Chronic immune stimulation as a contributing cause of chronic disease in opiate addiction including multi-system ageing.
Evidence of immune stimulation has been noted in opiate dependent patients for many decades. Documented changes have included lymphadenopathy, round cell infiltration of the hepatic portal triads, diffuse peri-bronchitis, hyperglobulinaemia, lymphocytosis, monocytosis, systemic cytokine stimulation, and cytokine and chemokine activation within the neuraxis. A parallel literature describes an elevated list of chronic degenerative disease as common in such patients including neurodegenerative conditions, atherosclerosis, nephrosclerosis, hepatic fibrosis and cirrhosis, chronic obstructive and fibrotic lung disease, osteoporosis, chronic periodontitis, various cancers, hair greying, and stem cell suppression. All of these disorders are now known to have an important immunological role in their pathogenic pathways. The multisystem nature of these myriad changes strongly suggest that the ageing process itself is stimulated in these patients. The link between the immunostimulation on the one hand and the elevated and temporally advanced nature of the chronic degenerative diseases on the other appears not to have been made in the literature. Moreover as immunostimulation is also believed to be an important, potent and principal contributor to the ageing process it appears that experimental and studies of this putative link are warranted. Verification of such an hypothesis would also carry management implications for dose and duration of chronic pain and addiction treatment, pharmacotherapeutic selection, and novel treatments such as long term naltrexone implant therapy and heroin trials.
Reece
Albert Stuart
AS
School of Psychiatry and Clinical Neurosciences, University of Western Australia, Australia. sreece@bigpond.net.au
D000375:Aging / Q000276:immunology*; D002908:Chronic Disease; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D009293:Opioid-Related Disorders / Q000150:complications* / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology
D051193:Toll-Like Receptors