Vaginal bleeding in a newborn as initial presentation of uterus didelphys.

Vaginal bleeding of the newborn is described as a normal phenomenon, occurring physiologically in a subset of baby girls as a response to decreased oestrogen levels in the postnatal period compared with in utero exposure. Here, we present the case of heavy vaginal bleeding prompting an evaluation via transabdominal ultrasound, which was ultimately diagnostic for uterus didelphys. We suggest that neonates with uterus didelphys are predisposed to heavy bleeding due to relatively larger amount of the endometrial tissue in two cavities. While diagnosis of Müllerian anomalies is typically made in adulthood, an earlier diagnosis facilitates timely medical and surgical intervention and prompts screening for concurrent and associated conditions. In summary, we recommend routine consideration of transabdominal ultrasound to investigate abnormal vaginal bleeding in the newborn.

Octreotide and low-fat breast milk in postoperative chylothorax.

Chylothorax is a rare complication following cavo-pulmonary connection and can lead to significant morbidity in infants and young children. We report here the case of a 3-month-old infant who underwent bilateral cavo-pulmonary connections, and developed severe chylothorax refractory to the usual conservative and surgical treatments. His chylothorax resolved after using a combination of parenteral octreotide (Sandostatin, Novartis Pharmaceuticals, East Hanover, NJ) and low-fat breast milk.

Histamine antagonizes tumor necrosis factor (TNF) signaling by stimulating TNF receptor shedding from the cell surface and Golgi storage pool.

Tumor necrosis factor (TNF) activates pro-inflammatory functions of vascular endothelial cells (EC) through binding to receptor type 1 (TNFR1) molecules expressed on the cell surface. The majority of TNFR1 molecules are localized to the Golgi apparatus. Soluble forms of TNFR1 (as well as of TNFR2) can be shed from the EC surface and inhibit TNF actions. The relationships among cell surface, Golgi-associated, and shed forms of TNFR1 are unclear. Here we report that histamine causes transient loss of surface TNFR1, TNFR1 shedding, and mobilization of TNFR1 molecules from the Golgi in cultured human EC. The Golgi pool of TNFR1 serves both to replenish cell surface receptors and as a source of shed receptor. Histamine-induced shedding is blocked by TNF-alpha protease inhibitor, an inhibitor of TNF-alpha-converting enzyme, and through the H1 receptor via a MEK-1/p42 and p44 mitogen-activated protein kinase pathway. Cultured EC with histamine-induced surface receptor loss become transiently refractory to TNF. Histamine injection into human skin engrafted on immunodeficient mice similarly caused shedding of TNFR1 and diminished TNF-mediated induction of endothelial adhesion molecules. These results both clarify relationships among TNFR1 populations and reveal a novel anti-inflammatory activity of histamine.