Celiac disease and type I (Insulin-Dependent) diabetes mellitus in childhood: Follow-up study

Lorini, Renata; Scotta, M. S.; Cortona, L.; Avanzini, Maria Antonietta; Vitali, Letizia; Giacomo, Costantino De; Scaramuzza, Andrea; Severi, F

doi:10.1016/1056-8727(96)00056-6

Cited by 33 publications

(24 citation statements)

References 22 publications

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“…It is thought that the malabsorption associated with type I autoimmune polyglandular syndrome is due to CD. Two case studies (57,111) have been reported of autoimmune polyglandular syndrome and CD. Based upon the HLA haplotype analysis (DQ8 predominance), the association may represent genetic predisposition rather than casual association.…”

Section: Autoimmune Endocrine Disorders and CDmentioning

confidence: 99%

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Celiac Disease-Associated Autoimmune Endocrinopathies

Kumar

Rajadhyaksha

Wortsman

2001

Clin Diagn Lab Immunol

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3Celiac disease (CD) is an autoimmune disorder induced by gluten intake in genetically susceptible individuals. It is characterized by the presence of serum antibodies to endomysium, reticulin, gliadin, and tissue transglutaminase. The incidence of CD in various autoimmune disorders is increased 10-to 30-fold in comparison to the general population, although in many cases CD is clinically asymptomatic or silent. The identification of such cases with CD is important since it may help in the control of type I diabetes or endocrine functions in general, as well as in the prevention of long-term complications of CD, such as lymphoma. It is believed that CD may predispose an individual to other autoimmune disorders such as type I diabetes, autoimmune thyroid, and other endocrine diseases and that gluten may be a possible trigger. The onset of type I diabetes at an early age in patients with CD, compared to non-CD, and the prevention or delay in onset of diabetes by gluten-free diet in genetically predisposed individuals substantiates this antigen trigger hypothesis. Early identification of CD patients in highly susceptible population may result in the treatment of subclinical CD and improved control of associated disorders.Autoimmunity as a concept evolved from the beginning of this century, when Ehrlich and Morgenroth (26) introduced the phenomenon of "horror autotoxicus," i.e., fear of selfpoisoning. Subsequently, many diseases were recognized with etiology arising from the abnormal reaction of the immune system to self antigens. These observations laid the foundation for establishing postulates that are characteristic of an autoimmune disease (4, 7). Since then, several hypotheses have been put forward regarding the mechanisms of autoimmunity (22,76,84,110,118).In general, autoimmune disorders can be classified as either organ specific or non-organ specific. In organ-specific autoimmune diseases, the autoantibodies are specifically directed against antigens localized in a particular organ and are often detected in circulation. Examples of organ-specific autoimmunity include Hashimoto's thyroiditis, type I diabetes, and myasthenia gravis.In contrast, the non-organ-specific autoimmune disorders are characterized by the presence of autoantibodies directed against ubiquitous antigens (not specific to a particular organ). This results in the involvement of several organs and is often characterized by the presence of specific circulating immune complexes. Non-organ-specific autoimmunity includes diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and scleroderma.Epidemiologic studies have shown that genetic factors are involved in host susceptibility to autoimmune disease. For example, the concordance rate of a particular autoimmune diseases is much higher in monozygotic twins in comparison to fraternal twins (17). Moreover, this incidence is much higher in organ-specific autoimmune disorders in comparison to nonorgan-specific disorders. Thus, in Grave's thyrotoxicosis, Hashimoto's disease, a...

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Section: Autoimmune Endocrine Disorders and CDmentioning

confidence: 99%

“…Addison's disease is an autoimmune disorder characterized by the presence of autoantibodies to antigens in the adrenal cortex (57,111). Adrenal cortex antibodies are directed against the steroidogenic enzyme 21-hydroxylase (36,41,95).…”

Section: Autoimmune Endocrine Disorders and CDmentioning

confidence: 99%

Celiac Disease-Associated Autoimmune Endocrinopathies

Kumar

Rajadhyaksha

Wortsman

2001

Clin Diagn Lab Immunol

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“…The prevalence of both hypoand hyperthyroidism was not different from that of controls, while the prevalence of autoimmune thyroid disease with euthyroidism was 13% in patients and 4.7% in controls (32). In a different study, investigators performed thyroid antibody tests and thyroid echography in 47 patients with CD and 91 healthy controls and found that CD patients had a three-to fourfold increase in the incidence of thyroid autoimmunity (30). Moreover, other studies have reported an association of idiopathic hypoparathyroidism with CD.…”

