Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to assess the relationship between IL-6 gene polymorphism at -174(G>C) and the coincidence of celiac and autoimmune thyroid diseases with type 1 diabetes mellitus (DM1) in children. 200 children with DM1 aged 13.23+/-3.54 years and 172 healthy controls were analyzed. The IL-6 gene -174(G>C) polymorphism at the promoter region of the gene was analyzed by the PCR-RFLP method. The genotype distribution was significantly different in diabetic children as compared to the healthy controls (p=0.01). In DM1 patients GC heterozygotes were the most common (52.5%), while CC homozygotes accuted for 29% and GG homozygotes only for 18% of cases. In contrast, GG homozygotes were much more frequent among healthy children (31%). Besides, the GG homozygotes were significantly more frequent among diabetic children with celiac disease (p=0.04) in relation to those without autoimmune complications. In children with autoimmune thyroiditis, the distribution of the IL-6 genotypes was similar to that seen in diabetic patients without autoimmune complications (p=0.24). The results of our study suggest that the diabetic children, who have IL-6 gene -174GG genotype may have an increased risk for celiac disease development.
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PMID:Interleukin 6 -174(G>C) gene polymorphism is related to celiac disease and autoimmune thyroiditis coincidence in diabetes type 1 children. 1869 34

There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. However, the mechanism underlying TRAIL effect is not well defined. In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. Furthermore, transfer of these cells into CBA/J mice prior to mTg-primed splenocyte injection could markedly reduce the frequency and severity of EAT development. CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. These findings reveal a novel mechanism by which TRAIL could inhibit autoimmune disease.
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PMID:Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. 1900 14

Thyroid hormones modulate the immune system and metabolism, influence insulin secretion, and cause decreased glucose tolerance. Thyroid hormones have been described to change the incidence of spontaneous autoimmune thyroiditis in Bio-Breeding/Worcester (BB) rats but it is unknown how these hormones affect the development of type 1 diabetes mellitus (T1DM). The aim was to investigate the influence of changes in thyroid function during postnatal development on the prevalence of T1DM in BB rats and the influence of T3 on the beta cell mass in non-diabetic Wistar rats. BB rats were treated with sodium iodine (NaI) or thyroid stimulating hormone (TSH) neonatally or with tri-iodo-thyronine (T3) during adolescence. At the age of 19 weeks the incidence of T1DM and the degree of insulitis were evaluated. The influence of T3 treatment on the beta cell mass was evaluated in Wistar rats by unbiased stereological methods. The incidence of T1DM in control BB rats was 68% at the age of 19 weeks. NaI and T3 reduced the incidence, whereas TSH had no effect. In Wistar rats T3 treatment increased the beta cell mass per bodyweight. The modulation of thyroid function during postnatal development may thus affect the precipitation of T1DM in genetically susceptible individuals.
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PMID:Iodine and tri-iodo-thyronine reduce the incidence of type 1 diabetes mellitus in the autoimmune prone BB rats. 1902 Oct 14

The aim of the study was to evaluate the natural course and potential risk factors of autoimmune thyroiditis (AIT) and thyroid dysfunction, and their influences on growth and glycemic control in children and adolescents with type 1 diabetes mellitus (T1D). The study comprised 148 subjects (age range 1-21 years; males 51%) with T1D. During the interval of 12 years serum levels of thyroid peroxidase (anti-TPO) and thyroglobulin (anti-TG) autoantibodies, thyroid-stimulating hormone (TSH) and tyroksine (T4), were screened annually. Height, weight, body mass index (BMI), glycosylated hemoglobin (HbA1c), insulin dose and the number of severe hypoglycemic episodes, were recorded every 3 months. The mean follow-up was 7 +/- 4.1 years. Prevalence of AIT in subjects with T1D was 15.5%. It was significantly higher in girls (21.9% vs. 9.3%; p = 0.03). The mean age at AIT onset was 11.5 +/- 5.2 years. The mean interval between negative and positive AIT screening was 2.5 +/- 2.3 years. Cumulative incidence of AIT after 6 years of T1D duration was significantly higher in girls (30% vs. 15%; p = 0.03). Prevalence of hypothyroidism was 8.1% with no significant differences in sex distribution. Prevalence of hypothyroidism among subjects with elevated serum thyroid antibodies was 52.2% with significant male preponderance (85.7% vs. 37.5%; p = 0.005). There were no subjects who developed hypothyroidism in absence of thyroid antibodies. Cumulative incidence of hypothyroidism after 3 years from the moment of thyroid antibodies appearance was 55% with significant male preponderance (85% vs. 40%; p = 0.005). The mean interval between T1D onset and hypothyroidism development was 3.3 +/- 2.5 years, and between thyroid antibodies appearance and hypothyreoidism development was 1.7 +/- 1.2 years. The mean age at hypothyroidism onset was 12.7 +/- 5.3 years. There were no differences in growth and metabolic control between patients with and without AIT. The results of the present study confirmed frequent occurrence of AIT and thyroid dysfunction in subjects with T1D. The number of newly diagnosed subjects with AIT reached the peak at the age of puberty. Girls were significantly more predisposed to AIT at any age while amongst subjects with elevated thyroid antibodies boys developed hypothyroidism more frequently. Annual screening of thyroid antibodies in all patients with T1D is recommended, while serum TSH level should be measured in patients with detected thyroid antibodies.
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PMID:Epidemiology and clinical characteristics of thyroid dysfunction in children and adolescents with type 1 diabetes. 1940 37

