scholarly journals Inflammatory Biomarkers are Correlated with Some Forms of Regressive Autism Spectrum Disorder

2019 ◽  
Vol 9 (12) ◽  
pp. 366 ◽  
Author(s):  
Margherita Prosperi ◽  
Letizia Guiducci ◽  
Diego G. Peroni ◽  
Chiara Narducci ◽  
Melania Gaggini ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Developmental Delay ◽  
Plasminogen Activator Inhibitor ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Inflammatory Biomarkers ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Gi Symptoms ◽  
Pai 1

Background: Several studies have tried to investigate the role of inflammatory biomarkers in Autism Spectrum Disorder (ASD), and their correlations with clinical phenotypes. Despite the growing research in this topic, existing data are mostly contradictory. Methods: Eighty-five ASD preschoolers were assessed for developmental level, adaptive functioning, gastrointestinal (GI), socio-communicative and psychopathological symptoms. Plasma levels of leptin, resistin, plasminogen activator inhibitor-1 (PAI-1), macrophage chemoattractant protein-1 (CCL2), tumor necrosis factor-alfa (TNF-α), and interleukin-6 (IL-6) were correlated with clinical scores and were compared among different ASD subgroups according to the presence or absence of: (i) GI symptoms, (ii) regressive onset of autism. Results: Proinflammatory cytokines (TNF-α, IL-6 and CCL2) were lower than those reported in previous studies in children with systemic inflammatory conditions. GI symptoms were not correlated with levels of inflammatory biomarkers except for resistin that was lower in ASD-GI children (p = 0.032). Resistin and PAI-1 levels were significantly higher in the group with “regression plus a developmental delay” onset (Reg+DD group) compared to groups without regression or with regression without a developmental delay (p < 0.01 for all). Conclusions: Our results did not highlight the presence of any systemic inflammatory state in ASD subjects neither disentangling children with/without GI symptoms. The Reg + DD group significantly differed from others in some plasmatic values, but these differences failed to discriminate the subgroups as possible distinct ASD endo-phenotypes.

Attention deficit hyperactivity disorder (ADHD) symptoms, comorbid psychopathology, behaviour problems and gastrointestinal symptoms in children and adolescents with autism spectrum disorder

2021 ◽  
pp. 1-11
Author(s):  
Geraldine Leader ◽  
Roisín Moore ◽  
June L. Chen ◽  
Aoife Caher ◽  
Sophia Arndt ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Children And Adolescents ◽  
Short Form ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Behaviour Problems ◽  
Adhd Symptoms ◽  
Hyperactivity Disorder ◽  
Gi Symptoms ◽  
Comorbid Psychopathology

Abstract Objectives: The study aims to investigate attention deficit hyperactivity disorder (ADHD) symptoms, gastrointestinal (GI) symptoms, comorbid psychopathology and behaviour problems in children and adolescents with autism spectrum disorder (ASD). Methods: Parents of 147 children and adolescents with ASD aged 6–18 years completed the Conners 3 Parent-Short Form, Gastrointestinal Symptom Inventory, Behavior Problems Inventory-Short Form and Autism Spectrum Disorder-Comorbid for Children. Results: Fifty-six per cent of children and adolescents had a comorbid diagnosis of ADHD, yet over 70% presented with clinically significant ADHD symptoms. Forty per cent of participants received a diagnosis of ADHD before ASD and 25.6% received a diagnosis of ASD first. Relationships were found between ADHD symptoms and comorbid psychopathology, GI symptoms, and behaviour problems. Conclusions: The outcomes suggest that ADHD is being underestimated as a comorbid disorder of ASD. This may have implications on treatment and interventions for children and adolescents who have a diagnosis of both ASD and ADHD.

Differential Mechanisms of Plasminogen Activator Inhibitor-1 Gene Activation by Transforming Growth Factor-β and Tumor Necrosis Factor-α in Endothelial Cells

2001 ◽  
Vol 86 (12) ◽  
pp. 1563-1572 ◽  
Author(s):  
Yan Chen ◽  
Joanne Sloan-Lancaster ◽  
David Berg ◽  
Mark Richardson ◽  
Brian Grinnell ◽  
...  
Keyword(s):  
Map Kinases ◽  
Transforming Growth Factor ◽  
Gene Activation ◽  
Plasminogen Activator Inhibitor ◽  
Transforming Growth Factor Β ◽  
Promoter Activation ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Pai 1

SummaryPlasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor (SERPIN) specific for tissue-type and urokinase-like plasminogen activators. High plasma PAI-1 activity is a risk factor for thrombotic diseases. Due to the short half-life of PAI-1, regulation of PAI-1 gene expression and secretion of active PAI-1 into the blood stream is important for hemostatic balance. We have investigated transcriptional control of PAI-1 gene expression in bovine aortic endothelial cells (BAECs) and human cell lines using PAI-1 5’ promoter-luciferase reporter assays. Contrary to the cytokine-induced up-regulation of PAI-1 mRNA and protein levels, we found that only transforming growth factor-β (TGF-β) was efficient in inducing PAI-1 promoter activation. Tissue necrosis factor-α (TNF-α) induced a small luciferase activity with the 2.5 kb PAI-1 promoter, but not with the PAI-800/4G/5G and p3TP-lux promoters. Next we investigated whether a lack of response to TNF-α was due to deficient signaling pathways. BAECs responded to TNF-α with robust NFκB promoter activation. TGF-β activated the p38 MAP kinase, while TNF-α activated both the SAPK/JNK and p38 MAP kinases. The ERK1/2 MAP kinases were constitutively activated in BAECs. BAEC therefore responded to TNF-α stimulation with activation of the MAP kinases and the NFκB transcriptional factors. We further measured the messenger RNA stability under the influence by TGF-β and TNF-α and found no difference. PAI-1 gene activation by TNF-α apparently is yet to be defined for the location of the response element and/or the signaling pathway, while TGF-β is the most important cytokine for PAI-1 transcriptional activation through its 5’ proximal promoter.

scholarly journals Rickets treatment improves more than bone health in toddler with autism spectrum disorder: A brief report

2019 ◽  
Vol 7 ◽  
pp. 2050313X1987002 ◽  
Author(s):  
Leah D Stalnaker ◽  
Priya Prasher ◽  
Susan Flesher
Keyword(s):  
Autism Spectrum Disorder ◽  
Vitamin D ◽  
Case Report ◽  
Effective Treatment ◽  
Vitamin D Deficiency ◽  
Developmental Delay ◽  
Bone Health ◽  
Children With Autism ◽  
Autism Spectrum ◽  
Spectrum Disorder

Children with autism spectrum disorder have been found to have lower levels of vitamin D than their peers. Our case report supports the hypothesis that vitamin D may be an effective treatment for developmental delay in autism. In addition, we review the literature surrounding vitamin D deficiency as a potential cause of autism spectrum disorder and the role that vitamin D may play in treatment.

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