Neonatal Visual Evoked Potentials in Infants Born to Mothers Prescribed Methadone.

Neonatal Visual Evoked Potentials in Infants Born to Mothers Prescribed Methadone.

Filed under: Drug and Alcohol Rehabilitation

Pediatrics. 2013 Feb 18;
McGlone L, Hamilton R, McCulloch DL, Boulton R, Bradnam MS, Weaver LT, Mactier H

OBJECTIVE:Drug misuse in pregnancy is associated with impaired infant visual development. Pilot data showed abnormal flash visual evoked potentials (VEPs) in neonates exposed to methadone in utero, but results were confounded by intrauterine growth restriction, gestation, and ongoing drug misuse. This large cohort study aimed to clarify the effects on neonatal flash VEPs of maternal drug misuse in pregnancy, including prescription of substitute methadone and subsequent development of neonatal abstinence syndrome.METHODS:This was a prospective cohort study. Flash VEPs were recorded within 3 days of birth from 100 healthy infants of drug-misusing mothers prescribed substitute methadone during pregnancy and 50 comparison infants matched for birth weight, gestation, and socioeconomic deprivation. VEP morphology was classified as mature, typical, or immature, and amplitudes and implicit times of the major waveform components measured. Drug exposure was determined by maternal history, maternal and infant urine, and meconium toxicology.RESULTS:VEPs from maternal drug-exposed infants were more likely to be of immature waveform (P < .001) and were smaller in overall amplitude (median 27 µV vs 39 µV, P < .001) compared with non-drug-exposed infants. Most infants were exposed to illicit drugs in addition to prescribed methadone; differences in VEP parameters were independently associated with maternal prescribed methadone and persisted after correcting for birth weight, cigarette smoking, and excess in utero alcohol exposure.CONCLUSIONS:In utero exposure to prescribed substitute methadone is associated with altered flash VEPs in the newborn period and these infants may warrant early clinical visual assessment. HubMed – drug

Severe DRESS Syndrome Managed With Therapeutic Plasma Exchange.

Filed under: Drug and Alcohol Rehabilitation

Pediatrics. 2013 Feb 18;
Alexander T, Iglesia E, Park Y, Duncan D, Peden D, Sheikh S, Ferris M

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare but increasingly described phenomenon of immune activation and organ dysfunction in association with a wide variety of medications. This reaction shows a broad spectrum of clinical presentation and severity, ranging from mild to lethal. Treatment strategies of immune suppression appear be helpful in some cases, but treatment failures occur frequently with reported mortality rates of 5% to 10%. We present a pediatric case of DRESS syndrome associated with either lamotrigine or bupropion, leading to multiorgan involvement and life-threatening complications of respiratory failure and cardiac arrest. After failing to improve with removal of these medications and administration of systemic corticosteroids, our patient showed dramatic, sustained clinical response to therapeutic plasma exchange. To our knowledge, this is the first reported case of therapeutic plasma exchange used for life-threatening DRESS syndrome in a pediatric patient. This case suggests needed research for this therapeutic option in life-threatening DRESS syndrome resistant to high-dose steroids.
HubMed – drug

Dynamics of Anemia in Relation to Parasitic Infections, Micronutrient Status, and Growing Age in South-Central Cote d’Ivoire.

Filed under: Drug and Alcohol Rehabilitation

J Infect Dis. 2013 Feb 18;
Righetti AA, Adiossan LG, Ouattara M, Glinz D, Hurrell RF, N’goran EK, Wegmüller R, Utzinger J

Background.?Parasitic diseases (e.g., malaria and helminthiases) exert enormous burdens on public health and social wellbeing. Moreover, parasitic infections are important causes of anemia in tropical Africa, exacerbated by lack of diversified diet, inflammatory and genetic diseases. There is a paucity of longitudinal studies monitoring the dynamics of anemia in relation to the aforementioned parameters.Methods.?We designed a 14-month prospective longitudinal study in three cohorts (i.e., infants aged 6-23 months, 6-8 year-old children, and women aged 15-25 years), in the Taabo health demographic surveillance system located in south-central Côte d’Ivoire. Parasitological, hematological, and micronutrient data were obtained at repeated cross-sectional surveys, utilizing standardized, quality-controlled methods.Results.?We found that young age, Plasmodium and Schistosoma infections, cellular iron deficiency, and stunting were significantly negatively associated with hemoglobin concentration. Moreover, iron status biomarkers (i.e., ferritin and soluble transferrin receptor) were significantly associated with inflammatory parameters.Conclusions.?Our results call for effective prevention and control measures targeting parasitic diseases and iron deficiency. These measures might include the distribution of long-lasting insecticidal nets, intermittent preventive treatment for malaria, regular anthelmintic drug administration, and improved intake of bioavailable iron, coupled with health and nutritional education, improved hygiene, water, and sanitation.
HubMed – drug

Diacylglycerol glycerol acyltransferase-1 localizes hepatitis C virus NS5A protein to lipid droplets and enhances NS5A interaction with the viral capsid core.

Filed under: Drug and Alcohol Rehabilitation

J Biol Chem. 2013 Feb 18;
Camus G, Herker E, Modi AA, Haas JT, Ramage HR, Farese RV, Ott M

The triglyceride-synthesizing enzyme acyl CoA:diacylglycerol acyltransferase 1 (DGAT1) plays a critical role in hepatitis C virus (HCV) infection by recruiting the HCV capsid protein, core, onto the surface of cellular lipid droplets (LDs). Here, we find a new interaction between the non-structural protein NS5A and DGAT1, and show that the trafficking of NS5A to LDs depends on DGAT1 activity. DGAT1 forms a complex with NS5A and core and facilitates the interaction between both viral proteins. A catalytically inactive mutant of DGAT1 (H426A) blocks the localization of NS5A, but not core, to LDs in a dominant-negative manner, and impairs the release of infectious viral particles, underscoring the importance of DGAT1-mediated translocation of NS5A to LDs in viral particle production. We propose a model whereby DGAT1 serves as a cellular hub for HCV core and NS5A proteins, guiding both onto the surface of the same subset of LDs, those generated by DGAT1. These results highlight the critical role of DGAT1 as a host factor for HCV infection and as a potential drug target for antiviral therapy.
HubMed – drug

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