Monday, November 21, 2005

Types of Asthma and Their Clinical Features

as presented by Brigette Hales, M.Sc.

There are three forms of asthma known, for all of which the underlying causes have not been entirely elucidated.

Allergic asthma, also known as extrinsic asthma, may begin during childhood and persist into adulthood. It is linked to an immune response, as is the case with allergic reactions (1). Non-allergic asthma is considered late-onset asthma, presenting typically during adulthood. Also referred to as intrinsic asthma, it is triggered by factors unrelated to allergies and the resulting symptoms – at least partially reversible with medication – are not associated with an allergic reaction, meaning it is not considered an immune response (2) . Occupational asthma is typically associated with exposure to fumes, gases, dust or other substances harmful to the airways while working, causing onset, or recurrence of asthmatic symptoms. Occupational asthma can be either allergic or non-allergic in nature, and can be more prevalent in persons with a previous family history of allergies or asthma (3).

Typical symptoms are similar across all forms of asthma and generally include wheezing, shortness of breath, chest tightness, coughing, as well as potential runny nose, nasal congestion and eye irritation, depending on the severity and form of the asthma attack (4). Severity of this disease varies by the individual, and requires equally diverse treatment options to meet the medical needs of each asthmatic.

Mechanism of Asthma

The airway constriction that is characteristic of asthma is influenced by a number of physiological and environmental factors, including increased bronchial contractility, altered permeability of the bronchial mucosa, humoral and cellular mediators of inflammation, dysfunctional neural regulation and exposure to environmental stimuli (allergens) (5).

Although the exact underlying causes of asthma are not entirely understood, asthma has been primarily described as an inflammatory disease. It can be triggered by degranulation of mast cells with the release of several immune mediators in the lower respiratory tract, leading to contraction of bronchial smooth muscle tissues and subsequent constriction of the airway. This is further exacerbated by edema within the airway, inflammation mediated by the immune response, and the increased secretion of mucus (6). The degranulation of mast cells has been linked to a class of immunoglobulins known as IgE – specific antibodies with a high affinity for receptors found on the surface of these asthma and allergy-related immune cells (7). Persons suffering from both asthma and allergies typically have atopy – a higher propensity to form the IgE antibody (8). Although asthma is not considered hereditary, atopy is an inherited trait (9), with several of the causative genes having been located on the human chromosomes (18). Overall, asthma is caused by a combination of allergic and non-allergic mechanisms, either developed over time or due to a genetic predisposition.


(1) Barnes, P. G., S. 2000. Asthma: Second Edition, Second Edition ed. Martin Dunitz Ltd., London, UK.
(2) Asthma and Allergy Foundation of America Website -
(3) American Academy of Allergy, Asthma and Immunology Website - (2005)
(4) 2003. DrugDigest - Asthma Drugs & Vitamins Website -,20041,5,00.html. E-Drug Digest
(5) Pinto Pereira, L. M., F. A. Orrett, and M. Balbirsingh. 1996. Physiological perspectives of therapy in bronchial hyperreactivity. Can J Anaesth 43:700-13.
(6) Kuby, J. 1997. Hypersensitive Reactions - Immune Effector Mechanisms, p. 413-442. In D. Allen (ed.), Immunology: Third Edition, Third Edition ed. W.H. Freeman and Company, New York
(7) Nadel, J. A., and W. W. Busse. 1998. Asthma. Am J Respir Crit Care Med 157:S130-8
(8) Kay, A. 2002. The cells and mediators of allergic inflammation. Clin Exp All Rev 2:8-12.
(9) Global Initiative for Asthma Website Glossary -

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