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

25-Hydroxy vitamin D (25(OH)D) deficiency is linked with predisposition to autoimmune type 1 diabetes and multiple sclerosis. Our objective was to assess the relationship between serum 25(OH)D levels and thyroid autoimmunity. Subjects included students, teachers and staff aged 16-60 years (total 642, 244 males, 398 females). Serum free thyroxine, thyroid-stimulating hormone (TSH), and thyroid peroxidase autoantibodies (TPOAb), intact parathyroid hormone and 25(OH)D were measured by electrochemiluminescence and RIA, respectively. Thyroid dysfunction was defined if (1) serum TSH > or = 5 microU/ml and TPOAb>34 IU/ml or (2) TSH > or = 10 microU/ml but normal TPOAb. The mean serum 25(OH)D of the study subjects was 17.5 (sd 10.2) nmol/l with 87 % having values < or = 25 nmol/l. TPOAb positivity was observed in 21 % of subjects. The relationship between 25(OH)D and TPOAb was assessed with and without controlling for age and showed significant inverse correlation (r - 0.08, P = 0.04) when adjusted for age. The prevalence of TPOAb and thyroid dysfunction were comparable between subjects stratified according to serum 25(OH)D into two groups either at cut-off of < or = 25 or >25 nmol/l or first and second tertiles. Serum 25(OH)D values show only weak inverse correlation with TPOAb titres. The presence of such weak association and narrow range of serum 25(OH)D did not allow us to interpret the present results in terms of quantitative cut-off values of serum 25(OH)D. Further studies in vitamin D-sufficient populations with wider range of serum 25(OH)D levels are required to substantiate the findings of the current study.
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PMID:Prevalence of vitamin D deficiency and its relationship with thyroid autoimmunity in Asian Indians: a community-based survey. 1920 20

Individuals with Turner syndrome (TS) are prone to develop autoimmune conditions such as coeliac disease (CD), thyroiditis and type 1 diabetes (T1DM). The objective of the present study was to examine TS of various karyotypes for autoantibodies and corresponding diseases. This was investigated in a prospective cross-sectional study of Danish TS patients (n = 107, median age 36.7 years, range: 6-60 years). A medical history was recorded and a blood sample was analysed for autoantibodies against gliadin, transglutaminase, adrenal cortex, intrinsic factor, anti-thyroid peroxidase (anti-TPO) and glutamic-acid-decarboxylase 65 (GAD-65). Autoantibodies were present in 58% (n = 61) of all patients, whereof 18% (11) had autoantibodies targeting more than one organ. Patients with autoantibodies were significantly older than those without (P = 0.001). Anti-TPO was present in 45% (48) of patients, of whom 33% (16) were hypothyroid. Overall, 18% (19) presented with CD autoantibodies, of whom 26% (five) had CD. Anti-TPO and CD autoantibodies co-existed in 9% (10). Immunoglobulin A deficiency was found in 3% (three) of patients, who all had CD autoantibodies without disease. Among four patients with anti-GAD-65 none had T1DM, but two were classified as having T2DM. One patient had adrenocortical autoantibodies but not adrenal failure. Autoantibodies against intrinsic factor were absent. Anti-GAD-65 was increased in isochromosomal karyotypes (3/23 versus 1/84, P = 0.008) with no other association found between autoantibodies and karyotype. In conclusion, TS girls and women face a high prevalence of autoimmunity and associated disease with a preponderance towards hypothyroidism and CD. Thus, health care providers dealing with this patient group should be observant and test liberally for these conditions even before clinical symptoms emerge.
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PMID:Increased prevalence of autoimmunity in Turner syndrome--influence of age. 1929 6

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

Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing beta cells and is characterised by the presence of insulitis and &and beta-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimoto's or Graves' disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA), 4 to 9% present with coeliac disease (CD), 0.5% have Addison's disease (AD), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimoto's thyroiditis), TSH receptor (for Graves' disease), parietal cell or intrinsic factor (for AIG /PA), tissue transglutaminase (for CD), and 21-hydroxylase (for AD). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimoto's hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves' hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.
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PMID:Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. 2000 14

