HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Figures All Versions of this Article: db06-0880v1 56/5/1189    most recent Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pietropaolo, M. Articles by Kuller, L. H. Search for Related Content PubMed PubMed Citation Articles by Pietropaolo, M. Articles by Kuller, L. H. Social Bookmarking                What's this?

Heterogeneity of Diabetes Mellitus. Unraveling a Dispute: Is Systemic Inflammation Related To Islet Autoimmunity?

¹Laboratory of Immunogenetics, The Brehm Center for Type 1 diabetes and Analysis, Division of Metabolism, Endocrinology & Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109
²Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261

Correspondence: maxtp{at}umich.edu

Diabetes mellitus is an emblematic example of a heterogeneous disease. Systemic inflammation has emerged as a prominent factor in the Type 2 diabetes (T2DM) pathoetiology, but it remains ill defined in Type 1 diabetes (T1DM). There is a wide spectrum of associations between inflammatory responses and diabetic syndromes. At one end of this spectrum there is T1DM for which there is convincing evidence that chronic inflammation of pancreatic islets is a central aspect of disease pathogenesis. At the opposite end, is T2DM that is clearly associated with systemic inflammation, which could be either the cause or simply mark the underlying pathology. Accumulating evidence has substantiated that a subgroup of adult patients clinically diagnosed with T2DM exhibit autoantibody responses to islet autoantigens. The presence of these immunologic abnormalities is associated with a severe insulin secretory defect and the absence of signs of systemic inflammation as documented by plasma C-reactive protein and fibrinogen levels that are comparable with those of control populations. Islet autoantibody evaluation should be part of the diagnostic assessment for clinically diagnosed T2DM not only because it might predict the rate of progression to insulin requirement in adult populations but also to identify a pathogenically distinct disease phenotype characterized by the absence of systemic inflammation and its related disorders. A more appropriate characterization of this subgroup of clinically diagnosed T2DM diabetes of autoimmune pathogenesis, will promote future research into the etiology, natural history as well as treatment.

CiteULike

Del.icio.us

Digg

Reddit

Technorati