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  • 1
    ISSN: 1432-0428
    Keywords: Autoantibodies ; glutamate decarboxylase ; islet cell antibodies ; insulin ; thyroid peroxidase ; coeliac disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sera obtained at diagnosis from 273 children (0–14 years) with insulin-dependent diabetes mellitus (IDDM) were studied to compare different autoantibody levels. The subjects comprise 75% of all incident cases in New South Wales, Australia, for a 2-year period (ascertainment 〉99% complete). Antibodies against glutamate decarboxylase were measured by radioimmunoprecipitation, insulin autoantibodies (on 176 sera collected within 4 days of initiation of insulin therapy) by radioimmunoassay, thyroid peroxidase and antigliadin IgA antibodies by enzyme-linked immunoassay, and anti-endomysial IgA and islet cell antibodies by indirect immunofluorescence. Reference ranges for anti-glutamate decarboxylase and insulin autoantibodies were determined in a group of non-diabetic children. Of the sera 69% were positive for anti-glutamate decarboxylase, 65% for insulin autoantibodies, 71% for islet cell antibodies (⩾20 Juvenile Diabetes Foundation units), 10% for anti-thyroid peroxidase, 2.6% for antigliadin and 3.0% for anti-endomysial antibodies. Islet cell antibodies and insulin autoantibodies were both negative in 13.7% of the sera, while only 5.8% were negative for all three of islet cell antibodies, insulin autoantibodies and anti-glutamate decarboxylase. There was a higher frequency of anti-glutamate decarboxylase among girls than boys (75% vs 63%, p=0.03) and a negative correlation between the level of insulin autoantibodies and age at diagnosis (r=−0.41, p〈0.0001). A higher frequency of antithyroid peroxidase was found with increasing age (p=0.05). Higher titres of islet cell antibodies were associated with a higher frequency of both anti-glutamate decarboxylase (p〈0.0001) and insulin autoantibodies (p=0.003). Five children (1.8%) with clear elevations of antigliadin and anti-endomysial antibodies were found to have asymptomatic coeliac disease by small bowel biopsy.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Key words Autoantibodies ; glutamate decarboxylase ; islet cell antibodies ; insulin ; thyroid peroxidase ; coeliac disease.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sera obtained at diagnosis from 273 children (0–14 years) with insulin-dependent diabetes mellitus (IDDM) were studied to compare different autoantibody levels. The subjects comprise 75 % of all incident cases in New South Wales, Australia, for a 2-year period (ascertainment 〉 99 % complete). Antibodies against glutamate decarboxylase were measured by radioimmunoprecipitation, insulin autoantibodies (on 176 sera collected within 4 days of initiation of insulin therapy) by radioimmunoassay, thyroid peroxidase and antigliadin IgA antibodies by enzyme-linked immunoassay, and anti-endomysial IgA and islet cell antibodies by indirect immunofluorescence. Reference ranges for anti-glutamate decarboxylase and insulin autoantibodies were determined in a group of non-diabetic children. Of the sera 69 % were positive for anti-glutamate decarboxylase, 65 % for insulin autoantibodies, 71 % for islet cell antibodies (≥ 20 Juvenile Diabetes Foundation units), 10 % for anti-thyroid peroxidase, 2.6 % for antigliadin and 3.0 % for anti-endomysial antibodies. Islet cell antibodies and insulin autoantibodies were both negative in 13.7 % of the sera, while only 5.8 % were negative for all three of islet cell antibodies, insulin autoantibodies and anti-glutamate decarboxylase. There was a higher frequency of anti-glutamate decarboxylase among girls than boys (75 % vs 63 %, p = 0.03) and a negative correlation between the level of insulin autoantibodies and age at diagnosis (r = –0.41, p 〈 0.0001). A higher frequency of anti-thyroid peroxidase was found with increasing age (p = 0.05). Higher titres of islet cell antibodies were associated with a higher frequency of both anti-glutamate decarboxylase (p 〈 0.0001) and insulin autoantibodies (p = 0.003). Five children (1.8 %) with clear elevations of antigliadin and anti-endomysial antibodies were found to have asymptomatic coeliac disease by small bowel biopsy. [Diabetologia (1994) 37: 1113–1120]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Diabetes ; autoimmunity ; autoantibodies ; islet cell antibodies ; Nauru
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Among the population of Nauru there is a high prevalence of diabetes with onset in early adult life. To ascertain whether autoimmunity to islet cell antigens contributes to this diabetes, a population survey of serum autoantibodies was performed. Subjects were grouped into euglycaemic control subjects, those with impaired glucose tolerance, and those with diabetes subdivided according to duration of disease. No subject was positive by immunofluorescence for islet cell autoantibodies. Various other autoantibodies to nuclear, thyroid and gastric autoantigens were detectable, at comparable frequencies in the three groups. This population study on Nauruan subjects selected to include those in the early phases of disease negates a contribution from islet cell autoimmunity, and thus supports the concept that the disease is the Type 2 (non-insulin-dependent) type.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Glutamic acid decarboxylase ; Type 1 (insulin-dependent) diabetes mellitus ; HLA-DR ; HLA-DQ ; Hong Kong ; Korea ; Japan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antibodies to glutamic acid decarboxylase, previously known as the 64 kD antigen, appear to be more predictive of Type 1 (insulin-dependent) diabetes mellitus in Caucasoids than other autoantibodies to islet cell antigens. However, seropositivity to glutamic acid decarboxylase is not universal at the onset of Type 1 diabetes and the prevalence in Asians is low compared to Caucasoid patients. This suggests the involvement of multiple pancreatic autoantigens in the Type 1 diabetes autoimmune process or, genetic differences within and between ethnic groups that contribute to the heterogeneous autoimmune response to glutamic acid decarboxylase or both. Alternatively some cases of Type 1 diabetes could have an aetiology unrelated to autoimmunity. This study examined the differential