Oseltamivir treatment and prophylaxis in a neonatal intensive care unit during a 2009 H1N1 influenza outbreak.

OBJECTIVE: To evaluate safety of oseltamivir in neonates with significant comorbidities in a level-III neonatal intensive care unit during an outbreak of 2009 H1N1 influenza. STUDY DESIGN: We performed a retrospective chart review of neonates who received oseltamivir for treatment and prophylaxis of influenza during the outbreak. RESULT: A total of 11 neonates received twice daily dosing and 21 neonates received once daily dosing (12 to 25 mg per dose) for treatment and prophylaxis of influenza, respectively. Age ranged from 2 days to 11.4 months (mean, 2.1 months). Corrected gestational age and weight at initiation of oseltamivir ranged from 32 to 86 weeks (mean, 41 weeks) and 775 to 8635 g (mean, 3074 g), respectively. All had complex underlying conditions. Oseltamivir was well tolerated. Neurologic adverse effects or mortality attributable to oseltamivir were not identified. Mild rash and gastrointestinal signs in four infants resolved without oseltamivir discontinuation. Three showed a transient rise in transaminases; all returned to baseline after completing therapy. CONCLUSION: Oseltamivir appears to be well tolerated in preterm and term neonates and infants with complex underlying conditions. More studies are needed to determine optimal dosing for treatment and prophylaxis in this vulnerable age group.

Hypercholesterolemia superimposed by experimental hypertension induces differential distribution of collagen and elastin.

We studied the mural distribution of collagen types I and III and tropoelastin in enhanced experimental atherogenesis induced in rabbits by hyperlipidemia superimposed by hypertension. Animals were fed a high-cholesterol diet for 5 weeks and also subjected to midthoracic aortic coarctation for 4 weeks. Serum cholesterol levels were increased and blood pressure was elevated proximal to the coarctation. Foam cell lesions developed in the aorta proximal to the coarctation. In situ hybridization and immunohistochemistry showed that gene expression of collagen types I and III and tropoelastin was upregulated, with a differential distribution across the arterial wall. New collagen type I was mainly distributed in the intima, the outer media, and the adventitia. New collagen type III was spread more uniformly across the wall, including the adventitia, whereas tropoelastin was mainly localized in intimal foam cell lesions. Morphometric data showed an increase in wall thickness. These results suggest that collagen types I and III play a role in remodeling of the aortic wall in response to hypertension. The remarkable involvement of the adventitia in this response indicates that the adventitia is an important component of the arterial wall. Tropoelastin is closely associated with foam cell lesion formation, suggesting a role for this component in atherogenesis as well.