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  • 1
    Electronic Resource
    Electronic Resource
    Serum zinc concentration during childhood (1977)
    Springer
    European journal of pediatrics 126 (1977), S. 199-202 
    Details
    ISSN: 1432-1076
    Keywords: Zinc ; Serum ; Normal values ; Children ; Infants ; Cord blood ; Adults
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum zinc concentrations in subjects of different ages were estimated by neutron activation analysis to obtain reliable reference values for the diagnosis of primary or secondary zinc deficiency during childhood. In these healthy individuals a small age-dependent variation of the mean values was found. Serum zinc concentrations were lower in cord blood (mean value: 880×10−9 g/ml) and in infants (mean value: 820×10−9 g/ml) than in adults (mean value 1178×10−9 g/ml). In comparison to these values, the serum zinc concentration in a patient with secondary zinc deficiency and 4 patients with acrodermatitis enteropathica was reduced to about 25% of normal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00477045
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The selenium state of healthy children (1977)
    Springer
    European journal of pediatrics 125 (1977), S. 81-88 
    Details
    ISSN: 1432-1076
    Keywords: Selenium ; Glutathione peroxidase ; Normal values ; Blood ; Infants ; Children ; Milk ; Nutrition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The selenium concentration of serum is age-dependent. The median value at birth ( $$\tilde x$$ =50×10−9g/ml) amounts to half of the median value of adults ( $$\tilde x$$ =102×10−9g/ml). After a decrease in early infancy to $$\tilde x$$ =34×10−9g/ml it steadily increases to $$\tilde x$$ =58×10−9g/ml in the second half of the first year, to $$\tilde x$$ =82×10−9g/ml in 1–5 year old children, and to $$\tilde x$$ =92×10−9g/ml in school children. The activities of the selenium containing enzyme glutathione peroxidase of erythrocytes are also reduced in early infancy (x=7.2±0.36 U37/g Hb), whereas the enzyme activities of cord blood erythrocytes (x=8.72±0.76 U37/g Hb) are in the same range as those of older children or adults. The selenium content of some commercially available milk formulas for infants are lower than those of human and cow's milk.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00470608
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Atypical vitamin B12-unresponsive methylmalonic aciduria in a sibship with severe progressive encephalomyelopathy: A new genetic disease? (1996)
    Springer
    European journal of pediatrics 155 (1996), S. 398-403 
    Details
    ISSN: 1432-1076
    Keywords: Methylmalonic aciduria ; Vitamin B12 ; GABA ; Cerebrospinal fluid ; Encephalomyelopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report on two siblings, a girl of 7 years and a boy of 2 years, who presented in infancy with hypotonia, athetoid movements, myopathy and severe developmental delay. The progressive clinical course was characterized by ophthalmoplegia, pyramidal tract signs, loss of visual contanct and failure to thrive. The older sister died at the age of 7 years. The younger brother followed an almost identical clinical course. MRI of the brain revealed bilateral hypodensities and atrophy of the putamen. Neurophysiological investigations were consistent with peripheral neuropathy. Investigations for neurometabolic disorders in urine, plasma and CSF of both patients revealed a consistent increase of methylmalonic acid in urine, plasma and CSF as well as borderline low free GABA in CSF. Except for an inconstant elevation of lactate in the boy, metabolic acidosis, hypoglycaemia, episodic ketoacidosis, or hyperammonaemia, the usual concomitants of organoacidopathies, were absent in both children. Homocystinuria was excluded. Methylmalonic aciduria did not respond to antibiotic treatment, vitamin B12 therapy nor dietary protein restriction. Incorporation of [14C]propionate into protein in cultured fibroblasts was pathologically but inconsistently decreased. Both patients' cell lines showed only minimal response to hydroxocobalamin and normal methylmalonyl-CoA mutase activity. Conclusion Even though the definitive undorlying enzymatic defect in this sibship remains obscure our results suggest a new genetic disorder. This report illustrates that hitherto undescribed metabolic disorders remain to be elucidated even in long investigated areas of intermediary metabolism such as methylmalonic aciduria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01955272
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Atypical vitamin B12-unresponsive methylmalonic aciduria in a sibship with severe progressive encephalomyelopathy: a new genetic disease? (1996)
    Springer
    European journal of pediatrics 155 (1996), S. 398-403 
    Details
    ISSN: 1432-1076
    Keywords: Key words Methylmalonic ; aciduria ; Vitamin B12 ; GABA ; Cerebrospinal fluid ; Encephalomyelopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report on two siblings, a girl of 7 years and a boy of 2 years, who presented in infancy with hypotonia, athetoid movements, myopathy and severe developmental delay. The progressive clinical course was characterized by ophthalmoplegia, pyramidal tract signs, loss of visual contact and failure to thrive. The older sister died at the age of 7 years. The younger brother followed an almost identical clinical course. MRI of the brain revealed bilateral hypodensities and atrophy of the putamen. Neurophysiological investigations were consistent with peripheral neuropathy. Investigations for neurometabolic disorders in urine, plasma and CSF of both patients revealed a consistent increase of methylmalonic acid in urine, plasma and CSF as well as borderline low free GABA in CSF. Except for an inconstant elevation of lactate in the boy, metabolic acidosis, hypoglycaemia, episodic ketoacidosis, or hyperammonaemia, the usual concomitants of organoacidopathies, were absent in both children. Homocystinuria was excluded. Methylmalonic aciduria did not respond to antibiotic treatment, vitamin B12 therapy nor dietary protein restriction. Incorporation of [14C]propionate into protein in cultured fibroblasts was pathologically but inconsistently decreased. Both patients’ cell lines showed only minimal response to hydroxocobalamin and normal methylmalonyl-CoA mutase activity. Conclusion Even though the definitive underlying enzymatic defect in this sibship remains obscure our results suggest a new genetic disorder. This report illustrates that hitherto undescribed metabolic disorders remain to be elucidated even in long investigated areas of intermediary metabolism such as methylmalonic aciduria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01955272
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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