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Adult combined GH, prolactin, and TSH deficiency associated with circulating PIT-1 antibody in humans
- Source :
- Journal of Clinical Investigation. January 1, 2011, Vol. 121 Issue 1, p113, 7 p.
- Publication Year :
- 2011
-
Abstract
- The pituitary-specific transcriptional factor-1 (PIT-1, also known as POU1F1), is an essential factor for multiple hormone-secreting cell types. A genetic defect in the PIT-1 gene results in congenital growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) deficiency. Here, we investigated 3 cases of adult-onset combined GH, PRL, and TSH deficiencies and found that the endocrinological phenotype in each was linked to autoimmunity directed against the PIT-1 protein. We detected anti-PIT-1 antibody along with various autoantibodies in the patients' sera. An ELISA-based screening revealed that this antibody was highly specific to the disease and absent in control subjects. Immunohistochemical analysis revealed that PIT-1-, GH-, PRL-, and TSH-positive cells were absent in the pituitary of patient 2, who also had a range of autoimmune endocrinopathies. These clinical manifestations were compatible with the definition of autoimmune polyendocrine syndrome (APS). However, the main manifestations of APS-I--hypoparathyroidism and Candida infection--were not observed and the pituitary abnormalities were obviously different from the hypophysitis associated with APS. These data suggest that these patients define a unique 'anti-PIT-1 antibody syndrome,' related to APS.<br />Introduction The pituitary-specific transcriptional factor-1 (PIT-1, also known as POU1F1), plays a pivotal role in regulating the expressions of growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone β (TSHβ). PIT-1 [...]
Details
- Language :
- English
- ISSN :
- 00219738
- Volume :
- 121
- Issue :
- 1
- Database :
- Gale General OneFile
- Journal :
- Journal of Clinical Investigation
- Publication Type :
- Academic Journal
- Accession number :
- edsgcl.245821596
- Full Text :
- https://doi.org/10.1172/JCI44073