Children etiology

The etiology of enuresis is poorly understood, but there is a clear genetic link. The incidence in children from families in whom there are no members with enuresis, where one parent had enuresis as a child, and where both parents had enuresis as children are 14%, 44%, and 77%, respectively. Loci for enuresis have been located on chromosomes 12,13, and 22. Sleep disorders are not considered major contributors with the exception of sleep apnea. Enuresis occurs in all sleep stages in proportion to the time spent in each stage. However, a small proportion of individuals are not aroused from sleep by bladder distention and have uninhibited bladder contractions preceding enuresis. 

Blatt, S. J., Homann, E. (1992). Parent-child interaction in the etiology of dependent and self-critical depression. Clinical Psychology Review, 12, 47-91. 

Although the etiological relationship between TS and ADHD is in dispute, it is clear that those individuals with both TS and ADHD are at a much greater risk for a variety of untoward outcomes (Carter et al., 2000). Uninformed peers frequently tease individuals with TS. They are often regarded as less likeable, more aggressive, and more withdrawn than their classmates (Bawden et al., 1998). These social difficulties are amplified in a child with TS who also has ADHD. In such cases, their level of social skill is often several years behind their peers. 

Brent, D.A. and Kolko, D.J. (1998) Psychotherapy definitions, mechanisms of action, and relatioship to etiological models./. Abnorm Child Psycholo 26 17—25. 

Goodman R, Stevenson J. A twin study of hyperactivity, II The etiologic role of genes, family relationships, and perinatal adversity. J Child Psychol Psychiatry 1989 30 691-709. 

Gillis JJ, Gilger JW, Pennington BF. Attention deficit disorder in reading-disabled twins evidence for a genetic etiology. J Abnorm Child Psychol 1992 20 303-315. 

A 6-month-old child was breast-fed exclusively by a mother who had been a strict vegetarian for at least 7 years. He was totally unresponsive to stimuli. His hemoglobin was 5.7 g/dL, and his bone marrow aspirates showed megaloblastic changes in blood cells. His serum folate and iron were normal. His urine contained increased amounts of homocystine, methylmalonic acid, and glycine. Propose a reason for this infant s illness, and discuss its biochemical etiology. Discuss other possible reasons for the same or similar symptoms in a patient. Explain the abnormal serum and urine chemistries. 

About 75% of cases of hepatitis in the neonate are idiopathic giant cell hepatitis, a disorder of unknown etiology characterized by cholestatic jaundice. There is a familial trend that may reflect an autosomal recessive inheritance. Jaundice appears withm the first 2 weeks. The child initially appears well and gains weight. The liver and spleen then become enlarged and stools become pale. Serum aminotransferases are usually >400 U/L the prothrombin time is prolonged. Liver biopsy reveals characteristic giant cells with hepatocyte... 

Despite important contributions of research into the cause of AD, the complicated genetic, environmental, and immunologic mechanisms that produce AD are not completely understood. The hereditary component of AD s etiology is particularly strong, as children with one affected parent have a 60% likelihood of having an atopic disease. If both parents are afflicted, the child has an 80% chance of developing an atopic condition. Paternal AD and asthma are stronger contributors to this risk, in contrast to maternal history. Most patients with AD are found to have elevated eosinophils and serum... 

IDA is a leading cause of infant morbidity and mortality in the world. The age of the child can yield some clues to the etiology of the anemia. Age- and sex-adjusted norms need to be utilized in interpretation of lab results in pediatric patients. Primary prevention of IDA is the goal. A therapeutic trial of oral iron is the standard of care. EPO may be used in anemia of prematurity (AOP). 

Weidenheim KM, Goodman L, Dickson DW, GiUberg C, Rastam M, Rapin I (2001) Etiology and pathophysiology of autistic behaviour Clues from two cases with unusual variant of neuroaxonal dystrophy. J Child Neurol 16 809-819. 

In 1942 Calvin married Genevieve Jemtegaard. After their first child Elin s death, related to Rh factor incompatibility, Calvin and his wife were part of an interdisciplinary project that investigated the etiology of the disease. They helped to determine the composition and structure of the Rh factor, named elinin for their daughter. 

Pincus, J.H. (1972) Subacute necrotizing encephalomyelopa-thy (Leigh s disease) a consideration of clinical features and etiology. Dev. Med. Child Neurol. 14 87-101. 

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