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Medical advances in pediatric oncology have led to increases in survival but the long-term adverse effects of treatment in childhood cancer survivors have not yet been examined in depth. In this systematic review, we aimed to study the prevalence and risk factors of late-onset cardiomyopathy (LOCM) among survivors of childhood lymphoma treated with anthracyclines.
This article was published in the following journal.
Name: Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheorese
As more children survive acute myeloid leukemia (AML) it is increasingly important to assess possible late effects of the intensive treatment. Hearing loss has only sporadically been reported in survi...
The impacts of radiotherapy dose and exposed cardiac volume, select chemotherapeutic agents, and age at exposure on risk for late-onset cardiac disease in survivors of childhood cancer remain unresolv...
Taking into consideration the progress in cancer treatment, an increase in the number of adult survivors of childhood cancer is expected. These survivors will have received treatment that predisposes ...
Treatment for childhood acute lymphoblastic leukemia has evolved over the past five decades, with moderation of traditional chemotherapy and radiotherapy and the introduction of targeted immune-based ...
This study aimed to examine the level and predictors of knowledge of late effects risks from childhood cancer treatment in adolescent and young adult (AYA) survivors.
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...
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...
The purpose of this research study is to try and identify markers in childhood cancer survivors to help predict if they will develop late effects from their cancer treatment.
The goal of this study is to better characterize peripartum cardiomyoapthy or pregnancy-related cardiomyopathy by enrolling as many PPCM survivors as possible using both direct and web-bas...
While thoracic radiation therapy (TRT) has been a primary component in successful treatment of a variety of childhood and adult cancers, the exposure to this treatment has been associated ...
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.
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.
A behavior disorder originating in childhood in which the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity. Although most individuals have symptoms of both inattention and hyperactivity-impulsivity, one or the other pattern may be predominant. The disorder is more frequent in males than females. Onset is in childhood. Symptoms often attenuate during late adolescence although a minority experience the full complement of symptoms into mid-adulthood. (From DSM-IV)
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 ...