NT-Pro-B-Type Natriuretic Peptide Levels in Infants with Failure to Thrive due to Caloric Deprivation

Background. Brain natriuretic peptide and its inactive fragment N-terminal pro-BNP (N-BNP) are reliable markers of ventricular dysfunction in adults and children. We analyzed the impact of nutritional state on N-BNP levels in infants with failure to thrive (FTT) and in infants with severe heart failure (HF). The purpose of this study was to compare N-BNP levels in infants with FTT with infants with severe HF and healthy controls. Methods. In a retrospective cohort study, we compared N-BNP levels from all consecutive infants with FTT and bodyweight below the tenth percentile (caloric deprivation (CD) group) to infants with severe HF. Reference values from infants between 2 and 12 month were taken from the literature and healthy infants. Results. Our results show that infants with FTT (n = 15) had significantly (P < .001) elevated N-BNP values compared with the healthy infants (n = 23), 530 (119–3150) pg/mL versus 115 (15–1121) pg/mL. N-BNP values in this CD group are comparable to the median value of infants with severe HF (n = 12) 673 (408–11310) pg/mL. There is no statistical significant difference in age. Conclusion. Nutritional state has an important impact on N-BNP levels in infants with FTT. We could show comparable levels of N-BNP in infants with FTT and infants with severe HF

Beta-Blocker Therapy and Hemophagocytic Lymphohistiocytosis: A Case Report

Objective. The aim of this paper is to describe a fatal case of hemophagocytic lymphohistiocytosis (HLH) in a patient with severe heart failure, who was treated with low-dose propranolol. Patient and Interventions. We report on a 7-month-old boy with Downs syndrome who was born with an unbalanced, left dominant atrioventricular septal defect and aortic coarctation. Despite coarctation repair and pulmonary artery banding he developed intractable heart failure and fever of unknown origin. Since he remained in heart failure he received a trial of low-dose propranolol to stabilize his cardiopulmonary status, which resulted in unexpected immunomodulatory effects. Measurements and Main Result. Immunoactivation was evidenced by high concentrations of procalcitonin, soluble CD 25, tumor necrosis factor α, and interleukin 6 and 8. Propranolol resulting in hepatic compromise as indicated by high lactate dehydrogenase and alanine aminotransferase levels. A therapeutic switch from propranolol to the β1-receptor blocker metoprolol appeared to be instrumental in hemodynamic improvement and allowed discharge from hospital. However, the infant ultimately died from secondary inflammatory reactivation and intractable pulmonary obstructive disease. The autopsy results revealed HLH. Conclusion. Our case describes HLH secondary to heart failure and Downs syndrome. In this highly activated inflammatory state the beneficial hemodynamic effects of propranolol may be accompanied by immunomodulatory effects and the risk of acute liver failure. HLH occurs with a distinct pathophysiology, and specific treatment might be mandatory to increase the chance of survival