Low serum myeloperoxidase in autistic children with gastrointestinal disease

Low Serum Alpha-1 Antitrypsin (AAT) in Family Members of Individuals with Autism Correlates with PiMZ Genotype

Biomarker Insights ◽

10.4137/bmi.s1115 ◽

2009 ◽

Vol 4 ◽

pp. BMI.S1115 ◽

Cited By ~ 6

Author(s):

Anthony J. Russo ◽

Lauren Neville ◽

Christine Wroge

Keyword(s):

Gastrointestinal Disease ◽

Family Members ◽

Serum Levels ◽

Normal Serum ◽

Autistic Children ◽

Respiratory Problems ◽

Low Levels ◽

Alpha 1 Antitrypsin ◽

And Gender ◽

Low Serum

Aim Deficiency of Alpha-1-antitrypsin (AAT) can be a genetic condition that increases the risk of developing liver, lung and possibly gastrointestinal disease. Since many autistic children also have gastrointestinal disorders, this study was designed to measure serum concentration of AAT and establish AAT genotypes in autistic children, age and gender matched non-autistic siblings, parents and controls. Subjects and Methods We used an indirect ELISA with monoclonal IgG to AAT to measure AAT serum concentrations in 71 members from 16 families of individuals with autism and 18 controls (no family history of autism). We used a duplex polymerase chain reaction to detect M, S and Z alleles for alpha-1 antitrypsin expression in 52 members of 12 of the above families. Results A significantly high number of autistic family members had lower than normal serum levels of AAT when compared to controls. Autistic children with regressive onset had significantly lower levels of AAT compared to controls, and a significant number of autistic children with low serum AAT also had hyperbilirubinemia, gastrointestinal disease and respiratory problems. We also found that a significantly high number of these individuals had the PiMZ genotype and correspondingly low levels of serum alpha-1 antitrypsin. Discussion Knowing that low levels of alpha-1 antitrypsin may be inherited, and that low levels of AAT may be associated with GI disease in autistic children, genotyping autistic children may help identify individuals susceptible to developing digestive problems.

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Decreased Serum Hepatocyte Growth Factor (HGF) in Autistic Children with severe Gastrointestinal Disease

Biomarker Insights ◽

10.4137/bmi.s3656 ◽

2009 ◽

Vol 4 ◽

pp. BMI.S3656 ◽

Cited By ~ 10

Author(s):

A.J. Russo ◽

A. Krigsman ◽

B. Jepson ◽

Andrew Wakefield

Keyword(s):

Growth Factor ◽

Hepatocyte Growth Factor ◽

Gastrointestinal Disease ◽

Serum Levels ◽

Autistic Children ◽

Functional Connection ◽

Disease Symptoms ◽

Lymphoid Nodular Hyperplasia ◽

Lymphoid Nodules ◽

Hepatocyte Growth

Aim To assess serum Hepatocyte Growth Factor (HGF) levels in autistic children with severe gastrointestinal (GI) disease and to test the hypothesis that there is a relationship between GI pathology and HGF concentration. Subjects and Methods Serum from 29 autistic children with chronic digestive disease (symptoms for a minimum of 6–12 months), most with ileo-colonic lymphoid nodular hyperplasia (LNH—markedly enlarged lymphoid nodules) and inflammation of the colorectum, small bowel and/or stomach), and 31 controls (11 age matched autistic children with no GI disease, 11 age matched non autistic children without GI disease and 9 age matched non autistic children with GI disease) were tested for HGF using ELISAs. HGF concentration of autistic children with GI disease was compared to GI disease severity. Results Autistic children with GI disease had significantly lower serum levels of HGF compared to controls (autistic without GI disease; p = 0.0005, non autistic with no GI disease; p = 0.0001, and non autistic with GI disease; p = 0.001). Collectively, all autistic children had significantly lower HGF levels when compared to non autistic children (p < 0.0001). We did not find any relationship between severity of GI disease and HGF concentration in autistic children with GI disease. Discussion These results suggest an association between HGF serum levels and the presence of GI disease in autistic children and explain a potential functional connection between the Met gene and autism. The concentration of serum HGF may be a useful biomarker for autistic children, especially those with severe GI disease.