response to glutamic acid decarboxylase according to HLA-DR and -DQ genotypes, as determined by RFLP, in 49 white Australian and 44 Asian patients with Type 1 diabetes. Among Australians heterozygous for HLA-DR3, DR4, 85% were positive for antibodies to glutamic acid decarboxylase, significantly different (p = 0.039) from the prevalence of 48% in patients with at least one HLA-DR antigen other than DR3 or DR4. Also, among Australians, the presence of “low risk” HLA-DQ antigens, namely DQw5, DQw6 or DQw7, reduced the prevalence of antibodies to glutamic acid decarboxylase by 40% (p = 0.064). Among Asians with Type 1 diabetes and with antibodies to glutamic acid decarboxylase, HLA-DR9 was significantly (p = 0.037) increased in frequency, at 63% compared with 22% in those without glutamic acid decarboxylase antibodies, and the presence of a “low risk” HLA-DQ allele reduced the antibody rates by 87% (p = 0.003). These observations may reflect differential genetic/environmental interactions in Type 1 diabetes or differential persistence of glutamic acid decarboxylase antibodies in those with different genetic backgrounds.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 73 (1986), S. 620-623 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1437-160X
    Keywords: Collagen antibodies ; Arthritogenic epitopes ; Cyanogen bromide peptides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antibodies to human type II collagen were examined in the sera of 105 patients with rheumatoid arthritis (RA), 44 patients with systemic lupus erythematosus (SLE) and 11 patients who fulfilled the criteria of both diseases (RA-SLE overlap), using a solid-phase radioimmunoassay (RIA). The frequencies of antibodies to native and denatured human type II collagen were 20% and 27% in RA, 14% and 16% in SLE, and 45% and 36% in RA-SLE overlap. The specificity of the antibodies was further examined by inhibition with native and denatured type II collagen, by immunoblotting on native and denatured type II collagen, and by immunoblotting on cyanogen-bromide derived polypeptides of type II collagen. We could not identify any disease-specific patterns of reactivity. Thus, in the three disease groups the antibody response was polyclonal; there were antibody populations that reacted with native and/or denatured collagen, and epitopes could be assigned to at least three CB peptides, CB10.5, CB11 and CB8.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Rheumatology international 7 (1987), S. 267-269 
    ISSN: 1437-160X
    Keywords: Collagen antibodies ; HLA antigens ; Ross River virus disease ; Epidemic polyarthritis ; Rheumatoid arthritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antibody activity against collagen was measured in 53 samples of serum from 48 patients with active signs of epidemic polyarthritis (EPA) following infection with Ross River virus. Activity was higher against denatured collagen than against native collagen, but was within the normal range for each. Determination of HLA phenotypes permitted a search for any relationship between HLA type and differences in collagen antibody levels within the normal range. No relationship was detected with HLA antigens predominating in EPA or with HLA antigens that are associated with high collagen-antibody levels in rheumatoid arthritis (RA), which suggests that the latter associations may represent failure to control collagen antibody levels after the onset of RA. The findings also provide evidence against a role for nonspecific enhancement of humoral immune responses in the pathogenesis of EPA, and constitute a further point of distinction between EPA and RA.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1437-160X
    Keywords: Collagen antibodies ; Sulphated glycosaminoglycans ; Rheumatoid arthritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is uncertain whether the autoantibodies to type II collagen that occur frequently in the serum and synovial fluid of patients with rheumatoid arthritis (RA), but rarely in other articular diseases, are primary or secondary to cartilage damage. Hence, we measured antibodies in synovial fluid from patients with RA and other articular disease and related these to the concentration of sulphated glycosaminoglycans, as a measure of ongoing cartilage catabolism. Synovial fluids from 42 patients with RA and 30 patients with other articular diseases were studied. We found that levels of antibodies to native and denatured collagen were significantly higher in RA than in all other articular diseases, whereas concentrations of sulphated glycosaminoglycans were similar. The absence of any correlation between levels of sulphated glycosaminoglycans and antibodies to collagen weighs against the occurrence of such antibodies in RA as a secondary effect of cartilage damage.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Rheumatology international 8 (1989), S. 239-243 
    ISSN: 1437-160X
    Keywords: Collagen antibodies ; Active and inactive rheumatoid arthritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty-seven patients with classical or definite rheumatoid arthritis (RA) were studied prospectively over a period of 12 months to assess whether there was a relationship between disease activity and raised levels of antibodies to native or denatured type II collagen. Nineteen patients had inactive RA according to ARA criteria for disease remission and 18 had active RA throughout the study. At the beginning of the study the levels of collagen antibodies were comparable in each group. After 1 year, antibodies to denatured type II collagen in patients with inactive RA had declined to significantly lower levels whereas in patients with active RA the levels of antibodies fluctuated during the period of study and were not significantly different at the end. There was no relationship between levels of antibodies to type II collagen and any specific index of disease activity, severity of X-ray changes in the hands and feet, or progression over 1 year in X-ray changes. The finding of a decline in levels of antibodies to denatured type II collagen in inactive RA suggests that the anticollagen response is an integral component of the rheumatoid process and could have a primary or secondary role in pathogenesis.
    Type of Medium: Electronic Resource
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