Section: Gluten Sensitivity and Autoimmune Endocrine Disordersmentioning

confidence: 99%

“…In addition, nonendocrine diseases that have been described in autoimmune polyglandular syndrome include mucocutaneous candidiasis, vitiligo, alopecia, pernicious anemia, autoimmune hepatitis, primary biliary cirrhosis, and intestinal malabsorption. There have been several studies on a link between autoimune polyglandular syndrome (including type I diabetes), thyroiditis, and gluten sensitivity (l0, [29][30][31][32][33][34]. Therefore, gluten sensitivity may coexist with several extraintestinal diseases.…”

Section: Gluten Sensitivity and Autoimmune Endocrine Disordersmentioning

confidence: 99%

“…Autoimmune polyglandular syndrome is a rare endocrine disorder comprising a combination of at least two of the following autoimmune endocrine disorders: Addison's disease, autoimmune thyroid diseases, hypoparathyroidism, type I diabetes, or primary gonadal failure (29)(30). In addition, nonendocrine diseases that have been described in autoimmune polyglandular syndrome include mucocutaneous candidiasis, vitiligo, alopecia, pernicious anemia, autoimmune hepatitis, primary biliary cirrhosis, and intestinal malabsorption.…”

Section: Gluten Sensitivity and Autoimmune Endocrine Disordersmentioning

confidence: 99%

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The Immunology of Gluten Sensitivity beyond the Intestinal Tract

Vojdani

O'Bryan²,

Kellermann

2008

Eur J Inflamm

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Celiac disease and gluten-sensitive enteropathy are terms that have been used to refer to a disease process affecting the small bowel. However, evidence has been accumulated in literature demonstrating that gluten sensitivity or celiac disease can exist even in the absence of enteropathy, but affecting many organs. Based on overwhelming evidence, immunological pathogenesis has been demonstrated in the joint, the heart, thyroid, bone, and, in particular, the brain cerebellum and neuronal synapsin I. When blood samples of patients with celiac disease are tested against gliadin and different tissue antigens, in addition to gliadin antibody, a significant percentage of them exhibit elevation in antibodies against transglutaminase, heat shock protein, collagen, thyroid, myosin, endothelial cell, bone antigen (transglutaminase), myelin basic protein, cerebellar and synapsin. This elevation of autoantibodies in patients with celiac disease may result in neuroimmune disorders. In fact, in comparison to the general population, the incidence of various autoimmune disorders, including gluten ataxia, is increased up to 30-fold in patients with celiac disease. Therefore, immune evaluation of patients with gluten sensitivity or celiac disease, in addition to gliadin and transglutaminase, should include antibody measurement against thyroglobulin, thyroid peroxidase, heat shock protein, bone transglutaminase, myelin basic protein, cerebellar peptide and synapsin. This novel laboratory approach to gluten sensitivity and autoimmunity may enable clinicians to detect markers of autoimmune diseases. Early identification of gluten sensitive and celiac disease patients and implementation of a gluten-free diet may result in significant improvement and control of associated diseases.

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Enhancement of soluble CD23 serum levels and cell-surface CD23-expression in subjects at increased risk of Type 1 diabetes mellitus and in diabetic patients

et al. 1998

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The low affinity receptor for IgE, CD23, is expressed on lymphocytes among other cell types. The purpose of the present study was to assess serum sCD23 levels and CD23 expression on peripheral blood mononuclear cells (PBMC) in people at increased risk of developing Type 1 diabetes mellitus and in diabetic patients. Serum sCD23 levels were significantly higher in first-degree relatives of Type 1 patients (median: 3.2 U ml(-1)) (p < 0.001) and in newly diagnosed (median: 3.3 U ml(-1)) (p < 0.001) and long-standing (median: 2.5 U ml(-1)) (p = 0.01) Type 1 diabetic patients than in controls (median: 1.2 U ml(-1)). Newly diagnosed patients showed higher levels than those with long-standing disease (p = 0.026). Moreover the percentage of B cells expressing CD23 were significantly higher in first-degree relatives (median: 48.6%) (p < 0.001) and in newly diagnosed (median: 58%) (p < 0.001) and long-standing (median: 44.8%) (p = 0.03) Type 1 diabetic patients than in controls (median: 28.5%). The increased sCD23 levels and the increased number of cells expressing CD23 observed in subjects at increased risk of Type 1 diabetes and diabetic patients may be indicators of Th2 activity in Type 1 diabetes.

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Celiac disease and type I (Insulin-Dependent) diabetes mellitus in childhood: Follow-up study

Cited by 33 publications

References 22 publications

Celiac Disease-Associated Autoimmune Endocrinopathies

Celiac Disease-Associated Autoimmune Endocrinopathies

The Immunology of Gluten Sensitivity beyond the Intestinal Tract

Enhancement of soluble CD23 serum levels and cell-surface CD23-expression in subjects at increased risk of Type 1 diabetes mellitus and in diabetic patients

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