Traumatic brain injury (TBI) causes pituitary dysfunction, mainly featuring GH deficiency. Several mechanisms have been proposed to explain this post-traumatic dyspituitarism, including autoimmunity. We analyzed pituitary antibodies in 100 of US Service Members chosen for a history of TBI and hearing impairment, a concurrence typically seen after blast injuries. Each soldier provided two sera, one before (-1,765 to - 66 days) and one after (10 to 177 days) TBI. All 200 sera were screened by indirect immunofluorescence for binding to a human pituitary gland collected at autopsy. Positive sera were then tested by double indirect immunofluorescence for recognition of cells expressing GH, PRL, ACTH, LH, FSH, TSH, alpha-internexin (INA), vimentin, or glial fibrillary-acidic protein (GFAP). Sera were also tested by ELISA for recognition of native GH or recombinant INA. 63 of 200 sera (31 %) contained pituitary antibodies: of them, 33 (16%) recognized the adenohypophysis, 18 (9 %) the neurohypophysis, and 12 (6%) both lobes. In the adenohypophysis, TSH-secreting cells were the most common target (26 of 45, 58%), followed by INA expressing cells (17 of 45, 37%). In the neurohypophysis, 20 of 30 sera (67 %) recognized INA, 6 (20%) vimentin, and 4 (13%) GFAP-expressing cells. There was no temporal association between pituitary antibodies and TBI: of the sera recognizing TSH-secreting cells, half had antibodies in both the pre- and post-TBI serum (13 of 26, 50%), a quarter (6 of 26, 23%) in the pre-TBI serum, and a quarter (7 of 26, 27%) in the post-TBI serum. Similarly, of the sera recognizing INA-expressing cells, 2 (11.7%) had antibodies in both the pre- and post-TBI serum, 9 (53%) only in the pre-TBI serum, and 6 (35.2%) only in the post-TBI serum. INA antibodies measured by ELISA did not differ between the pre- and post-TBI time points. On the contrary, GH antibodies tended to increase after TBI, although not reaching statistical significance (p= 0.055). The study highlights a preferential recognition of TSH- and INA-expressing cells in TBI patients, which remains to be interpreted in the context of their endocrine dysfunctions. It also suggests that the appearance of GH antibodies after TBI contributes to the GH deficiency typically seen in these patients.

MON-450 Pituitary Antibodies In A Cohort Of Us Service Members With Traumatic Brain Injury

Di Dalmazi, Giulia;
2019

Abstract

Traumatic brain injury (TBI) causes pituitary dysfunction, mainly featuring GH deficiency. Several mechanisms have been proposed to explain this post-traumatic dyspituitarism, including autoimmunity. We analyzed pituitary antibodies in 100 of US Service Members chosen for a history of TBI and hearing impairment, a concurrence typically seen after blast injuries. Each soldier provided two sera, one before (-1,765 to - 66 days) and one after (10 to 177 days) TBI. All 200 sera were screened by indirect immunofluorescence for binding to a human pituitary gland collected at autopsy. Positive sera were then tested by double indirect immunofluorescence for recognition of cells expressing GH, PRL, ACTH, LH, FSH, TSH, alpha-internexin (INA), vimentin, or glial fibrillary-acidic protein (GFAP). Sera were also tested by ELISA for recognition of native GH or recombinant INA. 63 of 200 sera (31 %) contained pituitary antibodies: of them, 33 (16%) recognized the adenohypophysis, 18 (9 %) the neurohypophysis, and 12 (6%) both lobes. In the adenohypophysis, TSH-secreting cells were the most common target (26 of 45, 58%), followed by INA expressing cells (17 of 45, 37%). In the neurohypophysis, 20 of 30 sera (67 %) recognized INA, 6 (20%) vimentin, and 4 (13%) GFAP-expressing cells. There was no temporal association between pituitary antibodies and TBI: of the sera recognizing TSH-secreting cells, half had antibodies in both the pre- and post-TBI serum (13 of 26, 50%), a quarter (6 of 26, 23%) in the pre-TBI serum, and a quarter (7 of 26, 27%) in the post-TBI serum. Similarly, of the sera recognizing INA-expressing cells, 2 (11.7%) had antibodies in both the pre- and post-TBI serum, 9 (53%) only in the pre-TBI serum, and 6 (35.2%) only in the post-TBI serum. INA antibodies measured by ELISA did not differ between the pre- and post-TBI time points. On the contrary, GH antibodies tended to increase after TBI, although not reaching statistical significance (p= 0.055). The study highlights a preferential recognition of TSH- and INA-expressing cells in TBI patients, which remains to be interpreted in the context of their endocrine dysfunctions. It also suggests that the appearance of GH antibodies after TBI contributes to the GH deficiency typically seen in these patients.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11564/729183
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