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NotificationsNotify me of updates to TYPE 1 DIABETES MELLITUS AND AUTOIMMUNE GASTRITIS pp. 511-515
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Authors:  (Núria Alonso, Berta Soldevila, Eva María Martínez-Cáceres, Anna Sanmartí, Department of Endocrinology and Nutrition, Hospital Universitari “Germans Trias i Pujol”, Badalona, Spain, and others)
Type 1 diabetes mellitus (T1D) is an organ-specific autoimmune disease characterized by
T-cell-mediated destruction of pancreatic beta cells. Patients with T1D show an increased
prevalence of associated organ-specific autoimmune diseases: fifteen to 30% have
autoimmune thyroid disease (AITD), 4-9% celiac disease, 0.5-4% pernicious anemia and
around 0.5% Addison’s disease [1]. The overlap of different autoimmune disorders has led to
the concept of autoimmune polyendocrine syndrome (APS) with the clinical or subclinical
involvement of several organs in the same subject. APS2 is defined by the presence of
primary adrenocortical insufficiency of an autoimmune origin together with either
autoimmune thyroid disease (Schmidt syndrome) or T1D (Carpenter syndrome) in the same
individual. In these patients, other endocrine autoimmune disorders occur with increased
frequency, i.e. 1-25% pernicious anemia [2]. Each of these diseases has an associated
morbidity and may be detected in the preclinical phase by expression of autoantibodies.
Prospective studies have shown that autoantibodies are reliable and specific markers for
patients at risk of developing an autoimmune disease [3,4,5].
Autoimmune gastritis (type A) and pernicious anemia are common autoimmune diseases
with a respective prevalence of 2 and 0.15-1% in the general population and being 3- to 5-
fold increased in patients with T1D [6]. Autoimmune gastritis involves the fundus and body
of the stomach and spares the antrum and is characterized by the presence of circulating
autoantibodies to parietal cells (PCA) (60-85%) and to their secretory product, intrinsic factor (IFI) (30-40%). It is caused by a pathogenic CD4+ T cell response to the gastric proton
pump, H/K ATPase, an abundant heterodimeric membrane protein of parietal cells. Chronic
autoaggression to the gastric proton pump may result in decreased acid secretion,
hypergastrinemia and decreased iron absorption that can lead to iron deficiency anemia. In
the later stage of the disease, pernicious anemia may result from vitamin B12 deficiency [7].
In patients with T1D, PCA are found in 10-15% of children and 15-25% of adults [8].
Immunological risk factors that have been associated with PCA positivity include persistent
islet cell antibody positivity, glutamic acid decarboxylase (GAD)-65 antibody positivity, and
thyroid peroxidase autoantibody positivity [6]. The association with GAD-65 antibodies
might be explained by the fact that GAD-65 is not only present in the pancreas and brain but
can also be found in the thyroid gland and stomach.
The association between T1D and organ-specific autoimmune diseases can be explained
by the sharing of a common genetic background (HLA antigens) but also by a defective
immunoregulation or a poor ability to develop tolerance to autoantigens. In T1D patients, a
weak association has been observed between PCA positivity and the HLADQA10501B10301
haplotype linked to HLA-DR5 [9]. In mouse models of autoimmune
gastritis, four distinct genetic regions conferring susceptibility to autoimmune gastritis have
been identified and are called Gasa 1, 2, 3 and 4. Importantly, three of these four
susceptibility loci are non-major histocompatibility complex genes that colocalize with those
of T1D and this is the strongest concordance identified between any two autoimmune
diseases so far. It is therefore likely that a subset of genes contribute susceptibility to both
diabetes and gastritis in mice and humans [10]. 

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