ECE2023 Poster Presentations Pituitary and Neuroendocrinology (123 abstracts)
Tokyo Womens Medical University, Internal Medicine, Tokyo, Japan
Background: Growth hormone (GH) deficiency, which causes visceral obesity and non-alcohol fatty liver disease, increases cardiovascular event risks. High-sensitivity C-reactive protein (hs-CRP), an inflammatory marker associated with increased cardiovascular risk, reportedly decreased after GH supplementation in GH-deficient patients, however, the association between GH secretion and inflammation remains unclear.
Patients and Methods: We retrospectively investigated the association between GH secretion assessed using a GH-releasing peptide-2 (GHRP-2) test and serum hs-CRP level in the patients with non-functioning pituitary neuroendocrine tumor (NF-PitNET) and Rathkes cleft cyst (RCC). Patients with severe renal insufficiency, active inflammatory and malignant diseases, and a history of pituitary surgery, and under GH supplementation therapy were excluded.
Results: Among 171 patients (100 NF-PitNET and 71 RCC), 55 (32%) presented severe GHD. Serum hs-CRP levels were significantly higher in the patients with severe GHD than those without (754 [393-1330] vs 249 [113-537] ng/ml, P <0.001) and significantly correlated with peak GH response to GHRP-2 (r=-0.50, P <0.001). Peak GH response to GHRP-2 significantly estimated the hs-CRP levels independent of the atherosclerotic and metabolic parameters and other anterior hormone secretions (β = -0.334, P = 0.001). Severe GHD was significantly associated with high hs-CRP (> 1000 ng/ml) (adjusted odds ratio, 2.55; 95% confidence interval 1.15-5.70). In the 60 patients who received pituitary surgeries, the postoperative changes in peak GH response to GHRP-2 (β = -0.320, P = 0.025) significantly estimated those in serum hs-CRP levels independent of other anterior hormone secretions.
Conclusions: The negative association between GH secretion and serum hs-CRP levels suggested an important role of impaired GH secretion in the increased cardiovascular risks through the development of inflammation.