Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the FDA recommends imipramine hydrochloride (IMI) only for temporary relief of symptoms of enuresis nocturna (EN), the drug has been applied to a number of other pediatric situations, including the Hyperkinetic Syndrome (HS), childhood depression, somnambulism and pavor nocturnus, school phobia, petit mal epilepsy, allergies, autism, encorpresis and head-banging. We have reviewed the literature, with particular attention to the pharmacokinetics of IMI in children, and its putative mechanisms of action. The drug probably works through a number of different actions, and the futher delineation of these will be of considerable heuristic value. We review the toxic effects of IMI treatment and IMI poisoning in children, and the pediatric literature concerning other antidepressant drugs and lithium carbonate (Li).
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PMID:Imipramine and children: a review and some speculations about the mechanism of drug action. 40 23

Two patients with infantile autism by DSM-III criteria and with atypical bipolar symptomatology were treated with lithium carbonate. Both children demonstrated a significant response with levels above 1.0mEq/liter. Factors that may be useful in discovering patients with autism who may respond to lithium treatment include a family history of bipolar illness; extreme hyperactivity not responsive to a stimulant; a definite cyclic component to symptomatic behaviors; sustained laughter, irritability, or giddiness that is not stereotypic; and/or the presence of many or all of the symptom criteria for bipolar disorder.
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PMID:Lithium carbonate in the treatment of two patients with infantile autism and atypical bipolar symptomatology. 342 1

It has been previously suggested that large amounts of oxalate in plasma could play a role in autism by binding to the bilobal iron transport protein transferrin (hTF), thereby interfering with iron metabolism by inhibiting the delivery of iron to cells. By examining the effect of the substitution of oxalate for the physiologically utilized synergistic carbonate anion in each lobe of hTF, we sought to provide a molecular basis for or against such a role. Our work clearly shows both qualitatively (6 M urea gels) and quantitatively (kinetic analysis by stopped-flow spectrofluorimetry) that the presence of oxalate in place of carbonate in each binding site of hTF does indeed greatly interfere with the removal of iron from each lobe (in the absence and presence of the specific hTF receptor). However, we also clearly demonstrate that once the iron is bound within each lobe of hTF, neither anion can displace the other. Additionally, as verified by urea gels and electrospray mass spectrometry, formation of completely homogeneous hTF-anion complexes requires that all iron must first be removed and hTF then reloaded with iron in the presence of either carbonate or oxalate. Significantly, experiments described here show that carbonate is the preferred binding partner; i.e., even if an equal amount of each anion is available during the iron loading process, the hTF-carbonate complex is formed.
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PMID:Human serum transferrin: is there a link among autism, high oxalate levels, and iron deficiency anemia? 2415 9