Are attention deficit hyperactivity disorder and chronic fatigue syndrome allergy related? what is fibromyalgia?

Despite the progress made in the field of allergy-immunology in recent years, there are a group of diseases that the allergist-immunologist may be called on to manage in which their precise etiologies have not been identified but that appear to be initiated or exacerbated by allergic mechanisms. Attention deficit hyperactivity disorder (ADHD), chronic fatigue syndrome (CFS), and fibromyalgia (FM) fall into this category of disorders. Although the precise etiology of ADHD still remains unknown, the most prevalent theory is that it represents a neurobiologically based developmental disability leading to inadequate production of the neurotransmitter dopamine. In patients with CFS, there appears to be a fundamental dysfunction of the neuroendocrine-immunological system with deficiencies of immunological and neurological function, which, together with chronic viral infection, may lead to a sequence of events responsible for the symptoms of this disorder. FM appears to be a variant of CFS with a predominance of hypothalamic pituitary axis dysfunction. The disorder is characterized by chronic widespread pain and the finding of 11/18 tender points on examination. Now, there is emerging evidence to suggest that adverse reactions to foods or food components also may be associated with behavioral disturbances that may play a role in each of these disorders. An understanding of the interactive responses involved in the neuroendocrine-immunological network is essential for a comprehension of the pathophysiology of ADHD, CFS, and FM and the role of allergies appears to be an important triggering event in each of the disorders.

Developmental immunology: clinical application to allergy-immunology.

BACKGROUND: An increase in prevalence of allergic diseases has been seen at an unprecedented rate in many countries throughout the world. Associated with this increase in allergic disease has been a disturbing increase in morbidity and mortality of such diseases as asthma despite the availability of several new therapeutic agents over the past 2 to 3 decades. The search for both environmental factors, eg, new allergens, as well as biologic markers of genetic susceptibility, eg, respiratory viruses, has yielded considerable promise for an explanation for this rising prevalence of allergic disease. OBJECTIVE: To present a central unifying hypothesis based upon recent knowledge concerning the developing human immune system and its interaction with external environmental factors, particularly viral infections, as a basis for a clearer understanding of the changing faces of the allergic diseases throughout the lifespan of the individual. DATA SOURCES: English language articles were selected from PubMed, as well as selected abstracts that would have immediate, practical clinical implications. RESULTS: Review of the current literature strongly suggests a relationship between delayed acquisition of Th1 function in the allergy-prone infant, not only as a predictive marker of susceptibility to the development of allergic disease but also as an explanation for the unique vulnerability of these infants to viral infection, eg, bronchiolitis. Furthermore, viral infection during early development in the allergy-prone infant appears to facilitate allergic sensitization in early infancy. This interesting triad of immune deficiency, viral infection, and atopic genetic susceptibility may provide a basis for early detection of allergic disease and may offer new intervention strategies for the prevention of allergic and infectious disease in the young infant.

IgE and non-IgE food allergy.

BACKGROUND: Food allergy (FA) is characterized by an abnormal immunologic reactivity to food proteins. The gastro-intestinal tract serves not only a nutritive function but also is a major immunologic organ. Although previously thought to be triggered primarily by an IgE-mediated mechanism of injury, considerable evidence now suggests that non-IgE mechanisms may also be involved in the pathogenesis of FA. OBJECTIVE: To review the immunologic disturbances that occur in FA and to correlate these with the clinical manifestations expressed in affected target organs based upon a classification of IgE and non-IgE mechanisms. METHODS: Data collected from a computerized MEDLINE search were used for the analysis of the following topics: immediate GI hypersensitivity, oral allergy syndrome, acute urticaria and angioedema, acute bronchospasm, celiac disease, cow's milk enteropathy, dietary protein enterocolitis, breast milk colitis, proctolitis, proctitis, dermatitis herpetiformis, Heiner syndrome, eosinophilic gastroenteritis, atopic dermatitis, asthma, attention-deficit-hyperactivity disorder and behavioral disorders, as well as systems affected by mucosal associated lymphoid tissue-mediated injury of associated lymphoid tissues and the immunologic deviation to Th1 or Th2 mechanisms of FA. CONCLUSIONS: The results of this review allow the construction of a central, unifying hypothesis for a new classification of FA as follows: the clinical manifestations of FA, expressed in affected target organs, may be the result of immunologic injury mediated by interaction of food antigens with contiguous elements of mucosal associated lymphoid tissue. These appear to be modulated by relative imbalances of the Th1/Th2 paradigm, which may be the ultimate determinant governing the expression of FA as IgE-mediated, non--IgE-mediated, or mixed forms of IgE/non-IgE mechanisms of FA.