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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1997-4-8
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pubmed:abstractText |
Adrenal cortex antibodies (ACA) were measured by immunofluorescence in 8840 adult patients with organ-specific autoimmune diseases without overt hypoadrenalism. Sixty-seven (0.8%) patients were ACA-positive, with the highest prevalence in those with premature ovarian failure (8.9%). Forty-eight ACA-positive and 20 ACA-negative individuals were enrolled into a prospective study. Antibodies to steroid 21-hydroxylases (21-OH), steroid 17 alpha-hydroxylase (17 alpha-OH) and cytochrome P450 side chain cleavage enzyme (P450scc) were measured by immunoprecipitation assay. Human leucocyte antigens D-related (HLA-DR) genotyping was also carried out and adrenal function assessed by ACTH test. On enrollment, 75% of ACA-positive patients had a normal adrenal function, while 25% revealed a subclinical hypoadrenalism. 21-OH antibodies were positive in 91% of ACA-positive sera. Eleven patients were positive for steroid-cell antibodies by immunofluorescence, and 9 revealed a positivity for antibodies to 17 alpha-OH and/or P450scc. During the prospective study, overt Addison's disease developed in 21% and subclinical hypoadrenalism in 29% of ACA-positive patients, while 50% maintained normal adrenal function. Progression to Addison's disease was more frequent in patients with subclinical hypoadrenalism, high titers of ACA and higher levels of 21-OH antibodies, complement-fixing ACA and HLA-DR3 status. All 20 persistently ACA-negative patients were also negative for antibodies to 21-OH, 17 alpha-OH, and P450scc, and all maintained normal adrenal function during follow-up. In conclusion, the detection of ACA/21-OH antibodies in adults is a marker of low progression toward clinical Addison's disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-972X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
82
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
932-8
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:9062509-Addison Disease,
pubmed-meshheading:9062509-Adrenal Cortex,
pubmed-meshheading:9062509-Adult,
pubmed-meshheading:9062509-Autoantibodies,
pubmed-meshheading:9062509-Autoimmune Diseases,
pubmed-meshheading:9062509-Biological Markers,
pubmed-meshheading:9062509-Disease Progression,
pubmed-meshheading:9062509-Female,
pubmed-meshheading:9062509-Follow-Up Studies,
pubmed-meshheading:9062509-Humans,
pubmed-meshheading:9062509-Male,
pubmed-meshheading:9062509-Middle Aged,
pubmed-meshheading:9062509-Organ Specificity,
pubmed-meshheading:9062509-Prospective Studies,
pubmed-meshheading:9062509-Steroid 21-Hydroxylase
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pubmed:year |
1997
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pubmed:articleTitle |
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.
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pubmed:affiliation |
Chair of Clinical Immunology and Allergy, University of Padova, Italy.
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pubmed:publicationType |
Journal Article
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