Autoantibodies against recombinant human steroidogenic enzymes 21-hydroxylase, side-chain cleavage and 17alpha-hydroxylase in Addison's disease and autoimmune polyendocrine syndrome type III

Silva, R de Carmo; Kater, C.E.; Dib, S.A.; Laureti, Stefano; Forini, F.; Cosentino, A; Falorni, Alberto

doi:10.1530/eje.0.1420187

Cited by 52 publications

(24 citation statements)

References 45 publications

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“…Indirect immunofluorescence assays are expressed as the lowest 2-fold serial dilution of subject serum with a positive result. 21-hydroxylase antibody (21OHAb), 17␣-hydroxylase antibody and P450 side chain cleavage antibody (P450sccAb) were measured using radiobinding assays to recombinant human 21OH, 17␣-hydroxylase and P450 side chain cleavage (P450scc) radiolabeled with 35 S as previously described (21,22). Antibody levels were expressed as relative indices (mean cpm unknown Ϫ mean cpm 2 negative standards)/(mean cpm positive standard Ϫ mean cpm 2 negative standards), with the upper limit of normal defined as the mean ϩ 3 sd of 90 healthy controls.…”

Section: Assaysmentioning

confidence: 99%

Selective Theca Cell Dysfunction in Autoimmune Oophoritis Results in Multifollicular Development, Decreased Estradiol, and Elevated Inhibin B Levels

Welt

Falorni

Taylor

et al. 2005

The Journal of Clinical Endocrinology &Amp; Metabolism

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We describe the clinical course of three women with presumptive autoimmune oophoritis who developed multiple follicles but very low to undetectable estradiol levels. Multiple follicles developed spontaneously in all subjects and during pulsatile GnRH treatment for ovulation induction in subject 1. The development of multiple dominant follicles was accompanied by LH levels in the postmenopausal range and FSH levels at the upper limit for premenopausal women. Serum inhibin B levels were elevated appropriately in the setting of multifollicular development, but estradiol levels remained low. Measurement of estradiol precursors demonstrated androstenedione and estrone levels below the 95th percentile in normal women. Adrenal cortical antibodies, and antibodies to 21-hydroxylase and P450 side chain cleavage enzymes were identified in all subjects. All subjects met the criteria for premature ovarian failure during follow-up. Subject 1 later developed adrenal failure, whereas subject 3 had adrenal failure at the time of the study. These subjects elucidate the hormonal pattern in autoimmune oophoritis, before the full criteria for premature ovarian failure are met. The elevated inhibin A and B levels, which accompany the development of multiple small and dominant follicles in these women, suppress FSH relative to LH levels, virtually independent of estradiol. These data provide further evidence for an important role of inhibin B and inhibin A in the negative feedback control of FSH. In addition, the normal inhibin A and inhibin B production in the absence of estradiol precursors and estradiol provide insight into the selective dysfunction of the theca cells in autoimmune oophoritis.

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Section: Assaysmentioning

confidence: 99%

Selective Theca Cell Dysfunction in Autoimmune Oophoritis Results in Multifollicular Development, Decreased Estradiol, and Elevated Inhibin B Levels

Welt

Falorni

Taylor

et al. 2005

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…[122][123][124][125][126][127] Sera of polyglandular and Addison's disease also react to a lesser extent with side chain cleavage enzyme and 17-alpha hydroxylase (CYP17). Antibodies to recombinant CYP21, CYP17, and side chain cleavage enzymes were not found in isolated POF.…”

Section: Antigensmentioning

confidence: 99%

Ovarian Autoimmune Disease and Ovarian Autoantibodies

Luborsky

2002

Journal of Women's Health & Gender-Based Medicine

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Detection of specific autoantibodies remains the most practical clinical and research marker of autoimmune disease. The lack of consensus on ovary specific antibodies as a marker for ovarian autoimmunity has clinical and research consequences. The objective of this review is to summarize the evidence for ovarian autoimmunity and the detection of ovary specific autoantibodies in humans. Evidence favors the presence of an autoimmune disease of the ovary. Ovarian autoantibodies are associated primarily with premature ovarian failure (POF) and unexplained infertility. Variations in detection of ovarian autoantibodies are likely to be due to study design elements such as antibody test format, antigen preparation, and criteria for study and comparison groups. In addition, multiple targets appear to be involved in ovarian autoimmunity including ovarian cellular elements and oocyte related antigens. Many studies only assess one target antigen, leaving individuals with ovarian autoimmunity unidentified. The next most significant advance in characterizing ovarian autoimmunity will be definitive identification of the specific antigens and development of standardized tests based on use of specific antigens.

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“…The DQ2 and DQ8 molecules responsible for the increased susceptibility to type I diabetes and other autoimmune diseases are devoid of an aspartate-57 residue. Residue 57 DQ␤ seems to be critical for peptide binding, T-cell recognition, and stability of the MHC class heterodimer on the cell surface (24). Peptides that have the favorable sequences of amino acids, fulfilling the stringent conditions of the DQ2 peptide binding pockets, will bind avidly and generate a Th2 cell response, which in turn leads to maturity and proliferation of the antibody response.…”

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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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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Autoantibodies against recombinant human steroidogenic enzymes 21-hydroxylase, side-chain cleavage and 17alpha-hydroxylase in Addison's disease and autoimmune polyendocrine syndrome type III

Cited by 52 publications

References 45 publications

Selective Theca Cell Dysfunction in Autoimmune Oophoritis Results in Multifollicular Development, Decreased Estradiol, and Elevated Inhibin B Levels

Selective Theca Cell Dysfunction in Autoimmune Oophoritis Results in Multifollicular Development, Decreased Estradiol, and Elevated Inhibin B Levels

Ovarian Autoimmune Disease and Ovarian Autoantibodies

Celiac Disease-Associated Autoimmune Endocrinopathies

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