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B Laboratory Findings
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Cytogenetic analysis should always be performed even though most patients will have simple trisomy for chromosome 21 to detect unbalanced translocations; such patients may have a parent with a balanced translocation, and there will be a substantial recurrence risk of Down syndrome in future offspring
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FRAGILE X MENTAL RETARDATION
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ESSENTIALS OF DIAGNOSIS
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Mental retardation in males Learning disabilities or mental retardation in females Large testes after puberty Expanded trinucleotide repeat in the FMR1 gene
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The presence of a fetus with Down syndrome can be detected in many pregnancies in the early second trimester through screening maternal serum for -fetoprotein and certain hormones ( multiple marker screening ) and by detecting increased nuchal thickness on fetal ultrasound The risk of bearing a child with Down syndrome increases exponentially with the age of the mother at conception and begins a marked
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Clinical Findings
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A Symptoms and Signs
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This X-linked condition accounts for more cases of mental retardation in males than any condition except Down syn-
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CMDT 2008
Sutherland GR et al Fragile X syndrome and other causes of Xlinked mental handicap In: Emery and Rimoin s Principles and Practice of Medical Genetics, 5th ed Rimoin DL et al (editors) Churchill Livingstone, 2007 Terracciano A et al Fragile X syndrome Am J Med Genet C Semin Med Genet 2005 Aug 15;137(1):32 7 [PMID: 16010677]
drome; about 1 in 4000 to 1 in 6000 males is affected; the condition also affects intellectual function in females about 50% less frequently than in males
B Laboratory Findings
The first marker for this condition was a small gap, or fragile site, evident near the tip of the long arm of the X chromosome Subsequently, the condition was found to be due to expansion of a trinucleotide repeat (CGG) near a gene called FMR1 All individuals have some CGG repeats in this location, but as the number increases beyond 52, the chances of further expansion during spermatogenesis or oogenesis increase Being born with one FMR1 allele with 200 or more repeats results in mental retardation in most men, and in about 60% of women The more repeats, the greater the likelihood that further expansion will occur during gametogenesis; this results in anticipation, in which the disorder can worsen from one generation to the next Affected (heterozygous) women show no physical signs other than early menopause, but they may have learning difficulties or frank retardation Affected males show macroorchidism (enlarged testes) after puberty, large ears and a prominent jaw, a high-pitched voice, and mental retardation Some males show evidence of a mild connective tissue defect, with joint hypermobility and mitral valve prolapse Men who are not retarded but carry an increased number of CGG repeats in the FMR1 locus (premutation carriers) are at increased risk for developing intention tremor, ataxia, or both Likewise, women who are premutation carriers (55 200 CGG repeats) are at increased risk for premature ovarian failure and mild cognitive or behavioral abnormalities Male and female premutation carriers are at risk for the development of tremor and ataxia beyond middle age Because of the relatively high prevalence of premutation carriers in the general population, older people in whom any of these problems develop should undergo testing of the FMR1 locus
GAUCHER DISEASE
ESSENTIALS OF DIAGNOSIS
Deficiency of -glucocerebrosidase Anemia and thrombocytopenia Hypersplenism
Clinical Findings
A Symptoms and Signs
Gaucher disease has an autosomal recessive pattern of inheritance A deficiency of -glucocerebrosidase causes an accumulation of sphingolipid within phagocytic cells throughout the body Anemia and thrombocytopenia are common and may be symptomatic; both are due primarily to hypersplenism, but marrow infiltration with Gaucher cells may be a contributing factor Cortical erosions of bones, especially the vertebrae and femur, are due to local infarctions, but the mechanism is unclear Episodes of bone pain (termed crises ) are reminiscent of those in sickle cell disease A hip fracture in a patient with a palpable spleen especially in a Jewish person of Eastern European origin suggests the possibility of Gaucher disease Two uncommon forms of Gaucher disease, called type II and type III, involve neurologic accumulation of sphingolipid and a variety of neurologic problems Type II is of infantile onset and has a poor prognosis Heterozygotes for Gaucher disease may be at increased risk for developing Parkinson disease
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