Variations in disease patterns are influenced by inborn factors such as genetic background, sex, and ethnicity. It is also clear that acquired life experiences, some of which are common to all (e.g., aging) and some that are unique to individuals (e.g., illnesses, habits, diet, and toxin and environmental exposures), may combine in a stochastic manner to alter tissue and influence vulnerability to injury. Disease vulnerabilities and characteristics are determined not only by who you are at birth, but also by whom you have become. When applied to vascular inflammatory diseases, these variables may be most relevant with regard to regional differences in endothelial cells, subendothelial matrix, vascular smooth muscle, and the response of each to a variety of experiences or injuries. Recovery from injury will, in turn, be dependent on an effective immune response. The response should eliminate the cause of injury and also effectively down-regulate the immune response, so that further injury does not result from the immune response itself. Although it is likely that acquired changes in the vessel wall play a role in determining disease patterns, it is also likely that acquired changes in immune function may be required for disease expression. Certain vasculitides are clearly age- and sex-biased. Age and sex influences may be related to a variety of factors, including changes in hormonal function. To solve the mysteries of disease patterns in vasculitis will require more complete studies of the differences that exist in structure, chemistry, and response to injury of targeted vessels and tissues, compared with sites that are spared. Conducting studies to elucidate gene and protein expression profiles of targeted versus spared sites will be a complex but necessary task.
Disclosure of Interest None Declared
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