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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This chapter aims to describe ways in which autoimmunity can be prevented or reversed and 'self-tolerance' re-established. To this end we have largely restricted our overview to the two main autoimmune disease models with which we are involved, i.e. IDDM in NOD mice and EAT in H-2k mice although, where appropriate and to demonstrate a particular point, other models are mentioned. The chapter has been divided into sections covering protection afforded by 1) transgenes, 2) autoantigen and 3) by reagents targetting T-cell surface molecules. Where established, the mechanism by which protection or tolerance is achieved is described but where, as in most cases, it is unknown the possibilities are discussed. Investigations using T-cell lines and clones and on islet regeneration which are currently being followed as part of a comprehensive approach to the study of autoimmunity are included as separate sections and their relevance discussed.
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PMID:Tolerance induction as a therapeutic strategy for the control of autoimmune endocrine disease in mouse models. 759 Aug 17

We have compared the prevalence of Eating Disorders in a population of 69 out-patients with Insulin-Dependent Diabetes Mellitus including a sample of diabetic young women (average year: 23 years) with two control populations (45 medicine out-patients and 54 girl students). The diabetic population didn't present no more eating disorders--measured by self-report questionnaires (EAT, BITE) than the control population. In a sample of 40 diabetic subjects--having participated in a diagnostic structured interview (LENTCA) based on DSM-III-R criteria: nobody has anorexia nervosa, one woman has bulimia nervosa, the lifetime prevalence of bulimia nervosa not otherwise specified was 21% for men and 43% for women. Bulimia Disorders--measured by self report questionnaire (BITE) and noncompliance were linked with poor glycemic control.
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PMID:[Eating disorders and metabolic balance in a population++ of young adults with insulin-dependent diabetes]. 761 27

The revolution in molecular techniques has allowed dissection of the autoimmune response in a way impossible to imagine 10 yr ago. There have been spectacular advances in our understanding of self-tolerance mechanisms and how these may fail, combined with a detailed comprehension of antigen presentation, functional T cell subsets, and TCR utilization in autoimmunity, albeit usually in animal models that resemble, but do not exactly duplicate, human diseases. More gradually, these findings are being translated to thyroid autoimmunity, where the major achievement of the last decade has been the molecular characterization of the three main thyroid autoantigens. This in turn has allowed epitope identification, although again the only clear data so far have come from animal models of EAT. Another advance has been the recognition that the thyrocyte is not a helpless target of autoaggression, being capable of expressing a wide array of immunologically active molecules, which may exacerbate or diminish the autoimmune response. In 1983, there was considerable excitement at the discovery of the first of these phenomena, namely MHC class II expression, but its possible role in autoantigen presentation remains to be defined. By analogy with pancreatic beta-cells, and based on our own data, we believe that class II-expressing thyrocytes have little, if any, such role and suspect that instead this may be a mechanism for inducing peripheral tolerance. Defining the contribution of thyrocytes to the intrathyroidal autoimmune response, whether from released cytokines or surface-bound molecules, will be crucial to our future understanding, as well as holding the promise that these thyroid-derived products might be therapeutic targets. Despite molecular developments in HLA analysis, there have been no really major improvements in our understanding of the immunogenetics of thyroid autoimmunity, equivalent to those made in type 1 diabetes mellitus. The available data suggest strongly that non-MHC genes play an important role in susceptibility, and novel approaches will be required to identify these. On the other hand, we know more about the importance of environmental and endogenous (most probably hormonal) factors in thyroid autoimmunity. Understanding the basic immunological changes in the postpartum period is still poor, however, as most studies to date have concentrated on epidemiology and clinical delineation. As PPTD undergoes spontaneous remission, elucidation of these mechanisms has clear implications for treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Autoimmune thyroid disease: further developments in our understanding. 770 81

Background Adolescents with type 1 diabetes mellitus (T1DM) are at an increased risk of eating disturbances. The aim of this study was to evaluate whether the risk of a disordered eating behavior (DEB) also applies to the well sibling sharing the same environment. Methods Well siblings were included if they were 10-18 years old, had a sibling with a T1DM diagnosis for at least 6 months and lived with the sibling during the illness. The control group was comprised of healthy participants recruited from the outpatient clinic with no family history of T1DM. Participants completed a four-part questionnaire concerning their eating behaviors that was developed by the study team. This survey aimed to evaluate the dietary habits and eating patterns. All participants completed the Eating Attitudes Test-26 (EAT-26) and a 24-h food dietary recall. Any participant with a high EAT-26 score or that seemed to be at risk according to the questionnaire was re-evaluated. Results Eight cases (33.3%) in the well sibling group had either a total and/or subgroup pathological score. Three of them were found to have DEB and one case was diagnosed with anorexia nervosa (AN). In the control group, five cases (17.2%) had either a total and/or subgroup pathological score. Three of these cases were found to have DEB, no cases were diagnosed with an eating disorder. There were no statistically significant differences in the EAT-26 scores between the groups. Conclusions Although a direct relationship was not observed, the probability of having a pathologic EAT-26 score was higher in the group with a sibling with T1DM.
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PMID:Can having a sibling with type 1 diabetes cause disordered eating behaviors? 2987 93