Endocrinology Metabolism

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By J. M. Saudubray, H. Ogier de Baulny, C. Charpentier (auth.), Dr. John Fernandes, Professor Jean-Marie Saudubray, Professor Georges Van den Berghe (eds.)

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Sample text

Liver size 2. Characteristic time schedule of hypoglycemia (unpredictable, postprandial, or after fasting) 3. Association with lactic acidosis 4. Association with hyperketosis or hypoketosis Other clinical signs of interest are hepatic failure, vascular hypotension, dehydration, short stature, neonatal body size (head circumference, weight, height), and evidence of encephalopathy, myopathy, or cardiomyopathy. Liver size can be used to separate the hypoglycemias into two large groups, as discussed below.

Disorders with disturbances of organic- and aminoacid metabolism are numerous. PDH deficiency presents frequently with peripheral neuropathy, intermittent ataxia, and slight or moderate hyperlactacidemia (see "Hyperlactacidemias" above). Several respiratorychain disorders first cause ataxia, intention tremor, dysarthria, epilepsy, myopathy, and (eventually) various multivisceral failures. 3-Hydroxyacyl-CoAdehydrogenase deficiency, L-2-hydroxyglutaric aciduria, 3-methylglutaconic aciduria, MMA, and PA disturb organic-acid excretion significantly, though sometimes only slightly and intermittently.

Mucopolysaccharidosis types I and II, mucolipidosis type III, oligosaccharidosis, Austin disease, Niemann-Pick disease type C, Gaucher disease type III, and lactosyl ceramidosis are usually easy to recognize. Mucolipidosis type IV, which causes major visual impairment by the end of the first year of life, sometimes associated with dystonia, presents with characteristic cytoplasmic membranous bodies in cells. In SanFilippo syndrome, coarse facies and bone changes may be very subtle or absent. Peroxisomal disorders may present at this age, with progressive mental deterioration, retinitis pigmentosa, and deafness, very similar to Usher syndrome type II.

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