The genetic basis of autoantibody production is largely unknown outside of associations located in the major histocompatibility complex (MHC) human leukocyte antigen (HLA) region. The aim of this study is the discovery of new genetic associations with autoantibody positivity using genome-wide association scan single nucleotide polymorphism (SNP) data in type 1 diabetes (T1D) patients with autoantibody measurements. We measured two anti-islet autoantibodies, glutamate decarboxylase (GADA, n = 2,506), insulinoma-associated antigen 2 (IA-2A, n = 2,498), antibodies to the autoimmune thyroid (Graves') disease (AITD) autoantigen thyroid peroxidase (TPOA, n = 8,300), and antibodies against gastric parietal cells (PCA, n = 4,328) that are associated with autoimmune gastritis. Two loci passed a stringent genome-wide significance level (p<10(-10)): 1q23/FCRL3 with IA-2A and 9q34/ABO with PCA. Eleven of 52 non-MHC T1D loci showed evidence of association with at least one autoantibody at a false discovery rate of 16%: 16p11/IL27-IA-2A, 2q24/IFIH1-IA-2A and PCA, 2q32/STAT4-TPOA, 10p15/IL2RA-GADA, 6q15/BACH2-TPOA, 21q22/UBASH3A-TPOA, 1p13/PTPN22-TPOA, 2q33/CTLA4-TPOA, 4q27/IL2/TPOA, 15q14/RASGRP1/TPOA, and 12q24/SH2B3-GADA and TPOA. Analysis of the TPOA-associated loci in 2,477 cases with Graves' disease identified two new AITD loci (BACH2 and UBASH3A).
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PMID:Genome-wide association analysis of autoantibody positivity in type 1 diabetes cases. 2182 93

Postpartum thyroiditis (PPT) is the occurrence of de novo autoimmune thyroid disease, excluding Graves' disease, in the first year postpartum. The incidence of PPT is 5.4% in the general population, and it is increased in individuals with other autoimmune diseases such as type 1 diabetes mellitus. The classic presentation of PPT of hyperthyroidism followed by hypothyroidism is seen in 22% of cases. The majority of women with PPT experience an isolated hypothyroid phase (48%), with the remainder experiencing isolated thyrotoxicosis (30%). Up to 50% of women who are thyroid antibody positive (thyroid peroxidase antibody and/or thyroglobulin antibody) in the first trimester will develop PPT. Symptoms are more common in the hypothyroid phase of PPT and include fatigue, dry skin, and impaired memory. Despite multiple studies exploring the relationship between PPT and postpartum depression, or postpartum depression in thyroid antibody-positive euthyroid women, the data are conflicting, and no firm conclusions can be reached. Long-term follow-up of women who had an episode of PPT reveals a 20-40% incidence of permanent primary hypothyroidism. In a single study, selenium administration significantly decreased the incidence of PPT, but replication of the findings is needed before the recommendation can be made that all pregnant thyroid peroxidase antibody-positive women receive selenium. The indication for treating the hyperthyroid phase of PPT is control of symptoms, whereas treatment of the hypothyroid phase of PPT is indicated for symptomatic relief as well as in women who are either breastfeeding or attempting to conceive.
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PMID:Approach to the patient with postpartum thyroiditis. 2231 89

The aim of this study was to assess the association between pancreatic and thyroid autoimmunity (TA) and determine impact of thyroid antibodies on statural growth. Seventy-two children with type 1 diabetes mellitus (TIDM) and no clinical evidence of thyroid disorders were evaluated: glycated haemoglobin (A1c), thyroid peroxidase antibodies (TPOAb), glutamic acid decarboxylase antibody (GADA), tyrosine phosphatase antibodies (IA2A), and thyroid-stimulating hormone (TSH). The score of standard deviation for height (SDS) was calculated. There were 72 patients, 38 (52.7%) boys and 34 (47.2%) girls, with a mean age of 10.89 +/- 4.26 years and a mean duration of T1DM of 3.41 +/- 2.56 years. TPOAb were present in 23.6% of patients; 12.5% of subjects were positive for GADA and 41.6% for IA2A. Patients with TA had more prevalent GADA and IA2A (23.5% vs. 9%, p < 0.001, and 58.8% vs. 36.3%, p < 0.001, respectively). A1c was higher in patients with TA (9.7% +/- 2.05% vs. 8.6% +/- 2.11%, p = 0.05). TA was associated with lower SDS (0.26 vs. 0.98, p = 0.043). TSH was higher in patients with TA (3.39 vs. 2.15 microU/mL, p < 0.05). Logistic regression analysis revealed that a negative SDS for height was independently associated with duration of diabetes (p = 0.049) and TSH (p = 0.027) but not with birth weight, A1c, and TPOAb. In conclusion, TA was found in 23.6% TIDM children. Patients with TA had significantly higher prevalence of GADA and IA2A and significantly higher A1c vs. patients without TA. Our data suggest significant association between TA and height in children with T1DM. SDS was independently associated with diabetes duration and TSH.
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PMID:Thyroid autoimmunity in 72 children with type 1 diabetes mellitus: relationship with pancreatic autoimmunity and child growth. 2315

