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Survivors of childhood central nervous system (CNS) tumors experience high rates of treatment-related neurologic sequelae. Whether survivors continue to be at increased risk for new events as they age is unknown.
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Neurocognitive impairment in survivors of childhood cancer may be associated with direct neurotoxicity, as well as indirect effects of systemic health complications. We evaluated associations among tr...
Every day 43 children are newly diagnosed with cancer. Fortunately, almost 90% of these childhood cancer patients will survive. However, 60-90% of these survivors will experience late effects, health ...
The cardiac and vascular late sequelae in long-term survivors of childhood cancer (CVSS)-study aimed to quantify the prevalence of cardiovascular risk factors (CVRF) and cardiovascular disease (CVD) i...
An increased risk of becoming overweight has been reported for childhood cancer survivors (CCSs), in particular leukemia survivors, although the evidence is inconclusive.
Survivors of childhood cancer are at increased risk for late effects of cancer therapy, but evidence suggests that adherence to follow-up care is suboptimal. Here, we review the barriers to adherence,...
Advances in cancer therapies have led to increasing numbers of adult survivors of pediatric malignancy. Unfortunately, treatment of childhood cancer continues to require agents designed t...
This feasibility study will determine the psychometric adequacy of a newly developed instrument - Needs Assessment Survey of Adult Childhood Cancer Survivors. Additionally the study will ...
The purpose of this study is to develop a mechanism for utilizing the comprehensive clinical database of childhood cancer survivors at Childrens Hospital Los Angeles (CHLA) for research pu...
Survivors of childhood cancer often suffer treatment-related toxicities, including chronic health conditions, high symptom burden and emotional distress, and decremented functional status ...
RATIONALE: A patient's genes may affect the risk of developing complications, such as congestive heart failure, heart attack, stroke, and second cancer, years after undergoing cancer treat...
Rare congenital metabolism disorders of the urea cycle. The disorders are due to mutations that result in complete (neonatal onset) or partial (childhood or adult onset) inactivity of an enzyme, involved in the urea cycle. Neonatal onset results in clinical features that include irritability, vomiting, lethargy, seizures, NEONATAL HYPOTONIA; RESPIRATORY ALKALOSIS; HYPERAMMONEMIA; coma, and death. Survivors of the neonatal onset and childhood/adult onset disorders share common risks for ENCEPHALOPATHIES, METABOLIC, INBORN; and RESPIRATORY ALKALOSIS due to HYPERAMMONEMIA.
A syndrome characterized by multiple system abnormalities including DWARFISM; PHOTOSENSITIVITY DISORDERS; PREMATURE AGING; and HEARING LOSS. It is caused by mutations of a number of autosomal recessive genes encoding proteins that involve transcriptional-coupled DNA REPAIR processes. Cockayne syndrome is classified by the severity and age of onset. Type I (classical; CSA) is early childhood onset in the second year of life; type II (congenital; CSB) is early onset at birth with severe symptoms; type III (xeroderma pigmentosum; XP) is late childhood onset with mild symptoms.
Pathological conditions (Disorder, SYNDROME, or DISEASE) whose SIGNS AND SYMPTOMS manifest late in the life of an individual.
A group of recessively inherited diseases that feature progressive muscular atrophy and hypotonia. They are classified as type I (Werdnig-Hoffman disease), type II (intermediate form), and type III (Kugelberg-Welander disease). Type I is fatal in infancy, type II has a late infantile onset and is associated with survival into the second or third decade. Type III has its onset in childhood, and is slowly progressive. (J Med Genet 1996 Apr:33(4):281-3)
Autosomal recessive metabolic disorder caused by mutations in PROPIONYL-COA CARBOXYLASE genes that result in dysfunction of branch chain amino acids and of the metabolism of certain fatty acids. Neonatal clinical onset is characterized by severe metabolic acidemia accompanied by hyperammonemia, HYPERGLYCEMIA, lethargy, vomiting, HYPOTONIA; and HEPATOMEGALY. Survivors of the neonatal onset propionic acidemia often show developmental retardation, and intolerance to dietary proteins. Late-onset form of the disease shows mild mental and/or developmental retardation, sometimes without metabolic acidemia.
Pediatrics is the general medicine of childhood. Because of the developmental processes (psychological and physical) of childhood, the involvement of parents, and the social management of conditions at home and at school, pediatrics is a specialty. With ...
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Neurology - Central Nervous System (CNS)
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