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21-Hydroxylase (21-OH) Autoantibody ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
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Cat. No. Size Price


R21E/96R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Sandwich ELISA, Biotin-labelled antibody

Applications

Serum

Sample Requirements

50 μl/well

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Range

100-0,3 u/ml

Limit of Detection

0,13 u/ml

Intra-assay (Within-Run)

4,8 %

Inter-assay (Run-to-Run)

6,2 %

Summary

Research topic

Autoimmunity

Summary

Autoimmune destruction of the adrenal cortex is the most common cause of Addison’s disease and autoantibodies to the adrenal specific enzyme steroid 21-OH hydroxylase are important markers of adrenal autoimmunity. This can be the case if the disease presents as Addison’s disease or as part of the autoimmune polyglandular syndromes (APS) type I or type II.

References to Product

References

  • E. S. Husebye et al Consensus Statement on the Diagnosis, Treatment and Follow-up of Patients with Primary Adrenal Insufficiency J Intern Med. 2014 275(2):104-15
  • G. Coco et al Estimated Risk for Developing Autoimmune Addison’s Disease in Patients with Adrenal Cortex Autoantibodies J. Clin. Endocrinol. Metab. 2006 91: 1637-1645
  • H. Tanaka et al Steroid 21-Hydroxylase Autoantibodies: Measurements with a New Immunoprecipitation Assay J. Clin. Endocrinol. Metab. 1997 82: 1440-1446
  • J. Furmaniak and B. Rees Smith Editorial: Adrenal and Gonadal Autoimmune Diseases J. Clin. Endocrinol. Metab. 1995 80: 1502 – 1505
  • S. Chen et al Autoantibodies to Steroidogenic Enzymes in Autoimmune Polyglandular Syndrome, Addison’s Disease, and Premature Ovarian Failure J. Clin. Endocrinol. Metab. 1996 81: 1871-1876
References to Summary

References to 21-hydroxylase

  • Smith BR, Furmaniak J. Adrenal and gonadal autoimmune diseases. J Clin Endocrinol Metab. 1995 May;80 (5):1502-5
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