Clinical Hypnosis for Pediatric Gastrointestinal Disorders: A Practical Guide for Clinicians.

Functional abdominal pain disorders (FAPDs) are common in the pediatric population and are associated with a significant reduction in quality of life. Bidirectional communication of the brain-gut axis plays an important role in pain generation and perception in FAPDs. There is a paucity of data on the best approach to treat this group of disorders, with no Food and Drug Administration (FDA)-approved drugs and scarce research to substantiate the use of most medications. Use of hypnosis in pediatric FAPDs is supported by evidence and has long-term benefits of up to at least 5 years beyond completion of treatment, highlighting the importance of incorporating this therapy into the care of these patients. The mechanisms by which clinical hypnosis is beneficial in the treatment of FAPDs is not completely understood, but there is growing evidence that it impacts functioning of the brain-gut axis, potentially through influence on central pain processing, visceral sensitivity, and motility. The lack of side effects or potential for significant harm and low cost makes it an attractive option compared to pharmacologic therapies. This review addresses current barriers to clinical hypnosis including misconceptions among patients and families, lack of trained clinicians, and questions around insurance reimbursement. The recent use of telemedicine and delivery of hypnosis via audio-visual modalities allow more patients to benefit from this treatment. As the evidence base for hypnosis grows, acceptance and training will likely increase as well. Further research is needed to understand how hypnosis works and to develop tools that predict who is most likely to respond to hypnosis. Studies on cost-effectiveness in comparing hypnosis to other therapies for FAPDs will increase evidence for appropriate healthcare utilization. Because hypnosis has applications beyond pain and is child-friendly with minimal to no risk, hypnosis could be an important therapeutic tool in the wider pediatric gastrointestinal population.

Redefining short bowel syndrome in the 21st century.

In 1968, Wilmore and Dudrick reported an infant sustained by parenteral nutrition (PN) providing a potential for survival for children with significant intestinal resections. Increasing usage of TPN over time led to some patients developing Intestinal Failure Associated Liver Disease (IFALD), a leading cause of death and indication for liver/intestinal transplant. Over time, multidisciplinary teams called Intestinal Rehabilitation Programs (IRPs) began providing meticulous and innovative management. Usage of alternative lipid emulsions and lipid minimization strategies have resulted in the decline of IFALD and an increase in long-term and transplant-free survival, even in the setting of ultrashort bowel (< 20 cm). Autologous bowel reconstructive surgeries, such as the serial tapering enteroplasty procedure, have increased the likelihood of achieving enteral autonomy. Since 2007, the number of pediatric intestinal transplants performed has sharply declined and likely attributed to the newer innovations healthcare. Recent data support the need for changes in the listing criteria for intestinal transplantation given the overall improvement in outcomes. Over the last 50 y, the diagnosis of short bowel syndrome has changed from a death sentence to one of hope with a vast improvement of quality of life and survival.

Neonatal iron overload and tissue siderosis due to gestational alloimmune liver disease.

BACKGROUND & AIMS: Gestational alloimmune liver disease is the main cause of the neonatal hemochromatosis phenotype, wherein severe neonatal liver disease is associated with iron overload and extrahepatic tissue siderosis. How fetal liver disease produces extrahepatic siderosis is not known. We hypothesized that fetal liver injury causes deficient hepcidin production and poor regulation of placental iron flux. Under the resulting conditions of iron overload, the tissue pattern of extrahepatic siderosis is determined by the normal expression of proteins involved in the import of non-transferrin-bound iron and the export of cellular iron. METHODS: Liver and extrahepatic tissues from infants with gestational alloimmune liver disease were examined and compared to normal age-appropriate tissues. RESULTS: Serum iron indices indicate iron overload and excess non-transferrin bound iron in gestational alloimmune liver disease. The diseased liver showed significantly reduced hepcidin, hemojuvulin, and transferrin gene expression compared to the normal fetal and neonatal liver. Those extrahepatic tissues that are typically involved in pathological siderosis in neonatal hemochromatosis, whether from normal or diseased newborns, consistently expressed solute carrier family 39 (zinc transporter), member 14 (ZIP14) for non-transferrin-bound iron uptake and expressed little ferroportin for iron export. CONCLUSIONS: Excess non-transferrin-bound iron in gestational alloimmune liver disease may result from fetal liver injury that causes reduced synthesis of key iron regulatory and transport proteins. Whereas, the pattern of extrahepatic siderosis appears to be determined by the normal capacity of various tissues to import non-transferrin-bound iron and not export cellular iron.