TAILIEUCHUNG - Understanding Growth Failure in Children With Homozygous Sickle-Cell Disease

Most SCHIP enrollees lived in families with a working adult (80 percent to 87 percent of enrollees, depending on the study State) who worked full time (63 percent to 74 percent). Although the study States permitted coverage for families with incomes up to as much as 250 percent of the FPL, nearly two-thirds to three-quarters of new enrollees lived in families with incomes equal to or below 150 percent of the FPL. Most new SCHIP enrollees were white (55 percent to 78 percent), but a significant proportion of SCHIP enrollees were black or Hispanic. Compared with white enrollees, minority children enrolled in SCHIP had lower incomes and poorer health status. They also. | Articles Understanding Growth Failure in Children With Homozygous Sickle-Cell Disease T l Journal of Pediatric Oncology Nursing 28 2 67-74 2011 by Association of Pediatric Hematology Oncology Nurses Reprints and permission dOi 1043454210382421 http SAGE Erin L. Bennett RN MSN1 Abstract Sickle-cell disease is the most prevalent genetic hematologic condition in the United States. Numerous studies have demonstrated poor growth and delayed maturation in children with homozygous sickle-cell disease however the pathophysiology remains inadequately understood. Affected children have normal weight and length at birth and then around 6 months of age their growth patterns begin to diverge from the norm. The growth deficits experienced by these children remain a problem with clinical significance and intangible consequences. A review of literature has provided insight into the multifactorial basis of the growth failure experienced by this population. It is important that nurses and health care providers are familiar with the growth patterns unique to sickle-cell disease and recognize their role in clinical practice. Keywords sickle-cell disease growth nutrition Overview of Sickle-Cell Disease Sickle-cell disease SCD is a chronic genetically inherited hemoglobinopathy caused by a point mutation in which valine replaces glutamic acid at the sixth position of the P-globin chain on chromosome 11. The mutation results in the production of sickle hemoglobin Hb S which differs from normal hemoglobin Hb A by its polymerization into a fragile and sickled shape under altered conditions. While in utero fetal hemoglobin Hb F is the most abundant type. Shortly after birth and possibly even during the later months of gestation the amount of circulating Hb F diminishes and Hb A replaces it. Once the transition from fetal to adult hemoglobin is nearly complete individuals with sickle cell begin to experience the sequelae of their

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