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Approach to the patient with hypo-/hyperkalaemia

10.1093/med/9780199592548.003.0034_update_001 ◽

2018 ◽

Author(s):

Charles S. Wingo ◽

I. David Weiner

Keyword(s):

Differential Diagnosis ◽

Drug Administration ◽

Serum Potassium ◽

Gastrointestinal Disease ◽

Large Population ◽

Clinical History ◽

Population Based ◽

Electrolyte Disorder ◽

Laboratory Values ◽

Low Serum

The differential diagnosis and approach to patients with high or low serum potassium are described. Patients with either abnormality have an increased mortality in large population-based studies. Most have significant renal, cardiovascular, endocrine, liver, or gastrointestinal disease. They are frequently taking prescription or other drugs and the evaluation of their electrolyte disorder should not be conducted in isolation, but within the context of their disease or diseases. The presence of isolated hypokalaemia or hyperkalaemia in the absence of these other diseases or any apparent drug administration should prompt the clinician to re-consider the clinical history and the reported laboratory values.

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Low serum Alpha-1 Antitrypsin Associated with Anti-PR-3 AncA in Autistic Children with GI Disease

Genomics Insights ◽

10.4137/gei.s2918 ◽

2009 ◽

Vol 2 ◽

pp. GEI.S2918 ◽

Cited By ~ 8

Author(s):

A.J. Russo ◽

A. Krigsman ◽

B. Jepson ◽

Andrew Wakefield

Keyword(s):

Digestive Disease ◽

Serum Levels ◽

High Serum ◽

Autistic Children ◽

Severity Of Disease ◽

High Severity ◽

Nodular Hyperplasia ◽

Alpha 1 Antitrypsin ◽

Lymphoid Nodular Hyperplasia ◽

Low Serum

Aim To assess the possible relationship between serum alpha-1 antitrypsin (AAT) levels and anti-neutrophil cytoplasmic antibodies (ANCA) in autistic children with severe GI disease and to test the hypothesis that there is an association between low serum AAT levels, the presence of ANCA and inflammatory GI disease seen in some autistic children. Subjects and Methods Serum from 40 autistic children with chronic digestive disease (many with ileo-colonic lymphoid nodular hyperplasia (LNH) and inflammation of the colorectum, small bowel and/or stomach), and 41 controls (21 age matched autistic children with no GI disease and 20 age matched children without autism or GI disease) were tested using ELISAs designed to quantitate ANCA (anti-PR3), AAT and PR3 levels. Results We found that a significant number of autistic children with chronic digestive disease had anti-PR3 ANCA, high serum PR3 and high severity of disease when compared to controls. This same group of autistic children had low serum levels of AAT compared to controls, which also correlated with the presence of anti-PR3 ANCA, high serum PR3, as well as the severity of intestinal disease, particularly LNH and severe erythema. Discussion These results suggest a relationship between low AAT levels, ANCA and severity of GI disease seen in a subpopulation of ASD individuals. We suggest that low AAT levels may result in high levels of PR3, which may, in turn be associated with the presence of ANCA.

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Relationship between Celiac Disease Markers and Gastrointestinal Disease in Children with Autism

Immunology and Immunogenetics Insights ◽

10.4137/iii.s3662 ◽

2010 ◽

Vol 2 ◽

pp. III.S3662

Author(s):

A.J. Russo

Keyword(s):

