variability in the dose of intravenous vitamin E given to very low birth weight infants.

OBJECTIVE: Vitamin E is required by very low birth weight (VLBW) infants to prevent vitamin E deficiency. However, prolonged intravenous intakes of vitamin E >4 international units (IU)/kg/day often yield potentially toxic serum tocopherol levels. This study was designed to assess the frequency of potentially inadequate or excessive doses of intravenous vitamin E in parenteral nutrition for VLBW infants in the US. STUDY DESIGN: A questionnaire was sent to the 100 neonatal-perinatal training program centers listed in the 2003 directory (American Academy of Pediatrics (AAP)). Using the information provided for each neonatal unit, we calculated the doses of vitamin E (IU/kg/day) that would have been given to infants with body weights of 0.5, 1.0 and 1.5 kg in that unit. The doses were then recoded as inadequate if less than recommended (2.8 IU/kg/day, maximum 7 IU/day) by the American Society for Clinical Nutrition and the AAP, and excessive if >4 IU/kg/day, and frequencies were compared using chi2 analysis. RESULTS: The 65 centers that responded were predominantly among those that offered the highest level of subspecialty neonatal intensive care (level IIID). The predicted dose of vitamin E had a median value of 2.8 IU/kg/day for all three weights, and was no significantly different among the three weights. VLBW infants with weights of 0.5, 1.0 and 1.5 kg were predicted to receive doses <2.8 IU/kg/day in 12, 12 and 19% of the neonatal intensive care units (NICUs), respectively, and doses >4 IU/kg/day in 40, 31 and 10% of the NICUs, respectively. Excessive doses were significantly associated with body weight, with more frequent excessive doses at lower weight (p=0.0008). CONCLUSION: This survey showed a lack of uniformity of dosing of intravenous vitamin E in VLBW infants. The smallest infants (<1.0 kg) were receiving excessive, potentially toxic doses of vitamin E in a significant number of NICUs in the US in 2003.

Dose-Response Relationship, Drug↗

PubMed2004

Craniosynostosis.

Skull deformity in infants continues to be a diagnostic and therapeutic challenge. Deformational plagiocephaly is a common and somewhat benign cause of skull deformity in infants that must be distinguished from the more serious craniosynostosis, which occurs alone or as a syndrome. Examining an infant's head from above can help the physician distinguish true lambdoid synostosis from deformational plagiocephaly. In infants with lambdoid synostosis, the posterior bossing is in the parietal area contralateral to the flat part of the head. Deformational plagiocephaly causes frontal bossing ipsilateral to the flat part of the head. In infants with lambdoid synostosis, the ear is displaced posteriorly toward the fused suture. In infants with deformational plagiocephaly, the ear is displaced anteriorly. Isolated sagittal synostosis is the most common type of craniosynostosis. Of the more than 150 craniosynostosis syndromes, Crouzon's disease and Apert's syndrome account for the majority of cases. The diagnosis of craniosynostosis relies on physical examination, plain radiography, and computed tomography. Untreated progressive craniosynostosis leads to inhibition of brain growth, and an increase in intracranial and intraorbital pressure. Infants should be evaluated as soon as they are diagnosed.

Cranial Sutures↗

PubMed2004

What is the appropriate intravenous dose of vitamin E for very-low-birth-weight infants?

The Committee on Fetus and Newborn of the American Academy of Pediatrics (AAP) has endorsed 1 to 2 mg/dl as the normal range of serum tocopherol level. Our Cochrane review has shown that vitamin E supplementation resulting in levels >3.5 mg/dl, but not < or =3.5 mg/dl, significantly reduces the risk for severe retinopathy among very-low-birth-weight (VLBW) infants examined but increases the risks of sepsis and of necrotizing enterocolitis among infants treated for >1 week. As a fixed daily intravenous dose of vitamin E results in an inverse relationship between serum level and birth weight and is a risk for both low and high serum tocopherol levels, a dose adjusted for current weight appears more judicious than a fixed dose per day. Based on currently available data the AAP and the American Society for Clinical Nutrition currently recommend a routine intake of 2 ml/kg/day of MVI Pediatric (2.8 IU/kg/day) in VLBW infants (maximum of 5 ml/day or 7 IU/day).

Body Weight↗

PubMed2002

Lactoferrin in the preterm infants' diet attenuates iron-induced oxidation products.

Free radical injury is thought to play a significant role in the pathogenesis of several disease processes in low birth weight premature infants including retinopathy of prematurity and necrotizing enterocolitis. Because iron is a known catalyst in free radical-mediated oxidation reactions, the objectives of the present in vitro studies were to determine whether after exposure to air 1) iron present in infant formula, or that added to human milk or formula as medicinal iron or as iron contained in human milk fortifier, increases free radical and lipid peroxidation products; and 2) recombinant human lactoferrin added to formula or human milk attenuates iron-mediated free radical formation and lipid peroxidation. Before adding medicinal iron to formula and human milk, significantly more ascorbate and alpha-hydroxyethyl radical production and more lipid peroxidation products (i.e. thiobarbituric acid reactive substances, malondialdehyde, and ethane) were observed in formula. After the addition of medicinal iron to either formula or human milk, further increases were observed in free radical and lipid peroxidation products. When iron-containing human milk fortifier was added to human milk, free radicals also increased. In contrast, the addition of apo-recombinant human lactoferrin to formula or human milk decreased the levels of oxidative products when medicinal iron or human milk fortifier was present. We speculate that the presence of greater concentration of iron and the absence of lactoferrin in formula compared with human milk results in greater in vitro generation of free radicals and lipid peroxidation products. Whether iron-containing formula with lactoferrin administered enterally to preterm infants will result in less free radical generation in vivo has yet to be established.

Apoproteins↗