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Autism Studies and Related Medical Conditions, January 2009 - TACA

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Abstract:<br />

Impaired social interaction, communication <strong>and</strong> imaginative skills characterize autistic<br />

syndromes. In these syndromes urinary peptide abnormalities, derived from gluten,<br />

gliadin, <strong>and</strong> casein, are reported. They reflect processes with opioid effect. The aim of<br />

this single blind study was to evaluate effect of gluten <strong>and</strong> casein-free diet for children<br />

with autistic syndromes <strong>and</strong> urinary peptide abnormalities. A r<strong>and</strong>omly selected diet <strong>and</strong><br />

control group with 10 children in each group participated. Observations <strong>and</strong> tests were<br />

done before <strong>and</strong> after a period of 1 year. The development for the group of children on<br />

diet was significantly better than for the controls.<br />

Kidd PM.: <strong>Autism</strong>, an extreme challenge to integrative medicine. Part: 1: The<br />

knowledge base. Altern Med Rev. 2002 Aug;7(4):292-316.<br />

Kidd PM.: <strong>Autism</strong>, an extreme challenge to integrative medicine. Part 2: medical<br />

management. Altern Med Rev. 2002 Dec;7(6):472-99.<br />

Hadjivassiliou M, Grunewald RA, Davies-Jones GA: Gluten sensitivity as a<br />

neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. [No abstract<br />

available]<br />

Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, S<strong>and</strong>ers<br />

DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM: The humoral<br />

response in the pathogenesis of gluten ataxia. Neurology 2002 Apr 23;58(8):1221-6.<br />

Abstract: Department of Clinical Neurology, The Royal Hallamshire Hospital, Sheffield,<br />

UK. m.hadjivassiliou@sheffield.ac.uk<br />

OBJECTIVE: To characterize humoral response to cerebellum in patients with gluten<br />

ataxia. BACKGROUND: Gluten ataxia is a common neurologic manifestation of gluten<br />

sensitivity. METHODS: The authors assessed the reactivity of sera from patients with<br />

gluten ataxia (13), newly diagnosed patients with celiac disease without neurologic<br />

dysfunction (24), patients with other causes of cerebellar degeneration (11), <strong>and</strong><br />

healthy control subjects (17) using indirect immunocytochemistry on human cerebellar<br />

<strong>and</strong> rat CNS tissue. Cross-reactivity of a commercial IgG antigliadin antibody with<br />

human cerebellar tissue also was studied. RESULTS: Sera from 12 of 13 patients with<br />

gluten ataxia stained Purkinje cells strongly. Less intense staining was seen in some but<br />

not all sera from patients with newly diagnosed celiac disease without neurologic<br />

dysfunction. At high dilutions (1:800) staining was seen only with sera from patients<br />

with gluten ataxia but not in control subjects. Sera from patients with gluten ataxia also<br />

stained some brainstem <strong>and</strong> cortical neurons in rat CNS tissue. Commercial anti-gliadin<br />

antibody stained human Purkinje cells in a similar manner. Adsorption of the antigliadin<br />

antibodies using crude gliadin abolished the staining in patients with celiac disease<br />

without neurologic dysfunction, but not in those with gluten ataxia. CONCLUSIONS:<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 150

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