title: Psychoendocrine and psychoneuroimmunological mechanisms in the comorbidity of atopic eczema and attention deficit/hyperactivity disorder.
abstract: Epidemiological data indicate that atopic eczema (AE) in infancy significantly increases the risk for attention deficit/hyperactivity disorder (ADHD) in later life. The underlying pathophysiological mechanisms of this comorbidity are unknown. We propose that the release of inflammatory cytokines caused by the allergic inflammation and/or elevated levels of psychological stress as a result of the chronic disease interfere with the maturation of prefrontal cortex regions and neurotransmitter systems involved ADHD pathology. Alternatively, increased stress levels in ADHD patients may trigger AE via neuroimmunological mechanisms. In a third model, AE and ADHD may be viewed as two separate disorders with one or more shared risk factors (e.g., genetics, prenatal stress) that increase the susceptibility for both disorders leading to the co-occurrence of AE and ADHD. Future investigation of these three models may lead to a better understanding of the mechanisms underlying the observed comorbidity between AE and ADHD and further, to targeted interdisciplinary primary prevention and treatment strategies.
authors.affiliation: Department of Biopsychology, Technical University of Dresden, Dresden, Germany. buske@biopsych.tu-dresden.de
authors.forename: A
authors.initials: A
authors.lastname: Buske-Kirschbaum
authors.forename: J
authors.initials: J
authors.lastname: Schmitt
authors.forename: F
authors.initials: F
authors.lastname: Plessow
authors.forename: M
authors.initials: M
authors.lastname: Romanos
authors.forename: S
authors.initials: S
authors.lastname: Weidinger
authors.forename: V
authors.initials: V
authors.lastname: Roessner
mesh_terms: D001289:Attention Deficit Disorder with Hyperactivity / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology* / Q000523:psychology; D001923:Brain Chemistry; D015897:Comorbidity; D016207:Cytokines / Q000032:analysis / Q000502:physiology; D003876:Dermatitis, Atopic / Q000196:embryology / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology* / Q000523:psychology; D004298:Dopamine / Q000502:physiology; D005260:Female; D000091344:Filaggrin Proteins; D020022:Genetic Predisposition to Disease; D006179:Gyrus Cinguli / Q000276:immunology / Q000503:physiopathology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007073:Immunoglobulin E / Q000276:immunology; D007223:Infant; D007381:Intermediate Filament Proteins / Q000172:deficiency; D015213:Neuroimmunomodulation / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D017397:Prefrontal Cortex / Q000276:immunology / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011598:Psychoneuroimmunology; D012306:Risk; D012867:Skin / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins; D007073:Immunoglobulin E; D004298:Dopamine