Hashimoto's thyroiditis emerges in patients who have genetic preponderance such as SNPs of CTLA-4 and risk factors such as excess intake of iodine, pregnancy or postpartum period, and smoking. Such risk factors also affect the entire clinical course. One of the major outcomes in Hashimoto's thyroiditis appears to be increased in cardio-vascular risks through subclinical hypothyroidism and concomitant metabolic syndrome, but in most cases, treatment with L-T4 has little effects on cardio-vascular benefit or quality of life. The pregnant women also have risks for obstetric complications and postpartum thyroid dysfunction. The women who have anti-TPO antibodies, type 1 diabetes, or previous history of post-partum thyroid dysfunction are recommended to be measured their TSH. It is noteworthy that Hashimoto's thyroiditis is sometimes complicated with encephalopathy, papillary carcinoma, or IgG4-related thyroiditis. IgG4-related thyroiditis is partly similar but partly discerned from a variant of Hashimoto's thyroiditis. The pathogenetic roles of this variant on autoimmune-based thyroiditis remain unclear.
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PMID:[Hashimoto's thyroiditis(chronic thyroiditis), IgG4-related thyroiditis]. 2321 65

Kearns-Sayre syndrome is characterized by onset before 20 years, chronic progressive external opthalmoplegia, pigmentary retinal degeneration, and ataxia (and/or hearth block, and/or high protein content in the cerebrospinal fluid) in the presence of mtDNA rearrangements. Multiple endocrine dysfunction associated with this syndrome was rarely reported. In this paper, the Authors report on a female patient with Kearns-Sayre syndrome with large heteroplasmic mtDNA deletion, absence of cytochrome c oxidase in many muscle fibers, partial GH deficiency, hypothyroidism and subsequently insulin dependent diabetes mellitus (IDDM). Anti-thyroid peroxidase and antithyreoglobulin antibodies were present in high titer in serum while anti-islet cell antibodies were absent. The patient developed thyroiditis with Hashimoto encephalopathy. The presence of GH deficiency, autoimmune thyroiditis with hypothyroidism and IDDM distinguishes this case from others and confirms the association of Kearns-Sayre syndrome with multiple endocrine dysfunction. Hashimoto encephalopathy and anti-thyroideal antibodies suggest that in this patient, predisposed by a genetic factor (a mitochondrial deletion) anti-thyroideal antibodies may have contributed to the hypothyroidism and, by interfering with cerebral mitochondrial function, may have caused the encephalopathy. GH deficiency and IDDM can be attributed to oxidative phosphorylation deficiency but the autoimmunity may also have played a role in the production of glandular insufficiencies. It seems important to search for endocrine autoimmunity in every case of KSS.
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PMID:Multiple endocrinopathies (growth hormone deficiency, autoimmune hypothyroidism and diabetes mellitus) in Kearns-Sayre syndrome. 2394 15

We have previously reported the high levels of glutamic acid decarboxylase 65 autoantibodies (GAD65A) in patients with type 1 diabetes and autoimmune thyroid disease. Here we describe a 32-year-old Japanese female with a thirteen-year history of type 1 diabetes whose levels of GAD65A were elevated just after the emergence of anti-thyroid autoimmunity. At 19 years of age, she developed diabetic ketoacidosis and was diagnosed with type 1 diabetes. She had GAD65A, insulinoma-associated antigen-2 autoantibodies (IA-2A), and zinc transporter-8 autoantibodies (ZnT8A), but was negative for antibodies to thyroid peroxidase (TPOAb) and thyroglobulin (TGAb) at disease onset. ZnT8A and IA-2A turned negative 2-3 years after the onset, whereas GAD65A were persistently positive at lower level (approximately 40 U/mL). However, just after the emergence of TGAb at disease duration of 12.5 years, GAD65A levels were reelevated up to 5717 U/mL in the absence of ZnT8A and IA-2A. Her thyroid function was normal and TPOAb were consistently negative. She has a HLA-DRB1*03:01/*04:01-DQB1*02:01/*03:02 genotype. Persistent positivity for GAD65A might be associated with increased risk to develop anti-thyroid autoimmunity.
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PMID:Sequential elevation of autoantibodies to thyroglobulin and glutamic acid decarboxylase in type 1 diabetes. 2414 7


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