INBORN ERRORSIn 1982 the recorded number of human disorders
inherited in simple mendelian fashion/caused by a mutant single gene
amounts to 3,368
[McKusic, V.A., 'Mendelian Inheritance in Man', 6th ed.,Johns Hopkins Univ. Press, Baltimore, 1983].The clinical effects of the inborn errors of metabolism vary from lethality in utero or in early postnatal life, to very severe handicap [Tay-Sachs disease, Hurler's syndrome, homozzygous talassemia, Lesch-Nyan syndrome, Duchenne muscular dystrophy, Huntington's disease, etc.], to restricted life expectancy, to harmlessness. For most inborn errors,
therapy is virtually nonexistent, at present.'Of about 120,000 US babies born each year with a birth defect, 8,000 die during their first year of life......birth defects are the fifth-leading cause of years of potential life lost and contribute substantially to childhood morbidity and long-term disability."
[http://www.cdc.gov/nceh/cddh/BD/bdpghome.htm ]
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The mental retardation, from mild to
severe, is present in
a very high proportion of the most frequent
273 inborn diseases: ~ 33 %.
'An estimated 12 of every 1,000 US school children
have mental retardation'
[ http://www.cdc.gov/nceh/cddh/fact/mrfs.htm
]
Inborn-error d i s e a s e s l e a d i n g to d e a t h perinatal death: - alpha-thalassemia, tetrahydrobiopterin deficiency, hyperammonemia type I & type II, citrullinemia, osteogenesis imperfecta, osteopetrosis, Fanconi syndrome, multiple acyl-CoA dehydrogenation deficiency, erythropoietic porphyria, acute intermittent porphyria, coproporphyria, variegate porphyria, Wolman's disease.
death within 5 years: - nephrogenic diabetes insipidus, tyrosinemia type I, Hyperpipecolic acidemia, Maple syrup urine disease,isovaleric acidemia, 3-hydroxyisobutyril CoA hydrolase deficiency, 3-methyl-3-hydroxy-glutaric acidemia, methylmalonic acidemia, ethanolaminosis, homocysteinemia, hyper-b-alaninemia, carnosinuria, a- 1,4-glucosidase deficiency, a- 1,4-glucanbranching enzyme, inactive liver phosphorilase, galactosemia, triose-phosphate isomerase, folic acid deficiency, combined severe immunodeficiency, chronic granulomatous disease, Crigler-Najjar syndrome type I, sialic acid storage disorder, mucolipidosis, gangliosidosis, juvenile gangliosidosis, Tay-Sachs disease, Sandhoff's disease, sphingolipodystrophy, Gaucher's disease, Niemann-Pick disease type C, triglycerid storage disease, adrenoleukodystrophy, Zellweger's syndrome, Menkes' disease.
death at less than 50 years: - glucose-galactose maladsorption, Batter's syndrome, oxalosis type I, Ehler-Danlos syndrome, alaktasia, isolated pyruvate carboxylase deficiency, pyruvate kinase, mitochondrial myopathy, oculo-cranio-somatic-neuromuscular disease, Kearns-Sayre syndrome, Ophtalmoplegia plus, familial hyperuricemic nephropathy, Lesch-Nyhan syndrome, metachromatic leukodystrophy, Krabbe's disease, Fabry's disease, familial amaurotic idiocy, neuronal ceroid lipofuscinosis, cerebrotendinous xanthomatosis.
Sudden Infant Death Syndrome [SIDS] is the leading cause of death of children 1 month to 1 year of age. In the US 5,000 to 6,000 infant deaths are attributed to SIDS each year. Recent findings seems to attribute SIDS to a defect in the SCHAD, short-chain L-3-hydroxylacyl CoA dehydrogenase [inborn error of metabolism][Treacy, E.P. et al., 2000, J. Pediatr., 137(2), 257-259]