Search

Background: In neonatal chylothorax, thoracic lymphatic drainage is ineffective. The resultant effusions often require drainage, leading to a loss of immune components. Affected infants can be managed with formula or defatted human milk feedings low in long-chain triglycerides to decrease lymph production. We hypothesized that there is no significant difference in the immunological profile or antibacterial effect of full-fat and defatted human milk., Methods: Milk from lactating mothers was divided into 1 aliquot that was defatted via centrifugation with the full-fat aliquot as control. Macronutrient content was analyzed with mid-infrared spectroscopy. Flow cytometry was used to measure immune cell populations. Lactoferrin, lysozyme, immunoglobulin (Ig)A, and IgG values were determined using enzyme-linked immunosorbent assay. The antibacterial properties were determined by inoculating paired full-fat and defatted milk samples with Escherichia coli or Streptococcus pneumoniae bacteria and performing colony counts., Results: Compared with full-fat milk, defatted milk demonstrated decreased total energy and fat and increased carbohydrate concentrations. Defatted milk demonstrated a significant decrease in all immune cell populations. There was no difference in IgA, IgG, lysozyme, or lactoferrin concentrations. Both aliquots demonstrated equivalent growth inhibition of E. coli and S. pneumoniae., Conclusions: Unexpectedly, defatted human milk contained significantly less leukocytes than full-fat milk. IgA, IgG, lysozyme, and lactoferrin concentrations were preserved. The ability of defatted milk to inhibit bacterial growth was unaffected, suggesting that the antibacterial benefits of human milk remain after the defatting process. Further investigation regarding the clinical effect of leukocyte loss in defatted milk is warranted., (© 2019 American Society for Parenteral and Enteral Nutrition.)

Left ventricular non-compaction (LVNC) is a rare form of cardiomyopathy. This case reviews a woman with familial LVNC (EF 45%, NYHA class I, evidence of non-sustained ventricular tachycardia pre-pregnancy) who had significant decompensation with heart failure in the third trimester that required early delivery. Deterioration in symptoms and LV function 7 days after delivery required further hospitalization and aggressive treatment. Suppression of lactation with bromocriptine, together with standard heart failure management, has allowed recovery and return to full activities and work. Acknowledged adverse risk factors in LVNC are considered, and pre-pregnancy risk assessment is reviewed. There is no specific treatment for LVNC in pregnancy besides the usual management of dilated cardiomyopathy. This is the ninth case report of LVNC in pregnancy reported in the literature.