Celiac Disease ◽

Significant Relationship ◽

Gastrointestinal Disease ◽

Children With Autism ◽

Autistic Children ◽

Low Level ◽

Disease Markers ◽

Significant Difference ◽

Alpha 1 Antitrypsin

Aim This study was designed to determine if there is a relationship between celiac disease (CD) and the presence of gastrointestinal disease (GI) disease in children with autism. Subjects and Methods One hundred twenty-two children were tested for IgG and IgA anti-transglutaminase autoantibodies (55 autistic children with GI disease, 28 non autistic children with no GI disease, 30 autistic children with no GI disease, and 9 non autistic children with GI Disease). We also compared the presence/level of these autoantibodies to presence of anti-neutrophil cytoplasmic antibodies (ANCA) and level of Alpha-1 Antitrypsin (AAT). Results We did not find a significant difference in the level of anti-transglutaminase IgG or IgA in autistic children with GI disease compared to controls. However, we found a significant relationship between the presence of ANCA and low-level IgG anti-transglutaminase IgG in children with autism and GI disease. Discussion Although there appears to be no relationship between these celiac disease markers and the presence of GI disease in autistic children, these results suggest a possible association between sub diagnostic levels of anti-transglutaminase IgG and the presence of ANCA, and therefore, supports the hypothesis that there is a generalized autoimmune dysfunction in autistic children with GI disease.

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Fibronexus-Like Adhesion Sites are Present at the Invasive Zones of Human Epidermoid Carcinomas

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100053280 ◽

1982 ◽

Vol 40 ◽

pp. 106-109

Author(s):

Irwin I. Singer

Keyword(s):

Cell Cycle ◽

Serum Concentration ◽

Substrate Binding ◽

High Serum ◽

Adhesion Sites ◽

Substrate Adhesion ◽

Focal Contacts ◽

Adhesion Complex ◽

Low Serum

Our previous results indicate that two types of fibronectin-cytoskeletal associations may be formed at the fibroblast surface: dorsal matrixbinding fibronexuses generated in high serum (5% FBS) cultures, and ventral substrate-adhering units formed in low serum (0.3% FBS) cultures. The substrate-adhering fibronexus consists of at least vinculin (VN) and actin in its cytoplasmic leg, and fibronectin (FN) as one of its major extracellular components. This substrate-adhesion complex is localized in focal contacts, the sites of closest substratum approach visualized with interference reflection microscopy, which appear to be the major points of cell-tosubstrate adhesion. In fibroblasts, the latter substrate-binding complex is characteristic of cultures that are arrested at the G1 phase of the cell cycle due to the low serum concentration in their medium. These arrested fibroblasts are very well spread, flattened, and immobile.

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Development of Neural Structure and Function in Autism Spectrum Disorder: Potential Implications for Learning Language

American Journal of Speech-Language Pathology ◽

10.1044/2020_ajslp-19-00209 ◽

2020 ◽

Vol 29 (4) ◽

pp. 1783-1797

Author(s):

Kelly L. Coburn ◽

Diane L. Williams

Keyword(s):

Autism Spectrum Disorder ◽

Language Development ◽

Diffusion Tensor ◽

Autism Spectrum ◽

Language Intervention ◽

Spectrum Disorder ◽

Autistic Children ◽

Neural Structure ◽

Complex Information ◽

And Function

Purpose Neurodevelopmental processes that begin during gestation and continue throughout childhood typically support language development. Understanding these processes can help us to understand the disruptions to language that occur in neurodevelopmental conditions, such as autism spectrum disorder (ASD). Method For this tutorial, we conducted a focused literature review on typical postnatal brain development and structural and functional magnetic resonance imaging, diffusion tensor imaging, magnetoencephalography, and electroencephalography studies of the neurodevelopmental differences that occur in ASD. We then integrated this knowledge with the literature on evidence-based speech-language intervention practices for autistic children. Results In ASD, structural differences include altered patterns of cortical growth and myelination. Functional differences occur at all brain levels, from lateralization of cortical functions to the rhythmic activations of single neurons. Neuronal oscillations, in particular, could help explain disrupted language development by elucidating the timing differences that contribute to altered functional connectivity, complex information processing, and speech parsing. Findings related to implicit statistical learning, explicit task learning, multisensory integration, and reinforcement in ASD are also discussed. Conclusions Consideration of the neural differences in autistic children provides additional scientific support for current recommended language intervention practices. Recommendations consistent with these neurological findings include the use of short, simple utterances; repetition of syntactic structures using varied vocabulary; pause time; visual supports; and individualized sensory modifications.

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