[Chylothorax]. / Il chilotorace.

Chylothorax is the accumulation of chyle in the pleural space. In newborns the congenital form is often prenatal diagnosed, while the late variety originates to damage to the thoracic duct by cardiac surgery, diaphragmatic hernia, etc. Clinical presentation results from the accumulation of pleural fluid and the symptoms depends on the size of the effusion. The treatment needs both medical and surgical care. The pleural cavity should be drained via thoracocentesis, and total parenteral nutrition should be started. Afterward fat-free diet with the addition of medium-chain triglycerides could be initiate. Somatostatin and octreotide have been successfully employed, mainly in post-surgery chylothorax. Surgery should be considered when medical management fails. Some approaches are reported, and thoracic duct ligation, pleurodesis and pleuroperitoneal shunts are the most utilized. The prognosis of chylothorax depends on the etiology, and it is consequence of a variety of treatments that may influence the outcome.

Total parenteral nutrition in patients with short bowel syndrome.

Nowadays short bowel syndrome (SBS) is quite frequent, because of more aggressive surgical and medical approaches to the management of neonatal intra-addominal catastrophes. Intestinal rehabilitation can be reached in case of SBS with a strategy that merges nutritional, pharmacologic and surgical approaches to achieve the ultimate goal of enteral nutrition. Long-term clinical nutrition which combines total parenteral nutrition (TPN) and enteral nutrition is required for the adaptation process. Long-term TPN can, however, be associated with mechanical, septic and metabolic complications, most of which have been consistently reduced by a better understanding of the prerequisites for its application and by improvements in parenteral solutions. Parenteral nutrition associated cholestasis (PNAC) and liver disease (PNALD) remain indeed the most worrisome complications and bear with them a high mortality rate. Their prevention will further improve the role of TPN in patients with SBS. The etiology of PNAC and PNALD, although elusive, is thought to be multifactorial and proposed theories also include problems arising from lipid emulsions. Parenteral nutrition, that includes n-3 fatty acids, appear to diminish the extent of the inflammatory response thought to be responsible for PNAC and PNALD. This article will attempt to review the role of TPN in the rehabilitation process and discuss energy and macronutrients requirements.

Modulation of recombinant GABA receptor/channel subunits by domain-specific antibodies in Xenopus oocytes.

To study interaction of specific antibodies with the GABA receptor/channel, antisera were raised against the extracellular domains of the GABAA receptor/channel beta2 subunit, gamma2 subunit and the GABAC receptor/channel rho1 subunit. The specificity of the antibodies was characterized by immunocytochemistry and by Western blotting of transfected FDC-P1 cells expressing recombinant GABA receptor/channel subunits. The effects of the antibodies on whole-cell currents in Xenopus laevis oocytes expressing homomeric recombinant GABA receptor/channel beta2, gamma2, and rho1 were studied using two-microelectrode voltage clamp. In the absence of GABA, anti-alpha2, anti-gamma2, and anti-rho1 antisera elicited whole-cell currents in oocytes expressing beta2, gamma2, and rho1 subunits, respectively. The effect of antibody on channel activation was concentration-dependent. The whole-cell currents induced by anti-beta2 and anti-gamma2 were several-fold greater than those induced by application of 100 microm GABA. In Xenopus oocytes expressing recombinant rho1 subunits, GABA-induced whole-cell currents were inhibited by the anti-rho1 antibody. In contrast, the GABA-induced whole-cell currents were potentiated several-fold by anti-beta2 and anti-gamma2 antibodies in Xenopus oocytes expressing homomeric beta2 and gamma2 subunits. Our studies indicate that antibodies specific to the N-terminal domain of GABA receptor/channel subunits can modulate the neurotransmitter receptor function.