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GHRP-6

Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Quick Stats
Studies 702
Trials 0
Score 2
2008 pubmed

Antipituitary antibodies after traumatic brain injury: is head trauma-induced pituitary dysfunction associated with autoimmunity?

Tanriverdi. Fatih F; De Bellis. Annamaria A; Bizzarro. Antonio A; Sinisi. Antonio Agostino AA; Bellastella. Giuseppe G; Pane. Elena E; Bellastella. Antonio A; Unluhizarci. Kursad K; Selcuklu. Ahmet A; Casanueva. Felipe F FF; Kelestimur. Fahrettin F

Key Findings

  • Antipituitary antibodies (APAs) were found in 44.8% of TBI patients but in none of the healthy controls.
  • APA‑positive patients had a higher rate of hypopituitarism (46.2%) compared to APA‑negative patients (12.5%).
  • Higher APA titers correlated with a lower growth‑hormone response to a GHRH + GHRP‑6 stimulation test (r = 0.74).

Practical Outcomes

  • If you have a history of head trauma or suspect pituitary autoimmunity, GHRP‑6 may not raise your growth‑hormone levels as effectively. Testing for APA could help explain variable responses to GHRP‑6. For most healthy users, the study offers limited direct guidance, but it highlights that underlying pituitary health can influence peptide efficacy.

Summary

Three years after a head injury, almost half of the patients had antibodies that attack the pituitary gland. Those with the antibodies were more likely to have low hormone production, including a weaker growth‑hormone response when given a test that combines GHRH and the peptide GHRP‑6. This suggests that auto‑immune damage to the pituitary can blunt the GH‑boosting effect of GHRP‑6.

Abstract

Traumatic brain injury (TBI) is a devastating public health problem that may result in hypopituitarism. However, the mechanisms responsible for hypothalamic-pituitary dysfunction due to TBI are still unclear. Although the antibodies against neurons have been demonstrated in injured animal studies, investigations regarding the occurrence of antipituitary antibodies (APAs) in patients with TBI are lacking in the literature. In order to investigate whether autoimmune mechanisms could play a role in the pituitary dysfunction after TBI, we have planned this study aimed at investigating the presence of APA at the third year of TBI and association between the TBI-induced hypopituitarism and APA. Twenty-nine (25 males and 4 females; age 36.5+/-2.3 years) patients who had completed a 3-year follow-up after TBI were included in the present study. APA and pituitary function were evaluated in all the patients 3 years after TBI; moreover, APAs were tested also in sera of 60 age-/sex-matched normal controls. The APAs were investigated by an indirect immunofluorescence method. Results APAs were detected in 13 out of the 29 TBI patients (44.8%), but in none of the normal controls. Pituitary dysfunction development ratio was significantly higher in APA-positive patients (46.2%) when compared with APA-negative ones (12.5%; P=0.04). There was a significant association between APA positivity and hypopituitarism due to TBI (odds ratio: 2.25, 95% confidence intervals 1.1-4.6). Moreover, there was a significant positive correlation (r=0.74, P=0.004) between APA titer ratio and peak GH response to GHRH+GH related peptide (GHRP)-6 test, suggesting that high APA titers were associated with low GH response to GHRH+GHRP-6 test. This study shows for the first time the presence of the APA in TBI patients 3 years after head trauma. Moreover, present investigation indicates preliminary evidence that APA may be associated with the development of TBI-induced pituitary dysfunction, thus suggesting that autoimmunity may contribute in the development of TBI-induced hypopituitarism. The presence of the association between APA and TBI-induced hypopituitarism may provide a new point of view in this field and promote further clinical and experimental studies.

Study Information

Provider

pubmed

Year

2008

Date

2008-05-07T00:00:00.000Z

DOI

10.1530/eje-08-0050