MON-279 Correlation Between Haemolitic Complement Activity (CH50) and Growth Hormone Response to Stimulation in Adult Growth Hormone Deficiency: Preliminary Data

Abstract

It is known that GH, directly or via IGF-1 activity, influences many aspects of immune response; both humoral and cellular branches are modulated, but no data are available about complement function. CH50 is a screening assay for the activation of the classical complement pathway and it is sensitive to the reduction, absence and/or inactivity of any component of the pathway. The CH50 tests the functional capability of serum complement components of the classical pathway to lyse sheep red blood cells (SRBC) pre-coated with rabbit anti-sheep red blood cell antibody (haemolysin). On the other hand, a low inflammation is present in GH deficiency (GHD) and it is related to cardiovascular risk of such situation, also in partial forms.Therefore, we performed a cohort study in a group of adult GHD patients evaluating CH50 levels to further explore the pattern of inflammatory markers in this condition.We included 17 patients with total GHD (GH peak after stimulation with GHRH+arginine <9 ng/ml with BMI<30 or <4 ng/ml with BMI≥30 Kg/m2; n=15) or partial GHD (peak between 9 and 16 ng/ml with BMI<30 Kg/m2 n=2) with mean±SEM BMI 27.7±2.6 kg/m2 and mean±SEM age 52.5±2.6 ys. The etiology of GHD, assessed by MRI, was: primary empty sella (n=7); post-surgical (n=1) pituitary adenoma (n=4); idiopathic (n=4), pineal cyst (n=1); CH50 has been assayed by turbidimetric method. Mean±SEM CH50 of entire cohort was 50.75±2.5 U/l (normal range 12.5-100 U/ml); however, a significant inverse correlation was observed between GH AUC and CH50 levels (Spearman r=-0.49; p=0.04).This datum joint to our previous observations about increased free light chains of immunoglobulins in GHD, substantiating the hypothesis of chronic low-grade inflammation affecting this condition, which in turn could negatively influence GH secretion. These data could be of interest especially in patients recognized as “idiopathic” GHD, where no pituitary morphologic alterations or anamnestic information (previous surgery, trauma or irradiation) were found. However, these data cannot be conclusive and further studies are needed to establish the causal relationships between these parameters, also in a greater cohort of patients.