We present the case of a 29.5-year-old girl with Down's syndrome, type 1 diabetes mellitus (DMT1), autoimmune thyroiditis and celiac disease starting on insulin pump therapy. After 22-month follow-up hemoglobin A1c dropped from 9% to 6.8%, even with a lower insulin requirement and no change in BMI.
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PMID:Insulin pump therapy for type 1 diabetes treatment in a girl with Down's syndrome. 1959 63

CD40 is a tumor necrosis factor receptor superfamily member expressed by immune and non-immune cells. CD40:CD154 interactions mediate T-dependent B cell responses and efficient T cell priming. Thus, CD40 is a likely candidate to play roles in autoimmune diseases in which activated T and B cells cause pathology. Diseases in which CD40 plays a pathogenic role include autoimmune thyroiditis, type 1 diabetes, inflammatory bowel disease, psoriasis, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. This review discusses the role of CD40:CD154 interaction in human and mouse autoimmunity, human polymorphisms associated with disease incidence, and disrupting CD40:CD154 interactions as an autoimmune therapy.
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PMID:CD40 and autoimmunity: the dark side of a great activator. 1959 12

To evaluate the prevalence of PTPN22 C1858T polymorphism in young type 1 diabetes patients with or without autoimmune thyroiditis. Genotyping was performed in 209 controls and 243 patients diagnosed with diabetes at median age of 8.6 years. Diabetes-related autoimmunity was assessed at diagnosis of the disease, while thyroid-related autoimmunity was determined at diabetes onset and at annual intervals up to 15 years of follow-up. The 1858T allele frequency was 15.2% in patients and 10.5% in controls (odds ratio 1.53, p = 0.037). 1858T positive patients were significantly younger at diagnosis of diabetes than those without this allele (p = 0.003). No association was found between C1858T polymorphism and diabetes-related autoimmunity (p = 0.173) or thyroid autoimmune disease (p = 0.321), respectively. We conclude that PTPN22 1858T allele is an independent risk factor for type 1 diabetes and associated with younger age at the onset of the disease. However, no association with concomitant thyroid autoimmunity was found.
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PMID:PTPN22 1858T allele is associated with younger age at onset of type 1 diabetes and is not related to subsequent thyroid autoimmunity. 2043 87

Combined pegylated interferon and ribavirin therapy for chronic hepatitis C infection cause a wide range of side effects, including flu-like syndrome, hematological abnormalities, cardiovascular symptoms, gastrointestinal symptoms, pulmonary dysfunction, depression, and retinopathy. Interferon-alpha has been shown to be related to the development of various autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, autoimmune thyroid disease, and type 1 diabetes mellitus (DM). Type 1 DM and thyroid disease respectively develop in 0.08-2.61% and 10-15% of patients treated with combined interferon-alpha and ribavirin for chronic hepatitis C. The coexistence of type 1 DM and autoimmune thyroiditis was rarely reported. We report a case of a 33-year-old female patient with chronic hepatitis C who simultaneously developed diabetic ketoacidosis and autoimmune thyroiditis after treatment with pegylated interferon-alpha 2b and ribavirin.
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PMID:[Occurrence of diabetic ketoacidosis and autoimmune thyroiditis in a patient treated with pegylated interferon-alpha 2b and ribavirin for chronic hepatitis C]. 2060 4

Patients with type 1 diabetes (T1D) are at increased risk for developing other autoimmune diseases, most commonly autoimmune thyroiditis and celiac disease. Few reports have described the association of systemic lupus erythematosus and T1D in the literature. To the best of our knowledge, this is the first report of lupus nephritis in a child with T1D.
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PMID:Lupus nephritis in a child with type I diabetes mellitus. 2105 67

Although the MHC class II 'u' haplotype is strongly associated with type 1 diabetes (T1D) in rats, the role of MHC class II in the development of tissue-specific autoimmune diseases including T1D and autoimmune thyroiditis remains unclear. To clarify this, we produced a congenic strain carrying MHC class II 'a' and 'u' haplotypes on the Komeda diabetes-prone (KDP) genetic background. The u/u homozygous animals developed T1D similar to the original KDP rat; a/u heterozygous animals did develop T1D but with delayed onset and low frequency. In contrast, none of the a/a homozygous animals developed T1D; about half of the animals with a/u heterozygous or a/a homozygous genotypes showed autoimmune thyroiditis. To investigate the role of genetic background in the development of thyroiditis, we also produced a congenic strain carrying Cblb mutation of the KDP rat on the PVG.R23 genetic background (MHC class II 'a' haplotype). The congenic rats with homozygous Cblb mutation showed autoimmune thyroiditis without T1D and slight to severe alopecia, a clinical symptom of hypothyroidism such as Hashimoto's thyroiditis. These data indicate that MHC class II is involved in the tissue-specific development of autoimmune diseases, including T1D and thyroiditis.
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PMID:Role of major histocompatibility complex class II in the development of autoimmune type 1 diabetes and thyroiditis in rats. 2191 39


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