I. Adrenal Cortex and Steroid 21-Hydroxylase Autoantibodies in Adult Patients with Organ-Specific Autoimmune Diseases: Markers of Low Progression to Clinical Addison’s Disease

Betterle, Corrado; Volpato, M; Smith, Bernard Rees; Furmaniak, Jadwiga; Chen, Shu; Greggio, Nella Augusta; Sanzari, M.; Tedesco, Francesco; Pedini, B.; Boscaro, Marco; Presotto, Fabio

doi:10.1210/jcem.82.3.3819

Cited by 40 publications

(60 citation statements)

References 9 publications

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“…Furthermore, a good agreement between the results of ACA (measured by indirect immunofluorescence) and 21-OH autoantibodies (Abs) indicates that 21-OH Abs are the major component of the ACA (56)(57)(58)(59)(60). Consequently, 21-OH/ ACA have been shown to be markers of progression towards overt AAD in ACA-positive adults and children as described above (31)(32).…”

Section: Adrenal Autoantigensmentioning

confidence: 92%

“…ACA have also been found in subjects without clinical AAD with a prevalence varying from 0.3% in patients with vitiligo to 48% in those with idiopathic hypoparathyroidism (31,32). It has been shown that the presence of complement-fixing ACA is a marker for a high risk of progression to clinical AAD (33).…”

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

“…Subsequently, it has been reported that ACA in some patients without clinical AAD can disappear spontaneously or after corticosteroid therapy with restoration of the previous impaired adrenal function (35). However, recent follow-up studies of 58 ACA-positive patients (children and adults) indicated that ACA were persistent markers of progression towards overt or subclinical AAD (31,32). The risk of progression to AAD was high in the group of ACA-positive children (cumulative risk of 100% at 11 years) (32) compared with a lower risk in the group of ACA-positive adults (cumulative risk of 31.6% at 11 years) (31).…”

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

“…However, recent follow-up studies of 58 ACA-positive patients (children and adults) indicated that ACA were persistent markers of progression towards overt or subclinical AAD (31,32). The risk of progression to AAD was high in the group of ACA-positive children (cumulative risk of 100% at 11 years) (32) compared with a lower risk in the group of ACA-positive adults (cumulative risk of 31.6% at 11 years) (31). In the case of ACA-positive adults the presence of a high titer of antibodies and HLA-DR3 were additional risk factors for clinical AAD (31).…”

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

“…The followup of these patients revealed a high risk of gonadal failure in females but not in males (43,44). Furthermore, steroid cell autoantibodies have also been found in 7.3% of patients with POF without AAD (44) and these patients have a high risk of development of clinical AAD (31,32).…”

Section: Autoantibodies and Autoantigensmentioning

confidence: 99%

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Adrenal and ovarian autoimmunity

Betterle

Volpato²

1998

European Journal of Endocrinology

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Section: Adrenal Autoantigensmentioning

confidence: 92%

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

Section: Aca In Patients Without Clinical Aadmentioning

confidence: 99%

Section: Autoantibodies and Autoantigensmentioning

confidence: 99%

See 3 more Smart Citations

Adrenal and ovarian autoimmunity

Betterle

Volpato²

1998

European Journal of Endocrinology

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Primary Ovarian Insufficiency

Cooper¹,

Covington²,

Nelson³

2010

Amenorrhea

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A 30-year-old woman presents with a history of no menses since she stopped taking oral contraceptives 6 months ago in order to conceive. She had undergone puberty that was normal in both timing and development, with menarche at 12 years of age. At 18 years of age, she started taking oral contraceptives for irregular menses. She reports stress at work. Her weight is 59 kg, and her height 1.66 m; her body-mass index (the weight in kilograms divided by the square of the height in meters) is 21.3. There is no galactorrhea, hirsutism, or acne. The pelvic examination is normal, a pregnancy test is negative, the prolactin level is normal, and the follicle-stimulating hormone (FSH) level is in the menopausal range. How should she be evaluated and treated? THE CLINICAL PROBLEMThe ovary is unique in the endocrine system in that an entirely new secretory structure is developed within it each month -the graafian follicle, which arises from a microscopic primordial follicle. Menopause, defined as the permanent cessation of menses, results from the depletion of potentially functional primordial follicles. The mean (±SD) age at the time of natural menopause is 50±4 years. 1 Menopause before the age of 40 years is considered to be premature.Primary ovarian insufficiency is the preferred term for the condition that was previously referred to as premature menopause or premature ovarian failure; other terms used for this condition include primary ovarian failure and hypergonadotropic hypogonadism, as well as the misnomer, gonadal dysgenesis. 2,3 The condition is considered to be present when a woman who is less than 40 years old has had amenorrhea for 4 months or more, with two serum FSH levels (obtained at least 1 month apart) in the menopausal range. 4,5 The condition differs from menopause in that there is varying and unpredictable ovarian function in approximately 50% of cases, and about 5 to 10% of women conceive and deliver a child after they have received the diagnosis. 4,6-9 Thus, the term "primary ovarian insufficiency," as originally suggested by Albright, meets the need to describe a continuum of impaired ovarian function rather than a dichotomous state. 2,3 This term may also be less stigmatizing than the terms that were used previously.Address reprint requests to Dr. Nelson at the Integrative Reproductive Medicine Unit, NICHD-Intramural Research Program on Reproductive and Adult Endocrinology, CRC, Rm. 1-3330, 10 Center Dr., MSC-1103, Bethesda, MD 20892, or at lawrence_nelson@nih.gov. Dr. Nelson reports being an inventor on three United States patents directed to MATER (a potential antigen in autoimmune primary ovarian insufficiency) and its applications (U.S. patent numbers 7,189,812; 7,217,811; and 7,432,067), as well as one pending United States patent application (U.S. patent application number 11/586,160) and foreign counterparts. No other potential conflict of interest relevant to this article was reported. Primary ovarian insufficiency occurs through two major mechanisms: follicle dysfunction and foll...

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Diagnosis and management of Addison’s disease during pregnancy

Ambrosi

Barbetta

Morricone

2003

J Endocrinol Invest

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Although primary adrenal failure is considered a rare condition, recent epidemiological studies indicate a rising incidence of the disease owing to the increase of autoimmune disorders. Addison's disease may be a life-threatening condition and the occurrence of pregnancy has been considered as a dangerous event. Nowadays, adrenal insufficiency during pregnancy is associated with high incidence of serious fetal and maternal complications, as fetal death in utero and post-partum adrenal crises, only if the disorder is not recognized and adequately treated. In this article pathophysiological aspects, clinical features and guidelines of management of pregnancy in Addison's disease are reviewed.

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I. Adrenal Cortex and Steroid 21-Hydroxylase Autoantibodies in Adult Patients with Organ-Specific Autoimmune Diseases: Markers of Low Progression to Clinical Addison’s Disease

Cited by 40 publications

References 9 publications

Adrenal and ovarian autoimmunity

Adrenal and ovarian autoimmunity

Primary Ovarian Insufficiency

Diagnosis and management of Addison’s disease during pregnancy

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