Auto-Antibodies in Addison's Disease

Anderson, John R.; Goudie, R. B.; Gray, Kathleen; Timbury, G.C.

doi:10.1016/s0140-6736(57)91687-2

Cited by 169 publications

(43 citation statements)

References 4 publications

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“…21 More than 80% of patients with autoimmune Addison's disease possess serum antibodies that recognize the adrenal cortex (adrenal cortex antibodies, ACAs). 22 All women identified to date with histological evidence of autoimmune oophoritis possess ACA; paradoxically, the major target of ACA, 21-hydroxylase (CYP21A2), [22][23][24] is not expressed in the ovary. In addition to autoantibodies to CYP21A2, autoantibodies to two other steroidogenic enzymes, P450 side chain cleavage (CYP11A1) and 17a-hydroxylase (CYP17), which convert cholesterol to pregnenolone, and progesterone to 17-hydroxyprogesterone, respectively, are present.…”

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

Ovarian autoimmune disease: clinical concepts and animal models

et al. 2014

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The ovary is not an immunologically privileged organ, but a breakdown in tolerogenic mechanisms for ovary-specific antigens has disastrous consequences on fertility in women, and this is replicated in murine models of autoimmune disease. Isolated ovarian autoimmune disease is rare in women, likely due to the severity of the disease and the inability to transmit genetic information conferring the ovarian disease across generations. Nonetheless, autoimmune oophoritis is often observed in association with other autoimmune diseases, particularly autoimmune adrenal disease, and takes a toll on both society and individual health. Studies in mice have revealed at least two mechanisms that protect the ovary from autoimmune attack. These mechanisms include control of autoreactive T cells by thymus-derived regulatory T cells, as well as a role for the autoimmune regulator (AIRE), a transcriptional regulator that induces expression of tissue-restricted antigens in medullary thymic epithelial cells during development of T cells. Although the latter mechanism is incompletely defined, it is well established that failure of either results in autoimmune-mediated targeting and depletion of ovarian follicles. In this review, we will address the clinical features and consequences of autoimmune-mediated ovarian infertility in women, as well as the possible mechanisms of disease as revealed by animal models.

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Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

Ovarian autoimmune disease: clinical concepts and animal models

et al. 2014

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“…Adrenal-cortex autoantibodies (ACA) were first demonstrated by a complement-fixation test (29) and later by the indirect immunofluorescence technique using cryostat sections of human adrenal-cortex glands (30). These techniques allowed the detection of ACA in 36-60% of patients with AAD but also in 7-10% of those with tuberculosis, as reviewed by Betterle et al (6).…”

Section: Adrenal-cortex Autoantibodies In Patients With Clinical Aadmentioning

confidence: 99%

Adrenal and ovarian autoimmunity

Betterle

Volpato²

1998

European Journal of Endocrinology

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“…Adrenal cortex autoantibodies (ACA) are polyclonal immunoglobulins of the IgG class that react with the cytoplasm of adrenal cortex cells (11) and their major specific target autoantigen has been identified to be the steroid 21-hydroxylase (21-OH) (9,12,13). ACA, when present, are markers of clinical, subclinical or potential AD (4,9).…”

Section: Introductionmentioning

confidence: 99%

Autoantibodies to steroidogenic enzymes in patients with premature ovarian failure with and without Addison's disease

Prà

Chen²,

Furmaniak³

et al. 2003

European Journal of Endocrinology

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Design: Adrenal cortex autoantibodies (ACA), steroid-producing cell autoantibodies (StCA) and autoantibodies (Abs) to steroidogenic enzymes in three groups of patients with premature ovarian failure (POF), 15 with autoimmune Addison's disease (AD), 26 with non-adrenal autoimmune diseases and 31 with isolated POF, have been assessed. Methods: ACA and StCA were measured using an immunofluorescence technique. Abs to 21-hydroxylase (21-OH), to 17a-hydroxylase (17a-OH) and to cytochrome P450 side-chain cleavage (P450scc) were measured using an immunoprecipitation assay. Results: Seventy-three percent of patients with POF and AD were positive for StCA, 93% for 17a-OH and/or P450scc Abs, 93% for ACA and 100% for 21-OH Abs. Among patients with POF and nonadrenal autoimmune diseases, 8% were positive for StCA, 12% for 17a-OH and/or P450scc Abs, and 8% and 12% for ACA and 21-OH Abs respectively. StCA, 17a-OH and/or P450scc Abs were all found in 10% of patients with isolated POF, and 13% had ACA and 21-OH Abs. All StCA-, 17a-OH-and/or P450scc Abs-positive patients were also positive for ACA and 21-OH Abs. Two patients with isolated POF who were ACA and 21-OH Ab positive developed AD 3 and 5 years after the onset of POF. Conclusion: This study has shown that, when POF is associated with AD, StCA, 17a-OH and/or P450scc Abs are present in the majority of patients, while in the other two groups these Abs are detectable in a much lower proportion of patients. Measurement of ACA/21-OH Abs in some patients with POF may be important in identifying patients at risk of developing overt AD.

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Auto-Antibodies in Addison's Disease

Cited by 169 publications

References 4 publications

Ovarian autoimmune disease: clinical concepts and animal models

Ovarian autoimmune disease: clinical concepts and animal models

Adrenal and ovarian autoimmunity

Autoantibodies to steroidogenic enzymes in patients with premature ovarian failure with and without Addison's disease

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